Department of Health and Human Services U.S. PUBLIC HEALTH SERVICE National Institute of Dental and Craniofacial Research
Suggested Citation
U.S. Department of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Rockville, MD: U.S. Department of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health, 2000.
ii Message from Donna E. Shalala Secretary of Health and Human Services
The intent of this first-ever Surgeon General’s Report on Oral Health is to alert Americans to the full meaning of oral health and its importance to general health and well-being. Great progress has been made in reducing the extent and severity of common oral diseases. Successful prevention measures adopted by communities, individuals, and oral health professionals have resulted in marked improvements in the nation’s oral and dental health. The terms oral health and general health should not be interpreted as separate entities. Oral health is integral to general health; this report provides important reminders that oral health means more than healthy teeth and that you cannot be healthy without oral health. Further, the report outlines existing safe and effective disease prevention measures that everyone can adopt to improve oral health and prevent disease. However, not everyone is experiencing the same degree of improvement. This Surgeon General’s report addresses the inequities and disparities that affect those least able to muster the resources to achieve optimal oral health. For whatever the reason, ignoring oral health problems can lead to needless pain and suffering, causing devastating complications to an individual’s well- being, with financial and social costs that significantly diminish quality of life and burden American society. For a third decade, the nation has developed a plan for the prevention of disease and the pro- motion of health, including oral health, embodied in the U.S. Department of Health and Human Services document, Healthy People 2010. This Surgeon General’s Report on Oral Health empha- sizes the importance of achieving the Healthy People goals to increase quality of life and eliminate disparities. As a nation, we hope to address the determinants of health—individual and environ- mental factors—in order to improve access to quality care, and to support policies and programs that make a difference for our health. We hope to prevent oral diseases and disorders, cancer, birth defects, AIDS and other devastating infections, mental illness and suicide, and the chronic diseases of aging. We trust that this Surgeon General’s report will ensure that health promotion and disease pre- vention programs are enhanced for all Americans. This report proposes solutions that entail part- nerships—government agencies and officials, private industry, foundations, consumer groups, health professionals, educators, and researchers—to coordinate and facilitate actions based on a National Oral Health Plan. Together, we can effect the changes we need to maintain and improve oral health for all Americans.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL iii
Foreword
The growth of biomedical research since World War II has wrought extraordinary advances in the health and well-being of the American people. The story is particularly remarkable in the case of oral health, where we have gone from a nation plagued by the pains of toothache and tooth loss to a nation where most people can smile about their oral health. The impetus for change—to take on the challenge of addressing oral diseases as well as the many other health problems that shorten lives and diminish well-being—led to the postwar growth of the National Institutes of Health. In 1948 the National Institute of Dental Research—now the National Institute of Dental and Craniofacial Research—joined the National Cancer Institute and the National Heart, Lung, and Blood Institute as the third of the National Institutes of Health. The Institute’s research initially focused on dental caries and studies demonstrating the effec- tiveness of fluoride in preventing dental caries, research that ushered in a new era of health promo- tion and disease prevention. The discovery of fluoride was soon complemented by research that showed that both dental caries and periodontal diseases were bacterial infections that could be pre- vented by a combination of individual, community, and professional actions. These and other appli- cations of research discoveries have resulted in continuing improvements in the oral, dental, and craniofacial health of Americans. Today, armed with the high-powered tools, automated equipment, and imaging techniques of genetics and molecular and cell biology, scientists have set their sights on resolving the full array of craniofacial diseases and disorders, from common birth defects such as cleft lip and palate to the debilitating chronic oral-facial pain conditions and oral cancers that occur later in life. The National Institute of Dental and Craniofacial Research has served as the lead agency for the development of this Surgeon General’s Report on Oral Health. As part of the National Institutes of Health, the Institute has had ready access to ongoing federal research and the good fortune to work collaboratively with many other agencies and individuals, both within and outside government. The establishment of a Federal Coordinating Committee provided a formal mechanism for the exchange of ideas and information from other departments, including the U.S. Department of Agriculture, Department of Education, Department of Justice, Department of Defense, Department of Veterans Affairs, and Department of Energy. Active participation in the preparation and review of the report came from hundreds of individuals who graciously gave of their expertise and time. It has been a pleasure to have had this opportunity to prepare the report, and we thank Surgeon General David Satcher for inviting us to participate. Despite the advances in oral health that have been made over the last half century, there is still much work to be done. This past year we have seen the release of Healthy People 2010, which emphasizes the broad aims of improving quality of life and eliminating health disparities. The recently released U.S. General Accounting Office report on the oral health of low-income popula- tions further highlights the oral health problems of disadvantaged populations and the effects on their well-being that result from lack of access to care. Agencies and voluntary and professional organizations have already begun to lay the groundwork for research and service programs that directly and comprehensively address health disparities. The National Institutes of Health has joined these efforts and is completing an agencywide action plan for research to reduce health dis- parities. Getting a healthy start in life is critical in these efforts, and toward that end, a Surgeon
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL v Foreword
General’s Conference on Children and Oral Health, The Face of a Child, is scheduled for June 2000. Many other departmental and agency activities are under way. The report concludes with a framework for action to enable further progress in oral health. It emphasizes the importance of building partnerships to facilitate collaborations to enhance educa- tion, service, and research and eliminate barriers to care. By working together, we can truly make a difference in our nation’s health—a difference that will benefit the health and well-being of all our citizens. Ruth L. Kirschstein MD Harold C. Slavkin DDS Acting Director Director National Institutes of Health National Institute of Dental and Craniofacial Research
vi ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Preface from the Surgeon General U.S. Public Health Service
As we begin the twenty-first century, we can be proud of the strides we have made in improving the oral health of the American people. At the turn of the last century, most Americans could expect to lose their teeth by middle age. That situation began to change with the discovery of the properties of fluoride, and the observation that people who lived in communities with naturally fluoridated drinking water had far less dental caries (tooth decay) than people in comparable com- munities without fluoride in their water supply. Community water fluoridation remains one of the great achievements of public health in the twentieth century—an inexpensive means of improving oral health that benefits all residents of a community, young and old, rich and poor alike. We are fortunate that additional disease prevention and health promotion measures exist for dental caries and for many other oral diseases and disorders—measures that can be used by individuals, health care providers, and communities. Yet as we take stock of how far we have come in enhancing oral health, this report makes it abundantly clear that there are profound and consequential disparities in the oral health of our citi- zens. Indeed, what amounts to a “silent epidemic” of dental and oral diseases is affecting some pop- ulation groups. This burden of disease restricts activities in school, work, and home, and often sig- nificantly diminishes the quality of life. Those who suffer the worst oral health are found among the poor of all ages, with poor children and poor older Americans particularly vulnerable. Members of racial and ethnic minority groups also experience a disproportionate level of oral health prob- lems. Individuals who are medically compromised or who have disabilities are at greater risk for oral diseases, and, in turn, oral diseases further jeopardize their health. The reasons for disparities in oral health are complex. In many instances, socioeconomic fac- tors are the explanation. In other cases, disparities are exacerbated by the lack of community pro- grams such as fluoridated water supplies. People may lack transportation to a clinic and flexibility in getting time off from work to attend to health needs. Physical disability or other illness may also limit access to services. Lack of resources to pay for care, either out-of-pocket or through private or public dental insurance, is clearly another barrier. Fewer people have dental insurance than have medical insurance, and it is often lost when individuals retire. Public dental insurance programs are often inadequate. Another major barrier to seeking and obtaining professional oral health care relates to a lack of public understanding and awareness of the importance of oral health. We know that the mouth reflects general health and well-being. This report reiterates that gen- eral health risk factors common to many diseases, such as tobacco use and poor dietary practices, also affect oral and craniofacial health. The evidence for an association between tobacco use and oral diseases has been clearly delineated in every Surgeon General’s report on tobacco since 1964, and the oral effects of nutrition and diet are presented in the Surgeon General’s report on nutrition (1988). Recently, research findings have pointed to possible associations between chronic oral infections and diabetes, heart and lung diseases, stroke, and low-birth-weight, premature births. This report assesses these emerging associations and explores factors that may underlie these oral- systemic disease connections. To improve quality of life and eliminate health disparities demands the understanding, compas- sion, and will of the American people. There are opportunities for all health professions, individu- als, and communities to work together to improve health. But more needs to be done if we are to make further improvements in America’s oral health. We hope that this Surgeon General’s report
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL vii Preface will inform the American people about the opportunities to improve oral health and provide a plat- form from which the science base for craniofacial research can be expanded. The report should also serve to strengthen the translation of proven health promotion and disease prevention approaches into policy development, health care practice, and personal lifestyle behaviors. A framework for action that integrates oral health into overall health is critical if we are to see further gains.
David Satcher MD, PhD Surgeon General
viii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL CHAPTER 3
Acknowledgments
This report was prepared by the Department of PROJECT TEAM Health and Human Services under the direction of Caswell A. Evans DDS, MPH the National Institutes of Health, National Institute Project Director and Executive Editor of Dental and Craniofacial Research. Assistant Director, Los Angeles County Department of Health Services, Los Angeles, CA Ruth L. Kirschstein MD Dushanka V. Kleinman DDS, MScD Acting Director, National Institutes of Health, DHHS, Co-Executive Editor Bethesda, MD Assistant Surgeon General, USPHS Harold C. Slavkin DDS Deputy Director, National Institute of Dental and Director, National Institute of Dental and Craniofacial Craniofacial Research, National Institutes of Health, Research, National Institutes of Health, DHHS, DHHS, Bethesda, MD Bethesda, MD William R. Maas DDS, MPH, MS David Satcher MD, PhD Assistant Surgeon General, Chief Dental Officer, Assistant Secretary for Health and Surgeon General, USPHS Office of Public Health and Science, Office of the Director, Division of Oral Health, Centers for Disease Secretary, Washington, DC Control and Prevention, DHHS, Atlanta, GA Nicole Lurie MD, MSPH Joan S. Wilentz MA Principal Deputy Assistant Secretary for Health, Office Science Writer and Editor, Bethesda, MD of Public Health and Science, Office of the Secretary, Roseanne Price ELS Washington, DC Editor, Silver Spring, MD Beverly L. Malone PhD, RN, FAAN Marla Fogelman Deputy Assistant Secretary for Health, Office of Public Editor, Silver Spring, MD Health and Science, Office of the Secretary, Washington, DC Arthur Lawrence PhD CONTRIBUTORS Assistant Surgeon General, USPHS, Deputy Assistant Margo Adesanya DDS Secretary for Health (Operations), Office of Public Staff Scientist, National Institute of Dental and Health and Science, Office of the Secretary, Craniofacial Research, National Institutes of Health, Washington, DC DHHS, Bethesda, MD Kenneth Moritsugu MD, MPH Alfredo Aguirre DDS, MS Deputy Surgeon General, USPHS, Office of the Director and Associate Professor, Advanced Oral and Surgeon General, Office of the Secretary, Maxillofacial Pathology, State University of New York at Buffalo School of Dental Medicine, Buffalo, NY Washington, DC ✳ Allan S. Noonan MD, MPH Ronald Andersen PhD, MA Captain, USPHS, Office of the Surgeon General, Wasserman Professor of Health Services and Professor Office of the Secretary, Washington, DC of Sociology, University of California Los Angeles School of Public Health, Los Angeles, CA
✳Indicates Coordinating Author
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL ix Acknowledgments
Jay R. Anderson DMD, MHSA ✳Chester W. Douglass DMD, PhD Chief Dental Officer, Division of Community and Professor and Chair, Department of Oral Health Policy Migrant Health, Bureau of Primary Health Care, and Epidemiology, Harvard School of Dental Medicine, Health Resources and Services Administration, DHHS, Boston, MA Rockville, MD M. Ann Drum DDS, MPH Kenneth J. Anusavice PhD, DMD Captain, USPHS, Acting Director, Division of Research, Associate Dean for Research, Chair, Department of Education and Training, Maternal and Child Health Dental Biomaterials, University of Florida College of Bureau, Health Resources and Services Administration, Dentistry, Gainesville, FL DHHS, Rockville, MD ✳Kathryn A. Atchison DDS, MPH Thomas F. Drury PhD Professor and Associate Dean for Research, University Senior Scientist, National Institute of Dental and of California Los Angeles School of Dentistry, Los Craniofacial Research, National Institutes of Health, Angeles, CA DHHS, Bethesda, MD James Bader DDS, MPH Burton L. Edelstein DDS, MPH Professor, University of North Carolina School of Director, Children’s Dental Health Project, American Dentistry, Chapel Hill, NC Academy of Pediatrics, Washington, DC Charles Bertolami DDS, D.Med.Sc. Frederick C. Eichmiller DDS Dean, University of California San Francisco School of Director, Paffenbarger Research Center, American Dentistry, San Francisco, CA Dental Association Health Foundation, National Aljernon Bolden DMD, MPH Institute of Standards and Technology, Director, Community Health Programs and Co- Gaithersburg, MD Director, Division of Dental Public Health, Boston Mary P. Faine MS, RD, CD University Goldman School of Dental Medicine, Associate Professor and Director of Nutrition Boston, MA Education, University of Washington School of L. Jackson Brown DDS, PhD Dentistry, Seattle, WA Associate Executive Director, American Dental Denise J. Fedele DMD, MS Association, Chicago, IL Chief Professional Development and Research in Janet A. Brunelle MS Dental Care Clinical Research, Veterans Statistician (retired), National Institute of Dental and Administration Medical Health Care System, Craniofacial Research, National Institutes of Health, Department of Veterans Affairs, Perrypoint, MD DHHS, Bethesda, MD Christopher H. Fox DMD, DMSc Brian A. Burt BDS, MPH, PhD Director of Professional Relations, Europe, Colgate- Professor of Dental Public Health, Department of Palmolive Co., New Jersey Epidemiology, University of Michigan School of Public Philip C. Fox DDS Health, Ann Arbor, MI Director, Research and Development Affiliation, Nita Chainani-Wu DMD, MPH Amarillo Biosciences, Inc., Amarillo, TX University of California San Francisco School of Lawrence J. Furman DDS, MPH Dentistry, San Francisco, CA Captain, USPHS, Head, Department of Health Services, David W. Chen MD, MPH U.S. Merchant Marine Academy, Kings Point, NY Commander, USPHS, Deputy Director, Division of Isabel Garcia DDS, MPH Associated, Dental, and Public Health Professions, Captain, USPHS, Special Assistant for Science Transfer, Bureau of Health Professions, Health Resources and National Institute of Dental and Craniofacial Research, Services Administration, DHHS, Rockville, MD National Institutes of Health, DHHS, Bethesda, MD Joseph Ciardi PhD ✳Robert J. Genco DDS, PhD Consultant, National Institute of Dental and Distinguished Professor and Chair, Department of Oral Craniofacial Research, National Institutes of Health, Biology, State University of New York at Buffalo School DHHS, Bethesda, MD of Dental Medicine, Buffalo, NY Betty DeBerry-Summer DDS, MPH Gretchen Gibson DDS, MPH Captain, USPHS, Chief Dental Officer, Bureau of Director, Special Care Dental Clinics, Veterans Primary Health Care, Health Resources and Services Administration North Texas Healthcare Systems, Administration, DHHS, Bethesda, MD Department of Veterans Affairs, Dallas, TX Teresa A. Dolan DDS, MPH Professor and Associate Dean, University of Florida College of Dentistry, Gainesville, FL
x ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments
Sharon M. Gordon DDS, MPH Linda LeResche ScD Director, Office of Education, National Institute of Research Professor, University of Washington School Dental and Craniofacial Research, National Institutes of Dentistry, Seattle, WA of Health, DHHS, Bethesda, MD James Lipton DDS, PhD Catherine Hayes DMD, DMSc Captain, USPHS, Assistant Director for Training and Assistant Professor, Department of Oral Health Policy Career Development, National Institute of Dental and and Epidemiology, Harvard School of Dental Medicine, Craniofacial Research, DHHS, Bethesda, MD Boston, MA Reginald Louie DDS, MPH Alice M. Horowitz PhD Captain, USPHS, Regional Dental Consultant, Health Senior Scientist, National Institute of Dental and Resources and Services Administration, DHHS, San Craniofacial Research, National Institutes of Health, Francisco, CA DHHS, Bethesda, MD ✳Irwin D. Mandel DDS Herschel Horowitz DDS, MPH Professor Emeritus, Columbia University School of Consultant, Dental Research and Public Health, Dental and Oral Surgery, New York, NY Bethesda, MD Stephen E. Marcus PhD Jeffrey Hyman DDS, PhD Epidemiologist, National Cancer Institute, National Epidemiologist, National Institute of Dental and Institutes of Health, DHHS, Bethesda, MD Craniofacial Research, National Institutes of Health, Frank Martin DDS, MPH DHHS, Bethesda, MD Captain, USPHS, Assistant Chief, Dental Services Amid I. Ismail BDS, MPH, DrPH Branch (retired), Indian Health Service, DHHS, Professor, University of Michigan School of Dentistry, Rockville, MD Ann Arbor, MI Wendy E. Mouradian MD ✳Marjorie Jeffcoat DMD Director, Children’s Hospital and Regional Medical Rosen Professor and Chair, Department of Center, Departments of Pediatrics, Pediatric Dentistry, Periodontics, University of Alabama School of Medical History and Ethics, University of Washington, Dentistry, Birmingham, AL Seattle, WA Candace Jones RDH, MPH ✳Linda Niessen DMD, MPH, MPP Captain, USPHS, Director, Dental Diseases Prevention Professor, Baylor University College of Dentistry and Program, Indian Health Service, DHHS, Rockville, MD Vice President, DENTSPLY International, York, PA David Jones DDS, MPH Ruth E. Nowjack-Raymer RDH, MPH Captain, USPHS (retired), Rockville, MD Public Health Researcher, National Institute of Dental Judith A. Jones DDS, MPH and Craniofacial Research, National Institutes of Senior Research Associate, Veterans Administration Health, DHHS, Bethesda, MD Center for Health Quality, Outcomes and Economic Steven Offenbacher DDS, PhD, MMSc Research, Department of Veterans Affairs and, Professor and Director, Center for Oral and Systemic Associate Professor, Boston University Goldman Diseases, University of North Carolina, School of Dental Medicine, Bedford, MA Chapel Hill, NC Kaumudi J. Joshipura BDS, DSc H. Whitney Payne, Jr. DDS, MPH Assistant Professor, Harvard School of Dental Captain, USPHS, Chief of Dental Services, Federal Medicine, Boston, MA Correctional Institution, Federal Bureau of Prisons, Linda M. Kaste DDS, PhD Department of Justice, Seogoville, TX Associate Professor and Division Director, Division of Edward Peters DMD Dental Public Health and Oral Epidemiology, Medical Instructor in Oral Health and Epidemiology, University of South Carolina College of Dental Department of Oral Health Policy and Epidemiology, Medicine, Charleston, SC Harvard School of Dental Medicine, Boston, MA William Kohn DDS, MS Douglas E. Peterson DMD, PhD Captain, USPHS, Associate Director for Science, Professor and Head, Department of Oral Diagnosis, Division of Oral Health, Centers for Disease Control University of Connecticut School of Dental Medicine, and Prevention, DHHS, Atlanta, GA Farmington, CT Mary Sue Lancaster RN, MA Maryann Redford DDS, MPH Health Education Specialist, Centers for Disease Health Scientist Administrator, National Institute of Control and Prevention, DHHS, Atlanta, GA Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xi Acknowledgments
✳Susan Reisine PhD Amardeep Singh Thind MD, PhD Professor, University of Connecticut School of Dental Assistant Professor, University of California Los Medicine, Hartford, CT Angeles School of Public Health, Los Angeles, CA John Rossetti DDS, MPH Scott L. Tomar DMD, DrPH Captain, USPHS, Chief Dental Officer, Health Epidemiologist/Dental Officer, National Center for Resources and Services Administration, DHHS, Chronic Disease Prevention and Health Promotion, Rockville, MD Centers for Disease Control and Prevention, DHHS, ✳R. Gary Rozier DDS, MPH Atlanta, GA Professor, Department of Health Policy Benedict I. Truman MD, MPH Administration, University of North Carolina School Senior Scientist and Epidemiology Program Officer, of Public Health, Chapel Hill, NC Centers for Disease Control and Prevention, DHHS, Susan Runner DDS, MA Atlanta, GA Captain, USPHS, Branch Chief Dental Devices, Center William Wathen DMD for Devices and Radiological Health, Food and Drug Associate Dean, Center for Professional Development, Administration, Rockville, MD Baylor College of Dentistry, Dallas, TX John S. Rutkauskas DDS, MS ✳Jane A. Weintraub DDS, MPH Executive Director, American Association of Pediatric Lee Hysan Professor and Chair, Division of Oral Dentistry, Chicago, IL Epidemiology and Dental Public Health, University of Margaret Scarlett DMD California San Francisco School of Dentistry, San Captain, USPHS, Office of the Secretary, Office of Francisco, CA Public Health and Science, DHHS, Washington, DC ✳B. Alex White DDS, DrPH Don Schneider DDS, MPH Assistant Program Director, Economic, Social, and Captain, USPHS, Chief Dental Officer, Health Care Health Services Research, Kaiser Permanente Center Financing Administration, Center for Medicaid and for Health Research, Portland, OR State Operations, DHHS, Baltimore, MD Deborah Winn PhD Stephen T. Schultz DDS, MS, MPH Senior Investigator, National Institute of Dental and Lieutenant Commander, U.S. Navy, National Institute Craniofacial Research, National Institutes of Health, of Dental and Craniofacial Research, National DHHS, Bethesda, MD Institutes of Health, DHHS, Bethesda, MD Athanasios I. Zavras DMD, MS, DMSc Robert H. Selwitz DDS, MPH Assistant Professor, Department of Health Policy and Captain, USPHS, Senior Dental Epidemiologist, Epidemiology, Harvard School of Dental Medicine, National Institute of Dental and Craniofacial Research, Boston, MA National Institutes of Health, DHHS, Bethesda, MD Gerald Shklar DDS, MS SENIOR REVIEWERS Charles A. Brackett Professor of Oral Pathology, Clifton Dummett Sr. DDS Harvard School of Dental Medicine, Boston, MA Distinguished Professor Emeritus, University Charles Shuler DMD, PhD of Southern California School of Dentistry, Director, Center for Craniofacial Molecular Biology, Los Angeles, CA George and Mary Lou Boone Professor of Craniofacial Helen C. Rodriguez-Trias MD, FAAP Molecular Biology, University of Southern California Past-President, American Public Health Association, School of Dentistry, Los Angeles, CA Brookdale, CA Gary Slade BDSc, DDPH, PhD John Stamm DDS, DDPH, MScD Assistant Professor, University of North Carolina Dean, University of North Carolina School of School of Dentistry, Chapel Hill, NC Dentistry, Chapel Hill, NC Ronald P. Strauss DMD, PhD Professor, School of Dentistry and School of Medicine, University of North Carolina, Chapel Hill, NC REVIEWERS Lawrence Tabak DDS, PhD Michael C. Alfano DMD, PhD Senior Associate Dean for Research, University of Dean, New York University College of Dentistry, Rochester School of Medicine and Dentistry, New York, NY Rochester, NY Myron Allukian Jr. DDS, MPH George W. Taylor DMD, DrPH Director, Oral Health, Boston Public Health Assistant Professor of Dentistry, University of Commission, Boston, MA Michigan School of Dentistry, Ann Arbor, MI
xii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments
Alexia Antczak-Bouckoms DMD, ScD, MPH, MS Eli Capilouto DMD, MPH, ScD Assistant Professor of Medicine, Tufts University Dean, School of Public Health, University of Alabama School of Medicine, Medford, MA at Birmingham, Birmingham, AL Howard L. Bailit DMD, PhD Victoria A. Cargill MD, MSCE Health Policy and Primary Care Research Center, Medical Officer, Office of AIDS Research, National University of Connecticut Health Center, Institutes of Health, DHHS, Bethesda, MD Farmington, CT D. Walter Cohen DDS David Barmes BDSc, DDSc, MPH Chancellor Emeritus, Medical College of Pennsylvania, Special Expert for International Health, National Hahneman University, Philadelphia, PA Institute of Dental and Craniofacial Research, National Lois K. Cohen PhD Institutes of Health, DHHS, Bethesda, MD Director, Office of International Health, National Bruce J. Baum DMD, PhD Institute of Dental and Craniofacial Research, National Chief of Gene Therapy and Therapeutic Branch, Institutes of Health, DHHS, Bethesda, MD National Institute of Dental and Craniofacial Research, Robert J. Collins DMD, MPH National Institutes of Health, DHHS, Bethesda, MD Deputy Executive Director, International and Stephen C. Bayne MS, PhD American Associations for Dental Research, Professor, University of North Carolina School of Alexandria, VA Dentistry, Chapel Hill, NC Stephen B. Corbin DDS, MPH James D. Beck PhD Director of Health and Research Initiatives, Special Kenan Professor, University of North Carolina School Olympics, Inc., Washington, DC of Dentistry, Chapel Hill, NC James G. Corrigan PhD Eugenio Beltran DMD, MPH, MS, BrPH Evaluation Officer, National Institute of Dental and Senior Research Fellow, Division of Oral Health, Craniofacial Research, National Institutes of Health, Centers for Disease Control and Prevention, DHHS, DHHS, Bethesda, MD Atlanta, GA James J. Crall DDS, ScD Henning Birkedal-Hansen DDS, PhD Chairman, Department of Pediatric Dentistry, Scientific Director, National Institute of Dental and University of Connecticut School of Dental Medicine, Craniofacial Research, National Institutes of Health, Farmington, CT DHHS, Bethesda, MD Ananda P. Dasanayake BDS, MPH, PhD Karina Boehm MPH Associate Professor, Department of Oral Biology Chief, Health Promotion Branch, National Institute of University of Alabama School of Dentistry, Dental and Craniofacial Research, National Institutes Birmingham, AL of Health, DHHS, Bethesda, MD Dominick P. DePaola DDS, PhD William H. Bowen BDS, PhD President and CEO, The Forsyth Institute, Boston, MA Welscher Professor of Dentistry, School of Dentistry, Richard D’Eustachio DDS University of Rochester Medical Center, Rochester, NY Private Practice, Cherry Hill, NJ Norman S. Braveman PhD Ray Dionne DDS, PhD Associate Director for Clinical, Behavioral and Health Captain, USPHS, Clinical Director, National Institute Promotion Research, National Institute of Dental and of Dental and Craniofacial Research, National Craniofacial Research, National Institutes of Health, Institutes of Health, DHHS, Bethesda, MD DHHS, Bethesda, MD Marylin Dodd RN, PhD Bruce B. Brehm DMD, MPH Professor, University of California San Francisco Lieutenant Colonel, U.S. Army, Tri-Service Center School of Nursing, San Francisco, CA for Oral Health Studies, Uniformed Services University Scott Dubowsky DMD, FAGD of the Health Sciences, Department of Defense, Private Practice, Bayonne, NJ Bethesda, MD Robert Dumbaugh DDS, MPH Patricia S. Bryant PhD Dental Executive Director, Palm Beach County Health Director, Behavioral and Health Promotion Research, Department, Palm Beach, FL National Institute of Dental and Craniofacial Research, Joel Epstein DMD, MSD National Institutes of Health, DHHS, Bethesda, MD Research Associate Professor, Department of Oral Maria Teresa Canto MS, DDS, MPH Medicine, University of Washington School of Public Health Research Specialist, National Institute of Dentistry, Seattle, WA Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xiii Acknowledgments
Ronald Ettinger BDS, MDS, DDSc Ellen R. Gritz PhD Professor, Department of Prosthodontics and Dows Professor and Chair, Department of Behavioral Institute for Dental Research, University of Iowa, Science, M.D. Anderson Cancer Center, University of Iowa City, IA Texas, Houston, TX Raymond Fonseca DMD Kenneth A. Gruber PhD Dean, University of Pennsylvania School of Dental Chief, Chronic Diseases Branch, National Institute of Medicine, Philadelphia, PA Dental and Craniofacial Research, National Institutes Allan J. Formicola DDS of Health, DHHS, Bethesda, MD Dean, School of Dental and Oral Surgery, Columbia Kevin Hardwick DDS, MPH University, New York, NY Captain, USPHS, International Health Officer, National Jane L. Forrest Ed.D., RDH Institute of Dental and Craniofacial Research, National Assistant Dean, Dental Hygiene Research and Institutes of Health, DHHS, Bethesda, MD Instructional Technology, Director, National Center for Hazel J. Harper DDS, MPH Dental Hygiene Research, University of Southern Private Practice, Washington, DC California School of Dentistry, Los Angeles, CA John Hauth MD Robert T. Frame DMD, MS, CHE Professor, Interim Chairman and Director, Center for Assistant Under Secretary for Health for Dentistry, Research in Women’s Health, University of Alabama at Department of Veterans Affairs, Washington, DC Birmingham, Birmingham, AL Raul I. Garcia DMD Maxine Hayes MD, MPH Professor and Chair, Department of Health Policy, Assistant Secretary, Community and Family Health, Boston University Goldman School of Dental Washington State Department of Health, Olympia, WA Medicine, Boston, MA Marc W. Heft DMD, PhD Jay Alan Gershen DDS, PhD Professor and Director of the Claude Pepper Executive Vice Chancellor, University of Colorado Center, University of Florida College of Dentistry, Health Sciences Center, Denver, CO Gainesville, FL Michael Glick DMD Joseph Henry DDS, PhD, ScD Professor of Oral Medicine, Director, Programs Dean Emeritus, Howard University College of for Medically Complex Patients, University of Dentistry and Professor, Harvard School of Dental Pennsylvania School of Dental Medicine, Medicine, Boston, MA Philadelphia, PA Mark C. Herzberg DDS, PhD Barbara F. Gooch DMD, MPH Professor, University of Minnesota School of Dentistry, Dental Officer, Division of Oral Health, Centers for Minneapolis, MN Disease Control and Prevention, DHHS, Atlanta, GA Alan R. Hinman MD, MPH John Greene DMD, MPH Senior Consultant for Public Health Programs, Dean Emeritus, University of California San Francisco Taskforce for Child Survival and Development, School of Dentistry, San Rafael, CA Decatur, GA Deborah Greenspan BDS, DSc, ScD (hc), Cynthia Hodge DMD, MPH FDSRCS Ed (hon) Private Practice, Nashville, TN Professor of Clinical Oral Medicine, University of Dorthe Holst DDS, MPH California San Francisco School of Dentistry, San Professor, Department of Community Dentistry, Francisco, CA University of Oslo, Oslo, Norway John S. Greenspan BSc, BDS, PhD, FRCPath John P. Howe III MD Professor and Chair, Department of Stomatology, President, University of Texas Health Science Center at University of California San Francisco School of San Antonio, San Antonio, TX Dentistry, San Francisco, CA David Johnsen DDS, MS Robert O. Greer DDS, ScD Dean and Professor of Pediatric Dentistry, University Professor of Pathology and Medicine, University of of Iowa College of Dentistry, Iowa City, IA Colorado Health Sciences Center, Schools of Medicine Ralph Katz DMD, PhD and Dentistry, Denver, CO Professor, Department of Behavioral Science and David Grembowski PhD Community Health, University of Connecticut School Professor of Health Services and Dental Public Health of Dental Medicine, Farmington, CT Sciences, University of Washington, Seattle, WA H. Asuman Kiyak MA, PhD Director, Institute on Aging and Professor, University of Washington School of Dentistry, Seattle, WA
xiv ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments
Kenneth S. Kornman DDS, PhD Kathleen Mangskau RDH, MPA Chief Scientific Officer, Interleukin Genetics, Inc., Director, North Dakota Oral Health Program, North San Antonio, TX Dakota Department of Health, Bismarck, ND Eleni Kousvelari DDS, DSc Georgetta Manning-Cox DDS, MPH Health Scientist Administrator, National Institute of Chairman, Community Dentistry and Associate Dental and Craniofacial Research, National Institutes Professor, Howard University College of Dentistry, of Health, DHHS, Bethesda, MD Washington, DC Jayanth V. Kumar DDS, MPH Don Marianos DDS, MPH Assistant Director, Bureau of Dental Health, New York Consultant in Public Health, Pinetop, AZ State Department of Health, Albany, NY Gary C. Martin DDS, MPH Raymond Kuthy DDS, MPH Lieutenant Colonel, U.S. Air Force, Tri-Service Center Professor and Chair, Preventive and Community for Oral Health Studies, Uniformed Services University Dentistry, University of Iowa College of Dentistry, of the Health Sciences, Department of Defense, Iowa City, IA Bethesda, MD Ira Lamster DDS, MMSc Ricardo J. Martinez MD, MPH Professor and Vice Dean, Columbia University School Director, Division of Extramural Research, National of Dental and Oral Surgery, New York, NY Institute of Dental and Craniofacial Research, National Philip R. Lee MA, MD Institutes of Health, DHHS, Bethesda, MD Professor Emeritus of Social Medicine and Senior Richard Mascola DDS Advisor, Institute for Health Policy Studies, Private Practice, Jericho, NY University of California San Francisco School of Carolyn Beth Mazzella RN Medicine, San Francisco, CA Assistant Surgeon General, USPHS, Office of the PHS Racquel Z. LeGeros BS, MS, PhD Chief Nurse, Health Resources and Services Professor, Department of Dental Materials Science Administration, DHHS, Rockville, MD and Director, Research Center for Minority Oral Kim McFarland DDS, MS Health, New York University College of Dentistry, Dental Health Director, State of Nebraska, Nebraska New York, NY Department of Health, Lincoln, NE David Locker BDS, PhD J. Michael McGinnis MD Professor, Faculty of Dentistry, University of Toronto, Senior Vice President and Director, Health Group, The Toronto, Canada Robert Wood Johnson Foundation, Princeton, NJ Stuart Lockwood DDS, MPH Robert Mecklenburg DDS, MPH Dental Officer/Epidemiologist, Division of Oral Health, Coordinator, Tobacco and Oral Health Initiatives for Centers for Disease Control and Prevention, DHHS, the Tobacco Control Research Branch, National Cancer Atlanta, GA Institute, DHHS, Bethesda, MD Harold Löe DDS Roseann Mulligan DDS, MS Director Emeritus, National Institute of Dental and Professor and Chairman, Department of Dental Craniofacial Research, National Institutes of Health, Medicine and Public Health, University of Southern DHHS, Florida and Norway California School of Dentistry, Los Angeles, CA G.M. Nana Lopez DDS, MPH Juan M. Navia PhD Dental Program Manager, City of Austin, Austin, TX Professor Emeritus, University of Alabama at Mark D. Macek DDS, PhD, MPH Birmingham, Birmingham, AL Assistant Professor, Department of Oral Health Care Edward O’Neil PhD, MPA and Delivery, University of Maryland School of Professor, Dental Public Health and Hygiene, Director, Dentistry, Baltimore, MD Center for Health Professions, University of California, Dolores M. Malvitz DrPH San Francisco, San Francisco, CA Chief, Surveillance Investigations and Research Roy C. Page DDS, PhD Branch, Division of Oral Health, Centers for Disease Professor, Departments of Periodontics and Pathology, Control and Prevention, DHHS, Atlanta, GA Schools of Dentistry and Medicine, University of Dennis F. Mangan PhD Washington, Seattle, WA Chief, Infectious Disease and Immunity Branch, No-Hee Park DMD, PhD National Institute of Dental and Craniofacial Research, Dean, School of Dentistry, University of California National Institutes of Health, DHHS, Bethesda, MD Los Angeles, Los Angeles, CA
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xv Acknowledgments
Steven Perlman DDS, MScD Aubrey Sheiham BDS, PhD, DHC Associate Professor of Pediatric Dentistry, Boston Professor, Department of Epidemiology and Public University Goldman School of Dental Medicine, Health, University College London Medical School, Boston, MA London, England Poul Erik Petersen DDS, Dr Odont Sci, BA, MSc Cynthia Sherwood DDS Professor, University of Copenhagen, School of Private Practice, Independence, KS Dentistry, Copenhagen N, Denmark Mark D. Siegal DDS, MPH Kathy Phipps RDH, DrPH Chief, Bureau of Oral Health Services, Ohio Associate Professor, Oregon Health Sciences Department of Health, Columbus, OH University, Newport, OR Sol Silverman Jr. MA, DDS Scott Presson DDS, MPH Professor of Oral Medicine, University of California Captain, USPHS, Chief, Program Services Branch, San Francisco School of Dentistry, San Francisco, CA Division of Oral Health, Centers for Disease Control Susan F. Silverton MD, PhD and Prevention, DHHS, Atlanta, GA Assistant Professor and Enid Neidle Scholar, Francisco Ramos-Gomez DDS, MS, MPH University of Pennsylvania School of Dental Medicine, Associate Professor, Department of Growth and Philadelphia, PA Development, University of California San Francisco, Jeanne Sinkford DDS, MS, PhD San Francisco, CA Associate Executive Director, American Dental E. Diane Rekow DDS, PhD Education Association, Washington, DC Professor and Chair, Department of Orthodontics, Judy A. Small PhD University of Medicine and Dentistry of New Jersey, Chief, Craniofacial Anomalies and Injuries Branch, Newark, NJ National Institute of Dental and Craniofacial Research, Michael Rethman DDS, MS National Institutes of Health, DHHS, Bethesda, MD Colonel, U.S. Army, Chief of Periodontics, Tripler Christian Stohler DMD, Dr.Med.Dent Dental Clinic, Honolulu, HI William R. Mann Professor and Chair, Department of S. Timothy Rose DDS, MS Biologic and Materials Sciences, University of Private Practice, Appleton, WI Michigan School of Dentistry, Ann Arbor, MI Bruce Rothwell DMD, MSD George Stookey PhD Associate Professor and Chairman, University Executive Associate Dean, Indiana University School of Washington, Restorative/Hospital Dentistry, of Dentistry, Indianapolis, IN Seattle, WA Michael Till DDS, PhD Shirley B. Russell PhD Dean, University of Minnesota School of Dentistry, Professor and Chairperson, Department of Minneapolis, MN Microbiology, Associate Dean for Research, Meharry Richard Valachovic DMD, MPH Medical College, Nashville, TN Executive Director, American Dental Education Ann L Sandberg PhD Association, Washington, DC Chief, Neoplastic Diseases Branch, National Institute Clemencia M. Vargas DDS, MPH, PhD of Dental and Craniofacial Research, National Assistant Professor, University of Maryland School of Institutes of Health, DHHS, Bethesda, MD Dentistry, Baltimore, MD Charles Sanders DDS Rueben Warren DDS, MPH, DrPH Dean, Howard University College of Dentistry, Associate Administrator for Urban Affairs, The Agency Washington, DC for Toxic Substances and Disease Registry, DHHS, Michèle J. Saunders DMD, MS, MPH Atlanta, GA Endowed Professor of Clinical Dentistry, University of Reginald Wells PhD Texas Health Science Center, San Antonio, TX Deputy Commissioner, Administration for Children Crispian Scully MD, PhD, MDS and Families, Administration on Developmental Dean, Director of Studies and Research, International Disabilities, DHHS, Washington, DC Centers for Excellence in Dentistry and Eastman Terrie Wetle PhD Dental Institute for Oral Health Care Sciences, Deputy Director, National Institute on Aging, National University College of London, London, England Institutes of Health, DHHS, Bethesda, MD Leslie W. Seldin DDS, PC David A. Whiston DDS Private Practice, New York, NY Private Practice, Falls Church, VA
xvi ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments
Ardell Wilson DDS, MPH Claude Earl Fox MD, MPH Bureau Chief, State of Connecticut Department of Administrator, Health Resources and Services Public Health, Avon, CT Administration, DHHS, Rockville, MD Kenneth M. Yamada MD, PhD Patricia A. Grady PhD, RN, FAAN Branch Chief, Craniofacial Development Biology and Director, National Institute of Nursing Research, Regeneration, National Institute of Dental and National Institutes of Health, DHHS, Bethesda, MD Craniofacial Research, National Institutes of Health, Elizabeth Jacobson PhD DHHS, Bethesda, MD Deputy Director for Science, Center for Devices and Radiological Health, Food and Drug Administration, DHHS, Rockville, MD EDITORIAL AND PRODUCTION Wanda K. Jones Dr. P.H. ASSISTANTS Deputy Assistant Secretary for Health, Office of The Editorial Staff of the KEVRIC Company, Inc., Women’s Health, DHHS, Washington, DC Silver Spring, MD Lireka P. Joseph Dr. P.H. Captain, USPHS, Director, Office of Health and PROJECT ASSISTANTS Industry Programs, Center for Devices and Anne Breitenbach Radiological Health, Food and Drug Administration, Maurice Champagne MA DHHS, Rockville, MD Stephanie A. Dopson MSW, MPH Douglas B. Kamerow MD, MPH Katherine E. Krizek Assistant Surgeon General, USPHS, Director, Center Marco P. Maertens for Practice and Technology Assessment, Agency for Edith McAllister JD Healthcare Research and Quality, DHHS, Georgia A. McIntyre Rockville, MD Catherine McNish RDH, MHS Mireille B. Kanda MD, MPH Director of Health and Disability Services, Head Start Bureau, Agency for Children, Youth, and Families, FEDERAL COORDINATING DHHS, Washington, DC COMMITTEE Rod F. Kirk DDS Lois Albarelli Captain, USPHS, Chief, Dental Program, Federal Aging Services Program Specialist, Administration on Bureau of Prisons, Department of Justice, Aging, DHHS, Washington, DC Washington, DC Cheryl Austein-Casnoff MPH Kenneth W. Kizer MD, MPH Director, Public Health Policy, Office of the Assistant Under Secretary for Health (retired), Department of Secretary for Planning and Evaluation, DHHS, Veterans Affairs, Washington, DC Washington, DC William Kohn DDS William F. Benson Captain, USPHS, Associate Director for Science, Acting Principal Deputy Assistant Secretary for Aging Division of Oral Health, Centers for Disease Control (retired), Administration on Aging, DHHS, and Prevention, DHHS, Atlanta, GA Washington, DC Thomas M. Leiendecker DDS, MPH Mohandas Bhat BDS, MDS, DrPH Commander, U.S. Navy, Assistant Professor, Tri-Service Senior Science Advisor, Office of International Center for Oral Health Studies, Uniformed Services Health Programs, U.S. Department of Energy, University of the Health Sciences, Department of Germantown, MD Defense, Bethesda, MD Donna Blum MS, RD Lawrence McKinley DDS Nutritionist, Department of Agriculture, Captain, U.S. Navy, Senior Consultant for Dentistry, Alexandria, VA Tricare Management Activity, Department of Defense, Eric Bothwell DDS, MPH, PhD Falls Church, VA Captain, USPHS, Assistant Chief, Dental Services Edward Sondik PhD Branch (retired), Indian Health Service, DHHS, Director, National Center for Health Statistics, Rockville, MD Centers for Disease Control and Prevention, DHHS, C. Richard Buchanan DMD Hyattsville, MD Deputy Director for Dentistry, Department of Veterans Affairs, Washington, DC
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xvii Acknowledgments
Sue Swenson Ron J. Vogel Commissioner, Administration on Developmental Acting Deputy Administrator of the Food and Disabilities, Administration for Children and Families, Nutrition Programs, Food and Nutrition Service, DHHS, Washington, DC Department of Agriculture, Alexandria, VA Jeanette Takamura Assistant Secretary for Aging, Administration on Aging, DHHS, Washington, DC
xviii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents
Executive Summary 1 THE CHALLENGE, 4 THE CHARGE, 4 THE SCIENCE BASE FOR THE REPORT, 5 ORGANIZATION OF THE REPORT, 5 Part One: What Is Oral Health? 5 Part Two: What Is the Status of Oral Health in America? 6 Part Three: What Is the Relationship Between Oral Health and General Health and Well-being? 6 Part Four: How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? 7 Part Five: What Are the Needs and Opportunities to Enhance Oral Health? 9 MAJOR FINDINGS, 10 A FRAMEWORK FOR ACTION, 11 CONCLUSION, 13 REFERENCES, 13 PROJECT TEAM, 13 PART ONE WHAT IS ORAL HEALTH? 15 Chapter 1 The Meaning of Oral Health 17 THE CHALLENGE, 19 THE CHARGE, 19 THE SCIENCE BASE FOR THE REPORT, 19 ORGANIZATION OF THE REPORT, 20 What Is Oral Health? 20 What Is the Status of Oral Health in America? 20 What Is the Relationship Between Oral Health and General Health and Well-being? 20 How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? 21 What Are the Needs and Opportunities to Enhance Oral Health? 21 A Call to Action, 21 Chapter 2 The Craniofacial Complex 23 CONTACT AND COMMUNICATION, 23 Taste and Smell, 23 Touch, Temperature, and Pain, 24 Speech, 25 THE ORAL CAVITY, 25 The Oral Mucosa, 25 The Teeth, 26 The Salivary Glands, 26 The Immune System, 27
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xix Contents
CRANIOFACIAL ORIGINS, 28 Early Development, 29 Genetic Controls, 30 THE AGING OF CRANIOFACIAL TISSUES, 31 The Teeth, 31 The Jaws, 31 The Oral Mucosa, 32 Sensory and Motor Functioning, 32 The Salivary Glands, 32 FINDINGS, 32 REFERENCES, 33 PART TWO WHAT IS THE STATUS OF ORAL HEALTH IN AMERICA? 35 Chapter 3 Diseases and Disorders 37 DENTAL AND PERIODONTAL INFECTIONS, 37 Dental Caries, 37 Periodontal Diseases, 39 SELECTED MUCOSAL INFECTIONS AND CONDITIONS, 42 Oral Candidiasis, 42 Herpes Simplex Virus Infections, 43 Oral Human Papillomavirus Infections, 43 Recurrent Aphthous Ulcers, 43 ORAL AND PHARYNGEAL CANCERS AND PRECANCEROUS LESIONS, 44 Heightening the Risk, 44 Prevention and Management, 47 DEVELOPMENTAL DISORDERS, 47 Craniofacial Anomalies Caused by Altered Branchial Arch Morphogenesis, 47 Cranial Bone and Dental Anomalies, 48 Craniofacial Defects Secondary to Other Developmental Disorders, 49 Craniofacial Manifestations of Single-Gene Defects, 49 INJURY, 50 Sports, 50 Falls, 50 Motor Vehicle Collisions, 50 Violence, 51 SELECTED CHRONIC AND DISABLING CONDITIONS, 51 Sjögren’s Syndrome, 51 Acute and Chronic Oral-Facial Pain, 52 Temporomandibular Disorders, 52 A MIRROR, A MODEL, AND A BETTER UNDERSTANDING OF DISEASES AND DISORDERS, 53 FINDINGS, 53 REFERENCES, 53
xx ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents
Chapter 4 The Magnitude of the Problem 61 WHO HAS WHAT DISEASES AND CONDITIONS? 63 Dental Caries, Periodontal Diseases, and Tooth Loss, 63 Oral and Pharyngeal Cancers and Precancerous Lesions, 67 Selected Mucosal Infections and Diseases, 70 Developmental Disorders, 71 Injury, 72 Chronic and Disabling Conditions, 73 WHAT IS THE BURDEN OF DISEASE IN SELECTED POPULATIONS? CHALLENGES AND OPPORTUNITIES, 74 Racial and Ethnic Minorities, 74 Women’s Health, 77 Individuals with Disabilities, 78 UTILIZATION OF PROFESSIONAL CARE: WHAT DO WE KNOW ABOUT THE RELATIONSHIP OF ORAL HEALTH AND USE OF DENTAL SERVICES? 79 Dental Care Utilization, 80 Variation by Sex, Race/Ethnicity, Income, and Insurance, 81 Variation by Oral Health Status, 82 Reasons for Nonutilization, 83 Unmet Needs, 83 Outcomes of Appropriate Levels of Access and Utilization: An Example, 83 ORAL HEALTH STATUS IN CHANGING TIMES, 87 FINDINGS, 89 REFERENCES, 89 PART THREE WHAT IS THE RELATIONSHIP BETWEEN ORAL HEALTH AND GENERAL HEALTH AND WELL-BEING? 95 Chapter 5 Linkages with General Health 97 THE MOUTH AND FACE AS A MIRROR OF HEALTH AND DISEASE, 97 Physical Signs and Symptoms of Disease and Risk Factors, 97 Oral Manifestations of HIV Infection and of Osteoporosis, 101 Oral-fluid-based Diagnostics: The Example of Saliva, 103 Conclusion, 104 THE MOUTH AS A PORTAL OF ENTRY FOR INFECTION, 104 Oral Infections and Bacteremia, 104 Oral Infections as a Result of Therapy, 105 Infective Endocarditis, 107 Oral Infections and Respiratory Disease, 108 Oral Transmission of Infections, 108 Conclusion, 109
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xxi Contents
ASSOCIATIONS AMONG ORAL INFECTIONS AND DIABETES, HEART DISEASE/STROKE, AND ADVERSE PREGNANCY OUTCOMES, 109 The Periodontal Disease–Diabetes Connection, 109 The Oral Infection–Heart Disease and Stroke Connection, 115 Periodontal Disease and Adverse Pregnancy Outcomes, 120 Conclusion, 122 IMPLICATIONS OF THE LINKAGES, 122 FINDINGS, 123 REFERENCES, 123 Chapter 6 Effects on Well-being and Quality of Life 133 THE CULTURAL CONTEXT, 134 Cultural Models, 134 Combining Perspectives, 134 ORAL-HEALTH-RELATED QUALITY OF LIFE DIMENSIONS, 135 Functional Dimensions, 135 Psychosocial Dimensions, 137 Indirect Economic Costs, 142 RATINGS OF ORAL HEALTH, 144 Global Ratings, 144 Satisfaction Ratings, 144 ORAL-HEALTH-RELATED QUALITY OF LIFE MEASURES, 144 HEIGHTENED EXPECTATIONS, 146 FINDINGS, 146 REFERENCES, 147 PART FOUR HOW IS ORAL HEALTH PROMOTED AND MAINTAINED AND HOW ARE ORAL DISEASES PREVENTED? 153 Chapter 7 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease 155 WEIGHING THE EVIDENCE THAT INTERVENTIONS WORK, 155 PREVENTION AND CONTROL OF DENTAL CARIES, 158 Fluoride, 158 Fluoridation of Drinking Water, 160 School Water Fluoridation, 162 Dietary Fluoride Supplements, 162 Fluoride Mouthrinses, 165 Fluoride Varnishes, 165 Dental Sealants, 166 PREVENTION AND CONTROL OF PERIODONTAL DISEASES, 168 Community Programs to Prevent Gingivitis, 169 Prevention of Periodontitis, 169 Summary, 169 PREVENTION AND CONTROL OF ORAL AND PHARYNGEAL CANCERS, 169 Community-based Interventions, 170 Early Diagnosis of Oral and Pharyngeal Cancers, 171 Summary, 172 xxii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents
PREVENTION AND CONTROL OF CRANIOFACIAL BIRTH DEFECTS, 172 Summary, 173 PREVENTION AND CONTROL OF INTENTIONAL AND UNINTENTIONAL INJURY, 173 Craniofacial Injuries, 173 Summary: Prevention of Craniofacial Injuries, 176 ORAL HEALTH PROMOTION AND DISEASE PREVENTION KNOWLEDGE AND PRACTICES, 176 Dental Caries Prevention, 177 Periodontal Disease Prevention, 178 Oral Cancer Prevention and Early Detection, 178 Summary, 179 BUILDING UPON SUCCESS, 179 FINDINGS, 181 REFERENCES, 181 Chapter 8 Personal and Provider Approaches to Oral Health 189 INDIVIDUAL RESPONSIBILITY: PERSONAL APPROACHES TO ORAL HEALTH, 189 Daily Hygiene and Dental Caries Prevention, 189 Daily Hygiene and the Prevention of Periodontal Diseases, 190 Healthy Lifestyles, 190 Care Seeking, 190 PROVIDER-BASED CARE, 191 Risk Assessment, 192 Diagnostic Tests, 193 Oral Health Assessment, 193 Changing Approaches to Selected Diseases and Conditions, 196 Chronic Craniofacial Pain and Sensorimotor Conditions, 211 Temporomandibular Disorders, 211 Mucosal and Autoimmune Diseases, 212 FACTORS AFFECTING FUTURE HEALTH CARE PRACTICES, 212 Evidence-based Practice, 213 Clinical Practice Guidelines, 213 Science and Technology Contributions, 214 Broadening the Base for the Provision of Oral Health Care, 216 FINDINGS, 216 REFERENCES, 216 Chapter 9 Provision of Oral Health Care 223 COMPONENTS OF PROFESSIONAL CARE, 223 The Dental Component, 223 The Medical Component, 225 The Public Health Component, 225 Areas of Overlap, 227 EXPENDITURES FOR ORAL HEALTH CARE, 227 FINANCING AND REIMBURSEMENT, 229 Insurance, 229 The Changing Market, 231 Federal and State Programs, 233
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xxiii Contents
FACTORS AFFECTING THE CAPACITY TO MEET ORAL HEALTH NEEDS, 234 Numbers of Dental Personnel, 235 Sex and Racial/Ethnic Composition of Dental Personnel, 236 Student Indebtedness and Its Effects, 237 Personnel Needs for Faculty and Clinical Research, 238 Curriculum Needs, 238 Taking Care of Those Most in Need, 239 TWENTY-FIRST CENTURY CHALLENGES: WHAT LIES AHEAD? 239 FINDINGS, 240 REFERENCES, 241 PART FIVE WHAT ARE THE NEEDS AND OPPORTUNITIES TO ENHANCE ORAL HEALTH? 243 Chapter 10 Factors Affecting Oral Health over the Life Span 245 HEALTH IN THE CONTEXT OF SOCIETY, 245 Historical Models, 245 Contemporary Models, 246 CHANGING VULNERABILITIES THROUGHOUT LIFE, 249 Children, 249 Adolescents and Young Adults, 257 Midlife Adults, 258 Older Americans, 262 ACHIEVING ORAL HEALTH THROUGHOUT LIFE, 267 FINDINGS, 269 REFERENCES, 269 Chapter 11 Facing the Future 275 THE PAST AND PRESENT AS PROLOGUE, 275 The Pioneers, 275 Vital Statistics, 275 Health Improvement, 276 DIVERSITY OF DISEASES AND PATIENTS, 276 TRANSFORMING TREATMENTS, 276 TRANSFORMING HEALTH PROFESSIONAL EDUCATION, 276 TRANSFORMING HEALTH CARE, 277 ORAL HEALTH—NOT YET FOR ALL, 277 HOPE FROM SCIENCE AND TECHNOLOGY, 278 A FRAMEWORK FOR ORAL HEALTH, 280 REFERENCES, 281 Chapter 12 A Call to Action 283 MAJOR FINDINGS, 283 A FRAMEWORK FOR ACTION, 284 CONCLUSION, 287 Index 289
xxiv ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary
Publication of this first Surgeon General’s Report on and nourish the oral tissues, as well as provide con- Oral Health marks a milestone in the history of oral nections to the brain and the rest of the body. The health in America. The report elaborates on the genetic patterning of development in utero further meaning of oral health and explains why oral health reveals the intimate relationship of the oral tissues to is essential to general health and well-being. In the the developing brain and to the tissues of the face and course of the past 50 years, great progress has been head that surround the mouth, structures whose made in understanding the common oral diseases— location is captured in the word craniofacial. dental caries (tooth decay) and periodontal (gum) A major theme of this report is that oral health diseases—resulting in marked improvements in the means much more than healthy teeth. It means nation’s oral health. Most middle-aged and younger being free of chronic oral-facial pain conditions, oral Americans expect to retain their natural teeth over and pharyngeal (throat) cancers, oral soft tissue their lifetime and do not expect to have any serious lesions, birth defects such as cleft lip and palate, and oral health problems. scores of other diseases and disorders that affect the The major message of this Surgeon General’s oral, dental, and craniofacial tissues, collectively report is that oral health is essential to the general known as the craniofacial complex. These are tissues health and well-being of all Americans and can be whose functions we often take for granted, yet they achieved by all Americans. However, not all represent the very essence of our humanity. They Americans are achieving the same degree of oral allow us to speak and smile; sigh and kiss; smell, health. In spite of the safe and effective means of taste, touch, chew, and swallow; cry out in pain; and maintaining oral health that have benefited the convey a world of feelings and emotions through majority of Americans over the past half century, facial expressions. They also provide protection many among us still experience needless pain and against microbial infections and environmental suffering, complications that devastate overall health insults. and well-being, and financial and social costs that The craniofacial tissues also provide a useful diminish the quality of life and burden American means to understanding organs and systems in less society. What amounts to “a silent epidemic” of oral accessible parts of the body. The salivary glands are a diseases is affecting our most vulnerable citizens— model of other exocrine glands, and an analysis of poor children, the elderly, and many members of saliva can provide telltale clues of overall health or racial and ethnic minority groups (GAO 2000). (See disease. The jawbones and their joints function like box entitled “The Burden of Oral Diseases and other musculoskeletal parts. The nervous system Disorders.”) apparatus underlying facial pain has its counterpart The word oral refers to the mouth. The mouth in nerves elsewhere in the body. A thorough oral includes not only the teeth and the gums (gingiva) examination can detect signs of nutritional defi- and their supporting tissues, but also the hard and ciencies as well as a number of systemic diseases, soft palate, the mucosal lining of the mouth and including microbial infections, immune disorders, throat, the tongue, the lips, the salivary glands, the injuries, and some cancers. Indeed, the phrase the chewing muscles, and the upper and lower jaws. mouth is a mirror has been used to illustrate the Equally important are the branches of the nervous, wealth of information that can be derived from immune, and vascular systems that animate, protect, examining oral tissues.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 1 Executive Summary
New research is pointing to associations between detriment. Consequently, a second theme of the chronic oral infections and heart and lung diseases, report is that oral health is integral to general stroke, and low-birth-weight, premature births. health. You cannot be healthy without oral health. Associations between periodontal disease and dia- Oral health and general health should not be betes have long been noted. This report assesses interpreted as separate entities. Oral health is a these associations and explores mechanisms that critical component of health and must be included in might explain the oral-systemic disease connections. the provision of health care and the design of The broadened meaning of oral health parallels community programs. the broadened meaning of health. In 1948 the World The wider meanings of oral and health in no way Health Organization expanded the definition of diminish the relevance and importance of the two health to mean “a complete state of physical, mental, leading dental diseases, caries and the periodontal and social well-being, and not just the absence of diseases. They remain common and widespread, infirmity.” It follows that oral health must also affecting nearly everyone at some point in the life include well-being. Just as we now understand that span. What has changed is what we can do about nature and nurture are inextricably linked, and mind them. and body are both expressions of our human biology, Researchers in the 1930s discovered that people so, too, we must recognize that oral health and living in communities with naturally fluoridated general health are inseparable. We ignore signs and water supplies had less dental caries than people symptoms of oral disease and dysfunction to our drinking unfluoridated water. But not until the end
The Burden of Oral Diseases and Disorders differences continue into adolescence. One out of four children in America is born into poverty,and children living below the poverty line Oral diseases are progressive and cumulative and become more com- (annual income of $17,000 for a family of four) have more severe and plex over time.They can affect our ability to eat, the foods we choose, untreated decay. how we look,and the way we communicate.These diseases can affect economic productivity and compromise our ability to work at home,at Unintentional injuries,many of which include head,mouth,and school, or on the job.Health disparities exist across population groups neck injuries,are common in children. at all ages. Over one third of the U.S. population (100 million people) Intentional injuries commonly affect the craniofacial tissues. has no access to community water fluoridation. Over 108 million chil- Tobacco-related oral lesions are prevalent in adolescents who dren and adults lack dental insurance,which is over 2.5 times the num- currently use smokeless (spit) tobacco. ber who lack medical insurance. The following are highlights of oral Professional care is necessary for maintaining oral health, yet health data for children,adults,and the elderly.(Refer to the full report 25 percent of poor children have not seen a dentist before entering for details of these data and their sources.) kindergarten. Medical insurance is a strong predictor of access to dental care. Children Uninsured children are 2.5 times less likely than insured children to Cleft lip/palate,one of the most common birth defects,is esti- receive dental care.Children from families without dental insurance are mated to affect 1 out of 600 live births for whites and 1 out of 1,850 live 3 times more likely to have dental needs than children with either pub- births for African Americans. lic or private insurance.For each child without medical insurance,there Other birth defects such as hereditary ectodermal dysplasias, are at least 2.6 children without dental insurance. where all or most teeth are missing or misshapen,cause lifetime prob- Medicaid has not been able to fill the gap in providing dental lems that can be devastating to children and adults. care to poor children.Fewer than one in five Medicaid-covered children Dental caries (tooth decay) is the single most common chronic received a single dental visit in a recent year-long study period. childhood disease—5 times more common than asthma and 7 times Although new programs such as the State Children’s Health Insurance more common than hay fever. Program (SCHIP) may increase the number of insured children, many Over 50 percent of 5- to 9-year-old children have at least one will still be left without effective dental coverage. cavity or filling,and that proportion increases to 78 percent among 17- The social impact of oral diseases in children is substantial. year-olds. Nevertheless, these figures represent improvements in the More than 51 million school hours are lost each year to dental-related oral health of children compared to a generation ago. illness. Poor children suffer nearly 12 times more restricted-activity There are striking disparities in dental disease by income.Poor days than children from higher-income families.Pain and suffering due children suffer twice as much dental caries as their more affluent peers, to untreated diseases can lead to problems in eating, speaking, and and their disease is more likely to be untreated. These poor-nonpoor attending to learning.
2 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary of World War II were the investigators able to design The theme of prevention gained momentum as and implement the community clinical trials that pioneering investigators and practitioners in the confirmed their observations and launched a better 1950s and 1960s showed that not only dental caries approach to the problem of dental caries: prevention. but also periodontal diseases are bacterial infections. Soon after, adjusting the fluoride content of commu- The researchers demonstrated that the infections nity water supplies was pursued as an important pub- could be prevented by increasing host resistance to lic health measure to prevent dental caries. disease and reducing or eliminating the suspected Although this measure has not been fully imple- microbial pathogens in the oral cavity. The applica- mented, the results have been dramatic. Dental caries tions of research discoveries have resulted in contin- began to decline in the 1950s among children who uing improvements in the oral health of Americans, grew up in fluoridated cities, and by the late 1970s, new approaches to the prevention and treatment of decline in decay was evident for many Americans. dental diseases, and the growth of the science. The application of science to improve diagnostic, The significant role that scientists, dentists, den- treatment, and prevention strategies has saved bil- tal hygienists, and other health professionals have lions of dollars per year in the nation’s annual health played in the prevention of oral disease and disabili- bill. Even more significant, the result is that far fewer ty leads to a third theme of this report: safe and effec- people are edentulous (toothless) today than a gen- tive disease prevention measures exist that every- eration ago. one can adopt to improve oral health and prevent disease. These measures include daily oral hygiene
Adults Older Adults Most adults show signs of periodontal or gingival diseases. Twenty-three percent of 65- to 74-year-olds have severe peri- Severe periodontal disease (measured as 6 millimeters of periodontal odontal disease (measured as 6 millimeters of periodontal attachment attachment loss) affects about 14 percent of adults aged 45 to 54. loss).(Also, at all ages men are more likely than women to have more Clinical symptoms of viral infections, such as herpes labialis severe disease,and at all ages people at the lowest socioeconomic lev- (cold sores), and oral ulcers (canker sores) are common in adulthood, els have more severe periodontal disease.) affecting about 19 percent of adults 25 to 44 years of age. About 30 percent of adults 65 years and older are edentulous, Chronic disabling diseases such as temporomandibular disor- compared to 46 percent 20 years ago.These figures are higher for those ders, Sjögren’s syndrome, diabetes, and osteoporosis affect millions of living in poverty. Americans and compromise oral health and functioning. Oral and pharyngeal cancers are diagnosed in about 30,000 Pain is a common symptom of craniofacial disorders and is Americans annually; 8,000 die from these diseases each year. These accompanied by interference with vital functions such as eating,swal- cancers are primarily diagnosed in the elderly.Prognosis is poor.The 5- lowing,and speech.Twenty-two percent of adults reported some form year survival rate for white patients is 56 percent;for blacks,it is only 34 of oral-facial pain in the past 6 months.Pain is a major component of percent. trigeminal neuralgia, facial shingles (post-herpetic neuralgia), tem- Most older Americans take both prescription and over-the- poromandibular disorders,fibromyalgia,and Bell’s palsy. counter drugs. In all probability, at least one of the medications used Population growth as well as diagnostics that are enabling ear- will have an oral side effect—usually dry mouth.The inhibition of sali- lier detection of cancer means that more patients than ever before are vary flow increases the risk for oral disease because saliva contains undergoing cancer treatments. More than 400,000 of these patients antimicrobial components as well as minerals that can help rebuild will develop oral complications annually. tooth enamel after attack by acid-producing, decay-causing bacteria. Immunocompromised patients, such as those with HIV infec- Individuals in long-term care facilities are prescribed an average of tion and those undergoing organ transplantation,are at higher risk for eight drugs. oral problems such as candidiasis. At any given time, 5 percent of Americans aged 65 and older Employed adults lose more than 164 million hours of work each (currently some 1.65 million people) are living in a long-term care facil- year due to dental disease or dental visits. ity where dental care is problematic. For every adult 19 years or older without medical insurance, Many elderly individuals lose their dental insurance when they there are three without dental insurance. retire.The situation may be worse for older women,who generally have A little less than two thirds of adults report having visited a lower incomes and may never have had dental insurance. Medicaid dentist in the past 12 months. Those with incomes at or above the funds dental care for the low-income and disabled elderly in some poverty level are twice as likely to report a dental visit in the past 12 states, but reimbursements are low.Medicare is not designed to reim- months as those who are below the poverty level. burse for routine dental care.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 3 Executive Summary procedures and other lifestyle behaviors, community THE CHALLENGE programs such as community water fluoridation and This Surgeon General’s report has much to say about tobacco cessation programs, and provider-based the inequities and disparities that affect those least interventions such as the placement of dental able to muster the resources to achieve optimal oral sealants and examinations for common oral and pha- health. The barriers to oral health include lack of ryngeal cancers. It is hoped that this Surgeon access to care, whether because of limited income or General’s report will facilitate the maturing of the lack of insurance, transportation, or the flexibility to broad field of craniofacial research so that gains in take time off from work to attend to personal or fam- the prevention of craniofacial diseases and disorders ily needs for care. Individuals with disabilities and can be realized that are as impressive as those those with complex health problems may face addi- achieved for common dental diseases. tional barriers to care. Sometimes, too, the public, At the same time, more needs to be done to policymakers, and providers may consider oral ensure that messages of health promotion and dis- health and the need for care to be less important than ease prevention are brought home to all Americans. other health needs, pointing to the need to raise In this regard, a fourth theme of the report is that awareness and improve health literacy. general health risk factors, such as tobacco use and Even more costly to the individual and to socie- poor dietary practices, also affect oral and craniofa- ty are the expenses associated with oral health prob- cial health. The evidence for an association between lems that go beyond dental diseases. The nation’s tobacco use and oral diseases has been clearly delin- yearly dental bill is expected to exceed $60 billion in eated in almost every Surgeon General’s report on 2000 (Health Care Financing Administration 2000). tobacco since 1964, and the oral effects of nutrition However, add to that expense the tens of billions of and diet are presented in the Surgeon General’s report dollars in direct medical care and indirect costs of on nutrition (1988). All the health professions can chronic craniofacial pain conditions such as tem- play a role in reducing the burden of disease in poromandibular disorders, trigeminal neuralgia, America by calling attention to these and other risk shingles, or burning mouth syndrome; the $100,000 factors and suggesting appropriate actions. minimum individual lifetime costs of treating cranio- Clearly, promoting health and preventing dis- facial birth defects such as cleft lip and palate; the eases are concepts the American people have taken to costs of oral and pharyngeal cancers; the costs of heart. For the third decade the nation has developed autoimmune diseases; and the costs associated with a plan for the prevention of disease and the promo- the unintentional and intentional injuries that so tion of health, embodied in the U.S. Department of often affect the head and face. Then add the social Health and Human Services (2000) document, and psychological consequences and costs. Damage Healthy People 2010. As a nation, we hope to elimi- to the craniofacial complex, whether from disease, nate disparities in health and prevent oral diseases, disorder, or injury, strikes at our very identity. We see cancer, birth defects, AIDS and other devastating ourselves, and others see us, in terms of the face we infections, mental illness and suicide, and the chron- present to the world. Diminish that image in any way ic diseases of aging. To live well into old age free of and we risk the loss of self-esteem and well-being. pain and infirmity, and with a high quality of life, is Many unanswered questions remain for scien- the American dream. tists, practitioners, educators, policymakers, and the Scientists today take that dream seriously in public. This report highlights the research challenges researching the intricacies of the craniofacial com- as well as pointing to emerging technologies that may plex. They are using an ever-growing array of sophis- facilitate finding solutions. Along with the quest for ticated analytic tools and imaging systems to study answers comes the challenge of applying what is normal function and diagnose disease. They are com- already known in a society where there are social, pleting the mapping and sequencing of human, ani- political, economic, behavioral, and environmental mal, microbial, and plant genomes, the better to barriers to health and well-being. understand the complexities of human development, aging, and pathological processes. They are growing cell lines, synthesizing molecules, and using a new THE CHARGE generation of biomaterials to revolutionize tissue The realization that oral health can have a significant repair and regeneration. More than ever before, they impact on the overall health and well-being of the are working in multidisciplinary teams to bring new nation’s population led the Office of the Surgeon knowledge and expertise to the goal of understand- General, with the approval of the Secretary of Health ing complex human diseases and disorders. and Human Services, to commission this report.
4 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary
Recognizing the gains that have been made in disease quality assurance has been maintained by the prevention while acknowledging that there are popu- Centers for Disease Control and Prevention. Studies lations that suffer disproportionately from oral health of smaller populations are also included where rele- problems, the Secretary asked that the report “define, vant. In Chapter 5, tables present information on the describe, and evaluate the interaction between oral association of oral infections and systemic condi- health and health and well-being [quality of life], tions, and in Chapter 7, tables exhibit oral disease through the life span in the context of changes in prevention and health promotion measures. The society.” Key elements to be addressed were the published literature related to the development of determinants of health and disease, with a primary new technologies, their potential impact, and the focus on prevention and “producing health” rather need for further research are described in the course than “restoring health”; a description of the burden of addressing the requested futures orientation. of oral diseases and disorders in the nation; and the The report was generated with the advice and evidence for actions to improve oral health to be support of a Federal Coordinating Committee taken across the life span. The report also was to fea- composed of representatives of agencies with oral ture an orientation to the future, highlighting lead- health components and interests. The chapters were ing-edge technologies and research findings that can based on papers submitted by experts working under be brought to bear in improving the oral health of the guidance of a coordinating author for each individuals and communities. chapter. Independent peer review was conducted for all sections of the report at various stages in the process, and the full manuscript was reviewed by a THE SCIENCE BASE FOR THE REPORT number of senior reviewers as well as the relevant This report is based on a review of the published federal agencies. All who contributed are listed in the scientific literature. Standards established to Acknowledgments section of the full report. determine the quality of the evidence, based on the study design and its rigor, were used where appropriate. In addition, the strength of the ORGANIZATION OF THE REPORT recommendations, where they are made, is based on The report centers on five major questions, which evidence of effectiveness for the population of have been used to structure the report into five parts. interest. The scope of the review encompassed the international English literature. Recent systematic reviews of the literature are referenced, as are selected Part One: What Is Oral Health? review articles. A few referenced articles are in press, The meaning of oral health is explored in Chapter 1, and there are occasional references to recent abstracts and the interdependence of oral health with general and personal communications. health and well-being is a recurrent theme through- The science base in oral health has been evolving out the volume. over the past half century. Initial research in this area Chapter 2 provides an overview of the craniofa- was primarily in the basic sciences, investigating cial complex in development and aging, how the tis- mechanisms of normal development and pathology sues and organs function in essential life processes, in relation to dental caries and periodontal diseases. and their role in determining our uniquely human Prevention research has included controlled clinical abilities. Our craniofacial complex has evolved to studies, with and without randomization, as well as have remarkable functions and abilities to adapt, community trials and demonstration research. More enabling us to meet the challenges of an ever-chang- recent research has broadened the science base to ing environment. An examination of the various tis- include studies of the range of craniofacial diseases sues reveals elaborate designs that serve complex and disorders and is moving from basic science to needs and functions, including the uniquely human translational, clinical, and health services research. function of speech. The rich distribution of nerves, The clinical literature includes the full range of muscles, and blood vessels in the region as well as studies, from randomized controlled studies to case extensive endocrine and immune system connec- studies. Most of the literature includes cross-section- tions are indicators of the vital role of the craniofacial al and cohort studies, with some case-control studies. complex in adaptation and survival over a long life General reviews of the literature have been used for span. In particular, the following findings are noted: Chapters 2 through 10. Chapter 4 includes both pub- Genes controlling the basic patterning and lished and new analyses of national and state data- segmental organization of human development, and bases that have been carefully designed and for which specifically the craniofacial complex, are highly
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 5 Executive Summary conserved in nature. Mutated genes affecting human groups, as well as their dental visit behavior. The development have counterparts in many simpler findings include: organisms. Over the past five decades, major improve- There is considerable reserve capacity or ments in oral health have been seen nationally for redundancy in the cells and tissues of the craniofacial most Americans. complex, so that if they are properly cared for, the Despite improvements in oral health status, structures should function well over a lifetime. profound disparities remain in some population The salivary glands and saliva subserve tast- groups as classified by sex, income, age, and race/eth- ing and digestive functions and also participate in the nicity. For some diseases and conditions, the magni- mucosal immune system, a main line of defense tude of the differences in oral health status among against pathogens, irritants, and toxins. population groups is striking. Salivary components protect and maintain Oral diseases and conditions affect people oral tissues through antimicrobial components, throughout their life span. Nearly every American buffering agents, and a process by which dental has experienced the most common oral disease, den- enamel can be remineralized. tal caries. Conditions that severely affect the face and facial expression, such as birth defects, craniofacial Part Two: What Is the Status of Oral injuries, and neoplastic diseases, are more common Health in America? in the very young and in the elderly. Chapter 3 is a primer describing the major diseases Oral-facial pain can greatly reduce quality of and disorders that affect the craniofacial complex. life and restrict major functions. Pain is a common The findings include: symptom for many of the conditions affecting oral- Microbial infections, including those caused facial structures. by bacteria, viruses, and fungi, are the primary cause National and state data for many oral and of the most prevalent oral diseases. Examples include craniofacial diseases and conditions and for popula- dental caries, periodontal diseases, herpes labialis, tion groups are limited or nonexistent. Available state and candidiasis. data reveal variations within and among states in pat- The etiology and pathogenesis of diseases terns of health and disease among population groups. and disorders affecting the craniofacial structures Research is needed to develop better meas- are multifactorial and complex, involving an inter- ures of disease and health, to explain the differences play among genetic, environmental, and behavioral among population groups, and to develop interven- factors. tions targeted at eliminating disparities. Many inherited and congenital conditions affect the craniofacial complex, often resulting in dis- figurement and impairments that may involve many Part Three: What Is the Relationship body organs and systems and affect millions of chil- Between Oral Health and General Health dren worldwide. and Well-being? Tobacco use, excessive alcohol use, and Chapters 5 and 6 address key issues in the report’s inappropriate dietary practices contribute to many charge—the relationship of oral health to general diseases and disorders. In particular, tobacco use is a health and well-being. Chapter 5 explores the theme risk factor for oral cavity and pharyngeal cancers, of the mouth as reflecting general health or disease periodontal diseases, candidiasis, and dental caries, status. Examples are given of how oral tissues may among other diseases. signal the presence of disease, disease progression, or Some chronic diseases, such as Sjögren’s syn- exposure to risk factors, and how oral cells and fluids drome, present with primary oral symptoms. are increasingly being used as diagnostic tools. This Oral-facial pain conditions are common and is followed by a discussion of the mouth as a portal often have complex etiologies. of entry for infections that can affect local tissues and Chapter 4 constitutes an oral health status report may spread to other parts of the body. The final sec- card for the United States, describing the magnitude tions review the literature regarding emerging associ- of the problem. Where data permit, the chapter also ations between oral diseases and diabetes, heart dis- describes the oral health of selected population ease and stroke, and adverse pregnancy outcomes.
6 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary
The findings include: cancers contribute to premature death and can be Many systemic diseases and conditions have measured by years of life lost. oral manifestations. These manifestations may be the Oral and craniofacial diseases and condi- initial sign of clinical disease and as such serve to tions contribute to compromised ability to bite, chew, inform clinicians and individuals of the need for fur- and swallow foods; limitations in food selection; and ther assessment. poor nutrition. These conditions include tooth loss, The oral cavity is a portal of entry as well as diminished salivary functions, oral-facial pain condi- the site of disease for microbial infections that affect tions such as temporomandibular disorders, alter- general health status. ations in taste, and functional limitations of prosthet- The oral cavity and its functions can be ic replacements. adversely affected by many pharmaceuticals and Oral-facial pain, as a symptom of untreated other therapies commonly used in treating systemic dental and oral problems and as a condition in and of conditions. The oral complications of these therapies itself, is a major source of diminished quality of life. can compromise patient compliance with treatment. It is associated with sleep deprivation, depression, Individuals such as immunocompromised and multiple adverse psychosocial outcomes. and hospitalized patients are at greater risk for gen- Self-reported impacts of oral conditions on eral morbidity due to oral infections. social function include limitations in verbal and non- Individuals with diabetes are at greater risk verbal communication, social interaction, and inti- for periodontal diseases. macy. Individuals with facial disfigurements due to Animal and population-based studies have craniofacial diseases and conditions and their treat- demonstrated an association between periodontal ments may experience loss of self-image and self- diseases and diabetes, cardiovascular disease, stroke, esteem, anxiety, depression, and social stigma; these and adverse pregnancy outcomes. Further research is in turn may limit educational, career, and marital needed to determine the extent to which these asso- opportunities and affect other social relations. ciations are causal or coincidental. Reduced oral-health-related quality of life is Chapter 6 demonstrates the relationship between associated with poor clinical status and reduced oral health and quality of life, presenting data on the access to care. consequences of poor oral health and altered appear- ance on speech, eating, and other functions, as well Part Four: How Is Oral Health Promoted as on self-esteem, social interaction, education, career achievement, and emotional state. The chapter and Maintained and How Are Oral introduces anthropological and ethnographic litera- Diseases Prevented? ture to underscore the cultural values and symbolism The next three chapters review how individuals, attached to facial appearance and teeth. An examina- health care practitioners, communities, and the tion of efforts to characterize the functional and nation as a whole contribute to oral health. Chapter social implications of oral and craniofacial diseases 7 reviews the evidence for the efficacy and effective- reveals the following findings: ness of health promotion and disease prevention Oral health is related to well-being and qual- measures with a focus on community efforts in pre- ity of life as measured along functional, psychosocial, venting oral disease. It continues with a discussion of and economic dimensions. Diet, nutrition, sleep, the knowledge and practices of the public and health psychological status, social interaction, school, and care providers and indicates opportunities for broad- work are affected by impaired oral and craniofacial based and targeted health promotion. The findings health. include: Cultural values influence oral and craniofa- Community water fluoridation, an effective, cial health and well-being and can play an important safe, and ideal public health measure, benefits indi- role in care utilization practices and in perpetuating viduals of all ages and socioeconomic strata. acceptable oral health and facial norms. Unfortunately, over one third of the U.S. population Oral and craniofacial diseases and their (100 million people) are without this critical public treatment place a burden on society in the form of health measure. lost days and years of productive work. Acute dental Effective disease prevention measures exist conditions contribute to a range of problems for for use by individuals, practitioners, and employed adults, including restricted activity, bed communities. Most of these focus on dental caries days, and work loss, and school loss for children. In prevention, such as fluorides and dental sealants, addition, conditions such as oral and pharyngeal where a combination of services is required to
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 7 Executive Summary achieve optimal disease prevention. Daily oral disciplinary care is needed to manage the oral hygiene practices such as brushing and flossing can health–general health interface. Dentists, as primary prevent gingivitis. care providers, are uniquely positioned to play an Community-based approaches for the pre- expanded role in the detection, early recognition, and vention of other oral diseases and conditions, such as management of a wide range of complex oral and oral and pharyngeal cancers and oral-facial trauma, general diseases and conditions. require intensified developmental efforts. Nonsurgical interventions are available to Community-based preventive programs are reverse disease progression and to manage oral dis- unavailable to substantial portions of the under- eases as infections. served population. New knowledge and the development of There is a gap between research findings and molecular and genetically based tests will facili- the oral disease prevention and health promotion tate risk assessment and management and improve practices and knowledge of the public and the health the ability of health care providers to customize professions. treatment. Disease prevention and health promotion Health care providers can successfully deliv- approaches, such as tobacco control, appropriate use er tobacco cessation and other health promotion pro- of fluorides for caries prevention, and folate supple- grams in their offices, contributing to both overall mentation for neural tube defect prevention, high- health and oral health. light opportunities for partnerships between commu- Biocompatible rehabilitative materials and nity-based programs and practitioners, as well as col- biologically engineered tissues are being developed laborations among health professionals. and will greatly enhance the treatment options avail- Many community-based programs require a able to providers and their patients. combined effort among social service, health care, Chapter 9 describes the roles of dental practi- and education services at the local or state level. tioners and their teams, the medical community, and Chapter 8 explores the role of the individual and public health agencies at local, state, and national the health care provider in promoting and maintain- levels in administering care or reimbursing for the ing oral health and well-being. For the individual, costs of care. These activities are viewed against the this means exercising appropriate self-care and changing organization of U.S. health care and trends adopting healthy behaviors. For the provider, it regarding the workforce in research, education, and means incorporating the knowledge emerging from practice. the science base in a timely manner for prevention Dental, medical, and public health delivery and diagnosis, risk assessment and risk management, systems each provide services that affect oral and and treatment of oral diseases and disorders. The craniofacial health in the U.S. population. Clinical chapter focuses largely on the oral health care oral health care is predominantly provided by a pri- provider. The management of oral and craniofacial vate practice dental workforce. health and disease necessitates collaborations among Expenditures for dental services alone made a team of care providers to achieve optimal oral and up 4.7 percent of the nation’s health expenditures in general health. The findings include: 1998—$53.8 billion out of $1.1 trillion. These Achieving and maintaining oral health expenditures underestimate the true costs to the require individual action, complemented by profes- nation, however, because data are unavailable to sional care as well as community-based activities. determine the extent of expenditures and services Individuals can take actions, for themselves provided for craniofacial health care by other health and for persons under their care, to prevent disease providers and institutions. and maintain health. Primary prevention of many The public health infrastructure for oral oral, dental, and craniofacial diseases and conditions health is insufficient to address the needs of disad- is possible with appropriate diet, nutrition, oral vantaged groups, and the integration of oral and gen- hygiene, and health-promoting behaviors, including eral health programs is lacking. the appropriate use of professional services. Expansion of community-based disease Individuals should use a fluoride dentifrice daily to prevention and lowering of barriers to personal oral help prevent dental caries and should brush and floss health care are needed to meet the needs of the daily to prevent gingivitis. population. All primary care providers can contribute to Insurance coverage for dental care is improved oral and craniofacial health. Inter- increasing but still lags behind medical insurance.
8 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary
For every child under 18 years old without medical on barriers and ways to raise the level of oral health insurance, there are at least two children without for children and older Americans. The findings dental insurance; for every adult 18 years or older include: without medical insurance, there are three without The major factors that determine oral and dental insurance. general health and well-being are individual biology Eligibility for Medicaid does not ensure and genetics; the environment, including its physical enrollment, and enrollment does not ensure that and socioeconomic aspects; personal behaviors and individuals obtain needed care. Barriers include lifestyle; access to care; and the organization of health patient and caregiver understanding of the value and care. These factors interact over the life span and importance of oral health to general health, low determine the health of individuals, population reimbursement rates, and administrative burdens for groups, and communities—from neighborhoods to both patient and provider. nations. A narrow definition of “medically necessary The burden of oral diseases and conditions is dental care” currently limits oral health services for disproportionately borne by individuals with low many insured persons, particularly the elderly. socioeconomic status at each life stage and by those The dentist-to-population ratio is declining, who are vulnerable because of poor general health. creating concern as to the capability of the dental Access to care makes a difference. A complex workforce to meet the emerging demands of society set of factors underlies access to care and includes the and provide required services efficiently. need to have an informed public and policymakers, An estimated 25 million individuals reside in integrated and culturally competent programs, and areas lacking adequate dental care services, as resources to pay and reimburse for the care. Among defined by Health Professional Shortage Area (HPSA) other factors, the availability of insurance increases criteria. access to care. Educational debt has increased, affecting Preventive interventions, such as protective both career choices and practice location. head and mouth gear and dental sealants, exist but Disparities exist in the oral health profession are not uniformly used or reinforced. workforce and career paths. The number of under- Nursing homes and other long-term care represented minorities in the oral health professions institutions have limited capacity to deliver needed is disproportionate to their distribution in the popu- oral health services to their residents, most of whom lation at large. are at increased risk for oral diseases. Current and projected demand for dental Anticipatory guidance and risk assessment school faculty positions and research scientists is and management facilitate care for children and for not being met. A crisis in the number of faculty and the elderly. researchers threatens the quality of dental educa- Federal and state assistance programs for tion; oral, dental, and craniofacial research; and, ulti- selected oral health services exist; however, the scope mately, the health of the public. of services is severely limited, and their reimburse- Reliable and valid measures of oral health ment level for oral health services is low compared to outcomes do not exist and need to be developed, val- the usual fee for care. idated, and incorporated into practice and programs. Chapter 11 spells out in greater detail the prom- ise of the life sciences in improving oral health in the coming years in the context of changes in Part Five: What Are the Needs and American—and global—society. The critical role of Opportunities to Enhance Oral Health? genetics and molecular biology is emphasized. Chapter 10 looks at determinants of oral health in Chapter 12, the final chapter, iterates the themes the context of society and across various life stages. of the report and groups the findings from the earlier Although theorists have proposed a variety of models chapters into eight major categories. These findings, of health determinants, there is general consensus as well as a suggested framework for action to guide that individual biology, the physical and the next steps in enhancing the oral health of the socioeconomic environment, personal behaviors and nation, are presented below. lifestyle, and the organization of health care are key factors whose interplay determines the level of oral health achieved by an individual. The chapter provides examples of these factors with an emphasis
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 9 Executive Summary
MAJOR FINDINGS promoting measures. Similarly, not all health Oral diseases and disorders in and of themselves providers may be aware of the services needed to affect health and well-being throughout life. The improve oral health. In addition, oral health care is burden of oral problems is extensive and may be par- not fully integrated into many care programs. Social, ticularly severe in vulnerable populations. It includes economic, and cultural factors and changing pop- the common dental diseases and other oral infections ulation demographics affect how health services are such as cold sores and candidiasis that can occur at delivered and used, and how people care for any stage of life, as well as birth defects in infancy themselves. Reducing disparities requires wide- and the chronic facial pain conditions and oral can- ranging approaches that target populations at high- cers seen in later years. Many of these conditions and est risk for specific oral diseases and involves their treatments may undermine self-image and self- improving access to existing care. One approach esteem, discourage normal social interaction, cause includes making dental insurance more available to other health problems, and lead to chronic stress and Americans. Public coverage for dental care is depression as well as incur great financial cost. They minimal for adults, and programs for children have may also interfere with vital functions such as breath- not reached the many eligible beneficiaries. ing, food selection, eating, swallowing, and speaking More information is needed to improve and with activities of daily living such as work, America’s oral health and eliminate health dispari- school, and family interactions. ties. We do not have adequate data on health, dis- Safe and effective measures exist to prevent the ease, and health practices and care use for the U.S. most common dental diseases—dental caries and population as a whole and its diverse segments, periodontal diseases. Community water fluoridation including racial and ethnic minorities, rural popula- is safe and effective in preventing dental caries in tions, individuals with disabilities, the homeless, both children and adults. Water fluoridation benefits immigrants, migrant workers, the very young, and all residents served by community water supplies the frail elderly. Nor are there sufficient data that regardless of their social or economic status. explore health issues in relation to sex or sexual ori- Professional and individual measures, including the entation. Data on state and local populations, essen- use of fluoride mouthrinses, gels, dentifrices, and tial for program planning and evaluation, are rare or dietary supplements and the application of dental unavailable and reflect the limited capacity of the sealants, are additional means of preventing dental U.S. health infrastructure for oral health. Health serv- caries. Gingivitis can be prevented by good personal ices research, which could provide much needed oral hygiene practices, including brushing and information on the cost, cost-effectiveness, and out- flossing. comes of treatment, is also sorely lacking. Finally, Lifestyle behaviors that affect general health measurement of disease and health outcomes is need- such as tobacco use, excessive alcohol use, and ed. Although progress has been made in measuring poor dietary choices affect oral and craniofacial oral-health-related quality of life, more needs to be health as well. These individual behaviors are asso- done, and measures of oral health per se do not exist. ciated with increased risk for craniofacial birth The mouth reflects general health and well- defects, oral and pharyngeal cancers, periodontal dis- being. The mouth is a readily accessible and visible ease, dental caries, and candidiasis, among other oral part of the body and provides health care providers health problems. Opportunities exist to expand the and individuals with a window on their general oral disease prevention and health promotion knowl- health status. As the gateway of the body, the mouth edge and practices of the public through community senses and responds to the external world and at the programs and in health care settings. All health care same time reflects what is happening deep inside the providers can play a role in promoting healthy body. The mouth may show signs of nutritional defi- lifestyles by incorporating tobacco cessation pro- ciencies and serve as an early warning system for dis- grams, nutritional counseling, and other health pro- eases such as HIV infection and other immune sys- motion efforts into their practices. tem problems. The mouth can also show signs of There are profound and consequential oral general infection and stress. As the number of sub- health disparities within the U.S. population. stances that can be reliably measured in saliva Disparities for various oral conditions may relate to increases, it may well become the diagnostic fluid of income, age, sex, race or ethnicity, or medical status. choice, enabling the diagnosis of specific disease as Although common dental diseases are preventable, well as the measurement of the concentration of a not all members of society are informed about or able variety of drugs, hormones, and other molecules of to avail themselves of appropriate oral-health- interest. Cells and fluids in the mouth may also be
10 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary used for genetic analysis to help uncover risks for Change perceptions regarding oral health and dis- disease and predict outcomes of medical treatments. ease so that oral health becomes an accepted com- Oral diseases and conditions are associated ponent of general health. with other health problems. Oral infections can be Change public perceptions. Many people con- the source of systemic infections in people with sider oral signs and symptoms to be less important weakened immune systems, and oral signs and symp- than indications of general illness. As a result, they toms often are part of a general health condition. may avoid or postpone needed care, thus exacerbat- Associations between chronic oral infections and ing the problem. If we are to increase the nation’s other health problems, including diabetes, heart dis- capacity to improve oral health and reduce health ease, and adverse pregnancy outcomes, have also disparities, we need to enhance the public’s under- been reported. Ongoing research may uncover mech- standing of the meaning of oral health and the rela- anisms that strengthen the current findings and tionship of the mouth to the rest of the body. These explain these relationships. messages should take into account the multiple lan- Scientific research is key to further reduction in guages and cultural traditions that characterize the burden of diseases and disorders that affect the America’s diversity. face, mouth, and teeth. The science base for dental Change policymakers’ perceptions. Informed diseases is broad and provides a strong foundation policymakers at the local, state, and federal levels are for further improvements in prevention; for other critical in ensuring the inclusion of oral health serv- craniofacial and oral health conditions the base has ices in health promotion and disease prevention pro- not yet reached the same level of maturity. Scientific grams, care delivery systems, and reimbursement research has led to a variety of approaches to improve schedules. Raising awareness of oral health among oral health through prevention, early diagnosis, and legislators and public officials at all levels of govern- treatment. We are well positioned to take these pre- ment is essential to creating effective public policy to vention measures further by investigating how to improve America’s oral health. Every conceivable develop more targeted and effective interventions avenue should be used to inform policymakers— and devising ways to enhance their appropriate adop- informally through their organizations and affilia- tion by the public and the health professions. The tions and formally through their governmental application of powerful new tools and techniques is offices—if rational oral health policy is to be formu- important. Their employment in research in genetics lated and effective programs implemented. and genomics, neuroscience, and cancer has allowed Change health providers’ perceptions. Too little rapid progress in these fields. An intensified effort to time is devoted to oral health and disease topics in understand the relationships between oral infections the education of nondental health professionals. Yet and their management, and other illnesses and con- all care providers can and should contribute to ditions is warranted, along with the development of enhancing oral health. This can be accomplished in oral-based diagnostics. These developments hold several ways, such as including an oral examination great promise for the health of the American people. as part of a general medical examination, advising patients in matters of tobacco cessation and diet, and referring patients to oral health practitioners for care A FRAMEWORK FOR ACTION prior to medical or surgical treatments that can dam- All Americans can benefit from the development of a age oral tissues, such as cancer chemotherapy or National Oral Health Plan to improve quality of life radiation to the head and neck. Health care providers and eliminate health disparities by facilitating collab- should be ready, willing, and able to work in collabo- orations among individuals, health care providers, ration to provide optimal health care for their communities, and policymakers at all levels of socie- patients. Having informed health care professionals ty and by taking advantage of existing initiatives. will ensure that the public using the health care sys- Everyone has a role in improving and promoting oral tem will benefit from interdisciplinary services and health. Together we can work to broaden public comprehensive care. To prepare providers for such a understanding of the importance of oral health and role will involve, among other factors, curriculum its relevance to general health and well-being, and to changes and multidisciplinary training. ensure that existing and future preventive, diagnos- tic, and treatment measures for oral diseases and dis- Accelerate the building of the science and evidence orders are made available to all Americans. The fol- base and apply science effectively to improve oral lowing are the principal components of the plan: health. Basic behavioral and biomedical research, clinical trials, and population-based research have
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 11 Executive Summary been at the heart of scientific advances over the past and on the ability of practitioners and the public to decades. The nation’s continued investment in apply research findings effectively. research is critical for the provision of new knowl- edge about oral and general health and disease for Build an effective health infrastructure that meets years to come and needs to be accelerated if further the oral health needs of all Americans and inte- improvements are to be made. Equally important is grates oral health effectively into overall health. The the effective transfer of research findings to the pub- public health capacity for addressing oral health is lic and health professions. However, the next steps dilute and not integrated with other public health are more complicated. The challenge is to understand programs. Although the Healthy People 2010 objec- complex diseases caused by the interaction of multi- tives provide a blueprint for outcome measures, a ple genes with environmental and behavioral vari- national public health plan for oral health does not ables—a description that applies to most oral dis- exist. Furthermore, local, state, and federal resources eases and disorders—and translate research findings are limited in the personnel, equipment, and facilities into health care practice and healthy lifestyles. available to support oral health programs. There is This report highlights many areas of research also a lack of available trained public health practi- opportunities and needs in each chapter. At present, tioners knowledgeable about oral health. As a result, there is an overall need for behavioral and clinical existing disease prevention programs are not being research, clinical trials, health services research, and implemented in many communities, creating gaps in community-based demonstration research. Also, prevention and care that affect the nation’s neediest development of risk assessment procedures for indi- populations. Indeed, cutbacks in many state budgets viduals and communities and of diagnostic markers have reduced staffing of state and territorial dental to indicate whether an individual is more or less sus- programs and curtailed oral health promotion and ceptible to a given disease can provide the basis for disease prevention efforts. An enhanced public formulating risk profiles and tailoring treatment and health infrastructure would facilitate the develop- program options accordingly. ment of strengthened partnerships with private prac- Vital to progress in this area is a better under- titioners, other public programs, and voluntary standing of the etiology and distribution of disease. groups. But as this report makes clear, epidemiologic and sur- There is a lack of racial and ethnic diversity in veillance databases for oral health and disease, the oral health workforce. Efforts to recruit members health services, utilization of care, and expenditures of minority groups to positions in health education, are limited or lacking at the national, state, and local research, and practice in numbers that at least match levels. Such data are essential in conducting health their representation in the general population not services research, generating research hypotheses, only would enrich the talent pool, but also might planning and evaluating programs, and identifying result in a more equitable geographic distribution of emerging public health problems. Future data collec- care providers. The effect of that change could well tion must address differences among the subpopula- enhance access and utilization of oral health care by tions making up racial and ethnic groups. More racial and ethnic minorities. attention must also be paid to demographic variables A closer look at trends in the workforce disclos- such as age, sex, sexual orientation, and socioeco- es a worrisome shortfall in the numbers of men and nomic factors in determining health status. Clearly, women choosing careers in oral health education and the more detailed information that is available, the research. Government and private sector leaders are better can program planners establish priorities and aware of the problem and are discussing ways to targeted interventions. increase and diversify the talent pool, including eas- Progress in elucidating the relationships between ing the financial burden of professional education, chronic oral inflammatory infections, such as peri- but additional incentives may be necessary. odontitis, and diabetes and glycemic control as well as other systemic conditions will require a similar Remove known barriers between people and oral intensified commitment to research. Rapid progress health services. This report presents data on access, can also occur with efforts in the area of the natural utilization, financing, and reimbursement of oral repair and regeneration of oral tissues and organs. health care; provides additional data on the extent of Improvements in oral health depend on multidisci- the barriers; and points to the need for public-private plinary and interdisciplinary approaches to biomed- partnerships in seeking solutions. The data indicate ical and behavioral research, including partnerships that lack of dental insurance, private or public, is one among researchers in the life and physical sciences, of several impediments to obtaining oral health care
12 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary and accounts in part for the generally poorer oral vital tissues and functions that are critical to total health of those who live at or near the poverty line, health and well-being across the life span. The mouth lack health insurance, or lose their insurance upon as a mirror of health or disease, as a sentinel or early retirement. The level of reimbursement for services warning system, as an accessible model for the study also has been reported to be a problem and a disin- of other tissues and organs, and as a potential source centive to the participation of providers in certain of pathology affecting other systems and organs has public programs. Professional organizations and gov- been described in earlier chapters and provides the ernment agencies are cognizant of these problems impetus for extensive future research. Past discover- and are exploring solutions that merit evaluation. ies have enabled Americans today to enjoy far better Particular concern has been expressed about the oral health than their forebears a century ago. But the nation’s children, and initiatives such as the State evidence that not all Americans have achieved the Children’s Health Insurance Program, while not man- same level of oral health and well-being stands as a dating coverage for oral health services, are a positive major challenge, one that demands the best efforts of step. In addition, individuals whose health is physi- public and private agencies and individuals. cally, mentally, and emotionally compromised need comprehensive integrated care. REFERENCES Use public-private partnerships to improve the oral Health Care Financing Administration (HCFA). health of those who still suffer disproportionately National Health Expenditures projections: 1998- 2008. Office of the Actuary. http://www.hcfa.gov/ from oral diseases. The collective and complementa- stats/NHE-Proj/. 2000 Apr 25. ry talents of public health agencies, private industry, U.S. Department of Health and Human Services social services organizations, educators, health care (USDHHS). Healthy People 2010 (Conference providers, researchers, the media, community lead- Edition, in two volumes). Washington; 2000 Jan. ers, voluntary health organizations and consumer U.S. General Accounting Office (GAO). Oral health in groups, and concerned citizens are vital if America is low-income populations. GAO/HEHS-00-72. 2000 not just to reduce, but to eliminate, health disparities. Apr. This report highlights variations in oral and general health within and across all population groups. Increased public-private partnerships are needed to PROJECT TEAM educate the public, to educate health professionals, Caswell A. Evans DDS, MPH to conduct research, and to provide health care serv- Project Director and Executive Editor Assistant Director, Los Angeles County Department ices and programs. These partnerships can build and of Health Services strengthen cross-disciplinary, culturally competent, Dushanka V. Kleinman DDS, MScD community-based, and community-wide efforts and Co-Executive Editor demonstration programs to expand initiatives for Deputy Director, National Institute of Dental and health promotion and disease prevention. Examples Craniofacial Research, National Institutes of Health of such efforts include programs to prevent tobacco William R. Maas DDS, MPH, MS use, promote better dietary choices, and encourage Chief Dental Officer, U.S. Public Health Service the use of protective gear to prevent sports injuries. Director, Division of Oral Health, In this way, partnerships uniting sports organiza- Centers for Disease Control and Prevention tions, schools, the faith community, and other groups Harold C. Slavkin DDS and leaders, working in concert with the health com- Director, National Institute of Dental and munity, can contribute to improved oral and general Craniofacial Research, National Institutes of Health Joan S. Wilentz MA health. Science Writer and Editor Roseanne Price ELS CONCLUSION Editor The past half century has seen the meaning of oral Marla Fogelman health evolve from a narrow focus on teeth and gin- Editor giva to the recognition that the mouth is the center of July 2000
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 13
PART ONE
What Is Oral Health?
The two chapters that follow explore the answer to this question, an answer that continues to evolve throughout the report. Oral health means more than healthy teeth and the absence of disease. It involves the ability of individuals to carry out essential functions such as eating and speaking as well as to contribute fully to society. Chapter 1, the introduction, explains how the meaning of oral health has developed in tandem with progress in understanding the two chief dental diseases—dental caries and periodontal diseases—which historically have been the major preoccupation of patients, providers, and research investigators alike. There is a marvelous success story here regarding the role of fluoride in preventing dental caries and the research that proved that dental caries and periodontal diseases are infections and can be prevented. These investigations were complemented by studies of the tissues of the mouth and adjacent areas—the craniofacial complex. Chapter 2 describes the tissues and organs of the craniofacial complex, providing a primer and guide to their essential features that emphasizes the ways they contribute to the richness of human experience, and at the same time protect and nurture the human body.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 15
CHAPTER 31
The Meaning of Oral Health
The intent of this first-ever Surgeon General’s report scores of other diseases and disorders that affect the on oral health is to alert Americans to the full mean- oral, dental, and craniofacial tissues, collectively ing of oral health and its importance in relation to known as the craniofacial complex. These are tissues general health and well-being. Great progress has whose functions we often take for granted, yet they been made in reducing the extent and severity of represent the very essence of our humanity. They common oral diseases, and recent history has seen allow us to speak and smile; sigh and kiss; smell, marked improvements in the nation’s oral and dental taste, touch, chew, and swallow; cry out in pain; and health, thanks to successful prevention measures convey a world of feelings and emotions through adopted by communities, individuals, and oral health facial expressions. They also provide protection professionals. However, not everyone is experiencing against microbial infections and environmental the same degree of improvement. What amounts to a insults. “a silent epidemic” of dental and oral diseases is The craniofacial tissues also provide a useful affecting some population groups—a burden of dis- means to understanding organs and systems in less ease that restricts activities in school, work, and accessible parts of the body. The salivary glands are a home, and often significantly diminishes the quality model of other exocrine glands, and an analysis of of life. saliva can provide telltale clues of overall health or The word oral, both in its Latin root and in com- disease. The jawbones are examples of other skeletal mon usage, refers to the mouth. The mouth includes parts. The nervous system apparatus underlying not only the teeth and the gums (gingiva) and their facial pain has its counterpart in nerves elsewhere in supporting connective tissues, ligaments, and bone, the body. but also the hard and soft palate, the soft mucosal tis- A thorough oral examination can detect signs of sue lining of the mouth and throat, the tongue, the nutritional deficiencies as well as a number of sys- lips, the salivary glands, the chewing muscles, and temic diseases, including microbial infections, the upper and lower jaws, which are connected to the immune disorders, injuries, and some cancers. skull by the temporomandibular joints. Equally Indeed, the phrase the mouth is a mirror has been important are the branches of the nervous, immune, used to illustrate the wealth of information that can and vascular systems that animate, protect, and nour- be derived from examining oral tissues. ish the oral tissues, as well as provide the connec- New research is pointing to associations between tions to the brain and the rest of the body. The genet- chronic oral infections and heart and lung diseases, ic patterning of development in utero further reveals stroke, and low-birth-weight, premature births. the intimate relationship of the oral tissues to the Associations between periodontal disease and developing brain and to the tissues of the face and diabetes have long been noted. This report assesses head that surround the mouth, structures whose these associations and explores mechanisms location is captured in the word craniofacial. that might explain these oral-systemic disease A major theme of this report is that oral health connections. means much more than healthy teeth. It means In parallel with the broadened meaning of oral being free of chronic oral-facial pain conditions, oral health, the meaning of health has evolved. The stan- and pharyngeal (throat) cancers, oral soft tissue dard definition of health, “freedom from disease, lesions, birth defects such as cleft lip and palate, and defect, or pain,” defines what health is not, rather
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 17 The Meaning of Oral Health than what it is. A more positive definition, one that tic, treatment, and prevention strategies has saved the World Health Organization established in 1948, billions of dollars per year in the nation’s annual states that health is a complete state of physical, men- health bill. Even more significant, the result is that tal, and social well-being, and not just the absence of far fewer people are edentulous (toothless) today infirmity. than a generation ago. The broadened meaning of oral health parallels The theme of prevention gained momentum as the broadened meaning of health. In 1948 the World pioneering investigators and practitioners in the Health Organization expanded the definition of 1950s and 1960s showed that not only dental caries health to mean “a complete state of physical, mental, but also periodontal diseases are bacterial infections. and social well-being, and not just the absence of The researchers demonstrated that the infections infirmity.” It follows that oral health must also could be prevented by increasing host resistance to include well-being. Just as we now understand that disease and reducing or eliminating the suspected nature and nurture are inextricably linked, and mind microbial pathogens in the oral cavity. The applica- and body are both expressions of our human biology, tions of research discoveries have resulted in contin- so, too, we must recognize that oral health and uing improvements in the oral health of Americans, general health are inseparable. We ignore signs and new approaches to the prevention and treatment of symptoms of oral disease and dysfunction to our dental diseases, and the growth of the science. detriment. Consequently, a second theme of the The significant role that scientists, dentists, den- report is that oral health is integral to general tal hygienists, and other health professionals have health. You cannot be healthy without oral health. played in the prevention of oral disease and disabili- Oral health and general health should not be ty leads to a third theme of this report: safe and effec- interpreted as separate entities. Oral health is a tive disease prevention measures exist that every- critical component of health and must be included in one can adopt to improve oral health and prevent the provision of health care and the design of disease. These measures include daily oral hygiene community programs. procedures and other lifestyle behaviors, community The wider meanings of oral and health in no way programs such as community water fluoridation and diminish the relevance and importance of the two tobacco cessation programs, and provider-based leading dental diseases, caries (tooth decay) and the interventions such as the placement of dental periodontal diseases. They remain common and sealants and examinations for common oral and pha- widespread, affecting nearly everyone at some point ryngeal cancers. It is hoped that this Surgeon in the life span. What has changed is what we can do General’s report will facilitate the maturing of the about them. broad field of craniofacial research so that gains in At the start of the twentieth century, most the prevention of craniofacial diseases and disorders Americans expected to be toothless by age 45, and can be realized that are as impressive as those most were. Expectations have changed, and most achieved for common dental diseases. people now assume that they will maintain their At the same time, more needs to be done to teeth over their lifetime, and take active measures to ensure that messages of health promotion and dis- do so. Researchers in the 1930s discovered that peo- ease prevention are brought home to all Americans. ple living in communities with naturally fluoridated In this regard, a fourth theme of the report is that water supplies had less dental caries than people general health risk factors, such as tobacco use and drinking unfluoridated water. But not until the end poor dietary practices, also affect oral and craniofa- of World War II were the investigators able to design cial health. The evidence for an association between and implement the community clinical trials that tobacco use and oral diseases has been clearly delin- confirmed their observations and launched a better eated in almost every Surgeon General’s report on approach to the problem of dental caries: prevention. tobacco since 1964, and the oral effects of nutrition Soon after, adjusting the fluoride content of commu- and diet are presented in the Surgeon General’s report nity water supplies was pursued as an important pub- on nutrition (1988). All the health professions can lic health measure to prevent dental caries. play a role in reducing the burden of disease in Although this measure has not been fully imple- America by calling attention to these and other risk mented, the results have been dramatic. Dental caries factors and suggesting appropriate actions. began to decline in the 1950s among children who Clearly, promoting health and preventing disease grew up in fluoridated cities, and by the late 1970s, are concepts the American people have taken to declines in decay were evident for many Americans. heart. For the third decade the nation has developed The application of oral science to improved diagnos- a plan for the prevention of disease and the promo-
18 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Meaning of Oral Health tion of health, embodied in the U.S. Department of autoimmune diseases; and the costs associated with Health and Human Services (2000) document, the unintentional and intentional injuries that so Healthy People 2010. As a nation, we hope to elimi- often affect the head and face. Then add the social nate disparities in health and prevent oral diseases, and psychological consequences and costs. Damage cancer, birth defects, AIDS and other devastating to the craniofacial complex, whether from disease, infections, mental illness and suicide, and the chron- disorder, or injury, strikes at our very identity. We see ic diseases of aging. To live well into old age free of ourselves, and others see us, in terms of the face we pain and infirmity, and with a high quality of life, is present to the world. Diminish that image in any way the American dream. and we risk the loss of self-esteem and well-being. Scientists today take that dream seriously in pur- Many unanswered questions remain for scien- suing the intricacies of the craniofacial complex. tists, practitioners, educators, policymakers, and the They are using an ever-growing array of sophisticat- public. This report highlights the research challenges ed analytic tools and imaging systems to study nor- as well as pointing to emerging technologies that may mal function and diagnose disease. They are com- facilitate finding solutions. Along with the quest for pleting the mapping and sequencing of human, ani- answers comes the challenge of applying what is mal, microbial, and plant genomes, the better to already known in a society where there are social, understand the complexities of human development, political, economic, behavioral, and environmental aging, and pathological processes. They are growing barriers to health and well-being. cell lines, synthesizing molecules, and using a new generation of biomaterials to revolutionize tissue repair and regeneration. More than ever before, they THE CHARGE are working in multidisciplinary teams to bring new The realization that oral health can have a significant knowledge and expertise to the goal of understand- impact on the overall health and well-being of the ing complex human diseases and disorders. nation’s population led the Office of the Surgeon General, with the approval of the Secretary of Health and Human Services, to commission this report. THE CHALLENGE Recognizing the gains that have been made in disease This Surgeon General’s report has much to say about prevention while acknowledging that there are popu- the inequities and disparities that affect those least lations that suffer disproportionately from oral health able to muster the resources to achieve optimal oral problems, the Secretary asked that the report “define, health. The barriers to oral health include lack of describe, and evaluate the interaction between oral access to care, whether because of limited income or health and health and well-being [quality of life], lack of insurance, transportation, or the flexibility to through the life span in the context of changes in take time off from work to attend to personal or fam- society.” Key elements to be addressed were the ily needs for care. Individuals with disabilities and determinants of health and disease, with a primary those with complex health problems may face addi- focus on prevention and “producing health” rather tional barriers to care. Sometimes, too, the public, than “restoring health”; a description of the burden policymakers, and providers may consider oral of oral diseases and disorders in the nation; and the health and the need for care to be less important than evidence for actions to improve oral health to be other health needs, pointing to the need to raise taken across the life span. The report also was to fea- awareness and improve health literacy. ture an orientation to the future, highlighting lead- Even more costly to the individual and to socie- ing-edge technologies and research findings that can ty are the expenses associated with oral health prob- be brought to bear in improving the oral health of lems that go beyond dental diseases. The nation’s individuals and communities. yearly dental bill is expected to exceed $60 billion in 2000 (Health Care Financing Administration 2000). However, add to that expense the tens of billions of THE SCIENCE BASE FOR THE REPORT dollars in direct medical care and indirect costs of This report is based on a review of the published chronic craniofacial pain conditions such as scientific literature. Where appropriate, standards temporomandibular disorders, trigeminal neuralgia, established to determine the quality of the evidence, shingles, or burning mouth syndrome; the $100,000 based on the study design and its rigor, were used. In minimum individual lifetime costs of treating cranio- addition, the strength of the recommendations, facial birth defects such as cleft lip and palate; the where they are made, is based on evidence of costs of oral and pharyngeal cancers; the costs of effectiveness for the population of interest. The scope
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 19 The Meaning of Oral Health of the review encompassed the international English complex in development and aging, how the tissues literature. Recent systematic reviews of the literature and organs function in essential life processes, and are referenced, as are selected review articles. A few their role in determining our uniquely human abili- referenced articles are in press, and there are ties. The later chapters elaborate further on the occasional references to recent abstracts and personal meaning of oral health. Of particular importance is communications. the discussion of oral health in relation to well-being The science base in oral health has been evolving and quality of life described in Chapter 6. over the past half century. Initial research in this area was primarily in the basic sciences, investigating mechanisms of normal development and pathology What Is the Status of Oral Health in in relation to dental caries and periodontal diseases. America? Prevention research has included controlled clinical Chapter 3 is a primer describing the major diseases studies, with and without randomization, as well as and disorders that affect the craniofacial complex. community trials and demonstration research. More Chapter 4 constitutes an oral health status report recent research has broadened the science base to card on the noninstitutionalized civilian population include studies of the range of craniofacial diseases of the United States, describing the magnitude of the and disorders and is moving from basic science to problem. It is based on the most recent national and translational, clinical, and health services research. state data available for a range of craniofacial dis- The clinical literature in the oral health sciences eases, disorders, and conditions. In general, the includes the full range of studies, from randomized national data provide information categorized by sex, controlled studies to case studies. Most of the litera- age, income (poor versus nonpoor), and broad racial ture includes cross-sectional and cohort studies, with and ethnic categories. In addition, the chapter some case-control studies. General reviews of the lit- includes a profile of the oral and general health of erature have been used for Chapters 2 through 10. selected population groups. These include racial and Chapter 4 includes both published and new analyses ethnic groups such as African Americans, Hispanics, of national and state databases that have been care- Asians, Native Hawaiians and Other Pacific Islanders, fully designed and for which quality assurance has and American Indians/Alaska Natives. The health been maintained by the Centers for Disease Control status of women and individuals with disabilities is and Prevention. Studies of smaller populations are highlighted. Although it is clearly desirable to also included where relevant. In Chapters 5 and 7, describe the health status of additional populations, evidence tables are presented for the discussion of data are insufficient or lacking for groups defined by the association of oral infections and systemic condi- sexual orientation or rural residency or categorized tions and for oral disease prevention and health pro- as homeless, migrant workers, or incarcerated. As an motion measures, respectively. Experts in the respec- initial step toward understanding the burden of dis- tive fields contributed to the report, and independent ease in relation to the provision of care, available data expert peer review was conducted for all sections of on the number of dental visits are provided. the report. The published literature related to the development of new technologies, their potential impact, and the need for further research are What Is the Relationship Between described in the course of addressing the requested Oral Health and General Health and futures orientation. Well-being? Chapters 5 and 6 address key issues in the charge— ORGANIZATION OF THE REPORT the relationship of oral health to general health and The report centers on five major questions, which well-being. Chapter 5 explores the theme of the have been used to structure the report into five parts. mouth as a mirror that in some measure can reflect general health or disease status. Examples are given of how oral tissues may signal the presence of dis- What Is Oral Health? ease, disease progression, or risk factor exposure lev- The meaning of oral health is discussed in the open- els, and how oral cells and fluids are increasingly ing pages of this chapter, and the interdependence of being used as diagnostic tools. This is followed by a oral health with general health and well-being is, as discussion of the mouth as a portal of entry for infec- noted, a recurrent theme throughout the volume. tions that can affect local tissues and may spread to Chapter 2 provides an overview of the craniofacial other parts of the body. The next section reviews the
20 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Meaning of Oral Health literature regarding emerging associations between and trends regarding the workforce in research, edu- oral diseases and disorders and diabetes, heart dis- cation, and practice. ease and stroke, and adverse pregnancy outcomes. Chapter 6 demonstrates the relationship between oral health and quality of life, presenting data on the What Are the Needs and Opportunities to consequences of poor oral health and altered appear- Enhance Oral Health? ance on speech, eating, and other functions, as well Chapter 10 looks at determinants of oral health in as on self-esteem, social interaction, education, career the context of society and across various life stages. achievement, and emotional state. Anthropological and Although theorists have proposed a variety of models ethnographic literature is introduced to underscore of health determinants, there is general consensus the cultural values and symbolism attached to facial that individual biology, the physical and socio- appearance and teeth. economic environment, personal behaviors and lifestyle, and the organization of health care are key factors whose interplay determines the level of oral How Is Oral Health Promoted and health achieved by an individual. The chapter Maintained and How Are Oral Diseases provides examples of these factors and, in the latter Prevented? half, illustrates their varying effects at different stages The next three chapters review how individuals, of the life span, with an emphasis on children and health care practitioners, communities, and the older Americans. Barriers and ways to raise the level nation as a whole contribute to oral health. Chapter of oral health that can be achieved at each life stage 7 reviews the evidence for the efficacy and effective- are presented. ness of oral health promotion and disease prevention Chapter 11 spells out in greater detail the prom- measures with a focus on community efforts in pre- ise of the life sciences in improving oral health in the venting dental disease. It continues with a discussion coming years in the context of changes in of the need to expand efforts in such areas as oral American—and global—society. The critical role of cancer prevention. genetics and molecular biology is emphasized. Chapter 8 explores the role of the individual and the health care provider in promoting and maintain- ing oral health and well-being. For the individual, A Call to Action this means exercising appropriate self-care and Chapter 12, the final chapter, summarizes the major adopting healthy behaviors. For the provider, it findings of the report and suggests actions to guide means incorporating the knowledge emerging from the next steps in enhancing the oral health of the the science base in a timely manner for prevention nation. The need for partnerships between public and diagnosis, risk assessment and risk management, and private sectors in carrying out a proposed and treatment of oral diseases and disorders. The National Oral Health Plan is emphasized. To ensure chapter focuses largely on the oral health care progress, these partnerships need to include individ- provider. The management of oral and craniofacial ual patients and the general public and to reflect all health and disease necessitates collaborations among population groups in the nation. All the health care a team of care providers to achieve optimal oral and disciplines need to be involved, along with industry, general health. academia, and government, as well as health care Chapter 9 describes the roles of dental practi- organizations, health professional associations, tioners and their teams, the medical community, and health insurers, and patient groups. United by the public health agencies at local, state, and national evidence that oral health is essential to general health levels in administering oral health care or reimburs- and well-being, the combined forces and collective ing for the costs of care. These activities are viewed wisdom of all interested parties and stakeholders can against the changing organization of U.S. health care make optimal oral health a reality for all people.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 21 Ophthalmic Branch
Olfactory Nerve
Thalamus
Processing Center
Olfactory Bulb
Olfactory Nerve Filaments
Trigeminal Nerve
Maxillary Branch
Mandibular Branch
Spinal Cord Tongue Nerves Taste Buds CHAPTER 32
The Craniofacial Complex
The first line a child draws on a face is usually the CONTACT AND COMMUNICATION mouth. The mouth is the center of communication and contact. Along with the eyes, ears, and nose, it is positioned near the brain, ensuring close integration Taste and Smell and coordination. We use the craniofacial complex— The developmental process by which vital nerve cen- the oral, dental, and the other craniofacial tissues ters came to be concentrated in the head, mouth, and that house the organs of taste, vision, hearing, and teeth began early in evolution. Even paramecia have smell—to experience and interact with the world mouths, as do worms, bugs, and all more complex around us. These sense organs have evolved to serve organisms. The mouth appears in the human embryo as superb information processors and aids to sur- during the third week of development. By the thir- vival. At the most elemental level, they enable us to teenth or fourteenth week, the fetal mouth can open sense our environment—from alerting us to preda- in response to stimulation of the lower lip. During tors or poisons to recognizing family, friends, or the next 2 months, the fetus will practice protruding prospective mates. and then pursing the lips, eventually achieving the Our ability to act on the nerve signals from these ability to suck vigorously at 29 weeks. In the mean- organs results from the abundant supply of paired time, inspiratory gasps, tongue movements, lip curl- cranial nerves that innervate the craniofacial tissues. ing, and swallowing responses will have been estab- No place in the body is as rich in both the number of lished (Wilentz 1968). sensory nerves and the ratio of motor nerves to mus- At birth, the taste buds are found on the roof of cle fibers as the face, and, within it, the mouth and the mouth and in the throat, as well as on the tip, teeth. The nerve circuits not only trigger protective sides, and back of the tongue. Taste buds, such as reflexes to make us blink, gape, and start in surprise, those on the tip of the tongue, are particularly subject but also enable us to perform countless functions we to wear and tear, and may be replaced every 2 weeks. take for granted. We speak and taste and chew and The total number of buds diminishes over time, but swallow. We express our feelings through smiles and there appears to be considerable reserve capacity, so scowls; we grimace and cry out in pain; we murmur there is normally little loss in the sense of taste as we endearments and kiss our loved ones. age. Beyond the special senses of vision, hearing, It has been said that taste is 90 percent smell, and taste, and smell, the craniofacial complex includes to some extent that is true. The taste cells that line nerve endings sensitive to the body’s position in the buds respond to only five known qualities: sweet, space and to touch, pressure, temperature, and pain. sour, salty, bitter, and glutamate. The experience of In sum, if the brain is the command-and-control cen- taste is a complex mixture of smell, temperature, ter of the body, evolution has ensured that the staff taste, and texture. reporting from the field and carrying out orders are The day-old newborn responds to sweet stimuli. stationed a strategic few inches away, in the craniofa- Suckling, the first oral function following the cry, is cial complex. enhanced by the presence of lactose, the sugar in breast milk. Liquids sweetened with sugar or honey have been used widely after birth to stimulate appetite, and later to wean children from breast-
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 23 The Craniofacial Complex feeding. The ability to recognize a sweet taste clearly receptors in the facial skin, joints, muscle, and oral has survival value, enabling the recognition and soft tissues, relayed to an image of the body mapped selection of carbohydrates—a vital source of energy. onto the sensory cortex of the brain, accounts for the The other taste modalities are also physiological- finesse with which we can discriminate the qualities ly important. A sour taste, for example, can signal an and precise location of these sensations. In particular, unripe fruit. However, sour substances may be the periodontal ligament, which anchors the teeth in involved in more subtle biochemistry, such as main- the jaws, is a tactilely sensitive tissue providing taining the body’s ion balance. They also satisfy thirst important feedback with regard to mastication and promote digestion by stimulating the secretion of (chewing) and dental occlusion (bite). As a test of saliva. A bitter taste is sufficiently unpleasant to this sensibility, a human hair placed between the tips evoke aversion, a useful response given that many of the fingers will rarely be sufficient to stimulate the bitter-tasting plant alkaloids are toxic. A salty taste nerve endings, but the same hair placed between the indicates the presence of sodium, which is essential lips or incisors will instantly be felt. to maintaining the fluid balance between cells and Pain and thermal sensitivity in the teeth are the extracellular compartment. transmitted through nerve endings in the pulp. Humans probably began as herbivores before the Because the pulp is in a narrow canal composed of advent of hunting and gathering and retained taste- connective tissue, blood vessels, and nerves and sur- discriminating ability as an evolutionary advantage. rounded by hard tissue, any infection or inflamma- The combination of taste and smell remains impor- tion that would normally cause tissue to swell creates tant not only for the maintenance of an optimal diet pressure on the pulpal nerves. That pressure, along (Young 1977), but also clearly for the pleasures of with bacterial or immune system products that stim- eating. ulate the nerve endings, produces the severe pain of Unlike taste cells, olfactory cells can respond to pulpal infections. many thousands of odorants, including ones that Neuroscientists have long studied oral-facial have been newly synthesized. Millions of olfactory pain, not only because of its importance in oral dis- receptors line a postage-stamp-sized area in the ease, but also because it provides an accessible model upper part of the nose, the olfactory epithelium. of pain elsewhere in the body. These investigations Although some smells may be judged universally as have greatly enriched our understanding of the basic unpleasant or foul, others are subject to learning and mechanisms of pain perception and modulation. cultural conditioning. For example, a ripe Roquefort They have helped delineate the complex pathways cheese may delight some people, but repel others. and multiple transmitters that convey pain signals to The primary receptor cells of the olfactory sys- the brain and spinal cord, as well as the mechanisms tem are neurons with fine hairs at one end that proj- and molecules that can modulate and inhibit noci- ect into the olfactory epithelium to pick up the olfac- ceptive input. These studies have also exploited new tory stimulus. The cells translate the stimulus to brain-imaging techniques to confirm the wide distri- nerve impulses transmitted to the brain along the bution of pain pathways and relay centers in the cere- two olfactory nerves—one from each nostril. bral hemispheres and cerebellum. Olfactory neurons have the unusual ability to regen- This research has generated new approaches to erate (although recent studies suggest that neurons the control of acute and chronic pain. These in other parts of the adult brain may also have this approaches include the use of nonsteroidal, anti- ability (Johansson et al. 1999). Olfactory pathways inflammatory drugs and long-acting local anesthetics are widely distributed in the brain, relaying to emo- for acute oral and dental pain, and the use of more tional and cognitive centers in the cortex. These con- potent drugs, drug combinations, and other kinds of nections undoubtedly account for the ability of odors therapies to treat chronic pain. Researchers have to stir old memories as well as stimulate a range of emphasized the importance of adequate pain control feelings, from fear to sexual arousal. in patients with chronic pain conditions. Otherwise, the constant barrage of signals can effect long-term changes in the brain that actually worsen the pain Touch, Temperature, and Pain (producing hyperalgesia) and cause normally non- The mouth also contains large numbers of nerve end- painful stimuli to be perceived as painful (a condition ings, similar to those found elsewhere in the body, called allodynia). Unrelieved chronic pain may also that are sensitive to touch (mechanoreceptors), hot suppress the immune system. and cold temperatures (thermoreceptors), and pain Recently, investigators discovered a link between (nociceptors). The dense concentration of these certain taste sensations, pain, and temperature. Their
24 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Craniofacial Complex findings indicate that capsaicin, the ingredient that palate is hard, formed by underlying bone, and serves makes hot peppers taste hot, binds to a receptor on as a shield against trauma to the face and head. The the surface of nociceptors that also responds to nox- posterior palate is soft, composed of muscles and ious heat. The researchers have cloned the gene for connective tissue that blend into the walls of the the capsaicin receptor (called vanilloid receptor 1); pharynx. Hanging from the rear of the soft palate is they believe it is involved in several chronic pain con- the uvula, a mass of muscle and connective tissue. ditions, especially those where inflammation plays a Under the tongue is the floor of the mouth, com- role, such as viral and diabetic neuropathy, rheuma- posed primarily of muscle and salivary glands. The toid arthritis, and oral mucositis pain caused by can- paired tonsils and adenoids, important components cer chemotherapy or radiation (Caterina et al. 1997). of the immune system, lie at the sides of the palate There is evidence that the prevalence of a num- and within the nasopharynx, respectively. ber of pain conditions varies by gender and that men The pharynx opens into channels leading either and women respond differently to different analgesic to the lungs for respiration or the esophagus for fur- drugs. These findings have prompted studies aimed ther digestion and passage to the stomach. This is a at determining whether there are sex differences in point of vulnerability: should food or some other pain anatomy and neurochemistry and whether (and obstruction lodge in the airway, it could lead to death how) nociception is affected by sex hormones. by asphyxiation. Externally, the oral cavity is bounded by the maxilla (the upper jaw bone), attached to the crani- Speech um, and the mandible (the lower jaw), attached to Human speech and language are the faculties that the temporal bone of the skull by the temporo- most distinguish us from other higher primates; they mandibular joint. are also the links that bind people together in diverse social groups and cultures. The Oral Mucosa Central to speech are laryngeal mechanisms involving the vocal cords. Equally critical are the res- Except for the teeth, the oral tissues are covered by a piratory system, the pharynx, and the nasal and oral mucous membrane called the oral mucosa, which cavities. The tongue is the most important structure varies in color from pink to brownish purple, of the peripheral speech mechanisms, working in depending on an individual’s skin color. Like skin, conjunction with the lips, teeth, and palate to pro- the oral mucosa acts as a major barrier against chem- duce a rich repertoire of sounds. Abnormalities in ical irritants and mechanical forces; it can even with- oral structures, from missing or malformed teeth and stand temperatures that would be painful to the skin. malocclusion to cleft lip and palate, can seriously In areas subject to chewing forces and food move- affect articulation. The movements of speech are ments, the surface layer is relatively hard, composed orchestrated by brain centers that coordinate the of epithelial cells filled with insoluble keratin, the muscles of mastication, facial expression, and jaw fibrous protein found in skin, nails, hair, and animal movements. horn. Elsewhere—in the mucosal lining of the Hearing impairments can also affect speech. To cheeks, for example—the surface layers are softer learn to speak, children must be able to hear others and more flexible, enabling the mobility we need to and monitor the feedback from their own voices. speak, chew, and make facial expressions. To aid in Congenital deafness and the serious hearing defects their barrier function, surface mucosal cells are associated with some craniofacial syndromes (see square-shaped and closely juxtaposed, with special- Chapter 3) can severely compromise speech ized organelles and cell products that promote cell- acquisition. cell adherence. The cells can also secrete sticky mol- ecules to plug gaps between them and further impede penetration by damaging chemicals or microorgan- THE ORAL CAVITY isms. Still another type of oral mucosa forms the peb- The mouth is the gateway to the body, performing bly surface of the back and sides of the tongue. dozens of functions that place high demands on its Lining the depths of these surface “papillae” are the unique hard and soft tissues. The point of entry is the taste buds. lips, which open into the oral cavity. The cheeks form Interestingly, the epithelium that lines the gingi- the sides of the cavity, and the roof is formed by the val surface completely lacks a keratin layer, yet this palate, which separates the mouth from the nose “naked” epithelium lies next to one of the most dense above and the pharynx (throat) behind. The anterior concentrations of bacteria to be found in the body.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 25 The Craniofacial Complex
Thus there is an opportunity for infectious agents or small particles and mixes it with saliva to form a their byproducts to penetrate the naked epithelial bolus for swallowing. barrier and initiate an inflammatory response, as hap- pens in gingival disease. Special cells in the basal layer of the oral mucosa The Salivary Glands generate replacements for surface cells as they Saliva is the mixed product of multiple salivary wear out. The painful oral ulcers and oral mucositis glands that lie under the mucosa. The three major that may develop in patients undergoing radiation glands are the paired parotid, submandibular, and or chemotherapy for head and neck cancer occur sublingual glands. The parotids, near the ears, secrete because these cancer-killing agents attack all a watery saliva into the mouth via ducts in the cells undergoing rapid turnover, whether healthy or cheeks. The walnut-sized submandibular glands lie cancerous. in the floor of the mouth and secrete a mucous fluid. The secretions of the almond-shaped sublingual The Teeth glands, also in the floor of the mouth but near the front, usually join with those of the submandibular The most prominent features of the oral cavity are the glands. Tiny minor salivary glands are scattered with- teeth. The 20 primary, or deciduous, teeth erupt gen- in the inner surfaces of the lips, cheeks, and soft and erally between 6 months and 2 to 3 years of age and hard palates; these secrete a mucinous saliva directly are succeeded by the permanent teeth beginning at onto the soft tissue surfaces. about age 6. The primary teeth enable infants to eat Saliva moistens food and provides mucinous pro- solid foods, aid speech development, and serve as teins to lubricate the bolus for ease of swallowing. placeholders for the permanent dentition. Keeping The combined movements of the tongue and cheeks primary teeth healthy is important, not only in spar- move the bolus to the back of the mouth. Saliva also ing an infant pain and disease, but also in preserving contains the enzyme amylase, which initiates the the dimensions of the dental arches and lessening the digestion of starch. By solubilizing food components risk of dental caries in the permanent teeth. A period and facilitating their interaction with the taste buds of mixed primary and permanent dentition occurs on the tongue and palate, saliva also contributes to from about ages 6 to 13. There are 28 to 32 perma- taste enhancement. nent teeth, depending on whether the 4 wisdom teeth (third molars), which are last to erupt, are pres- ent. Teeth are anchored in the jaws by the periodon- Tissue Protection tal ligament. This ligament connects the cervix The main function of saliva is not—as is commonly (neck) of the tooth, at the junction between the believed—to aid digestion, but to protect the integri- crown and root, to the gingiva. Below that, the liga- ty of the oral tissues. The moment a baby passes ment connects the outer layer of the tooth root, the through the birth canal and takes its first breath, cementum, to the adjacent alveolar bone (the part of microbes begin to take up residence in its mouth. the jaw bone that supports the tooth roots). Later, as the teeth erupt, additional bacteria establish The evolutionary forces that shaped the human colonies on tooth surfaces (Mandel 1989). Nearly mouth designed an apparatus for optimal food 500 species of microbes in all, most of which are not intake. The front four upper and lower incisor teeth harmful, will colonize the oral cavity (Kroes et al. are chisel-shaped for biting, cutting, and tearing and 1999). The microbes form a biofilm, in which their exert forces of 30 to 50 pounds. The canines, or numbers greatly exceed the number of human inhab- cuspids, are larger and stronger and have deeper itants on Earth. roots than the incisors; their conical cusps are Millions of years before there were toothbrushes, effective for ripping and tearing. The premolars, or dental floss, and water irrigators, evolutionary forces bicuspids, and the molars are designed for heavy generated protective mechanisms to combat poten- grinding and chewing, exerting forces as high as 200- tially harmful microbes. The physical flow of saliva plus pounds. The temporomandibular joint, the most helps to dislodge pathogens (viruses, bacteria, and complex synovial joint in the body, equips the yeast) from teeth and mucosal surfaces, just as tear- human jaw with extraordinary mobility, enabling ing and blinking, sneezing, and coughing and expec- movements in three dimensions. Its range of motion torating clear the eye, nose, and throat. Saliva can is controlled by three sets of muscles of also cause microbes to clump together so that they mastication—the masseter, temporalis, and pterygoid can be swallowed before they become firmly muscles (Oberg 1994). Chewing reduces food to attached. Saliva can destroy orally shed infected
26 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Craniofacial Complex white blood cells by virtue of its low salt content: the part because of the presence of a potent molecule, infected cells—of higher salt content—swell and epidermal growth factor (EGF) (Zelles et al. 1995). burst when exposed to fluids of lower salinity (Baron When swallowed, EGF can also protect the tissue et al. 1999). surfaces of the esophagus (Sarosiek et al. 1996). Salivary secretions, like tears and other exocrine Vascular endothelial growth factor (VEGF) has also gland secretions, are rich in antimicrobial compo- been identified in saliva. VEGF stimulates blood ves- nents. Certain molecules in saliva, such as lysozyme, sels and may contribute to the remarkable healing lactoferrin, peroxidase, and histatins, can directly kill capacity of oral tissues (Taichman et al. 1998, Zelles or inhibit a variety of microbes; the histatins are par- et al. 1995). ticularly potent antifungal agents (Xu et al. 1991). Several salivary proteins exhibit antiviral properties, Caries Protection including secretory leukocyte protease inhibitor Saliva also guards against dental caries (tooth decay), (SLPI), recently discovered to have the ability to the disease that has been the greatest threat to teeth. inhibit HIV from invading cells (Shugars and Wahl Caries is caused by bacteria that generate acids that 1998). attack tooth mineral (see Chapter 3). The buffering The ability of saliva to limit the growth of systems in saliva, augmented by the neutralizing pathogens, in some instances even preventing them components urea and ammonium, counter the acid from establishing a niche in the biofilm community formation. The physical flow of saliva also helps in the first place, is a major determinant of general as flush out sugars and food particles that are the bacte- well as of oral health. When salivary flow is compro- rial food source. Mineral salts in saliva—calcium and mised, the gateway to the body can open wide to phosphate—can remineralize tooth enamel, effec- local as well as to systemic pathogens. tively reversing the decay process. This regenerative function is greatly enhanced by the presence of fluo- Barrier and Buffering Properties ride in saliva. Finally, saliva forms a film on teeth Salivary components protect oral tissues in other made up of selectively adsorbed proteins that have a ways as well. Mucins have unique properties that high affinity for tooth mineral. This acquired pellicle enable them to concentrate on mucosal surfaces and is insoluble and limits the diffusion of acids into the provide an effective barrier against drying and physi- teeth and the dissolution of tooth mineral (Lamkin cal and chemical irritants (Tabak 1995). They act as and Oppenheim 1993). natural waterproofing, control the permeability of the tissue surfaces, and help limit penetration of potential irritants and toxins in foods and beverages, The Immune System as well as toxic chemicals and potential carcinogens The salivary glands and the oral mucosa, along with in tobacco and tobacco smoke and from other the body’s other mucosal linings and the lymphatic sources. This barrier function complements the bar- circulation, constitute a major component of the rier formed by the oral mucosa itself. The mucosa has body’s defense system—the mucosal immune system a specific permeability coefficient that can change (Mestecky 1987). When the area of the oral mucosa under various conditions of stress, nutritional status, is combined with the areas of the mucosal linings and and other challenges. passageways of the respiratory, gastrointestinal, uri- Saliva contains several effective buffering sys- nary, and genital tracts, the total represents the largest tems that can help maintain a normal pH when acidic surface area of the body—nearly 400 square meters, foods and beverages are introduced, thereby protect- or 200 times larger than the total skin area. ing oral tissues against acidic attack. When swal- The great majority of infectious diseases affect, lowed, these buffers protect the esophagus, helping or are acquired through, mucosal surfaces. Immune neutralize the reflux acids of conditions such as cells that line the mucous membranes throughout heartburn and hiatal hernia (Sarosiek et al. 1996). the body secrete antibodies targeted to specific disease-causing microbes (Mandel and Ellison 1985). Wound Healing The mucosal immune system works in concert with Saliva also contains molecules that nurture and pre- the bloodborne immune system to detect and dispose serve the oral tissues, even helping them to repair of foreign substances and invading microbes. and regenerate (Mandel 1989, Tabak 1995, Zelles et The two components of the immune system con- al. 1995). Experimental studies have shown that sist of molecules and cells that provide both broad wound healing is significantly enhanced by saliva, in and specific defense mechanisms. In the broad group
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 27 The Craniofacial Complex are some circulating white blood cells (monocytes Much of what we know about the immune sys- and granulocytes) associated with the inflammatory tem has come from studies of serum factors, but response. These cells migrate to a site of injury or research in the last two decades has generated much infection and move into damaged tissues manifest- new information about mucosal immunity (McGhee ing the four signs of inflammation: swelling, heat, and Kiyono 1999). The mucosal immune system can redness, and pain. The cells promote an increase in be divided into inductive and effector compartments. blood flow to begin the healing process, and they The nasal-associated lymphoreticular tissues (NALT) recruit other cells able to engulf and dispose of the in the nasopharyngeal area (which includes the ton- offending organism. sils) and the gut-associated lymphoreticular tissues The specific immune system is associated with (GALT) in gut tissue are inductive regions, where two major classes of immune cells: T cells and B cells. foreign invaders are encountered. If, for example, T cells react to antigens (proteins associated with infectious bacteria are swallowed, they can stimulate microbes or irritants) and can stimulate B cells to immune cells in GALT to circulate T and B cells make antigen-specific antibodies. These are the Y- through the lymph system to various effector sites in shaped molecules called immunoglobulins. the gastrointestinal and upper respiratory tracts and T cells are the instruments of cell-mediated in the salivary and other exocrine glands. The B cells immunity; they are able to detect telltale surface in the gland produce antibodies, designated S-IgA, to markers on diseased or foreign cells that distinguish which is attached a secretory component (Mestecky them from normal body cells. Some T cells can kill and Russell 1997). These antibodies are the domi- infected cells and cancer cells directly. T cells are also nant type found in saliva, tears, breast milk, and involved in the rejection of organ transplants. colostrum and in the gastrointestinal and genitouri- Certain T cells are memory cells, preserving the nary tracts. information from earlier encounters with specific The uses of the mucosal immune system extend pathogens. Thus they are able to initiate more rapid beyond its normal surveillance and defense func- and effective responses in the event of a repeat tions. The tissues can be used as routes for delivery encounter with the pathogen. Helper T cells assist in of oral (swallowed) or nasal (inhaled) vaccines, as activating killer T and B cells. It is the loss of helper sites for gene transfer to augment host defenses, and T cells that leads to the many infections that cause ill- as a means of invoking oral tolerance—the suppres- ness and death in HIV disease. Still another group of sion of overactive or inappropriate immune respons- T cells, suppressor T cells, moderates the activities of es that occur in chronic inflammatory and autoim- both B and T lymphocytes. mune diseases (Baum and O’Connell 1995, Activated T cells generate and release Hajishengallis and Michalek 1999). cytokines—potent families of proteins, such as the interleukins, that can stimulate immune cells to divide, migrate, attack, and engulf invaders or partic- CRANIOFACIAL ORIGINS ipate in the inflammatory response. Other cytokines The extraordinary successes of research in molecular include varieties of tumor necrosis factor and genetics over the past decade, coupled with the adhesins (proteins that facilitate the binding of National Institutes of Health’s project to map and immune cells to each other or to blood vessel lin- sequence the human genome, have proved to be a ings). Feedback mechanisms provide a system of boon in understanding craniofacial development. checks and balances to regulate cytokine production. The use of automated gene-sequencing equipment, The immune system interacts with the nervous the Internet availability of genome databases, and the and endocrine systems. For example, immune ability to transfer genes or create “knockout” ani- cytokines secreted into the brain can induce the fever mals—in which a gene of interest has been eliminat- associated with infection: the high temperature may ed—have greatly facilitated progress. The events that help destroy the infectious agent. The brain’s govern the transformation of a fertilized human egg response to stress also has repercussions for the cell into a healthy newborn with all organs and sys- immune system. The hypothalamus-pituitary-adre- tems in place are being unfolded at the molecular nal axis is a major pathway activated in response to level. Families of master and regulatory genes have stress, which results in the secretion of cortisol, the been identified, and their role in controlling how the stress hormone, from the adrenal glands. Cortisol body’s general shape and specialized tissues and promotes the body’s fight-or-flight mechanisms, but organs are formed is coming to light. via feedback loops, cortisol acts to depress immune reactions.
28 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Craniofacial Complex
Early Development bomeres, segments of future nerve tissue arranged in an orderly fashion so that the first two rhombomeres The Three Germ Cell Layers innervate branchial arch 1, and so on. During the formation of the midbrain and hind- By the time the face and the mouth are ready to form, brain, cranial neural crest cells migrate into the the human embryo is in the third week of develop- developing facial areas and differentiate into neu- ment. The embryo has evolved from a sphere to an ronal and nonneuronal tissues. The neuronal tissues oval two-layered disk with a head-to-tail orientation. include the clusters of nerve cells (ganglia) that lie The outer layer is the epiblast and will become the adjacent to the spinal cord, parts of the ganglia of ectodermal germ layer. A narrow groove, called the four cranial nerves, and two of the meningeal layers primitive streak, extends from the tail toward the of the brain. The nonneuronal tissues include major center of the disk, where it ends in a spot surround- bones, cartilage, the dentin and cementum of teeth, ing a small depression called the primitive pit. and the various types of connective tissues of the Epiblast cells migrate toward the streak and pit, craniofacial complex, as well as the muscles of the detach from the surface, and slip downward to form eye. The branchial arches give rise to the bones, car- the two additional germ cell layers, the mesoderm tilage, nerves, muscles, and blood supply of succes- and, below that, the endoderm. sive segments of the head and neck. The ectodermal layer gives rise to tissues that relate the body to the outside world: the nervous sys- The Face and Mouth tem; the sensory epithelium of the ears, nose, and eyes; skin, hair, nails, salivary glands, tonsils, and The branchial arches play a key role in the formation tooth enamel; and the pituitary, mammary, and sweat of the facial structures. Toward the end of the fourth glands. At the head end, the mesodermal layer gives week of gestation, a primitive mouth appears. This rise to a primitive connective tissue, called mes- “stomadeum” is flanked by a series of swellings, or enchyme, which will interact with the ectoderm to prominences, derived from the first pair of branchial form parts of the head and mouth. The remaining arches. A single frontonasal prominence forms the mesoderm develops into the muscle, cartilage, bone, upper border of the stomadeum. On either side of and subcutaneous skin tissue of the rest of the body. this prominence are two thickened regions of ecto- The mesoderm is also the origin of the vascular and derm—the nasal placodes. At the sides of the stom- urogenital systems (except for the bladder), the adeum and below it are pairs of maxillary and spleen, and the adrenal cortex. The innermost, endo- mandibular prominences. dermal layer provides the linings of the gut, the res- In the course of the next 3 weeks, differential piratory system, bladder, liver, pancreas, thyroid and growth and movements of the various prominences parathyroid glands, and parts of the middle ear. and fusions of tissues that come together at the mid- line will sculpt the bridge, crest, sides, and tip of the Neural Tube and Neural Crest nose, the upper and lower lips, and the upper and Further migrations and descending movements of lower jaws (Bhaskar and Orban 1990, Sadler and cells result in the formation of the notochord, a solid Langman 1995). cord of cells along the midline that will become the The external merger at the midline of a pair of backbone. The ectoderm above the notochord next prominences that helps to form the nose occurs thickens to form a neural plate. The sides of the plate inside the mouth as well, resulting in an intermaxil- curve up and inward to form a neural tube, beginning lary segment that will contribute to the formation of at the head, with fusion completed by the end of the the four upper incisors and parts of a small triangu- fourth week. The tail end of the tube will form the lar-shaped primary palate and the upper jaw. The spinal cord; the head end differentiates into the three bulk of the palate, the secondary palate, forms from parts of the primitive brain: the forebrain, midbrain, shelflike outgrowths of the maxillary prominences. and hindbrain. These growths appear in the sixth week, and in the What happens next is of central importance to following week fuse along the midline above the the craniofacial complex: cells that were at the edges tongue. (The tongue appears at approximately 4 of the neural plate break away to form neural crest weeks, the front two-thirds forming from the first cells, which migrate to the forebrain area and to the branchial arch, and the posterior third from parts of nearby branchial arches, a series of swellings on the second, third, and fourth branchial arches.) The either side of the embryo, adjacent to the hindbrain. palatal shelves also fuse with the primary palate The hindbrain becomes organized into eight rhom- along a triangular border called the incisive foramen.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 29 The Craniofacial Complex
This border is considered the line of division among come from detailed studies of species ranging from clefting abnormalities. Lateral cleft lip, cleft upper fruit flies, nematodes, and zebrafish to frog, chick, jaw, and clefts between the primary and secondary mouse, and human embryos. In many cases, the palates are associated with defects anterior to the simpler organism has been the source of discoveries incisive foramen. Cleft palate and cleft uvula occur of genes or developmental processes that are highly because of defects affecting closure of the palatal conserved in the course of evolution (Alberts et al. shelves posterior to the foramen (Bhaskar and Orban 1994). 1990, Sadler and Langman 1995). Research on the fruit fly, for example, has revealed that particular families of genes are respon- The Teeth sible for the fundamental head to thorax to tail pat- terning of the fly’s body. Another set of genes deter- Tooth development begins in the sixth week with the mines the back-to-front positioning of organs, and a appearance of an epithelial band lining the upper and third set subdivides this general body plan into a lower jaws. A part of the band develops into a dental series of discrete segments. With further develop- lamina, which forms a series of projections into the ment, yet another family of genes confers a position- jaw. These are the tooth buds and correspond to the al memory on the cells within a segment. These sites of deciduous teeth. The epithelial tissue of the “homeotic selector” genes ensure that cells in one bud develops into an enamel organ that forms a cap part of a particular segment “know” that they are des- over tissue that is differentiating in the jaw to become tined to be wings and not legs, or to be eyes and not the dental papilla. The two structures—the enamel antennae. In flies the homeotic genes are known as organ, derived from the epithelium, and the dental Hom genes. Their arrangement on the fly chromo- papilla, derived from neural crest mesenchyme— some is ordered with genes at one end of the chro- constitute the tooth germ. mosome specifying the developmental destiny of With further development, the tooth germ cells in the most anterior segments of the fly’s body assumes a bell shape and separates from the oral and genes at the other end specifying the fate of cells epithelium. At the same time, the internal epithelial in the most posterior segments. layer of the enamel organ undergoes a series of In the course of evolution, mammals have devel- infoldings that will shape the future crown of the oped four overlapping sets of positional memory tooth. gene clusters homologous to the fly’s single Hom Mineralization of the tooth begins at the late bell complex. The four mammalian Hox gene families are stage. The first mineralized tissue to form is dentin, ordered in a similar anterior-posterior fashion along which provides the foundation for the deposition of four different chromosomes. The mammalian genes enamel. The differentiation of the odontoblasts (the appear to operate like the Hom genes: they code for dentin-producing cells) depends on organizing DNA-binding proteins that control gene expression. influences from enamel organ cells. Thus the The similarity from fly to human is particularly evi- development of these two different hard tissues is a dent when maps of the expression domains of Hom mutually dependent process. genes in anterior segments of the fly embryo are com- As dentin is laid down, the odontoblasts move pared to maps of Hox gene expression as seen in the toward the center of the papilla, trailing thin cellular rhombomeres and branchial arches of mammals. processes, which become embedded in the mineral- Molecular genetic studies of flies and other non- ized matrix. When dentin formation is completed, mammalian species show some variation in how and dentin completely surrounds the pulp, protecting it when the basic body patterns and repeating segments from injury. The enamel layer of the tooth starts to are formed. Sometimes the head-to-tail pattern is laid form soon after the first dentin appears, synthesized down in the egg cell before fertilization—dictated by by special enamel-forming cells, or ameloblasts, egg polarity genes. Although egg polarity genes do which develop from the enamel organ. The tooth not operate in humans, mutations have been found root, and its outer layer of cementum, form only after in a human gene homologous to the fly egg polarity the crown erupts. gene and account for serious syndromes in which there are defects in anterior organs, such as the pitu- itary gland and heart. Genetic Controls None of these developmental controls work in Only in the last decade have scientists begun to isolation. Much remains to be understood about the understand how certain genes and gene families genetic clock that determines when and where devel- control embryonic development. Their findings have opmental genes act, how they interact, and what
30 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Craniofacial Complex mechanisms are used to sustain as well as terminate lifestyle (including medical and dental history) cre- their function. The systems that govern programmed ates a unique craniofacial portrait, one that inspired cell death are also important: normal development George Orwell to remark, “By the age of fifty, a man depends as much on the elimination of cells as it does gets the face he deserves.” on the orderly movement, proliferation, and differen- tiation of cells. When it comes to processes that control the The Teeth development of particular tissues or organs—bones, One of the more dramatic discoveries in biomedical skin, or heart—developmental biologists observe science in the twentieth century has been the realiza- that there is often an “organizer,” that is, a cell or set tion that tooth loss is not an inevitable consequence of cells that initiates the process. The organizer of aging, but the result of disease or injury. Aging induces changes in the behavior of neighboring cells through cell-cell interactions, so that these cells does produce a number of other dental changes, develop into the specified type—bone or skin or however. Teeth change in form and color with age. heart muscle. The interaction with the neighboring Wear and attrition alter the biting and chewing sur- cell is often in the form of a signaling molecule, such faces, as do food choices and oral habits. The altered as a growth factor (e.g., transforming growth factor surface structure produces a different pattern of light , epidermal growth factor, fibroblast growth factor) reflection in older teeth, resulting in some yellowing that attaches to a receptor on the surface membrane and a general loss of translucency (Mjor 1986). Fully of the recipient cell. This interaction is translated to formed enamel is acellular, hence there is no meta- the interior of the cell, where a chain of molecular bolic activity or turnover as occurs in skin, for exam- interactions eventually reaches the cell nucleus to ple. Dentin and cementum have limited cellular effect gene expression. One of the more startling dis- activity. In contrast, tooth pulp and periodontal liga- coveries of the past decade has been the finding that ment undergo relatively high levels of tissue a series of mutations, each associated with a change turnover. in only one nucleotide of the gene for the fibroblast Tooth surfaces can be eroded by chemical growth factor receptor—a so-called point muta- dissolution from fruit acids and from acids from tion—accounts for a range of organ defects seen in at sugars in foods such as soft drinks and candies. This least a half dozen craniofacial syndromes. destructive process can occur at any age, resulting in Interestingly, all these syndromes include craniosyn- ostosis, a premature closure of the bones that form loss of translucency as well as some tissue loss from the skull. demineralization (Zero 1996). Countering the erosive forces are the natural components in saliva that help remineralize the enamel surface, a process THE AGING OF CRANIOFACIAL that is enhanced when fluoride is present (see TISSUES “Caries Protection” above). Normal aging describes the developmental processes The cementum increases in thickness with age. that begin at conception, continue in childhood, and Gingival recession caused by normal aging exposes merge gradually into maturation and senescence. The the cementum to the oral environment (and is the milestones of development such as the age when origin of the expression “long in the tooth”). The children teethe, begin to walk, talk, enter puberty, exposed cementum can often be worn away mechan- attain their full height, and so on, are under genetic ically, exposing the underlying dentin, which can and hormonal controls, subject to important envi- then become hypersensitive. Dentin responds ronmental factors such as nutrition and exercise. through a series of protective changes that work to Despite the complexity and interrelationships of the variables involved, a reasonably accurate picture of close off the connections between dentin and nerves normal age-related changes in the craniofacial com- in the pulp, reducing transmission of painful stimuli. plex is emerging (Ship 1999). Barring major illness or injury, destructive The Jaws behaviors, or severe or unusual environmental cir- cumstances, the cells, tissues, and fluids of the face The bones of the maxilla and mandible that support and mouth are hardy survivors, eminently durable the teeth, called the alveolar processes, are, like bone and functional over a long life span. For any given elsewhere in the body, subject to cellular turnover individual the combination of life experience and in a coordinated process of bone resorption and
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 31 The Craniofacial Complex formation. Alveolar bone is well adapted to or a side effect of medication and not dismissed as a mechanical stresses, and changes continuously natural by-product of aging. during facial growth, tooth eruption, tooth wear, and The distribution of motor fibers in the craniofa- tooth loss. This lifelong adaptation makes cial tissues is also abundant and sufficiently fine- orthodontic treatments to reposition teeth in adults tuned to allow for a full range of movement of the possible. tongue, jaws, and oral-facial muscles. There is some Because the primary function of alveolar bone is loss of muscle tone in aging, along with changes in to support the teeth, the loss of teeth will lead to tongue shape and function in articulating specific bone atrophy, making prosthetic replacements diffi- speech sounds. Subtle changes may also occur in cult. The rate of bone loss is affected by both local preparing food for swallowing. As with sensory disease such as periodontal disease and systemic con- changes, these developments do not seriously inter- ditions such as osteoporosis (Bhaskar 1991). fere with motor function in healthy older adults.
The Oral Mucosa The Salivary Glands The oral mucosa appears to age in much the same Studies of normative aging indicate that individuals way as skin does. The oral epithelium thins and vary in the quantity of “whole” saliva they produce. becomes less hydrated, increasing vulnerability to Whole saliva consists of the secretions of the various injury. The rate of cell division is slower, but the basic salivary glands plus other oral contents, such as cells cell architecture and patterning of cell types through- shed from the mucosa. These individual patterns are out the oral cavity are maintained. It is not certain to consistent across the life span. In healthy adults, what extent these changes are a natural consequence there is no diminution in the production of saliva of aging; they may be due to altered protein synthe- from the major salivary glands in the course of aging. sis or lowered responsiveness to regulatory mole- This constancy may seem surprising given the cules. They may also be an effect of diminished vas- morphological changes documented in aging salivary cularity, which could limit cellular access to oxygen glands. Both the parotid and the submandibular and nutrients (Mjor 1986). glands lose between 20 and 30 percent of their essen- Overall immune system function deteriorates tial tissue volume in the course of aging. The loss pri- with age, and it is likely that mucosal immunity does marily affects the acinar components, the cells that as well. Such a decline could result in an increased secrete saliva. Increases in the number of ductal cells risk of transmission of infectious agents across the and in fat, vascular, and connective tissues compen- mucosa and probably contributes to delayed wound sate for this loss, however—evidence of the remark- healing in oral tissues with aging. able functional reserve capacity of the glands, which enables them to maintain a stable salivary output across the life span (Baum 1986). Sensory and Motor Functioning In contrast, studies of age-related changes in the The high density of sensory nerve endings in the chemistry of salivary secretions suggest that there are craniofacial tissues and their functional abilities are significant reductions in the concentration of mucins well-preserved in aging. There may be minor increas- from the submandibular gland (Navazesh et al. es in threshold detection levels or in judgments of 1992), which could result in reduced lubrication and intensity, but, for the most part, sensory cells can contribute to a sensation of mouth dryness. There are turn over or have a built-in reserve capacity that also subtle changes in the protective ability of sali- allows for near-optimal functioning in aging. The vary secretory IgA antibody (Smith et al. 1987). exception is olfaction, which declines in both men and women with age. This decrement in smell may FINDINGS lead to some dissatisfaction with how foods taste and Natural selection has served Homo sapiens well in increased use of flavor enhancers to compensate. But evolving a craniofacial complex with remarkable for most people, the ability to enjoy food is not functions and abilities to adapt, enabling the organ- appreciably diminished as time goes by. Any dramat- ism to meet the challenges of an ever-changing envi- ic change in sensory function—complaints of a con- ronment. An examination of the various tissues tinued unpleasant taste or smell or the sudden com- reveals elaborate designs that have evolved to serve plete loss of a sensory modality—should be taken the basic needs and functions of a complex mammal seriously as a sign of possible oral or systemic disease as well as those that are uniqely human, such as
32 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Craniofacial Complex speech. The rich distribution of nerves, muscles, and Johansson CB, Momma S, Clarke DL, Risling M, blood vessels in the region as well as extensive Lendahl U, Frisen J. Identification of a neural stem endocrine and immune system connections is an cell in the adult mammalian central nervous system. indication of the vital role of the craniofacial complex Cell 1999 Jan 8;96(1):25-34. in adaptation and survival over a long life span. In Kroes I, Lepp PW, Relman DA. Bacterial diversity with- particular, in the human subgingival crevice. Proc Natl Acad Sci USA 1999 Dec 7;96(25):14547-52. Genes controlling the basic patterning and Lamkin MS, Oppenheim FG. Structural features of sali- segmental organization of human development, and vary function. Crit Rev Oral Biol Med 1993;4(3- specifically the craniofacial complex, are highly con- 4):251-9. served in nature. Mutated genes affecting human Mandel ID. The role of saliva in maintaining oral home- development have counterparts in many simpler ostasis. J Am Dent Assoc 1989 Aug;119:298-304. organisms. Mandel ID, Ellison SA. The biological significance of There is considerable reserve capacity or the nonimmunoglobulin defense factors. In: Pruit K, redundancy in the cells and tissues of the craniofacial Tenovuo J, editors. The lactoperoxidase system. New complex, so that if they are properly cared for, the York: Marcel Dekker; 1985. p. 1-14. structures should function well over a lifetime. McGhee JR, Kiyono H. The mucosal immune system. In: Paul WE, editor. Fundamental immunology. 4th The salivary glands and saliva subserve tast- ed. New York: Lippincott-Raven; 1999. p. 909-45. ing and digestive functions and also participate in the Mestecky J. The common mucosal immune system and mucosal immune system, a main line of defense current strategies for induction of immune respons- against pathogens, irritants, and toxins. es in external secretions. J Clin Immunol 1987 Salivary components protect and maintain Jul;7(4):265-76. oral tissues through antimicrobial components, Mestecky J, Russell MW. Mucosal immunoglobulins buffering agents, and a process by which dental and their contribution to defense mechanisms: an enamel can be remineralized. overview. Biochem Soc Trans 1997 May;25(2):457- 62. Mjor IA. Age changes in the teeth. In: Holm-Pedersen P, REFERENCES Löe H, editors. Geriatric dentistry. Copenhagen: Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson Munksgaard; 1986. p. 94-101. JD. Cellular mechanisms of development. In: Navazesh M, Mulligan RA, Kipnis V, Denny PA, Denny Molecular biology of the cell. 3rd ed. New York: PC. Comparison of whole saliva flow rates and Garland; 1994. p. 1036-137. mucin concentrations in healthy Caucasian young Baron S, Poast J, Cloyd MW. Why is HIV rarely trans- and aged adults. J Dent Res 1992 Jun;71(6):1275-8. mitted by oral secretions? Saliva can disrupt orally Oberg S. Dissector for Netter’s atlas of human anatomy: shed, infected leukocytes. Arch Intern Med 1999 Feb discussions. Vol 2. Summit (NJ): Ciba-Geigy; 1994. 8;159(3):303-10. Sadler TW, Langman J. Langman’s medical embryology. Bhaskar SN. Maxilla and mandible (alveolar process). Baltimore: Williams & Wilkins; 1995. In: Bhaskar SN, editor. Orban’s oral histology and Sarosiek J, Scheurich CJ, Marcinkiewicz M, McCallum embryology. St. Louis (MO): Mosby Year Book; 1991. RW. Enhancement of salivary esophagoprotection: p. 239-59. rationale for a physiological approach to gastroe- Bhaskar SN, Orban BJ. Orban’s oral histology and sophageal reflux disease. Gastroenterology embryology. 11th ed. St. Louis (MO): Mosby Year 1996;110:675-81. Book; 1990. Chapter 1, Development of the face and Ship JA. The oral cavity. In: Hazzard WR et al., editors. oral cavity. Principles of geriatric medicine and gerontology. Baum BJ. Age changes in salivary glands and salivary New York: McGraw-Hill; 1999. secretions. In Holm-Pederson P, Löe H, editors. Shugars DC, Wahl SM. The role of the oral environment Geriatric dentistry. Copenhagen: Munksgaard; 1986. in HIV-1 transmission. J Am Dent Assoc 1998 p. 114-22. Jul;129(7):851-8. Baum BJ and O’Connell BC. The impact of gene thera- Smith DJ, Taubman MA, Ebersole JL. Ontogeny and py on dentistry. J Am Dent Assoc 1995:126:179-89. senescence of salivary immunity. J Dent Res 1987 Caterina MJ, Schumacher MA, Tominaga M, Rosen TA, Feb(2);66:451-6. Levine JD, Julius D. The capsaicin receptor: a heat- Tabak L. In defense of the oral cavity: structure, biosyn- activated ion channel in the pain pathway. Nature thesis, and functions of salivary mucins. Annu Rev 1997;389:816-24. Physiol 1995;57:547-64. Hajishengallis G, and Michalek SM. Current status of a mucosal vaccine against dental caries. Oral Microbiol Immunol 1999;14:1-20.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 33 The Craniofacial Complex
Taichman NS, Cruchley AT, Fletcher LM, Hagi-Pavli EP, Bethesda (MD): National Institutes of Health, Public Paleolog EM, Abrams WR, Booth V, Edwards RM, Health Service, U.S. Department of Health, Malamud D. Vascular endothelial growth factor in Education and Welfare Report no. NIH 77-1068; normal salivary glands and saliva: a possible role in 1977. p. 399-417. the maintenance of mucosal homeostasis. Lab Invest Zelles T, Purushotham KR, Macauley SP, Oxford GE, 1998 Jul;78(7):869-75. Humphreys-Beher MG. Saliva and growth factors: Wilentz J. The senses of man. New York: Thomas Y. the fountain of youth resides in us all. J Dent Res Crowell; 1968. 1995 Dec;74(12):1826-32. Xu T, Levitz SM, Diamond RD, Oppenheim FG. Zero DT. Etiology of dental erosion—extrinsic factors. Anticandidal activity of major human salivary his- Eur J Oral Sci 1996 Apr;104(2 Pt 2):162-77. tatins. Infect Immun 1991 Aug;59(8):2549-54. Young PT. Role of hedonic processes in development of sweet taste. In: Weiffenbach, JM, editor. Taste and development—the genesis of sweet preference.
34 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL PART TWO
What Is the Status of Oral Health in America?
To begin to answer this question, Chapter 3 guides the reader through a discussion of oral diseases and disorders in such categories as infections, inherited disorders, and neoplasms. Whether or not an individual succumbs to the disease or disorder in question depends on subtle interactions of genetic, environmental, and behavioral variables. Risk factors common to systemic diseases and disorders, such as tobacco use, excessive alcohol use, and inappropriate dietary practices, also contribute to many oral diseases and disorders. As more details on the causes of diseases unfold, specific strategies for disease prevention can be developed. Chapter 4 describes the magnitude of the problem facing the nation due to oral diseases and disorders. These conditions are prevalent and complex, and they affect individuals across the life span. Although major improvements have been seen nationally for most Americans, disparities exist in some population groups as classified by age, sex, income, and race/ethnicity. National and state-based epidemiologic data presented against the backdrop of demographic and socioeconomic variables provide some information on racial and ethnic minorities, but serious shortcomings exist. The paucity of data at national, state, and local levels extends to other populations, including indi- viduals with disabilities, those with alternate sexual orientation, migrant populations, and the homeless, and limits the capacity to fully document the magnitude of the problem and develop needed programs. The chapter provides a basis for understanding disparities in oral health by pre- senting available data on dental visits. More work is needed to understand the dimensions of oral health problems in the United States and the reasons for differences among populations.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 35
CHAPTER 3
Diseases and Disorders
As the gateway to the body, the mouth is challenged DENTAL AND PERIODONTAL by a constant barrage of invaders—bacteria, viruses, INFECTIONS parasites, fungi. Thus infectious diseases, notably The most common oral diseases are dental caries and dental caries and periodontal diseases, predominate the periodontal diseases. Individuals are vulnerable among the ills that can compromise oral health. to dental caries throughout life, with 85 percent of Injuries take their toll as well, with the face and head adults aged 18 and older affected. Periodontal dis- particularly vulnerable to sports injuries, motor vehi- eases are most often seen in maturity, with the major- cle crashes, violence, and abuse. Less common but ity of adults experiencing some signs and symptoms very serious are oral and pharyngeal cancers, with a by the mid-30s. Certain rare forms of periodontal dis- 5-year survival rate of hardly better than 50 percent ease affect young people. The major oral health suc- (Kosary et al. 1995). Birth defects and developmental cess story of the past half century is that both caries disorders frequently affect the craniofacial complex. and periodontal diseases can be prevented by a com- These appear most commonly as isolated cases of bination of individual, professional, and community cleft lip or palate, but clefting or other craniofacial measures. defects can also be part of complex hereditary dis- eases or syndromes. Additionally, acute and chronic pain can affect the oral-facial region, particularly in Dental Caries and around the temporomandibular (jaw) joint, and The word caries derives from the Latin for rotten, and accounts for a disproportionate amount of all types of many cultures early on posited a tooth worm as the pain that drive individuals to seek health care. cause of this rottenness. By the twentieth century, Many systemic diseases such as diabetes, arthri- caries came to describe the condition of having holes tis, osteoporosis, and AIDS, as well as therapies for in the teeth—cavities. This description, although not systemic diseases, can directly or indirectly compro- incorrect, is misleading. In actuality, a cavity is a late mise oral tissues. The World Health Organization’s manifestation of a bacterial infection. International Classification of Diseases and The bacteria colonizing the mouth are known as Stomatology currently lists more than 120 specific the oral flora. They form a complex community that diseases, distributed in 10 or more classes, that have adheres to tooth surfaces in a gelatinous mat, or manifestations in the oral cavity (WHO 1992). biofilm, commonly called dental plaque. A cariogenic This chapter concentrates on six major oral dis- biofilm at a single tooth site may contain one-half- ease categories: dental and periodontal infections; billion bacteria, of which species of mutans mucosal disorders; oral and pharyngeal cancers; streptococci are critical components. These bacteria developmental disorders; injuries; and a sampling of are able to ferment sugars and other carbohydrates to chronic and disabling conditions, including Sjögren’s form lactic and other acids. Repeated cycles of acid syndrome and oral-facial pain. generation can result in the microscopic dissolution of minerals in tooth enamel and the formation of an opaque white or brown spot under the enamel surface (Mandel 1979). Frequency of carbohydrate consumption (Gustafsson et al. 1954), physical
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 37 Diseases and Disorders characteristics of food (e.g., stickiness), and timing of been proportionately greater on the smooth surfaces food intake (Burt and Ismail 1986) also play a role. rather than on the pit-and-fissure surfaces character- The essential role of bacteria in caries initiation istic of chewing surfaces. The gingival tissues tend to was established in landmark experiments in the recede over time, exposing the tooth root to cario- 1950s. Investigators observed that germ-free ani- genic bacteria that can cause root caries. An impor- mals fed high-sugar diets remained caries-free until tant risk factor for root caries in older people is the the introduction of mutans streptococci (a particular use of medications that inhibit salivary flow, leading group of bacterial strains having a number of com- to dry mouth (xerostomia). mon characteristics, and which adhere tightly to the Saliva contains components that can directly tooth). Later experiments demonstrated the trans- attack cariogenic bacteria, and it is also rich in calci- missibility of the bacteria from mother to litter and um and phosphates that help to remineralize tooth from caries-infected to uninfected cage-mates enamel. Demineralization of enamel occurs when pH (Fitzgerald and Keyes 1960). Species of Lactobacillus, levels fall as a result of acid production by bacteria. It Actinomyces, and other acid-producing streptococci can be reversed at early stages if the local environ- within the plaque may also contribute to the process ment can counteract acid production, restoring pH to (Bowden 1990). neutral levels. Remineralization can occur through If the caries infection in enamel goes unchecked, the replacement of lost mineral (calcium and phos- the acid dissolution can advance to form a cavity that phates) from the stores in saliva. Fluoride in saliva can extend through the dentin (the component of the and dental plaque and the buffering capacity of sali- tooth located under the enamel) to the pulp tissue, va also contribute to this process. Indeed, it is now which is rich in nerves and blood vessels. The result- believed that fluoride exerts its chief caries-preven- ing toothache can be severe and often is accompanied tive effect by facilitating remineralization. Several by sensitivity to temperature and sweets. Treatment studies have demonstrated that remineralization requires endodontic (root canal) therapy. If untreat- results in an increase in tooth hardness and mineral ed, the pulp infection can lead to abscess, destruction content, rendering the tooth surface more resistant to of bone, and spread of the infection via the blood- subsequent acid attack (Larsen 1987, Linton 1996, stream. Retief 1983, Shannon 1978, Vissink et al. 1985, Dental caries can occur at any age after teeth White 1988). erupt. Particularly damaging forms can begin early, Overt caries lesions develop when there is insuf- when developing primary teeth are especially vulner- ficient time for remineralization between periods of able. This type of dental caries is called early child- acidogenesis, or when the saliva production is com- hood caries (ECC). Some 6 out of 10 children in the promised. Over 400 medications list dry mouth as a United States have one or more decayed or filled pri- side effect, notably some antidepressants, antipsy- mary teeth by age 5 (U.S. Department of Health and chotics, antihistamines, decongestants, antihyperten- Human Services, National Center for Health sives, diuretics, and antiparkinsonian drugs (Sreebny Statistics 1997). ECC may occur in children who are et al. 1992). The effects of xerostomia may be partic- given pacifying bottles of juice, milk, or formula to ularly severe in cancer patients receiving radiation to drink during the day or overnight. The sugar con- the head or neck because the rays can destroy sali- tents pool around the upper front teeth, mix with vary gland tissue rather than simply inhibiting sali- cariogenic bacteria, and give rise to rapidly progress- vary secretion. ing destruction (Ripa 1988). Other risk factors for The professional application of dental sealants ECC include arrested development of tooth enamel, (plastic films coated onto the chewing surfaces of chronic illness, altered salivary composition and vol- teeth) is an important caries-preventive measure that ume (resulting from the use of certain medications or complements the use of fluorides. The films prevent malnourishment), mouth breathing, and blockage of decay from developing in the pits and fissures of saliva flow in a bottle-fed infant (Bowen 1998, Seow teeth, channels that are often inaccessible to brushing 1998). and where fluoride may be less effective. Although there have been continuing reductions The rate of caries progression through enamel is in dental caries in permanent teeth among children relatively slow (Berkey 1988, Ekanayake 1987, and adolescents over the past few decades, caries Shwartz et al. 1984) and may be slower in patients prevalence in the primary dentition may have stabi- who have received regular fluoride treatment or who lized or increased slightly in some population groups consume fluoridated water (Pitts 1983, Shwartz et al. (Petersson and Bratthall 1996, Rozier 1995). 1984). Because a large percentage of enamel lesions Reductions in caries in permanent teeth also have remain unchanged over periods of 3 to 4 years, and
38 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders because progression rates through dentin are destruction of supporting tissue can cause the tooth comparably slow (Craig et al. 1981, Emslie 1959, to loosen and fall out, increases with age. Kolehmainen and Rytömaa 1977), the application of infection control and monitoring procedures to Gingivitis assess caries risk status, lesion activity status, Gingivitis is an inflammation of the gums character- evidence of lesion arrest, and evidence of lesion ized by a change in color from normal pink to red, remineralization over extended periods of time is with swelling, bleeding, and often sensitivity and ten- recommended. derness. These changes result from an accumulation Experts believe that the earlier mutans strepto- of biofilm along the gingival margins and the cocci are acquired in infancy, the higher the caries immune system’s inflammatory response to the risk. Most studies indicate that infants are infected release of destructive bacterial products. The early before their first birthday, around the time the first changes of gingivitis are reversible with thorough incisors emerge. However, one study found the medi- toothbrushing and flossing to reduce plaque. an age of acquisition to be 26 months, coinciding Without adequate oral hygiene, however, these early with the emergence of the primary molars (Bowen changes can become more severe, with infiltration of 1998, Caufield et al. 1993, Seow 1998). DNA finger- inflammatory cells and establishment of a chronic printing has demonstrated that the source of trans- infection. Biofilm on tooth surfaces opposite the mission is usually the mother (Caufield et al. 1993). openings of the salivary glands often mineralizes to It is not clear why some individuals are more sus- form calculus or tartar, which is covered by unmin- ceptible and others more resistant to caries. Genetic eralized biofilm—a combination that can exacerbate differences in the structure and biochemistry of local inflammatory responses (Mandel 1995). A gin- enamel proteins and crystals (Slavkin 1988), as well gival infection may persist for months or years, yet as variations in the quality and quantity of saliva and never progress to periodontitis. in immune defense mechanisms are among the fac- Gingival inflammation does not appear until the tors under study. Analysis of mutans streptococci biofilm changes from one composed largely of gram- genomes may also shed light, indicating which positive streptococci (which can live with or without species are particularly virulent and which genes oxygen) to one containing gram-negative anaerobes contribute to that virulence. (which cannot live in the presence of oxygen). Even the most protective genetic endowment Numerous attempts have been made to pinpoint and developmental milieu are unlikely to confer which microorganisms in the supragingival (above resistance to decay in the absence of positive person- the gum line) plaque are the culprits in gingivitis. al behaviors. These include sound dietary habits and Frequently mentioned organisms include good oral hygiene, including the use of fluorides, and Fusobacterium nucleatum, Veillonella parvula, and seeking professional care. There are indications, species of Campylobacter and Treponema. But as however, that some destructive oral habits are on the Ranney (1989) notes, “The complexity of the results rise, such as the use of smokeless (spit) tobacco defies any attempt to define a discrete group clearly products by teenage boys. Although the chief con- and consistently associated with gingivitis.” cern here lies in the long-term risk for oral cancers, Gingival inflammation may be influenced by spit tobacco that contains high levels of sugar is also steroid hormones, occurring as puberty gingivitis, associated with increased levels of decay of both pregnancy gingivitis, and gingivitis associated with crown and root surfaces (Tomar and Winn 1998). birth control medication or steroid therapy. The pres- ence of steroid hormones in tissues adjacent to Periodontal Diseases biofilm apparently encourages the growth of certain bacteria and triggers an exaggerated response to Like dental caries, the periodontal diseases are infec- biofilm accumulation (Caton 1989). Again, thorough tions caused by bacteria in the biofilm (dental oral hygiene can control this response. plaque) that forms on oral surfaces. The basic divi- Certain prescription drugs can also lead to gingi- sion in the periodontal diseases is between gingivitis, val overgrowth and inflammation. These include the which affects the gums, and periodontitis, which may antiepileptic drug phenytoin (Dilantin); cyclosporin, involve all of the soft tissue and bone supporting the used for immunosuppressive therapy in transplant teeth. Gingivitis and milder forms of periodontitis are patients; and various calcium channel blockers used common in adults. The percentage of individuals in heart disease. Treatment often requires surgical with moderate to severe periodontitis, in which the removal of the excess tissue followed by appropriate personal and professional oral health care.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 39 Diseases and Disorders
A form of gingivitis common 50 years ago but is that the disease process may not be continuous but relatively rare today is acute necrotizing ulcerative rather progresses in random bursts in which short gingivitis, also known as Vincent’s infection or trench periods of breakdown of periodontal ligament and mouth. This aggressive infection is characterized by bone alternate with periods of quiescence. These destruction of the gingiva between the teeth, sponta- episodes occur randomly over time and at random neous bleeding, pain, and oral odor. People under sites in the mouth. Part of the difficulty in determin- extreme stress have an increased susceptibility. ing the pattern of progression reflects variation in the Spirochetes and other bacteria have been found in sensitivity of the instruments used to measure the the connective tissue of those affected. An associa- loss of soft tissue and bone. The latest generation of tion between smoking and this type of gingivitis is probes finds evidence of both continuous and multi- well recognized and was demonstrated as early as ple-burst patterns of loss in different patients and at 1946 (Pindborg 1947, 1949). This condition has different times (Jeffcoat and Ready 1991). been seen in some HIV-positive patients (Murray Most researchers agree that periodontitis results 1994). Treatment requires a combination of profes- from a mixed infection but that a particular group of sional periodontal treatment and antibacterial thera- gram-negative bacteria are key to the process and py along with professional smoking cessation assis- markedly increase in the subgingival plaque. The tance as appropriate. bacteria most frequently cited are Porphyromonas gin- givalis, Prevotella intermedia, Bacteroides forsythus, Adult Periodontitis Treponema denticola, and Actinobacillus actino- The most common form of adult periodontitis is mycetemcomitans (Genco 1996). Their role in disease described as general and moderately progressing; a initiation and progression is determined in part by second form is described as rapidly progressing and their “virulence factors.” These include the ability to severe, and is often resistant to treatment. The mod- colonize subgingival plaque, generate products that erately progressive adult form is characterized by a can directly injure tissues, and elicit an inflammatory gradual loss of attachment of the periodontal liga- or immune response. The potentially noxious bacte- ment to the gingiva and bone along with loss of the rial products include hydrogen sulfide, polyamines, supporting bone. It is most often accompanied by the fatty acids butyrate and propionate, lipopolysac- gingivitis (Genco 1990). It is not necessarily preced- charide (also known as endotoxin), and a number of ed by gingivitis, but the gingivitis-related biofilm destructive enzymes. The interaction of this arsenal often seeds the subgingival plaque. The destruction with the host response is at the core of periodontal of periodontal ligament and bone results in the for- pathology (Genco 1992, Socransky and Haffajee mation of a pocket between the tooth and adjacent 1991, 1992). Sequencing of the genomes of several tissues, which harbors subgingival plaque. The cal- key periodontal pathogens is under way and should culus formed in the pocket by inflammatory fluids provide further insight into these pathogens as well and minerals in adjacent tissues is especially damag- as catalyze new treatment approaches. ing (Mandel and Gaffar 1986). The severity of periodontal disease is determined Delicate Balances. Neutrophils (a type of white blood through a series of measurements, including the cell) and antibodies are the major immune defenses extent of gingival inflammation and bleeding, the against bacterial attack. Neutrophils move to the site probing depth of the pocket to the point of resist- of infection, where they engulf bacteria and elaborate ance, the clinical attachment loss of the periodontal antibacterial agents and enzymes to destroy bacteria. ligament measured from a fixed point on the tooth Although stimulation of the immune system to attack (usually the cemento-enamel junction), and the loss the offending bacteria is generally protective, of adjacent alveolar bone as measured by x-ray immune hyperresponsiveness and hypersensitivity (Genco 1996). Severity is determined by the rate of can be counterproductive, leading to the destruction disease progression over time and the response of the of healthy tissue. Nevertheless, the neutrophil/anti- tissues to treatment. body axis is critical for full protection against peri- Adult periodontitis often begins in adolescence odontal diseases (Genco 1992). but is usually not clinically significant until the mid- Also important is the release of certain potent 30s. Prevalence and severity increase but do not molecules called cytokines and prostaglandins, accelerate with age (Beck 1996). One view proposes especially prostaglandin E2 (PGE2) which can that destruction occurs at a specific site during a contribute to tissue destruction. Cytokines are defined period, after which the disease goes into proteins secreted by immune cells that help regulate remission (Socransky et al. 1984). The current view immune responses and also affect bone, epithelial,
40 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders and connective tissues. Most prominent in periodontitis (Page 1995). It is important that epi- periodontal diseases are interleukin 1 (IL-1), tumor demiologic studies also take into consideration the necrosis factor (TNF- ), and interferon (IFN- ). fact that tobacco use, oral hygiene, professional pro- These cytokines mediate the processes of bone phylaxis, and routine dental care are correlated to resorption and connective tissue destruction. socioeconomic status, as are race and ethnicity. Sex is another factor. Males tend to have higher levels of Susceptibility and Resistance. PGE2 may play a central periodontal diseases, presumably because of a histo- role in the tissue destruction that occurs in peri- ry of greater tobacco use and differences in personal odontal diseases. Levels of PGE2 in periodontal tissue care and frequency of dental visits. However, female are low or undetectable in health, increase in gingivi- hormones may play a protective role (as they do in tis, and rise significantly in periodontitis. Now there protecting against osteoporosis) (Genco 1996). is increasing evidence that the level of PGE2 pro- Certain systemic diseases heighten susceptibility. duced in response to bacterial challenge (especially Epidemiological studies have confirmed that patients by endotoxin) can be used as a measure of suscepti- with diabetes mellitus, both type 1 and type 2, are bility (Offenbacher et al. 1993). more susceptible to periodontal diseases (Genco Presumably, the level of PGE2 production is sub- 1996). Measures such as the gingival index, pocket ject to genetic influence. Studies of identical and fra- depth, and loss of attachment are more severe if the ternal twins, either reared together or apart, provide diabetic patients are smokers (Bridges et al. 1996). evidence that genetic factors may indeed influence The likelihood of periodontal disease increases susceptibility or resistance to the common adult form markedly when diabetes is poorly controlled. In con- of periodontitis (Michalowicz 1994). Recently, a trast, periodontal diseases respond well to therapy commercial test for a genetic marker of susceptibility and can be managed successfully in patients with has been introduced. The marker is associated with well-controlled diabetes. Such therapy can result in increased production of a particular form of inter- improvements in the diabetic condition itself leukin 1 (IL-1 ) when stimulated by periodonto- (Mealey 1996) (see Chapter 5). pathic bacteria (Kornman et al. 1997). Newman There is some evidence that osteoporosis may be (1996) found that nonsmoking adults who are posi- a risk factor for periodontal disease. More clinical tive for the marker are 6 to 19 times more likely to attachment loss and edentulousness have been develop severe periodontitis. reported in osteoporotic than in nonosteoporotic Susceptibility to adult periodontitis has also been women (Jeffcoat and Chestnut 1993). Two studies in explored in relation to a variety of behavioral and 1996 showed that estrogen replacement therapy in demographic variables as well as to the presence of postmenopausal women not only gives protection other diseases. One of the strongest behavioral asso- against osteoporosis, but also results in fewer teeth ciations is with tobacco use. The risk of alveolar bone lost to periodontal disease (Grodstein et al. 1996, loss for heavy smokers is 7 times greater than for Jacobs et al. 1996). those who have not smoked (Grossi et al. 1995). The less common rapidly progressive form of Cigarette smoking also may impair the normal host adult periodontitis typically affects people in their response in neutralizing infection (Seymour 1991), early 20s and 30s. It is characterized by severe gingi- resulting in the destruction of healthy periodontal val inflammation and rapid loss of connective tissue tissues adjacent to the site of infection (Lamster and bone. Many patients have an inherent defect in 1992). Smokers also have decreased levels of salivary neutrophil response to infection. Several systemic and serum immunoglobulins to Prevotella intermedia diseases have been associated with this form of peri- and Fusobacterium nucleatum (Bennet and Reade odontal disease, including type 1 diabetes, Down 1982, Haber 1994) and depressed numbers of helper syndrome, Papillon-Lefevre syndrome, Chediak- T cells as well (Costabel et al. 1986). Finally, smok- Higashi syndrome, and HIV infection (Caton 1989). ing alters the cells that engulf and dispose of bacte- Specific bacteria associated with rapidly progressive ria—neutrophils and other phagocytes—affecting disease include Porphyromonas gingivalis, Prevotella their ability to clear pathogens (Barbour et al. 1997). intermedia, Eikenella corrodens, and Wolinella recta Epidemiologic studies have found that such (Scheutz et al. 1997). Most recently, mutations in the additional factors as increasing age, infrequent dental cathepsin C gene have been associated with the visits, low education level, low income, co-morbidi- Papillon-Lefevre syndrome (Hart et al. 1999) and ties, and inclusion in certain racial or ethnic popula- how the defect can result in periodontal disease tions are associated with increased prevalence of (Toomers et al. 1999).
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 41 Diseases and Disorders
Refractory Periodontitis. Refractory periodontitis is Defects in neutrophil function noted in both forms of not a specific form of disease, but refers to cases in the disease (Schenkein and Van Dyke 1994) may which patients continue to exhibit progressive dis- explain why patients are highly susceptible to other ease at multiple sites despite aggressive mechanical infections as well (Suzuki 1988). therapy to remove biofilm and calculus, along with the use of antibiotics. Refractory sites exhibit elevat- ed levels of a number of different bacteria, with the SELECTED MUCOSAL INFECTIONS dominant species different in different subjects. It is AND CONDITIONS not known whether variations in pathogenicity of the Like the skin, the mucosal lining of the mouth serves bacteria, defects in the subject’s defense systems, or to protect the body from injury. This lining is itself combinations of these factors are responsible for the subject to a variety of infections and conditions, refractory nature of the disease (Haffajee et al. 1988). ranging from benign canker sores to often fatal The adoption of new diagnostic technology to detect cancers. predominant bacterial species, followed by selective antibiotic treatment, may help resolve infection and Oral Candidiasis disease in these patients. Chronic hyperplastic candidiasis is a red or white Early-onset Periodontitis lesion that may be flat or slightly elevated and may adhere to soft or hard tissue surfaces, including den- The forms of periodontitis occurring in adolescents tal appliances. It is caused by species of Candida, and young adults generally involve defects in neu- especially Candida albicans, the most common fungal trophil function (Van Dyke et al. 1980). Localized pathogen isolated from the oral cavity. Normally, the juvenile periodontitis (LJP) mainly affects the first fungi are present in relatively low numbers in up to molar and incisor teeth of teenagers and young 65 percent of healthy children and adults and cause adults, with rapid destruction of bone but almost no no harm (McCullough et al. 1996). Problems arise telltale signs of inflammation and very little when there is a change in oral homeostatis—the nor- supragingival plaque or calculus. Actinobacillus actin- mal balance of protective mechanisms and resident omycetemcomitans has been isolated at 90 to 100 per- oral flora that maintain the health of the oral cavity— cent of diseased sites in these patients, but is absent so that defense mechanisms are compromised (Scully or appears in very low frequency in healthy or mini- et al. 1994). Under these circumstances the fungal mally diseased sites (Socransky and Haffajee 1992). organisms can overgrow to cause disease. A primary It is possible that the bacteria are transmitted among disruption in homeostasis occurs with the use of family members through oral contacts such as kiss- antibiotics and corticosteroids, which can markedly ing or sharing utensils, because the same bacterial change the composition of the oral flora. Deficiencies strain appears in affected family members. However, in the immune and endocrine systems are also evidence of a neutrophil defect argues for a genetic important. Indeed, the diagnosis of candidiasis in an component. Another organism frequently associated otherwise seemingly healthy young adult may be the with LJP is Capnocytophaga ochracea. Neither of first sign of HIV infection. Other causes of candidia- these bacteria dominate in the generalized adult form sis include cancer chemotherapy or radiotherapy to of the disease, where Porphyromonas gingivalis is con- the head and neck, xerostomia resulting from radia- sidered of greatest significance (Schenkein and Van tion to the head and neck, medications, chronic Dyke 1994). mucosal irritation, certain blood diseases, and other Prepubertal periodontitis is rare and can be systemic conditions. Also, tobacco use has been iden- either general or localized. The generalized form tified as a cofactor. begins with the eruption of the primary teeth and Candidiasis often causes symptoms of burning proceeds to involve the permanent teeth. There is and soreness as well as sensitivity to acidic and spicy severe inflammation, rapid bone loss, tooth mobility, foods. Patients may complain of a foul taste in the and tooth loss. The localized form of the disease is mouth. However, it can also be asymptomatic. less aggressive, affecting only some primary teeth. Genomic analysis of the Candida albicans genome is The infection involves many of the organisms associ- helping investigators identify numerous genes that ated with periodontitis, but the mix may differ some- code for virulence factors, including enzymes that what, with Actinobacillus actinomycetemcomitans, can facilitate adhesion to and penetration of mucous Prevotella intermedia, Eikenella corrodens, and several membranes. At the same time, researchers are explor- species of Capnocytophaga implicated (Caton 1989). ing novel gene technologies to increase production of
42 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders a family of native salivary proteins, the histatins, that Normally, the immune system mounts a success- have known anticandidal and other antimicrobial ful attack on the viruses, with symptoms abating by effects. the time neutralizing antibodies appear in the blood- The most common form of oral candidiasis is stream, in about 10 days. However, herpes viruses are denture stomatitis. It occurs when tissues are trau- notorious for their ability to avoid immune detection matized by continued wearing of ill-fitting or inade- by taking refuge in the nervous system, where they quately cleaned dental appliances and is described as can remain latent for years. In oral herpes the virus chronic erythematous candidiasis. Another form, commonly migrates to the nearby trigeminal gan- candidal angular cheilosis, occurs in the folds at the glion, the cluster of nerve cells whose fibers branch angles of the mouth and is closely associated with out to the face and mouth. In about 20 to 40 percent denture sore mouth (Tyldesley and Field 1995). of people who are virus-positive, the virus may reac- Other common forms of Candida infection are tivate, with infectious virus particles moving to the pseudomembranous candidiasis (thrush), which may oral cavity to cause recurrent disease (Scott et al. affect any of the mucosal surfaces, and acute erythe- 1997). matous candidiasis, a red and markedly painful vari- The usual site of a recurrent lesion is on or near ant commonly seen in AIDS patients. the lips. Recurrences are rarely severe, and lesions In most cases, Candida infection can be con- heal in 7 to 10 days without scarring (Higgins et al. trolled with antifungal medications used locally or 1993). The recurrences may be provoked by a wide systemically. Control is difficult, however, in patients range of stimuli, including sunlight, mechanical trau- with immune dysfunction, as in AIDS, or other ma, and mild fevers such as occur with a cold. chronic debilitating diseases. Often the organisms Emotional factors may play a role as well. become resistant to standard therapy, and aggressive approaches are necessary (Tyldesley and Field 1995). The spread of oral candidiasis to the esophagus or Oral Human Papillomavirus Infections lungs can be life-threatening and is one of the crite- There are more than 100 recognized strains of oral ria used to define frank AIDS (Samaranayake and human papillomavirus (HPV), a member of the Holmstrup 1989). papovavirus family, implicated in a variety of oral lesions (Regezi and Sciubba 1993). Most common are papillomas (warts) found on or around the lips Herpes Simplex Virus Infections and in the mouth. HPV is found in 80 percent of In any given year, about one-half-million Americans these oral squamous papillomas (de Villiers 1989). will experience their first encounter with the herpes The virus has also been identified in 30 to 40 percent simplex virus type 1 (HSV-1), the cause of cold sores. of oral squamous cell carcinomas (Chang et al. 1990) That first encounter usually occurs in the oral region and has been implicated in cervical cancer as well. and may be so mild as to go unnoticed. But in some Whether a cancer or nonmalignant wart develops people, particularly young children and young may depend on which virus is present or on which adults, infection may take the form of primary her- viral genes are activated. petic stomatitis, with symptoms of malaise, muscle Oral warts are most often found in children, aches, sore throat, and enlarged and tender lymph probably as a result of chewing warts on the hands. nodes, prior to the appearance of the familiar cold In adults, sexual transmission from the anogenital sore blisters. These blisters usually show up on the region can occur (Franchesi et al. 1996). lips, but any of the mucosal surfaces can be affected. In general, viral warts spontaneously regress Bright-red ulcerated areas and marked gingivitis may after 1 or 2 years. The immune system normally also be seen (Tyldesley and Field 1995). keeps HPV infections under control, as evidenced by Herpes viruses also cause genital infections, the increased prevalence of HPV-associated lesions in which are transmitted sexually. Both HSV-1 and HSV- HIV-infected patients and others with immuno- 2 have been found in oral and genital infections, with deficiency. HSV-1 predominating in oral areas and HSV-2 in gen- ital areas (Wheeler 1988). Herpes viruses have also been implicated as cofactors in the development of Recurrent Aphthous Ulcers oral cancers. Crowded living conditions can result in Recurrent aphthous ulcers (RAU), also referred to as greater contact with infected individuals, which aids recurrent aphthous stomatitis, is the technical term in transmission of HSV (Whitley 1992). for canker sores, the most common and generally
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 43 Diseases and Disorders mild oral mucosal disease. Between 5 and 25 percent general, people who are immunocompromised are of the general population is affected, with higher more susceptible to RAU, as are people with a variety numbers in selected groups, such as health profes- of blood diseases. sional students (Axéll et al. 1976, Embil et al. 1975, RAU itself does not give rise to other illnesses Ferguson et al. 1984, Kleinman et al. 1991, Ship but is uncomfortable. Symptomatic treatment 1972, Ship et al. 1967). includes topical analgesics, antibacterial rinses, topi- The disease takes three clinical forms: RAU cal corticosteroids, and a new prescription medica- minor, RAU major, and herpetiform RAU. The minor tion that reduces pain and healing time (Khandwala form accounts for 70 to 87 percent of cases. The sores et al. 1997, Ship 1996). are small, discrete, shallow ulcers surrounded by a red halo appearing at the front of the mouth or the tongue. The ulcers, which usually last up to 2 weeks, ORAL AND PHARYNGEAL CANCERS are painful and may make eating or speaking diffi- AND PRECANCEROUS LESIONS cult. About half of RAU patients experience recur- In 2000, oral or pharyngeal cancer will be diagnosed rences every 1 to 3 months; as many as 30 percent in an estimated 30,200 Americans and will cause report continuous recurrences (Bagan et al. 1991). more than 7,800 deaths (Greenlee et al. 2000). Over RAU major accounts for 7 to 20 percent of cases 90 percent of these cancers are squamous cell carci- and usually appears as 1 to 10 larger coalescent nomas—cancers of the epithelial cells. The most ulcers at a time, which can persist for weeks or common oral sites are on the tongue, the lips, and the months (Bagan et al. 1991). Herpetiform RAU has floor of the mouth. Oral cancer is the sixth most been reported as occurring in 7 to 10 percent of RAU common cancer in U.S. males and takes a dispropor- cases. The ulcers appear in crops of 10 to 100 at a tionate toll on minorities; it now ranks as the fourth time, concentrating in the back of the mouth and most common cancer among African American men lasting for 7 to 14 days (Bagan et al. 1991, Rennie et (Kosary et al. 1995). The prominent role of tobacco al. 1985). use, especially in combination with alcohol, in caus- RAU can begin in childhood, but the peak peri- ing these cancers is a major incentive to develop od for onset is the second decade (Lehner 1968). effective health promotion and disease prevention About 50 percent of close relatives of patients with efforts. RAU also have the condition (Ship 1965), and a high correlation of RAU has been noted in identical but not fraternal twins. Associations have been found Heightening the Risk between RAU and specific genetic markers (Scully and Porter 1989). Oral cancer develops as a clone from a single geneti- RAU has also been associated with hypersensi- cally altered cell (Solt 1981). It generally has a long tivities to some foods, food dyes, and food preserva- latency period and invariably develops from a pre- tives (Woo and Sonis 1996). Nutritional deficien- cancerous lesion on the oral mucosa, such as a white cies—especially in iron, folic acid, various B vita- leukoplakia, or more commonly, a reddish erythro- mins, or combinations thereof—have also been plakia (Mashberg 1978, Shklar 1986). Both kinds of reported, and improvements noted with suitable lesions are usually induced by tobacco use alone or in dietary supplements (Nolan et al. 1991). combination with heavy use of alcohol. The develop- The two factors that have been found to have the ment of squamous cell carcinoma from initial ery- strongest association with RAU are immunologic throplakia lesions has been well demonstrated exper- abnormality, possibly involving autoimmunity, and imentally. Silverman (1998) reported rates of malig- trauma (Lehner 1968, Ship 1996, Woo and Sonis nant transformation for leukoplakias of between 0.13 1996). and 17.5 percent. However, there is considerable Volunteers with and without a history of RAU debate as to the actual malignant potential of the were studied for their reaction to the trauma of a nee- leukoplakia lesion associated with the use of smoke- dle prick to the inner cheek tissue. No ulcers devel- less (spit) tobacco. Meaningful data for determining oped in non-RAU subjects, but nearly half of those a specific malignant transformation rate or relative prone to canker sores had a recurrence (Wray et al. risk of oral cancer due to smokeless tobacco use are 1981). difficult to obtain because of the confounding effects RAU also can occur in a number of systemic dis- of other habits such as concurrent smoking and alco- eases, including HIV infection, ulcerative colitis, hol consumption and because of the variations in Crohn’s disease, and Behçet’s disease (Ship 1996). In smokeless (spit) products and how they are used.
44 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders
Another oral precancerous lesion that has tration of tobacco carcinogens into oral tissues. That received attention is submucous fibrosis. It is com- observation may partly explain why the combined monly seen in India and Southeast Asia and is relat- use of tobacco and alcohol produces a greater risk for ed to betel nut use (Canniff et al. 1986). oral cancer than use of either substance alone. Early epidemiologic studies identified behaviors Indeed, tobacco and alcohol, working in tandem, are such as smoking and environmental factors such as thought to account for 75 to 90 percent of all oral and exposure to solar radiation and x-rays as causes of pharyngeal cancers in the United States (Blot et al. intraoral and lip cancers (Pindborg 1977). 1988). Researchers then sought experimentally to explain the mechanisms of initiation. In the 1980s and Viruses 1990s, investigators exploited the techniques of The role of viruses in causing cancer in animals was molecular biology and genetics to probe what was established early in the century when Rous showed going on deep inside the cell. These studies revealed that a virus, later named the Rous sarcoma virus an abundance of systemic and local factors, including (RSV), caused tumors in chickens. The issue of viral and fungal infections, that affect cell behavior. whether viruses could cause cancer in humans Some factors stimulate cell division and others remained unexplored until the mid-1970s, when inhibit it—even to the point of initiating a program Varmus and Bishop showed that RSV had a special of cell “suicide,” called apoptosis. How a given cell gene, which they called src (for sarcoma), that could behaves at any given time in its life cycle is the net transform the cell it infected into a malignant cell result of the signals it receives from neighboring cells (Bishop et al. 1978). It was an oncogene, or cancer- and molecules, from circulating factors in the blood causing gene. The researchers subsequently, and sur- or immune system, and from its own internal prisingly, discovered that src was not native to the controls. The following sections provide a brief virus, but had been picked up by some ancestor virus description of these factors and how they may from a chicken cell’s own genome, where src had pre- participate in enhancing the risk for the development sumably played a role in the chicken cell’s normal of oral cancers. growth and development. Somehow RSV was able to subvert src when it infected a chicken cell to cause Tobacco and Alcohol the cell to divide uncontrollably. Varmus and Bishop Tobacco and alcohol are the major risk factors for called the normal cellular src gene a proto-oncogene, oral cancers, and their effects have been studied for meaning that it had the potential to be converted to many years (Rothman and Keller 1972, Decker and an oncogene. Subsequent research led to the discov- Goldstein 1982). Tobacco contains substances that ery of other viruses that could cause tumors in ani- are frankly carcinogenic or act as initiators or pro- mals and revealed the presence of proto-oncogenes in moters of carcinogenesis. Among these are N- birds and mammals. These genes could also be con- nitrosonornicotine, 4-nitroquinoline-N-oxide, and verted to oncogenes, behaving exactly like those car- benzpyrene. The most damaging carcinogens are ried by cancer viruses. In 1982 an oncogene isolated found in the tars of tobacco smoke, but many forms from a human bladder cancer turned out to be virtu- of smokeless (spit) tobacco, including snuff, have ally identical to ras, the oncogene found in a rat sar- been implicated in the development of mouth cancer coma virus (Parada et al. 1982). (Advisory Committee to the Surgeon General 1986, Viruses that have been implicated in oral cancer International Agency for Research on Cancer 1985, include herpes simplex type 1 and human papillo- Winn 1984). Other habits that have been related to mavirus. Epstein-Barr virus, also a herpes virus, is oral cancer include chewing betel nut in the presence now accepted as an oncogenic virus responsible for of tobacco, as is done primarily in Southeast Asia Burkitt’s lymphoma, occurring primarily in Africa, (Hirayama 1966, Mehta et al. 1981), and, more and nasopharyngeal carcinoma, occurring primarily recently, using marijuana (Donald 1986). in China. HPV is a major etiologic agent in cervical The role of alcohol in oral carcinogenesis has cancer (Howley 1991), and has been found in associ- been demonstrated experimentally (Wight and ation with oral cancer as well (Sugerman and Ogden 1998) and appears to be related to its damag- Shillitoe 1997). HPV DNA sequences have been ing effect on the liver. Major metabolites of alcohol, found in oral precancerous lesions as well as in squa- such as acetaldehyde—a known carcinogen in ani- mous cell carcinomas (Adler-Storthz et al. 1986, mals—may also be important. Alcohol is also Syrjanen et al. 1988), and experimental evidence has thought to act as a solvent that facilitates the pene- shown that HPV-16 can be an important cofactor in
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 45 Diseases and Disorders oral carcinogenesis (Park et al. 1991, 1995). Herpes tions in the p53 gene detected in many types of can- simplex type 1 antibodies were demonstrated in cer (Greenblatt et al. 1994, Hollstein et al. 1991), patients with oral cancer, and herpes was found to including oral and pharyngeal cancer (Langdon and induce dysplasia (abnormal cellular changes) in the Partridge 1992, Somers et al. 1992). The p53 gene lips of hamsters when combined with the application has been called the “guardian of the genome” (Lane of tobacco tar condensate (Park et al. 1986). 1992) because of its ability to recognize damage to a More recently, human herpes virus 8, a newly cell’s DNA and stop the process of growth and divi- identified member of the herpes virus family, has sion until the damage is repaired. If repair is not pos- been found in Kaposi’s sarcoma, an otherwise rare sible, p53 can trigger apoptosis. Mutations in the p53 cancer occurring in patients with AIDS. These gene in oral cancer have been linked to smoking and tumors often appear initially within the oral cavity alcohol use (Brennan et al. 1995). (Epstein and Scully 1992). Other uncommon oral malignant tumors, such as Hodgkin’s lymphoma and Loss of Immunosurveillance and Control non-Hodgkin’s lymphoma, can also occur in the The immune system can, as first noted by Paul mouths of AIDS patients. Ehrlich in 1909, seek and destroy initial clones of In addition to viruses, infection with strains of transformed cancer cells (Ehrlich 1957). Ehrlich the fungus Candida albicans has been linked to the called this process immunosurveillance, and it has development of oral cancers via the fungal produc- been confirmed in experimental animals (Burnet tion of nitrosamines, which are known carcinogens. 1970, Shklar et al. 1990) and in humans with induced immunosuppression (Penn 1975). Genetic Derangements One mechanism of immunosurveillance involves Of the more than 50 known oncogenes, many have stimulating cytotoxic macrophages and lymphocytes been reported to be present in oral cancer, and mul- to migrate to the tumor site and release tumor necro- tiple oncogenes have been reported in oral and pha- sis factors and (Shklar and Schwartz 1988). ryngeal cancer (Spandidos et al. 1985). Some of these Another mechanism operative in oral cancer appears are Bcl-1, c-erb-B2, c-myc, ins-2, and members of the to be stimulation of Langerhans cells, a special group ras family (Berenson et al. 1989, Bos 1989, Riviere et of immune cells, in the oral mucosa (Schwartz et al. al. 1990, Somers et al. 1990, 1992). 1985). Other immune cells implicated in tumor The genetic derangements that can give rise to rejection are natural killer cells and lymphokine-acti- oral cancer, including many mutations associated vated killer cells (Reif 1997). with the transformation of proto-oncogenes, have There is an increased incidence of cancer in received notable attention (Sidransky 1995, Wong et patients with AIDS or other immunodeficient condi- al. 1996). In some instances a change in a single tions or with induced immunosuppression prior to nucleotide base—a point mutation—in a gene organ transplantation. encoding a proto-oncogene is enough to transform it In addition, there is evidence that smoking into an oncogene. Cancerous changes may also depresses the immune system (Chretien 1978), and involve alterations, deletions, and break points in this may be one of the ways in which smoking acts as chromosomes that affect the position of genes. a major risk factor in oral cancer. Mutations that disarm the cell’s DNA repair mechanisms, as well as mutations in tumor suppres- Growth Factors sor genes, which inhibit abnormal cell growth, play a Immune cells are potent generators of growth factors major role in cancer development. If an individual and other molecules that can stimulate other cells to inherits or acquires a mutation in one or more tumor- migrate and proliferate. This capacity is important in suppressor genes, for example, the loss of this pro- normal cell growth and turnover, in wound healing, tective mechanism reduces the number of other dele- and in coping with infection. Unfortunately, the terious changes needed for cancer to develop. release of growth factors can contribute to oral can- Tumor suppressor genes suspected to be mutated cer by stimulating keratinocyte (oral epithelial cell) in oral and pharyngeal cancers include those for Rb, proliferation (Aaronson 1991, Issing et al. 1993, p16 (MTS1, CDKN2, or IN4a), and p53. Todd et al. Wong 1993). Increased levels of transforming growth (1995) recently reported a novel oral tumor suppres- factor (TGF- ) and epidermal growth factor have sor gene, named “deleted in oral cancer-1 (doc-1).” Of been found in oral and pharyngeal cancers and there- the group of tumor suppressor genes, that coding for fore could serve as markers for malignancy (Grandis p53 is considered of major importance, with muta- and Tweardy 1993). Nicotine at high doses stimulates
46 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders the release of growth hormones, among other help to ameliorate the problems but often at great endocrine effects (Pomerleau and Pomerleau 1984, cost and over many years. Seyler et al. 1984, 1986). Although each developmental craniofacial dis- ease or syndrome is relatively rare, the number of children affected worldwide is in the millions. In Prevention and Management addition, craniofacial defects form a substantial com- Studies of experimental carcinogenesis are elucidat- ponent of many other developmental birth defects, ing the role of micronutrients in tumor development largely because they occur very early in gestation, and progression. Alpha tocopherol (vitamin E) also when many of the same genes that orchestrate the has been studied as an antioxidant in nutritional development of the brain, head, face, and mouth are approaches to the prevention or control of oral can- also directing the development of the limbs and cer. Antioxidants can trap free radicals, the highly many vital internal organs, such as the heart, lungs, reactive molecules that build up in cells and can and liver. damage DNA. The control of oral cancer and precan- By about the third week after fertilization, the cerous lesions has been demonstrated experimental- three germ layers of the embryo—the ectoderm, ly using a variety of antioxidant micronutrients, such endoderm, and mesoderm—have formed, as well as as retinoids, carotenoids, and glutathione, as well as the first of four sets of paired swellings—the alpha tocopherol. For example, it was found that branchial arches—that appear at the sides of the head alpha tocopherol inhibited tumor development and end of the embryo. (See Chapter 2 for more details on tumor angiogenesis (blood vessel formation) in ham- this process.) Some craniofacial defects result from sters, as well as the expression of TGF- , a potent failure of the arches to complete their morphogenet- ic development. Other craniofacial defects are the angiogenesis stimulator (Shklar and Schwartz 1996). result of the abnormal differentiation of cells derived Animal research and tissue culture studies using ani- from the ectoderm and endoderm or from ectomes- mal- and human-derived cancer cell lines have enchyme cells, which originate in a part of the ecto- shown combinations of micronutrients to be more derm (the neural crest), in interaction with future effective than single micronutrients and to work syn- connective tissue (the mesenchyme). ergistically. The nutrients not only were able to inhib- it experimental carcinogenesis, but also could com- pletely prevent tumor development and cause estab- Craniofacial Anomalies Caused by Altered lished squamous cell carcinomas to regress (Shklar Branchial Arch Morphogenesis and Schwartz 1993). The mechanisms of cancer con- trol by micronutrients are gradually becoming clari- Cleft Lip/Palate and Cleft Palate fied and involve common pathways of activity at the molecular level (Shklar and Schwartz 1994). Clinical The most common of all craniofacial anomalies—and studies in humans have shown an inhibitory effect on among the most common of all birth defects—are oral leukoplakia (Benner et al. 1993, Blot et al. 1993, clefts of the lip with or without cleft palate and cleft Garewal 1993, Garewal et al. 1990, Hong et al. 1986), palate alone; these occur at a rate of 1 to 2 out of suggesting a potential role for nutrients in the overall 1,000 births, resulting in over 8,000 affected new- prevention and management of early oral cancer and borns every year. Cleft lip/palate and cleft palate are precancerous leukoplakia. However, a recommenda- distinct conditions with different patterns of inheri- tion to employ such approaches clinically at this time tance and embryological origins (Lidral et al. 1997, is premature. Murray et al. 1997). The male to female ratio of cleft lip/palate is 2:1; the ratio for cleft palate alone is just the reverse, 1:2. DEVELOPMENTAL DISORDERS These anomalies result from the failure of the The importance of the face as the bearer of identity, first branchial arches to complete fusion processes character, intelligence, and beauty is universal. (Murray 1995, Robert et al. 1996). Clefting can occur Craniofacial birth defects, which can include such independently or as part of a larger syndrome that manifestations as cleft lip or palate, eyes too closely may include mental retardation and defects of the or widely spaced, deformed ears, eyes mismatched in heart and other organs. Not all cases of clefting are color, and facial asymmetries, can be devastating to inherited; a number of teratogens (environmental the parents and child affected. Surgery, dental care, agents that can cause birth defects) have been impli- psychological counseling, and rehabilitation may cated, as well as defects in essential nutrients such as
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 47 Diseases and Disorders folic acid. Smoking by the mother during pregnancy et al. 1997). The function of the gene is not yet also increases the risk. It is becoming increasingly known, but its identity will provide opportunities for evident that most diseases and disorders, not just prenatal diagnosis, gene therapy, and further under- craniofacial anomalies, result from interactions standing of craniofacial development. involving multiple genes and environmental factors. Infants with clefts have difficulty with vital oral The Pierre Robin Syndrome functions such as feeding, breathing, speaking, and Deficient development of the first-branchial-arch- swallowing. They are also susceptible to repeated res- derived mandibular portion results in the lower jaw’s piratory infections. As these children grow, they must being set far back in relation to the forehead. As a cope with the social consequences of a facial defor- result, the tongue is set back and may obstruct the mity, delayed and altered speech, frequent illness, posterior airway, compromising respiration (Elliott et and repeated surgeries that may persist through late al. 1995, Tomaski et al. 1995) and, in severe cases, adolescence. leading to inadequate aeration and failure to thrive. Current molecular epidemiology investigations The infant is also at risk for the development of cor have examined both syndromic and nonsyndromic pulmonale, an enlargement of the right ventricle of (isolated) cleft lip/palate and cleft palate. Linkage the heart that occurs secondarily to a chronic lung studies have identified a number of candidate genes condition. Cleft palate may be another consequence. (Lewanda and Jabs 1994), including MSX1, RAR, an X-linked locus, and the genes for TGF- 3 and TGF- . The pattern of inheritance in cleft lip/palate and The DiGeorge/Velocardiofacial Syndrome cleft palate suggests that between 2 and 20 genes may The primary defect in the DiGeorge syndrome results be involved, with one gene representing a major from altered development of the fourth branchial component in the development of the cleft. One of arch and the third and fourth pharyngeal pouches the common syndromic forms of cleft lip/palate, the (Goldmuntz and Emanuel 1997). Deficiencies affect- Van der Woude syndrome, is caused by an autosomal ing the thymus, parathyroid glands, and the great dominant form of inheritance at a locus on chromo- vessels that derive from these structures result. The some 1 (Sander et al. 1995). Future molecular genet- facial features are subtle and include a squared-off ic studies will be needed to provide the information nasal tip, small mouth, and widely spaced eyes. necessary for prenatal diagnosis, calculation of risk, Similar facial features, along with heart defects, are and potential gene therapy. seen in the velocardiofacial syndrome. Both syn- dromes are associated with deletions on the long arm The Treacher Collins Syndrome— of chromosome 22 (22q11) (Gong et al. 1997, Mandibulofacial Dysostosis Gottlieb et al. 1997). Further characterization of this Children with the Treacher Collins syndrome have chromosomal deletion region will provide informa- downward-sloping eyelids; depressed cheekbones; a tion on the specific gene(s) affected and its function large fishlike mouth; deformed ears with conductive in craniofacial development. deafness; a small, receding chin and lower jaw; a The thymus defects severely compromise cellular highly arched or cleft palate; and severe dental mal- immunity, depriving the body of thymus-derived T occlusion (Dixon 1996). These defects result from cells and paving the way for severe infectious disease. defective cranial neural crest cell differentiation, Inadequate or missing parathyroid glands cause migration, and proliferation (see Chapter 2). severe hypocalcemia (low blood calcium levels) and Consequently, the first branchial arch structures are seizures. The great vessel abnormalities alter cardiac deficient, and all derivative craniofacial components output and lead to compromised circulation to heart are affected. tissues. The underdeveloped facial structures can con- tribute to airway blockage and repeated upper respi- ratory infections, either of which can be fatal. The Cranial Bone and Dental Anomalies faulty development of the ears leads to a conductive Defects in the timing of developmental events can deafness. The severe facial deformities exacerbate the cause premature fusion of cranial bones. psychological difficulties these youngsters face. Impairments of tooth development can result from Investigators have identified the gene involved in interruptions of the developmental sequence at sev- an autosomal dominant form of the syndrome (Wise eral different stages.
48 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders
Craniosynostoses Craniofacial Defects Secondary to Other Some craniofacial anomalies are associated with so- Developmental Disorders called master genes that orchestrate a program by A number of genetic diseases occur in which cranio- which the embryo assumes its basic shape. facial defects are secondary to a more generalized Craniosynostosis, which occurs in approximately 1 structural or biochemical defect. out of 3,000 births, is one such anomaly. It results in the premature fusion of the cranial sutures, a danger- Osteogenesis Imperfecta ous condition that puts pressure on the developing brain. A number of diseases and syndromes, includ- Inherited mutations of collagen genes lead to a num- ing Crouzon’s, Apert’s, Boston-type craniosynostosis, ber of “brittle bone” diseases characterized by defects Pfeiffer’s, and Saethre-Chotzen, share this anomaly, in mineralized tissues that form from a collagen-rich but differ in other features, which can include struc- matrix. Osteogenesis imperfecta presents a spectrum tural defects such as webbing of the hands and feet as of deficiencies that includes fragile bones, clear or well as mental retardation. Boston-type craniosynos- blue sclera, deafness, loose ligaments, and painful tosis has been linked to MSX2, one of the master dentinogenesis imperfecta-like changes in the teeth. genes. Several of the other syndromes involve point mutations at one or another locus in genes that code Epidermolysis Bullosa—Recessive Dystrophic for fibroblast growth factor receptors (FGFR 1, 2, and Type 3) (Howard et al. 1997, Meyers et al. 1996). The gene defect in epidermolysis bullosa—recessive Collectively, these genes are associated with cell reg- dystrophic type—manifests as blisters or bullae that ulation, either through mediating growth factor appear shortly after birth on skin areas following effects or by serving as transcription factors (Cohen minor trauma. Mutations in keratin genes that con- 1997). tribute to the epithelial cell cytoskeleton have been correlated with this condition. Hereditary Hypodontia or Anodontia The oral manifestations include both mucosal Conditions of underdeveloped teeth (hypodontia) or bullae and altered teeth. Altered teeth with hypoplas- their complete absence (anodontia) have been corre- tic enamel develop and exhibit an increased suscepti- lated with specific genes, such as MSX1 and LEF1. bility to caries. Oral bullae develop from even the The complete absence of teeth alters the bony devel- slightest mucosal trauma. The condition is painful opment of the mandible and maxilla. and dangerous because of the constant risk that the bullae will become infected. Amelogenesis Imperfecta and Dentinogenesis Imperfecta Craniofacial Manifestations of Single-Gene Amelogenesis imperfecta and dentinogenesis imper- Defects fecta are linked to defects in structural genes that code for proteins essential to the development of In many craniofacial defects, mutations within a sin- tooth enamel (amelogenesis imperfecta) or dentin gle gene manifest as complex syndromes with varied (dentinogenesis imperfecta). The teeth are weak and organ and limb defects as well as facial anomalies. extremely sensitive to temperature and pressure. The ordinary forces of chewing are painful and can lead to Ectodermal Dysplasias further wear and pain. The ectodermal dysplasias (EDs) are a family of The enamel matrix genes include tuftelin, hereditary diseases first observed by Charles Darwin ameloblastin, and amelogenin; researchers have over a century ago. They involve defects in two or begun to link mutations in these genes with amelo- more tissues derived from the ectoderm—skin, hair, genesis imperfecta. Similarly, genes labeled DSP and teeth, nails, and sweat glands. The ectodermal struc- DPP have been characterized for dentin matrix and tures fail to differentiate properly owing to altered are associated with the inheritance of dentinogenesis epithelial-mesenchymal signaling. A gene, EDA, at an imperfecta. X-linked locus has been linked to the syndrome, and ongoing research is aimed at determining the func- tion of the gene and the molecular mechanism of the syndromes (Kere et al. 1996, Zonana et al. 1994).
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 49 Diseases and Disorders
More recently, investigators have discovered genes death in some age groups of the population (Kraus linked to autosomal (i.e., non-sex-linked) forms of and Robertson 1992). Cranial injuries in particular ED, displaying both dominant and recessive inheri- are a leading cause of mortality. Oral-facial injuries tance (Monreal et al. 1999). can bring disfigurement and dysfunction, greatly Oral manifestations of the ectodermal dysplasias diminishing the quality of life and contributing to are associated with the teeth. Alterations in tooth social and economic burdens (Reisine et al. 1989). development can include hypodontia, anodontia, The leading causes of oral and craniofacial and conically shaped teeth. injuries are sports, violence, falls, and motor vehicle collisions (Kraus and Robertson 1992). Oral cavity The Waardenburg Syndrome injuries may also be caused by foreign objects in food The Waardenburg syndrome has been subdivided (Hyman et al. 1993). into several types. All involve a variety of abnormali- ties in the position and appearance of the nose and Sports eyes, with pigment changes that may cause one eye to differ in color from the other. Other signs include Craniofacial sports injuries occur not only in contact deafness, a mildly protruding jaw, cleft lip and palate, sports, but also in individual activities such as bicy- and skeletal deformities (Reynolds et al. 1995). The cling, skating, and gymnastics, especially on trampo- syndrome is inherited in an autosomal dominant lines. Each sport predisposes its participants to a spe- manner with complete penetrance and variable cific array of extrinsic risk factors (Pinkham and expression. Specific genes associated with this syn- Kohn 1991). These include physical contact, projec- drome are members of the homeobox family that reg- tiles such as balls and pucks, and the quality of the ulate the transcription of other genes: Waardenburg playing field and equipment. In contact sports the type 1 with PAX3; Waardenburg type 2 with MITF, absence of protective equipment such as headguards 3q14.1; and Waardenburg type 3 with PAX3, 2q35 and mouthguards is a major risk factor. In a recent (Asher et al. 1996). survey of school-aged children in organized sports, football was the only sport in which the majority of Cleidocranial Dysplasia participants used mouthguards and headgear (Nowjack-Raymer and Gift 1996). The inheritance of a regulatory gene defect in clei- There are intrinsic risk factors as well, relating to docranial dysplasia leads to features that include characteristics of the individual participant. These delayed tooth eruption, supernumerary teeth, altered include age, sex, injury history, body size, aerobic fit- or missing collarbones, short stature, and possible ness and muscle strength, central motor control, and failure of cranial suture closure. The exact mecha- general mental ability (Taimela et al. 1990). nism of the associated gene, CBFA1, located on chro- mosome 6, has not been determined but appears to be essential for bone development. Falls Falls are a major cause of trauma to teeth, primarily INJURY to incisors. Unlike bone fractures, fractures of the The common perception is that injuries are random crowns of the teeth do not heal or repair, and affect- occurrences that are unpredictable and hence unpre- ed teeth often have an uncertain prognosis. Problems ventable. In actuality, experts in the field make the may develop later due to damage to the pulp. point that there are no basic scientific distinctions between injury and disease (Haddon and Baker 1981). Injuries have been categorized as “intention- Motor Vehicle Collisions al” and “unintentional.” People identified as being at The effects of motor vehicle collisions may range risk for certain injuries, as well as the causes of those from minor and reversible effects to long-term med- injuries, can be targeted for appropriate prevention ical, surgical, and rehabilitative consequences. Post- strategies. Such an approach is broadly applicable to traumatic headaches and chronic oral-facial pain can sports, falls, and motor vehicle injuries (unintention- occur. Neuromuscular and glandular damage may al) as well as to injuries caused by abusive and vio- cause short- or long-term problems with chewing, lent behaviors (intentional). swallowing, and tearing or result in facial tics or Injuries are a major public health problem, out- paralysis. ranking cancer and heart disease as a leading cause of
50 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders
Violence is no cure for Sjögren’s, and patients often carry eye- The family is the single most frequent locus of vio- drops and water bottles or saliva substitutes in an lence in Western society. Domestic violence includes attempt to provide symptomatic relief. Clinically, the child abuse, spousal and elder abuse, and abuse of reduction in salivary flow changes the bacterial flora, the disabled. Child abuse is of particular concern to which, in addition to the reduction in salivary pro- the oral health community because 65 percent of tective components, increases the risk of caries and cases involve head and oral-facial trauma candidiasis (Daniels and Fox 1992). Recent studies (Mathewson 1993, Needleman 1986) and dentists have indicated that there is a reduction in masticato- are required to report suspected cases of child abuse. ry function (Dusek et al. 1996) and an increased In the young child, head injury is the most common prevalence of periodontal disease (Najera et al. cause of death. Psychological trauma from abuse can 1997). In advanced stages the salivary glands may result in sleep disturbances, eating disorders, devel- swell because of obstruction and infection or lym- opmental growth failure in young children, and nerv- phatic infiltration. In both forms of the disease, other ous habits such as lip and fingernail biting and systems may eventually become affected. Nasal, thumb sucking. Effects may also include chronic laryngeal, and vaginal dryness may occur, as well as underachievement in school and poor peer relation- abnormalities in internal organs (Oxholm and ships (Mathewson 1993). In abusive families, physi- Asmussen 1996). cal neglect is commonplace, with inadequate provi- Diagnosis is difficult in the early stages, and sion of basic needs, including medical and oral health women often report that it took many years and con- care (Mathewson 1993). sultations with many specialists before they received the correct diagnosis. Diagnosis involves demonstra- tion of specific antibodies in the blood characteristic SELECTED CHRONIC AND DISABLING of an autoimmune disorder, a labial (minor) salivary CONDITIONS gland biopsy, and a series of eye tests to measure flow Oral, dental, or craniofacial signs and symptoms play rate and tissue characteristics. Confirmatory tests a critical role in autoimmune disorders such as include an evaluation of salivary flow and chemistry. Sjögren’s syndrome and in a number of chronic and Patients with Sjögren’s syndrome are at some risk disabling pain conditions. of developing diseases such as non-Hodgkin’s lym- phoma; clinical data indicate that such lymphomas develop in 5 percent of patients with Sjögren’s syn- Sjögren’s Syndrome drome (Moutsopoulos et al. 1978). Sjögren’s syndrome is one of several autoimmune dis- Histological examination shows that immune orders in which the body’s own cells and tissues are cells infiltrate the glands and cluster around the mistakenly targeted for destruction by the immune secretory elements, resulting in a breakdown of the system. Like other autoimmune conditions, Sjögren’s normal structure of the gland. The mechanisms by syndrome is more prevalent among women. The ratio which this occurs involve immune-cell-mediated of females to males affected is 9:1, with symptoms inflammation and stimulation of the salivary gland usually developing in middle age. There are an esti- cells themselves to produce tissue-destructive mole- mated 1 to 2 million individuals in the United States cules such as cytokines. Another hypothesis is that a with Sjögren’s syndrome (Talal 1992). viral infection of the glands may trigger the immune The disease occurs in two forms. Primary response that leads to autoimmunity, whereas genet- Sjögren’s involves the salivary and lacrimal (tear) ic or regulatory alterations might lead to abnormali- glands. In secondary Sjögren’s the glandular involve- ties in apoptosis (Fox and Speight 1996). ment is accompanied by the development of a con- In addition to saliva substitutes and artificial nective tissue or collagen disease, most often tears, some medications, such as pilocarpine and rheumatoid arthritis, lupus erythematosis, scleroder- cevimeline, are prescribed to increase salivary flow ma, or biliary cirrhosis. from the residual healthy gland tissue, again provid- The glandular involvement causes a marked ing symptomatic relief only. The problems that reduction in fluid secretion, resulting in xerostomia develop in the other organ systems are also treated and xerophthalmia (dry eyes). The constant oral dry- symptomatically. At advanced stages, steroids are ness causes difficulty in speaking, chewing, and swal- employed intermittently to alleviate problems. lowing; the dry eyes often itch and feel gritty. There
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 51 Diseases and Disorders
Acute and Chronic Oral-Facial Pain by multiple sclerosis, where it is assumed to be asso- Since the nineteenth century, when two dentists, ciated with lesions (multiple sclerosis “plaques”) in Horace Wells and Frederick Morton, demonstrated the brain stem. Medical treatment depends largely on the analgesic powers of nitrous oxide and ether, oral the use of a drug that has become a virtual specific, health investigators have been recognized leaders in the antiepileptic drug carbamazepine. For those the field of pain management worldwide. Their patients with no consequential adverse effects, it can analyses of the cells, pathways, and molecules control the disease. An alternative for chronic suffer- involved in the transmission and modulation of pain ers is the surgical removal of a small vein or artery have given rise to a growing variety of medications, that may be exerting pressure on the nerve root or often combined with other approaches, that can con- the selective destruction of the nerve fibers them- trol acute and chronic pain. Pain researchers today selves using chemical or electrical methods. In many stress that chronic pain can become a disease in itself, cases, these procedures can produce complete relief causing long-term detrimental changes in the nerv- from pain (Tyldesley and Field 1995). ous system. These changes may affect resistance to other diseases as well as effectively destroy quality of Temporomandibular Disorders life. Most people have experienced acute pain involv- ing teeth and the oral tissues at one time or another. Various etiological factors, including trauma, can give rise to pain and dysfunction in the temporo- Atypical Facial Pain mandibular joint and surrounding muscles, condi- tions collectively called temporomandibular disor- Atypical facial pain is characterized by a continuous ders (TMDs). The pain may be localized or radiate to dull ache on one or both sides, most frequently in the the teeth, head, ears, neck, and shoulders. Abnormal region of the maxilla (the upper jaw). The pain tends grating, clicking, or crackling sounds, known as to be episodic and is aggravated by fatigue, worry, or crepitus, in the joint often accompany localized pain. emotional upset. It is often accompanied by pain Pain is also found in response to clinical palpation of elsewhere in the body and depression. Once a dental the affected structures. TMDs are common, occur- cause can be ruled out, pain resolution depends on ring in as many as 10 million Americans. Although the successful use of antidepressants, psychotherapy, surveys indicate that both sexes are affected, the or both (Tyldesley and Field 1995). majority of individuals seeking treatment are women of childbearing age, a phenomenon suggesting that Tic Douloureux hormonal influences should be investigated. The oral-facial region is also subject to pain that can Several factors can contribute to the onset or be paroxysmal or continuous along a distinct nerve exacerbation of TMD symptoms. These factors distribution. The most frequently encountered of include certain developmental anomalies; injury to these oral facial neuralgias is tic douloureux, or the jaw from accidents or abuse; oral habits that trigeminal neuralgia, a disease of unknown etiology greatly stress the joint and musculature, such as affecting one, two, or all three branches of the tooth grinding (bruxism); jaw manifestations of sys- trigeminal nerve. The pain is highly intense and of a temic diseases such as fibromyalgia and arthritic dis- stabbing nature, and lasts for a few seconds. This eases; and some irreversible treatments for initial transient attack may be repeated every few minutes signs and symptoms. or several hours. There may be no precipitating fac- The multiplicity of factors that may cause or con- tor, or it may occur in response to a gentle touch or a tribute to TMDs has unfortunately led to a multiplic- breeze wafting across the face—a condition experts ity of treatments. Most of these treatments have not call allodynia, the feeling of pain in response to a nor- been tested in randomized controlled clinical trials. mally nonpainful stimulus. On other occasions, there During the 1970s and 1980s, many individuals may be a specific trigger zone. Although spontaneous underwent surgery, which proved unsuccessful in remission for weeks or months may occur, it is rarely many cases. permanent. Given the unknown, unpredictable Leading investigators have proposed standard- nature of tic douloureux, it is not surprising that fear ized research diagnostic criteria to clarify the kinds of of pain comes to dominate these patients’ lives, as pathology that can give rise to TMDs and to classify they avoid doing anything that might trigger an the most common forms of TMDs. Such criteria attack. could be used in designing clinical trials and could Trigeminal neuralgia generally occurs in later ultimately lead to better diagnostics, treatments, and life, but also occurs in younger individuals affected prevention. The criteria use two dimensions or axes:
52 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders axis I delineates various forms of joint or muscle interventions that can correct errors in the program. pathology; axis II explores pain-related disability and The continued sequencing of the genomes of micro- psychological status. The approach requires detailed bial pathogens involved in oral diseases also should clinical examinations and patient histories (Dworkin lead to new diagnostic and preventive approaches. and LeResche 1992). FINDINGS A MIRROR, A MODEL, AND A BETTER Microbial infections, including those caused UNDERSTANDING OF DISEASES AND by bacteria, viruses, and fungi, are the primary cause DISORDERS of the most prevalent oral diseases. Examples include Studying the diseases and disorders that affect cran- dental caries, periodontal diseases, herpes labialis, iofacial tissues can provide scientists with models of and candidiasis. systemic pathology. Because some craniofacial tis- The etiology and pathogenesis of diseases sues, such as bones, mucosa, muscles, joints, and and disorders affecting the craniofacial structures are nerve endings, have counterparts in other parts of the multifactorial and complex, involving an interplay body and these tissues are often more accessible to among genetic, environmental, and behavioral research analysis than deeper-lying tissues, factors. researchers studying craniofacial tissues can gain Many inherited and congenital conditions valuable insights into how cancer develops, the role affect the craniofacial complex, often resulting in dis- of inflammation in infection and pain, the effects of figurement and impairments that may involve many diet and smoking, the consequences of depressed body organs and systems and affect millions of chil- immunity, and the changes that can arise from a dren worldwide. mutated gene. Tobacco use, excessive alcohol use, and inappro- Other craniofacial tissues—teeth, gingiva, priate dietary practices contribute to many diseases tongue, salivary glands, and the organs of taste and and disorders. In particular, tobacco use is a risk fac- smell—are unique to the craniofacial complex. Study tor for oral cavity and pharyngeal cancers, periodon- of the diseases affecting these tissues has revealed a tal diseases, candidiasis, and dental caries, among wealth of information about their special nature as other diseases. well as the molecules and mechanisms that normally Some chronic diseases, such as Sjögren’s syn- operate for the protection, maintenance, and repair of drome, present with primary oral symptoms. all the oral, dental, and craniofacial tissues. When Oral-facial pain conditions are common and factors perturb these nurturing elements, the oral often have complex etiologies. health scale can tip toward disease. When those fac- tors stem from systemic diseases or disorders, the REFERENCES mouth can sometimes mirror the body’s ill health. Aaronson SA. Growth factors and cancer. Science 1991 Similarly underscoring the connection between oral Nov 22;254(5035):1146-53. and general health are studies suggesting that poor Adler-Storthz K, Newland JR, Tessin BA, Yeudall WA, dental health, mainly due to chronic dental infec- Shillitoe EJ. Human papillomavirus type 2 DNA in tions, may heighten the risk for both cardiovascular oral verrucous carcinoma. J Oral Pathol 1986 disease and stroke independently of factors such as Oct;15(9):472-5. social class and established cardiovascular risk fac- Advisory Committee to the Surgeon General. The health consequences of using smokeless tobacco. tors (Grau et al. 1997). The interplay between cran- Chapter 2, Carcinogenesis associated with smokeless iofacial and systemic health and disease has become tobacco use. Bethesda (MD): Public Health Service; a lively focus of interest and research, as discussed in 1986. NIH Pub. no. 86-2874. Chapter 5. Asher JH Jr, Harrison RW, Morell R, Carey ML, Current research on developmental disorders Friedman TB. Effects of PAX3 modifier genes on and diseases affecting the craniofacial complex is craniofacial morphology, pigmentation, and viability: facilitating and complementing the intense effort of a murine model of Waardenburg syndrome variation. the Human Genome Project to map and sequence all Genomics 1996 Jun;34(3):285-98. 100,000 genes. This goal should be accomplished Axéll T, Mörnstad H, Sundström B. The relation of the early in the twenty-first century and should begin to clinical picture to the histopathology of snuff dip- yield information on the genetic program that gov- per’s lesions in a Swedish population. J Oral Pathol 1976;5(4):229-36. erns morphogenesis, organ development, and disease etiology and pathogenesis, with the potential for
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Public Health Dent 1995;55(SI):292-301. Shklar G, Schwartz J. Tumor necrosis factor in experi- Samaranayake LP, Holmstrup P. Oral candidiasis and mental cancer regression with alphatocopherol, beta- human immunodeficiency virus infection. J Oral carotene, canthaxanthin, and algae extract. Eur J Pathol Med 1989;18:554-64. Cancer Clin Oncol 1988 May;24(5):839-50. Sander A, Murray JC, Scherpbier-Heddema T, Buetow Shklar G, Schwartz J. Oral cancer inhibition by KH, Weissenbach J, Zingg M, Ludwig K, Schmelzle micronutrients. The experimental basis for clinical R. Microsatellite-based fine mapping of the Van der trials. Eur J Cancer B Oral Oncol 1993 Jan;29B(1): Woude syndrome locus to an interval of 4.1 cM 9-16. between D1S245 and D1S414. Am J Hum Genet Shklar G, Schwartz JL. A common pathway for the 1995 Jan;56(1):310-8. destruction of cancer cells: experimental evidence Schenkein HA, Van Dyke TE. Early onset periodontitis: and clinical implications. Int J Oncol 1994;4:215-24. systemic aspects of etiology and pathogenesis. Shklar G, Schwartz JL. Vitamin E inhibits experimental Periodontol 2000 1994;6:7-25. carcinogenesis and tumour angiogenesis. Eur J Scheutz F, Matee MI, Andsager L, Holm AM, Moshi J, Cancer B Oral Oncol 1996 Mar;32B(3):114-9. Kagoma C, Mpemba N. Is there an association Shklar G, Schwartz JL, Trickler DP, Reid S. Prevention of between periodontal condition and HIV infection? J experimental cancer and immunostimulation by Clin Periodontol 1997 Aug;24(8):580-7. vitamin E (immunosurveillance). J Oral Pathol Med Schwartz JL, Frim Sr, Shklar G. RA can alter the distri- 1990 Feb;19(2):60-4. bution of ATPase-positive Langerhans cells in the Shwartz M, Gröndahl H-G, Pliskin JS, Boffa J. A longi- hamster cheek pouch in association with DMBA tudinal analysis from bite-wing radiographs of the application. Nutr Cancer 1985;7(1-2):77-84. rate of progression of approximal carious lesions Scott DA, Couter WA, Lamey PJ. Oral shedding of her- through human dental enamel. Arch Oral Biol pes simplex virus type 1: a review. J Oral Pathol Med 1984;29(7):529-36. 1997;26(10):441-7. Sidransky D. Molecular genetics of head and neck can- Scully C, Porter CR. Recurrent aphthous stomatitis: cer. Curr Opin Oncol 1995 May;7(3):229-33. current concepts of etiology, pathogenesis and man- Silverman S. Oral cancer. 4th ed. Hamilton, Ontario: agement. J Oral Pathol Med 1989;18:21-7. B.C. Decker; 1998. Scully C, el-Kabir M, Samaranayake LP. Candida and Slavkin H. Gene regulation in the development of the oral candidosis: a review. Crit Rev Oral Biol Med oral tissues. J Dent Res 1988;67:1142-9. 1994;5(2):125-57. Socransky SS, Haffajee AD. Microbial mechanisms in Seow WK. Biological mechanisms of early childhood the pathogenesis of destructive periodontal diseases: caries. J Public Health Dent 1998;26(Suppl 1):8-27. a critical assessment. J Periodontol Res 1991 Apr;26: Seyler LE Jr, Fertig J, Pomerleau O, Hunt D, Parker K. 195-212. The effects of smoking on ACTH and cortisol secre- Socransky SS, Haffajee AD. The bacterial etiology of tion. Life Sci 1984 Jan 2;34(1):57-65. destructive periodontal disease: current concepts. J Periodontol 1992 Apr;63(4 Suppl):322-31.
58 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders
Socransky SS, Haffajee AD, Goodson JM, Lindhe J. New U.S. Department of Health and Human Services, concepts of destructive periodontal disease. J Clin National Center for Health Statistics. National Periodontol 1984 Jan;11(1):21-32. Health and Nutrition Examination Survey III, 1988- Solt DB. Localization of gamma-glutamyl transpepti- 1994. CD-ROM series 11, no.1. Hyattsville (MD): dase in hamster buccal pouch epithelium treated National Center for Health Statistics, Centers for with 7, 12-dimethylbenz[a]anthracene. J Natl Disease Control and Prevention; 1997. Available Cancer Inst 1981 Jul;67(1):193-200. from National Technical Information Service (NTIS), Somers KD, Cartwright SL, Schechter GL. Springfield, VA. Amplification of the int-2 gene in human head and Van Dyke TE, Horoszewicz HU, Cianciola LJ, Genco RJ. neck squamous cell carcinomas. Oncogene 1990 Neutrophil chemotaxis dysfunction in human peri- Jun;5(6):915-20. odontitis. Infect Immun 1980 Jan;27(1):124-32. Somers KD, Merrick MA, Lopez ME, Incognito LS, Vissink A, ‘s-Gravenmade EJ, Gelhard TB, Panders AK, Schechter GL, Casey G. Frequent p53 mutations in Franken MH. Rehardening properties of mucin- or head and neck cancer. Cancer Res 1992;52(21): CMC-containing substitutes on softened human 5997-6000. enamel. Effects of sorbitol, xylitol and increasing vis- Spandidos DA, Lamothe A, Field JK. Multiple tran- cosity. Caries Res 1985;19(3):212-8. scriptional activation of cellular oncogenes in human Wheeler CE. The herpes simplex problem. J Am Acad head and neck solid tumors. Anticancer Res Dermatol 1988;18(1 Pt 2):163-8. 1985;5(2):221-4. White DJ. Reactivity of fluoride dentifrices with artifi- Sreebny LM, Yu A, Green A, Valdini A. Xerostomia in cial caries; II. Effects on subsurface lesions, F uptake, diabetes mellitus. Diabetes Care 1992 Jul;15(7): surface hardening, and remineralization. Caries Res 900-4. 1988;22:27-36. Sugerman PB, Shillitoe EJ. The high risk of human Whitley RJ. Neonatal herpes simplex virus infections: papillomaviruses and oral cancer: evidence for and pathogenesis and therapy. Pathol Biol (Paris) 1992 against a causal relationship. Oral Dis 1997;3:130- Sep;40(7):729-34. 47. Wight AJ, Ogden GR. Possible mechanisms by which Suzuki JB. Diagnosis and classification of the periodon- alcohol may influence the development of oral can- tal diseases. Dent Clin North Am 1988 cer—a review. Oral Oncol 1998;34:441-7. Apr;32(2):195-216. Winn DM. Tobacco chewing and snuff dipping: an asso- Syrjanen SM, Syrjanen KJ, Happonen RP. Human papil- ciation with human cancer. IARC Sci Publ lomavirus (HPV) DNA sequences in oral precancer- 1984;(57):837-49. ous lesions and squamous cell carcinoma demon- Wise CA, Chiang LC, Paznekas WA, Sharma M, Musy strated by in situ hybridization. J Oral Pathol 1988 MM, Ashley JA, Lovett M, Jabs EW. TCOF1 gene Jul;17(6):273-8. encodes a putative nucleolar phosphoprotein that Taimela S, Kujala UM, Osterman K. Intrinsic risk fac- exhibits mutations in Treacher Collins syndrome tors and athletic injuries. Sports Med 1990 Apr;9(4): throughout its coding region. Proc Natl Acad Sci 205-15. USA 1997 Apr 1;94(7):3110-5. Talal N. Sjögren’s syndrome: historical overview and Wong DT. TGF-alpha and oral carcinogenesis. Eur J clinical spectrum of disease. Rheum Dis Clin North Cancer B Oral Oncol 1993 Jan;30B(4):3-7. Am 1992 Aug;18(3):507-15. Wong DT, Todd R, Tsuji T, Donoff RB. Molecular biolo- Todd R, McBride J, Tsuji T, Donoff RB, Nagai M, Chou gy of human oral cancer. Crit Rev Oral Biol Med MY, Chiang T, Wong DT. Deleted in oral cancer-1 1996;7(4):319-28. (doc-1), a novel oral tumor suppressor gene. FASEB Woo SB, Sonis ST. Recurrent aphthous ulcers: a review J 1995 Oct;9(13):1362-70. of diagnosis and treatment. J Am Dent Assoc 1996 Tomar SL, Winn DM. Coronal and root caries among Aug;127(8):1202-13. U.S. adult users of chewing tobacco [abstract]. J World Health Organization (WHO). World Health Dent Res 1998;77(SI):256. Organization’s international classification of diseases Tomaski SM, Zalzal GH, Saal HM. Airway obstruction and stomatology, IDC-DA. 3rd ed. Geneva: WHO; in the Pierre Robin sequence. Laryngoscope 1995 1992. Feb;105(2):111-4. Wray D, Graykowski EA, Notkins AL. Role of mucosal Toomers C, James J, Wood AJ, et al. Loss of function injury in initiating recurrent aphthous stomatitis. Br mutations in the cathepsin C gene result in peri- Med J (Clin Res Ed) 1981 Dec 12;283(6306):1569- odontal disease and palmoplantar keratosis. Nat 70. Genet 1999 Dec;22:421-4. Zonana J, Jones M, Clarke A, Gault J, Muller B, Thomas Tyldesley WR, Field AE. Oral medicine. 4th ed. Oxford: NS. Detection of de novo mutations and analysis of Oxford University Press; 1995. their origin in families with X linked hypohidrotic ectodermal dysplasia. J Med Genet 1994 Apr;31(4): 287-92.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 59
CHAPTER 34
The Magnitude of the Problem
The range of oral, dental, and craniofacial diseases income groups are warranted. The relationship of and conditions that take a toll on the U.S. population oral health to the use of dental services is described. is extensive. This chapter provides highlights of dis- However, the effects of health care visits and of spe- eases and conditions affecting the U.S. population cific services rendered need further study. using available national and state data to describe the Most of the data in the figures and tables pre- burden of disease in the United States. To capture the sented in this chapter are derived from large, nation- dimensions and extent of these diseases and condi- ally representative surveys of the U.S. civilian, nonin- tions, the data are presented where possible by demo- stitutionalized population. These include complex graphic measures such as race/ethnicity, sex, age, sample surveys, such as the National Health and education, and economic status. Statistics and trends Nutrition Examination Survey (NHANES), which are presented for each of the six categories of oral dis- use a sample of individuals selected with known eases and disorders whose etiology and pathogenesis probability to estimate the prevalence of particular are described in Chapter 3: dental and periodontal characteristics and conditions in the nation as a infections, oral and pharyngeal cancers, mucosal whole. The multipurpose NHANES provides data on infections and conditions, developmental disorders, the frequency of the most common oral diseases and intentional and unintentional injuries, and chronic conditions. The most recent survey, NHANES III, and disabling conditions. Included are conditions as was conducted by the National Center for Health common as dental caries and periodontal diseases as Statistics (NCHS) of the Centers for Disease Control well as relatively rare clefting syndromes. Also men- between 1988 and 1994. Trained interviewers gath- tioned are conditions that are more common in cer- ered demographic, health, and related data from eli- tain demographic subpopulations—for example, gible households. Selected persons in these house- Sjögren’s syndrome and temporomandibular disor- holds were invited to a mobile examination center, ders, which are more common in women, and where they underwent multiple health assessments, injuries, which are more common in men. (See Box including an oral examination by a trained dentist 4.1 for a glossary of terms used in this chapter.) (NCHS 1996). Related surveys such as the National There is no single measure of oral health or the Health Interview Survey (NHIS) also use complex burden of oral diseases and conditions, just as there survey sampling and household interviews to obtain is no single measure of overall health or overall dis- health information about the U.S. population (Kovar ease. As a result, this chapter assembles clinical and 1989). The NHIS conducted in 1989 included data epidemiologic measures for specific conditions on oral-facial pain conditions; several of these sur- affecting the craniofacial structures. Note too that the veys have captured data on dental visits. The most chapter presents an incomplete picture. State-specif- extensive dental utilization survey that provides ic data on oral diseases are extremely limited. There demographic and socioeconomic data and data on is a paucity of national data on rare conditions as well reasons for not visiting a dentist was conducted in as on the health of selected populations and 1989. their subgroups. Some characteristics and unique Surveys conducted by the National Institute of needs of these populations are highlighted, and a Dental and Craniofacial Research of a probability number of questions raised. More extensive analyses sample of U.S. schoolchildren in 1979-80 and 1986- of the differences among racial/ethnic, sex, and 87 (Snowden and Miller-Chisholm 1992) used
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 61 The Magnitude of the Problem
similar oral examination procedures as in NHANES. Because school attendance is high in the United BOX 4.1 States, these surveys are considered representative of Glossary noninstitutionalized children throughout the United States and are used in this chapter. Complex sample survey. A survey of individuals selected with Record-based surveys are another approach to known probability to estimate the prevalence and/or extent of obtaining health data for the nation as a whole or for particular characteristics and conditions. selected broad areas. Mortality statistics are obtained dfs. The count (number) of decayed (untreated) or filled primary by determining the number of deaths in the United tooth surfaces per person. States and dividing that figure by the total U.S. pop- dft. The count (number) of decayed (untreated) or filled primary ulation as determined from U.S. Census data (Kovar teeth per person. 1989). Cancer statistics are derived from population- based cancer registries in selected large geographic DMFS. The count (number) of decayed (untreated),missing (due areas of the United States using reports of cancer to caries),or filled permanent tooth surfaces per person. occurrences from hospitals, doctors, and laborato- DMFT.The count (number) of decayed,missing (due to caries),1 or ries. This data system, maintained by the National filled permanent teeth per person. Cancer Institute, is called the Surveillance, Epidemiology.The study of the distribution and determinants of Epidemiology, and End Results program (Ries et al. disease frequency in human populations. 1999). Birth certificate registries in geographic areas and surveys of health care facilities provide valuable Incidence. The number of cases of a disease, or condition, that information from record-based systems about other occurs during a specified period of time. aspects of oral and craniofacial health such as birth Incidence rate. The number of cases of a disease, or condition, defects (Schulman et al. 1993). The Centers for that occurs during a specified period of time,per specified unit of Disease Control and Prevention’s Behavioral Risk and population. State Surveillance System provides essential state Loss of periodontal attachment.2 The distance from the data on edentulousness (Tomar 1997). In selected cementoenamel junction to the bottom of the gingival sulcus. cases, survey findings other than from national prob- ability surveys are used. State-specific data are pro- Mortality rate. The number of deaths during a stated period of time divided by the total number of persons in the population. vided for those conditions for which there are data from most states—that is, cancer mortality statistics Prevalence. The number of existing cases of a disease,or condi- and self-reports of edentulism. tion,at a designated point in time. Economic status is derived from annual income Prevalence rate. The number of existing cases of a disease, or data. Unless otherwise stated, “poor” is defined in condition, at a designated point in time, per the number of per- this chapter as an annual income below the U.S. sons in the population. poverty level. For both national and other surveys, Relative survival rate. Survival rates for persons with a partic- the race and ethnicity terms used in this report are ular disease or condition corrected for the expected occurrence of consistent with the terms used in the supporting death in persons in the age group. documentation as referenced in the text and cited in the reference list. Available national data for most Survival rate. The number of persons surviving over a specified conditions are limited primarily to Hispanic, non- time period divided by the number of persons alive at the start of Hispanic black, and non-Hispanic white populations, the time period. due to the sampling design of the national surveys. 1 In the Third National Health and Nutrition Examination Survey,the M (miss- The NHANES III oversampled Mexican Americans, ing) component of the DMFT (S) index reflects teeth (or tooth surfaces) miss- so the data from that survey are available for this sub- ing because of dental caries or periodontal disease. Teeth missing because of population of Hispanics. trauma, orthodontic treatment, or other non-disease-related reasons were not scored. 2 Periodontal disease status is assessed by measuring the distance from the gingival margin (FGM) to depth of the gingival sulcus, or pocket depth, and the distance from the gingival margin to the cementoenamel junction (FGM- CEJ).A third measure,loss of attachment,is determined by calculating the dif- ference between pocket depth and the FGM-CEJ distance.Loss of attachment is important because it serves as a measure of how much support from the tissues surrounding the tooth has been lost.
62 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem
WHO HAS WHAT DISEASES AND 2 to 9 have the highest number of primary teeth CONDITIONS? affected by dental caries (a mean of 2.4 decayed or filled teeth) compared to poor non-Hispanic blacks Dental Caries, Periodontal Diseases, and (mean 1.5) and non-Hispanic whites (mean 1.9). Tooth Loss Among the nonpoor, Mexican American 2- to 9-year- olds have the highest number of affected teeth (mean Dental Caries 1.8), followed by non-Hispanic blacks (1.3) and non- Hispanic whites (1.0). Dental caries is one of the most common childhood There are also differences by race/ethnicity and diseases. In this section, decayed refers to teeth with poverty level in the proportion of untreated decayed caries that have not been treated. The term filled teeth for all age groups. Poor Mexican American chil- refers to treated caries. Dental caries refers to both dren aged 2 to 9 have the highest proportion of decayed and filled teeth. Among 5- to 17-year-olds, untreated decayed teeth (70.5 percent), followed by dental caries is more than 5 times as common as a poor non-Hispanic black children (67.4 percent) reported history of asthma and 7 times as common as (Figure 4.3). Nonpoor children have lower propor- hay fever (Figure 4.1). Prevalence increases with age. The majority (51.6 percent) of children aged 5 to 9 years had at least one carious lesion or filling in the FIGURE 4.2 coronal portion of either a primary or a permanent A higher percentage of poor people than nonpoor have at least tooth. This proportion increased to 77.9 percent for one untreated decayed tooth 17-year-olds and 84.7 percent for adults 18 or older. 50 43.6 Additionally, 49.7 percent of people 75 years or older Poor 40 36.8 had root caries affecting at least one tooth (NCHS 34.4 Nonpoor 1996, NHANES III). 30 Despite progress in reducing dental caries, indi- 23.4 viduals in families living below the poverty level 20 17.3 experience more dental decay than those who are 11.3 economically better off. Furthermore, the caries seen of people Percentage 10 in these individuals is more likely to be untreated 0 than caries in those living above the poverty level 2 to 9 (primary 5 to 17 (primary 18+ (permanent (Figure 4.2); more than one third (36.8 percent) of teeth only) and permanent teeth) teeth only) poor children aged 2 to 9 have one or more untreat- Age ed decayed primary teeth, compared to 17.3 percent Source: NCHS 1996. of nonpoor children. In addition to poverty level, the proportion of teeth affected by dental caries also varies by age and FIGURE 4.3 race/ethnicity. Poor Mexican American children aged Poor children aged 2 to 9 in each racial/ethnic group have a higher percentage of untreated decayed primary teeth than nonpoor children FIGURE 4.1 Dental caries is one of the most common diseases among 80 70.5 5- to 17-year-olds 70 67.4 Caries 58.6 60 56.1 56.9 57.2 50 Asthma 11.1 40 37.3 8.0 Hay fever 30 Chronic 4.2 20 bronchitis that are untreated per child are untreated that 10 010203040506070 Percentage of decayed primary of decayed teeth Percentage Percentage of children and adolescents aged 5 to17 0 Non-Hispanic black Mexican American Non-Hispanic white Note: Data include decayed or filled primary and/or decayed, filled, or missing permanent teeth. Asthma, chronic bronchitis, and hay fever based on report of Poor children Nonpoor children household respondent about the sampled 5- to 17-year-olds. Source: NCHS 1996. Source: NCHS 1996.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 63 The Magnitude of the Problem tions of untreated decayed teeth, although the group Improvements have been noted over the past 25 with the lowest proportion (non-Hispanic whites) to 30 years with regard to dental caries. Among most still has an average of 37.3 percent of decayed teeth age groups, the average number of teeth per person untreated. affected by dental caries has decreased, and the aver- Poor adolescents aged 12 to 17 in each racial/eth- age number of teeth per person that show no signs of nic group have a higher percentage of untreated infection, as well as the proportion of the population decayed permanent teeth than the corresponding that is caries-free, has increased. nonpoor adolescent group (Figure 4.4). Poor Since 1971-74, major increases have been noted Mexican American (47.2 percent) and poor non- in the percentage of children and adolescents aged 5 Hispanic black adolescents (43.6 percent) have more to 17 who have never experienced dental caries in than twice the proportion of untreated decayed teeth their permanent teeth. Younger adults have experi- than poor non-Hispanic white adolescents (20.7 per- enced a decline in dental caries during this time cent). For nonpoor adolescents the proportion of period, as measured by the average number of teeth untreated decayed permanent teeth is highest in non- without decay or fillings (Figure 4.6). These trends Hispanic black adolescents (41.7 percent)—a pro- are not found among those 55 to 74 years of age. portion only slightly lower than for this group’s poor counterparts (43.6 percent). The mean number of permanent teeth affected by dental caries (decayed or FIGURE 4.5 Poor adults aged 18 and older have a higher percentage of filled) for this age group is similar among Mexican untreated decayed teeth than nonpoor adults Americans (2.7), non-Hispanic whites (2.5), and 50 non-Hispanic blacks (2.3). As income level increases, 46.7 46.9 the percentage of adolescents with decayed teeth 45 decreases and the proportion of decayed teeth that 40 have been filled increases (Vargas et al. 1998). 35 30.2 Adult populations (aged 18 and older) show a 30 similar pattern, with the proportion of untreated 27.0 decayed teeth higher among the poor than the non- 25 21.9 poor (Figure 4.5). Regardless of poverty level status, 20 adult non-Hispanic blacks and Mexican Americans 15 are untreated per person are untreated have higher proportions of untreated decayed teeth 10 8.6 than their non-Hispanic white counterparts. that teeth of decayed Percentage 5 0 FIGURE 4.4 Non-Hispanic black Mexican American Non-Hispanic white Poor children aged 12 to 17 in each racial/ethnic group have a Poor adults Nonpoor adults higher percentage of untreated decayed permanent teeth than nonpoor children Source: NCHS 1996. 50 47.2 45 43.6 41.7 FIGURE 4.6 40 Since 1971-74, the average number of permanent teeth without 35 decay or fillings has increased among 18- to 54-year-olds 30 20 19.6 25 23.1 18 20.7 Age 20 16 15.7 18-34 15 14 12.1 13.5 35-54 12.0 10 12
that are untreated per person are untreated that 55-64 10 10.6 5 9.6 65-74 Percentage of decayed permanent teeth of decayed Percentage 8 7.9 0 6 6.5 Average number of sound Average Non-Hispanic black Mexican American Non-Hispanic white per person permanent teeth 4 Poor children Nonpoor children 1971-74 1988-94 Survey year Source: NCHS 1996. Sources: NCHS 1975, 1996.
64 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem
The number of untreated decayed teeth per per- year-olds having this amount of loss or more. Figure son across all age groups has also declined. 4.8 displays these data in a different format and shows that a small but increasing percentage of the popula- Periodontal Diseases tion at each older age group has severe disease. The presence of periodontal disease is measured clin- At all ages, men are more likely than women to ically in several ways, one of which is by calculating have at least one tooth site with a 6 mm or more loss the loss of periodontal attachment. Figure 4.7 shows of attachment (Figure 4.9). In addition to age and that most adults 25 years and older have at least 2 sex, the prevalence of periodontal loss of attachment mm or more loss of attachment. The disease is more also varies by racial/ethnic group (Figure 4.10). A serious as the amount of attachment loss and number higher percentage of non-Hispanic black persons at of tooth sites affected increase. More severe disease each age group have at least one tooth site with 6 mm can be defined as having 4 mm or more loss of attach- or more of periodontal attachment loss as compared ment in at least one site. The percentage of adults to other groups. Within each racial/ethnic group, the with 6 mm or more loss of attachment at one or more highest percentage affected is found among individu- sites increases at older age groups, with 19.0 percent als 70 years and older. At every age, a higher propor- of 55- to 64-year-olds and 23.4 percent of 65- to 74- tion of those at the lowest socioeconomic status
FIGURE 4.7 The proportion of adults with at least one site with loss of periodontal attachment of 2 mm or more, 4 mm or more, and 6 mm or more increases with age 100 94.5 95.7 86.4 89.8 80 Loss of attachment 74.9 64.6 60.5 2 mm or more 60 54.9 50.2 4 mm or more 6 mm or more 40 37.3 38.0 29.5
Percentage of people Percentage 22.1 23.4 20 19.0 12.0 13.9 3.0 6.7 0.2 2.6 0 18-24 25-34 35-44 45-54 55-64 65-74 75+ Age group
Sources: Adapted from NCHS 1996, Burt and Eklund 1999.
FIGURE 4.8 FIGURE 4.9 Although older adults have more periodontal attachment loss Males are more likely than females to have at least one tooth than younger adults, severe loss is seen among a small site with 6 mm or more of periodontal loss of attachment percentage of individuals at every age 40 35.1 100 35 29.9 90 Age 30 25.0 26.2 80 18-44 25 70 45-64 20 18.1 17.7 65+ 60 15 13.6 9.8 9.5 50 10 Percentage of people Percentage 3.5 4.0 40 5 1.6 30 0 25-34 35-44 45-54 55-64 65-74 75+ 20 Age group Cumulative percentage of people Cumulative 10 Female Male 0 Sources: Adapted from NCHS 1996, Burt and Eklund 1999. 3 579 11 Loss of periodontal attachment (mm) Sources: Adapted from NCHS 1996, Burt and Eklund 1999.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 65 The Magnitude of the Problem
(SES) level have at least one site with attachment loss 35, has been reported to be 4 times more common in of 6 mm or more, compared to those at higher SES males than in females (Löe and Brown 1991); among levels (Figure 4.11) (Burt and Eklund 1999).1 13- to 17-year-olds, it has been found to be highest Gingivitis as measured by gingival bleeding, a among African Americans (10.0 percent), as com- sign of inflammation, is more evident among pared with Hispanics (5.0 percent) and whites (1.3 Mexican Americans (63.6 percent) than among non- percent) (Albandar et al. 1997). Hispanic blacks (55.7 percent) and non-Hispanic whites (48.6 percent) (Albandar et al. 1999). Tooth Loss and Edentulism Early-onset periodontitis, a severe, rapidly pro- Although teeth are lost for a number of reasons, gressive disease occurring in individuals under age including trauma, orthodontic treatment, and removal of third molars (wisdom teeth), most teeth FIGURE 4.10 are lost because of periodontal disease or dental Non-Hispanic blacks are more likely than other groups to have caries (Phipps and Stevens 1995, Neissen and at least one tooth site with 6 mm or more of periodontal loss Weyant 1989). By age 17, more than 7.3 percent of of attachment U.S. children have lost at least one permanent tooth 50 47.1 because of caries; by age 50, Americans have lost an 45 average of 12.1 teeth, including the third molars. 40 Men and women are nearly equally likely to be 35 31.2 32.0 edentulous. Overall, a higher percentage of individu- 30 28.2 als living below the poverty level are edentulous than 25 24.1 are those living above (Figure 4.12). Individuals with 20 16.9 incomes equal to or above twice the poverty level 15 12.4 have a rate of edentulism of 6.9 percent. This rate is Percentage of people Percentage 10 6.2 5.7 less than half the rate for those with incomes below 5 twice the poverty level (14.3 percent). 0 Although the overall rate of edentulism for adults 30-49 50-69 70+ 18 and older is approximately 10 percent (9.7 per- Age group cent), the rate increases with age, so that about a third Race/ethnicity (33.1 percent) of those 65 and older are edentulous. Non-Hispanic black Mexican American Non-Hispanic white Comparisons across race/ethnicity for the population Source: NCHS 1996. 18 years and older indicate that the edentulous rate
FIGURE 4.11 The percentage of adults with at least one tooth site with 6 mm or more of periodontal attachment loss is greater among persons of low socioeconomic status at all ages 40 37.8 36.2 35 30 25.8 25.5 25 21.8 23.3 20 16.8 18.4 19.2 15 11.7 17.5 17.2 10 6.5 8.1 Percentage of people Percentage 4.2 5 2.5 3.9 0.20.20.0 1.3 0 18-24 25-34 35-44 45-54 55-64 65-74 75+ Age group Socioeconomic status Low Middle High Sources: Adapted from NCHS 1996, Burt and Eklund 1999.
1In this section, income levels are defined as low (less than 185 percent of the U.S. poverty level or below), middle (185.1 percent to 350 percent of the poverty level), and high (350.1 percent of the poverty level or higher).
66 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem for non-Hispanic whites is 10.9 percent; for non- in the oral cavity and pharynx (throat) account for Hispanic blacks, it is 8.0 percent; and for Mexican about 30,200 cases, or 2.4 percent of all cancers, and Americans, 2.4 percent. Non-Hispanic whites, both about 7,800 Americans die from these cancers each poor and nonpoor, have the highest rates of eden- year (ACS 1999). The life of each person with these tulism compared to non-Hispanic blacks and cancers is shortened by an average of 16.5 years. The Mexican Americans. Of the three population groups, median age at diagnosis of oral and pharyngeal can- Mexican Americans are the least likely to lose all of cer is 64, and the rate of occurrence increases with their teeth, and the proportion of Mexican Americans age. More than 95 percent of oral cancers occur in who are edentulous varies only slightly by economic individuals aged 35 and older (Ries et al. 1999). status. A lower proportion of U.S. adults have lost all The overall 5-year survival rate for people with their natural teeth now than was the case two oral and pharyngeal cancers is 52 percent, which is decades ago (Figure 4.13). The decline is most pro- worse than that for—among others—cancers of the nounced at older ages. prostate, corpus and uterus, breast, bladder, larynx, Edentulism is one of a few conditions for which cervix, colon, and rectum in both blacks and whites state-specific data exist. These data reveal a wide (Ries et al. 1999). People with oral cancers detected variation in the percentages of the population aged at an early stage have a 5-year survival rate of 81.3 65 and older who have no teeth, from a low of 13.9 percent; however, only 35 percent of individuals with percent in Hawaii to a high of 47.9 percent in West oral and pharyngeal cancers are diagnosed at an early Virginia; this is more than a threefold difference stage. The 5-year survival rate drops to 21.6 percent (Table 4.1) (Tomar 1997). Reasons for these differ- ences are unknown at this time. FIGURE 4.13 Oral and Pharyngeal Cancers and The percentage of people without any teeth has declined among Precancerous Lesions adults over the past 20 years
50 Oral and Pharyngeal Cancers 45.6 Every year, about 1.2 million people develop cancer 40 in the United States (based on 2000 estimates). Sites Age 30 33.3 28.6 65-74 55-64 20 20.1 FIGURE 4.12 35-54
Percentage of people Percentage 18-34 Complete tooth loss varies by race/ethnicity and poverty status: 12.6 a higher percentage of poor and nonpoor non-Hispanic white 10 adults (18 and older) have no teeth compared with non-Hispanic 5.2 2.0 blacks and Mexican Americans 0 0.4 1971-74 1988-94 20 18.7 Survey years 18 Sources: NCHS 1975, 1996. 16 14 TABLE 4.1 12 Five states with highest and lowest percentages of 9.9 10 9.8 edentulous persons aged 65 and older
8 6.9 States with Highest Percentage States with Lowest Percentage
Percentage of people Percentage 6 Percentage Percentage 4 State Edentulous State Edentulous 2.1 2.2 West Virginia 47.9 Hawaii 13.9 2 Kentucky 44.0 California 16.2 0 Louisiana 43.0 Oregon 16.5 Non-Hispanic black Mexican American Non-Hispanic white Arkansas 39.2 Arizona 18.5 Poor adults Nonpoor adults Maine 37.8 Wisconsin 19.4 Source: NCHS 1996. Source: Tomar 1997.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 67 The Magnitude of the Problem among people diagnosed with advanced-stage can- Islanders (7.9 per 100,000), American Indians and cers (Ries et al. 1999). Compared to patients with Alaska Natives (6.4 per 100,000), and Hispanics (5.8 other types of cancer, oral and pharyngeal cancer per 100,000) have lower incidence rates than whites patients who survive have the highest rate of devel- and blacks (Wingo et al. 1999). opment of new cancers in the mouth or in other parts Figure 4.14 provides incidence rates for selected of the body (Winn and Blot 1985). racial/ethnic groups by sex. Males have higher inci- Incidence rates for oral and pharyngeal cancers dence rates than females; specifically, they are 2.6 are higher for black individuals than for whites: 12.5 times more likely to develop oral and pharyngeal cases versus 10.0, respectively, per 100,000 people cancers than women (Ries et al. 1999). The incidence each year. In the United States, Asians and Pacific rates of oral and pharyngeal cancers for black males are 39.6 percent higher than for white males (20.8 versus 14.9, FIGURE 4.14 respectively, per 100,000 males Males have higher incidence rates of oral and pharyngeal cancers than females per year). Rates for black and white females are the same (6.0 6.0 Black 20.8 per 100,000 females per year) 6.0 (Ries et al. 1999). Oral and pha- White 14.9 ryngeal cancers are the seventh Asian and 4.8 Female most common cancer among 11.6 Pacific Islander Male white males and the fourth most American Indian 3.5 and Alaska Native 10.2 frequently diagnosed cancer among black males (Figure 4.15) Hispanica 8.8 (Wingo et al. 1999). As for many other cancer 0 5 10 15 20 25 Rate per 100,000 sites, the overall 5-year survival rate for oral and pharyngeal can- Note: Age adjusted to the 1970 U.S. standard. a Data are unavailable for Hispanic females. cers is lower for blacks than for Sources: Adapted from Wingo et al. 1999; SEER Program, 1990-96, Ries et al. 1999. whites: 34 versus 56 percent
FIGURE 4.15 Cancers of the oral cavity and pharynx are the seventh most common cancers in white males and the fourth most common in black males
Prostate gland 147.3 Prostate gland 222.9
Lung & bronchus 73.1 Lung & bronchus 112.3
Colon/rectum 53.2 Colon/rectum 58.1
Urinary bladder 31.2 Oral cavity & pharynx 20.8
Lymphomas 20.2 Stomach 17.1
Melanoma of skin 17.0 Urinary bladder 15.6
Oral cavity & pharynx 14.9 Lymphomas 15.4
Leukemia 14.0 Pancreas 14.9
Kidney/renal 12.6 Kidney/renal 14.5
Pancreas 9.8 Esophagus 13.5
0 50 100 150 200 250 0 50 100 150 200 250 White males Black males Incidence rate per 100,000 Note: Age adjusted to the 1970 U.S. standard. Sources: Adapted from Wingo et al. 1999; SEER Program, 1990-96, Ries et al. 1999.
68 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem
(Ries et al. 1999) (Figure 4.16). However, only 19 cers of the pharynx generally have a worse survival percent of blacks with oral and pharyngeal cancers rate than those with cancers in oral cavity sites: 5- are diagnosed when the cancer is at the local, and year pharyngeal cancer survival rates range from 53.3 more easily treatable, stage, compared to 38 percent to 29.5 percent, depending on the subsite, whereas for whites (Figure 4.17). At every stage of diagnosis, oral cavity cancer survival rates range from 94.3 to the survival rate for blacks is lower than for whites 48.3 percent. The incidence of lip cancer, a highly (Figure 4.18). treatable cancer, is more common in whites than The occurrence of cancers in specific sites with- among blacks (1.2 per 100,000 persons per year in the oral cavity and pharynx varies by sex and compared to 0.1). race/ethnicity. A relatively rare subtype of pharyngeal Overall, the incidence rate for oral cavity and cancer, nasopharyngeal cancer, occurs more often in pharyngeal cancers is decreasing, with an estimated American males and females of Chinese descent than annual percentage decrease of 0.5 percent per year among other racial/ethnic groups (Miller et al. 1996). between 1973 and 1996. There are wide variations in Blacks are twice as likely as whites to develop cancers the incidence of site-specific cancers. The largest of the pharynx: 6.0 and 2.9 per 100,000 per year, respectively (Ries et al. 1999). Individuals with can- FIGURE 4.17 Blacks are less likely to be diagnosed with a localized oral or FIGURE 4.16 pharyngeal cancer than whites Five-year relative survival rates for selected cancers for 60 whites and blacks 54 88 50 Testis 96 89 White patients Thyroid 95 41 84 40 38 Black patients Prostate 93 68 Melanomas of skin 88 30 71 Breast (females) 86 Corpus & uterus, NOS 56 20 19 85 15 Hodgkin's 76 13 12 83 8 62 of people diagnosed Percentage 10 Urinary bladder 82 Cervix uteri 59 71 0 53 Localized Regional Distant Unstaged Larynx 66 52 Stage at diagnosis Colon 62 58 Source: Adapted from SEER Program, 1989-95, Ries et al. 1999. Kidney/renal 61 51 Rectum 60 Oral cavity & pharynx 34 56 FIGURE 4.18 41 Non-Hodgkin's 52 At every stage of diagnosis, the 5-year relative survival rates 47 for blacks with oral and pharyngeal cancers are lower than Ovary 50 33 for whites Leukemias 44 90 Brain & NOS 39 81.7 30 80 White patients Multiple myeloma 31 72.1 28 70 Black patients Stomach 22 19 11 60 Lung & bronchus 14 50 43.9 Esophagus 9 13 40 35.8 Liver & intrahepatic 3 6 30 28.3 surviving 5 years 23.2 22.9 Pancreas 4 4 of people Percentage 20 13.7 0102030405060708090100 10 Five-year relative survival rates 0 Localized Regional Distant Unstaged White patients Black patients Stage at diagnosis Note: NOS = not otherwise specified. Source: Kosary 1996. Source: Adapted from SEER Program, 1989-95, Ries et al. 1999.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 69 The Magnitude of the Problem annual declines in incidence were noted for lip can- lence of tobacco-related lesions increased with cer (–3.4 percent per year between 1973 and 1996) increasing duration and frequency of spit tobacco use. (Ries et al. 1999). In contrast, the incidence of In some American Indian tribes, both adolescent tongue cancer, the most common form of oral and males and females commonly use spit tobacco and pharyngeal cancer, may be increasing among young have an especially high frequency of spit tobacco men (Day et al. 1994). lesions. On a Sioux reservation, 37.0 percent of stu- Although overall mortality rates for oral and pha- dents in grades 7 through 12 used spit tobacco. Spit ryngeal cancers declined by 1.6 percent per year tobacco lesions occurred in over one third of those between 1973 and 1996, the 5-year survival rate for tobacco-using adolescents (CDC 1988). In another individuals with oral and pharyngeal cancers has study of Navajo adolescents, three fourths of male shown no improvement for the past 25 years (Ries adolescents (75.4 percent) and one half of female et al. 1999). adolescents (49.0 percent) used spit tobacco. Of Mortality statistics by state allow for analysis of Navajo adolescents who used spit tobacco, 25.5 per- deaths due to oral cavity and pharyngeal cancers. cent had spit tobacco lesions—29.6 percent of males Table 4.2 highlights the wide variation in mortality and 17.0 percent of females (Wolfe and Carlos 1987). found in the country. The highest rate is in the District of Columbia—6.7 per 100,000 population; this is nearly 5 times the lowest rate, 1.4 in Utah. Selected Mucosal Infections and Diseases Again, reasons for this variation need to be studied (Ries et al. 1999). Oral Herpes Simplex Virus Infections The prevalence of recurrent herpes lesions is estimat- Tobacco-related Lesions ed to be between 15 and 40 percent (Scully 1989). Tobacco use has been estimated to account for over The proportion of the U.S. population with herpes 90 percent of cancers of the oral cavity and pharynx simplex virus type 1 (HSV-1) antibodies is 68.2 per- (Peto et al. 1995) and thus represents the greatest cent (as evidenced by positive antibody titer). The single preventable risk factor for oral cancer. Both proportion reporting a history of herpes lesions in the smoking and spit (smokeless) tobacco (moist snuff past 12 months is 17.7 percent. The presence of anti- and chewing tobacco) are associated with a number of bodies and occurrence of herpes lesions vary by age other oral conditions, including oral mucosal lesions, (Figure 4.20). The frequency of recurrence also varies that may progress to oral cancer (Silverman 1998). greatly, ranging from once to several times per year. One type of tobacco-related lesion is seen in peo- Infection with the oral herpes simplex virus has ple who use spit tobacco. A national survey of U.S. been related to socioeconomic factors, with 75 to 90 schoolchildren in 1985-86 showed that 6.1 percent of percent of individuals from lower socioeconomic males and 0.1 percent of females used spit tobacco. The survey also showed that 34.9 percent of current snuff users aged 12 to 17 and 19.6 percent of current adolescent chewing tobacco users had a spit tobacco FIGURE 4.19 Tobacco-related oral lesions are more common in 12- to 17- lesion (Figure 4.19) (Tomar et al. 1997). The preva- year-olds who currently use spit tobacco
35 34.9 TABLE 4.2 Five states with highest and lowest oral and pharyngeal 30 Current user cancer mortality rates Former user 25 States with Highest Rates States with Lowest Rates 19.6 Mortality Rate per Mortality Rate per 20 State 100,000 Population State 100,000 Population 15 District of Columbia 6.7 Minnesota 2.0 Delaware 4.0 Wyoming 2.0 10 South Carolina 3.9 Colorado 2.0 5.6 6.0 5 Louisiana 3.5 North Dakota 1.8 of people with lesion Percentage Florida 3.4 Utah 1.4 0 Note: Ages adjusted to the 1970 standard population. Snuff user Chewing tobacco user Source:Ries et al.1999. Source: Adapted from Tomar et al. 1997.
70 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem populations developing antibodies by the end of the eral population can vary from 5 to 25 percent (Axéll first decade of life (Whitley 1993a,b). In comparison, et al. 1976, Embil et al. 1975, Ferguson et al. 1984, 30 to 40 percent of individuals from middle and Ship 1972, Ship et al. 1967). In NHANES III, 17.2 upper socioeconomic groups evidence antibodies by percent of persons reported having a recurrent aphthous the middle of the second decade of life. ulcer within the past 12 months, and occurrences were The prevalence of one or more herpes labialis most common among young adults (18 to 24 years lesions within the past 12 months is 8.4 percent for old) (Figure 4.21). In selected population groups, the non-Hispanic blacks, 16.2 percent for Mexican prevalence of recurrent aphthous ulcers can be as Americans, and 19.7 percent for non-Hispanic whites high as 50 to 60 percent (Miller and Ship 1977, Ship (NHANES III). et al. 1961, 1977).
Recurrent Aphthous Ulcers Other Mucosal Lesions Various epidemiologic studies of recurrent aphthous Other mucosal conditions contribute to the burden ulcers have indicated that the prevalence in the gen- of oral diseases. The following are among the most common: Oral candidiasis (commonly FIGURE 4.20 Herpes simplex type 1 virus infection is widespread, and oral herpes lesions called thrush) is a particular prob- (cold sores/fever blisters) are common lem for individuals with impaired immune function. A prevalence of 100 Age 88.9 9.4 percent has been reported in 90 8-11 renal transplant patients (King et 80 77.1 12-17 18-24 al. 1994); Samaranayake (1992) 70 65.5 25-44 reports prevalences between 43 60 45-64 and 93 percent among HIV-infect- 51.8 >65 50 ed patients. It is estimated that 3.6 43.1 40 percent of full denture wearers have candidiasis. Percentage of people Percentage 30 Denture stomatitis, a condi- 20 17.3 18.4 18.6 11.9 14.3 15.2 tion in which the mucosa under- 10 neath a denture becomes inflamed 0 and sometimes painful, affects 25.6 Positive antibody to HSV-1a Had oral herpes lesion in past 12 months percent of people aged 18 and older a Data not available for the 8- to 11-year-old age group. who have two full dentures. Source: NCHS 1996. Additionally, 32.2 percent of those with one full denture are affected, 26.7 percent of those with one or more partial den- FIGURE 4.21 A substantial percentage of the population, particularly tures, and 0.87 percent of those who do not have full among young adults, has experienced recurrent aphthous or partial dentures. lesions (canker sores) in the past 12 months Oral human papillomavirus infections, oral 30 and genital papillomas (or condyloma acuminata, 26.9 also called venereal warts), are especially common 25 among HIV-positive patients. Human papilloma- viruses may be associated with some oral leukopla- 20.1 20 18.4 19 kias with a high risk for malignant transformation (Palefsky et al. 1995). 15 14.4
10 8.4 Developmental Disorders
5 Numerous developmental disorders affect the oral, Percentage who experienced lesion who experienced Percentage dental, and craniofacial complex. These include con- 0 genitally missing teeth (all or specific tooth types); 8-11 12-17 18-24 25-44 45-64 >65 congenital problems involving tooth enamel, pulp, or Age group dentin; and craniofacial birth defects or syndromes. Source: Adapted from NCHS 1996.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 71 The Magnitude of the Problem
Cleft lip and palate are the most common congenital is more common in males (Burman 1985, Fraser and anomalies and may occur as isolated defects or as part Calnan 1961, Habib 1978, Owens et al. 1985). of other syndromes. Other craniofacial defects and syndromes that have been the focus of recent genet- Malocclusions ics research include ectodermal dsyplasia, Treacher Malocclusions can occur due to congenital or Collins syndrome, Apert’s syndrome, and Waarden- acquired misalignments (crowding) of the teeth or burg syndrome. Craniofacial defects and syndromes jaws. In a national study of individuals between 8 have many serious consequences including unusual and 50 years old, 25 percent were found to have no facial features; severe functional problems; and the crowding of the incisors (front teeth), whereas 11 need for extensive surgical, medical, and rehabilita- percent were found to have severe crowding tive interventions and prosthetic devices. (Brunelle et al. 1996). About 9 percent had a posteri- or crossbite, where there is poor contact of the back Cleft Lip/Palate upper and lower chewing surfaces. This crossbite was Oral clefts are one of the most common classes of most common in non-Hispanic whites. Severe over- congenital malformations in the United States, with jet—where the upper front teeth project far for- prevalence rates in the general population of 1.2 per ward—was found in approximately 8 percent of this 1,000 births for cleft lip with or without cleft palate population, with a similar percentage demonstrating and 0.56 per 1,000 births for cleft palate alone a severe overbite—where the front top and bottom (Schulman et al. 1993). These conditions affect facial teeth greatly overlap when the mouth is closed. Less appearance throughout life. than 5 percent of non-Hispanic whites had an open The rate of oral clefts for whites is more than 3 bite, an inability to bring the upper and lower front times that for blacks (1.7 versus 0.5 per 1,000 live teeth together. births) (Figure 4.22). Oral clefts are more common among North American Indians (3.7 per 1,000 births) (Lowry et al. 1989). Cleft palate occurs more fre- Injury quently in females, whereas cleft lip or cleft lip/palate Injuries to the head, face, and teeth are very com- mon. They can range in severity from the very mild to those that cause death. Although injuries have a FIGURE 4.22 major impact on oral health, data on the number and Cleft lip and cleft palate are among the most common severity of head and face injuries in the United States congenital malformations, and prevalence varies by race are very limited.2 Most of our knowledge about the number of injuries that occurs comes from more Hydrocephalus 0.73 0.85 severe injuries that involve a visit to the emergency room. Trisomy 21 0.61 0.99 In 1993 and 1994, there were 20 million visits Microcephalus 3.7 per year to emergency departments for craniofacial 1.07 injuries. Less serious injuries can be treated on an Obstruction kidney/ureter 0.87 outpatient basis. More than 5.9 million injuries in 1.12 1991 were treated by dentists in private offices (Gift Cleft lip & palate 0.54 1.7 and Bhat 1993). Overall, 25 percent of all persons aged 6 to 50 have had an injury that resulted in dam- Hip dislocation 1.35 1.9 age to one or more anterior teeth (Kaste et al. 1996a). Pyloric stenosis 0.72 An estimated 2.9 million emergency room visits for 2.4 all age groups related to tooth or mouth injuries 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 between 1997 and 1998. Twenty-five percent of these Prevalence per 1,000 live births injuries were seen in children under the age of 4 (NCHS 1997b). Whites Blacks Source: Schulman et al. 1993. The leading causes of head and face injuries that result in emergency room visits include falls, assaults,
2This section reports national data that should provide some estimation of the scope of craniofacial injuries in the population. However, the findings may not be directly comparable because they are from different sources at different times, and because those at risk for each type of injury are not quantified in most cases.
72 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem sports injuries, and motor vehicle collisions (De Wet mouth and chewing, headaches, and ear pain. Based 1981, Pinkham and Kohn 1991, Sane 1988). In the upon assessments of pain in or around the jaw joint, National Health Care Survey of emergency rooms, these disorders are estimated to affect 10 million assaults and falls each accounted for 31 percent of Americans (Lipton et al. 1993). visits related to head and face injury. Other studies Data from the few available population-based have reported that up to 19 percent of head and face epidemiologic studies indicate that the prevalence of injuries are sports-related (McDonald 1994), and 5 self-reported pain symptoms and clinical signs of percent of head and 19 percent of face injuries result TMD pain is between 5 and 15 percent, with peak from riding bicycles and tricycles (U.S. Consumer prevalence in young and middle-aged adults (20 to Product Safety Commission 1987). 40 years of age) (Von Korff 1995). There are differences in rates of emergency room Although physical signs associated with TMDs visits for head and face injuries among demographic have been shown to occur with nearly equal fre- groups. Males had higher rates than females, except quency among men and women, clinical studies have among older adults. The rates of injury were higher found that women in the third and fourth decades of for younger and older adults than for those in the life were much more likely than men of the same age middle years. to have sought care for reported facial pain in the tem- poromandibular region (Carlsson and LeResche 1995). Chronic and Disabling Conditions Sjögren’s Syndrome Sjögren’s syndrome, an autoimmune disorder that Oral-Facial Pain causes xerostomia (dry mouth), difficulty in swal- Oral-facial pain can greatly reduce quality of life. lowing, and xerophthalmia (dry eyes), is estimated to These types of pain may be due to tooth-related affect 1 to 2 million people in the United States (Talal infections, mucosal sores, and irritations, and may 1992). The diagnosis is most often made in women include burning sensations, pain in the jaw joint in middle age. One estimate of the average annual area, and aching pain across the face or cheek. Over incidence rate for Sjögren’s syndrome, based on the 39 million people, or 22 percent of adults 18 years of Olmsted County, Minnesota, medical database, is age and older in the civilian U.S. population, experi- about 3 to 5 cases per 100,000 population; this may enced at least one of five types of oral-facial pain dur- be low, however (Pillemer et al. 1995). As with most ing a recent 6-month period (Lipton et al. 1993). other autoimmune conditions (e.g., rheumatoid Based on the results of a national study of the preva- arthritis, systemic lupus erythematosis), Sjögren’s lence and distribution of oral-facial pain, it is esti- syndrome affects more women than men. The mated that during a 6-month period, 1 American female-to-male ratio depends on the study, but may adult in 8 (12.2 percent) suffers from toothache, 1 in be as high as 9:1 (Fox 1996). 12 (8.4 percent) from painful oral sores, 1 in 19 (5.3 percent) from jaw joint pain, and 1 in 71 (1.4 per- FIGURE 4.23 cent) from face or cheek pain (Lipton et al. 1993). Toothache is the most common source of oral-facial pain The prevalence of toothache and pain due to oral among adults sores decreases with age, whereas the prevalence of 14 burning mouth pain increases with age. Women are 12.5 12 12 twice as likely as men to report two specific types of oral-facial pain: jaw joint pain and face/cheek pain 10 8.9 7.8 (Figure 4.23). Non-Hispanic blacks and Hispanics 8 6.9 were slightly more likely to report toothache than 6 non-Hispanic whites (Lipton et al. 1993). Adults liv- 4 ing in poverty were more likely to report toothaches 3.5 2 1.9 than adults living above the poverty level (Vargas et per 1,000 persons Prevalence 0.9 0.8 0.6 al. 2000). 0 Toothache Oral sores Jaw joint Face/cheek Burning mouth Temporomandibular Disorders Pain category Female Male Symptoms of temporomandibular disorders (TMDs) vary but may include severe pain in the jaw muscu- Note: Data are for persons aged 18 and older looking back over the past 6 months. Sources: Adapted from NCHS 1989, Lipton et al.1993. lature, severe pain or difficulty when opening the
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 73 The Magnitude of the Problem
WHAT IS THE BURDEN OF DISEASE IN society, but relatively little systematic attention has SELECTED POPULATIONS? been focused on the oral health of blacks. Although CHALLENGES AND OPPORTUNITIES the overall oral health status of Americans has been improving, many oral diseases and conditions among The national data provide a broad-brush picture of blacks remain a serious problem—despite the fact America’s oral health. For selected populations, how- that for almost three decades these disparities have ever, oral health and disease status has a different been highlighted and recommendations made for profile. By 2050 about 50 percent of the U.S. popula- addressing health issues including research, educa- tion is expected to be Asian, non-Hispanic black, tion, human resources, and delivery systems Hispanic, and American Indian (Council of (National Dental Association 1972). These recom- Economic Advisers 1998). Currently available data mendations still represent opportunities for improve- for these groups present a picture of disease that is ment in the oral health status of African Americans. generally poorer than that for non-Hispanic whites. Baseline data for the Healthy People 2010 objec- These subgroups present a unique cluster of health, tives establish that, for children aged 2 to 4 years, socioeconomic, and cultural issues. At the same time, 24.0 percent of non-Hispanic blacks have experi- data for the subgroups within each of these categories enced dental caries in their primary teeth, compared are lacking. In addition to racial/ethnic groups, other to 15.0 percent for their non-Hispanic white coun- groups such as individuals with disabilities, the terparts. For children aged 6 to 8, there were no dif- homeless, incarcerated individuals, and migrant ferences among the races; but for 15-year-olds, a workers have unique needs and challenges. Cutting higher percentage of non-Hispanic blacks were across all subgroups are gender-specific health issues. affected than of whites. In addition the percentage of For improvements to be made in America’s overall people of all ages who had untreated caries was sub- health, a better understanding of the full dimension stantially higher for blacks than for whites—about of the problems faced by these populations and twice as many. Higher levels of gingivitis and peri- development of specific solutions are needed. This odontal loss of attachment were also seen in non- part of the chapter examines each subgroup in Hispanic blacks as compared to non-Hispanic whites. greater depth. A greater percentage of non-Hispanic blacks 18 years and older have missing teeth when compared to Racial and Ethnic Minorities non-Hispanic whites. Relative to non-Hispanic whites, however, non-Hispanic blacks aged 18 and Although there have been gains in oral health status older are less likely to have lost all their teeth (eden- for the population as a whole, they have not been tulism) regardless of whether they are poor. evenly distributed across subpopulations. Non- African American males have the highest inci- Hispanic blacks, Hispanics, and American Indians dence rate of oral cavity and pharyngeal cancers in and Alaska Natives generally have the poorest oral the United States compared with women and other health of any of the racial and ethnic groups in the racial/ethnic groups (Wingo et al. 1999). The distri- U.S. population. Other health statistics, such as life bution of oral cancer cases reveals that blacks also expectancy and infant mortality, indicate that the have a higher proportion of pharyngeal cancer than general health of these groups is varied and also poor oral cavity cancer compared to whites. Also, the 5- compared to other population groups (Council of year relative survival rate (1989-95) for oral cancer Economic Advisers 1998). To address the elimination was much lower among blacks than whites: 34 ver- of these disparities in health—and also in housing, sus 56 percent (American Cancer Society (ACS) education, and other indicators of social and eco- 1999). This latter finding may be related to the fact nomic well-being—the administration has launched that a high percentage of these cancers are diagnosed “The President’s Initiative on Race: One America in in later stages of disease in blacks as compared to the 21st Century.” Recommendations for improving whites (ACS 1999). the oral and general health status of racial and ethnic On the other hand, for several conditions, minorities are also a prominent feature of Healthy African Americans have a lower disease burden than People 2010, the goal-setting health agenda devel- do whites. The incidence rate for cleft lip and cleft oped for the decade by the USDHHS (2000). palate in African Americans is 0.54 per 1,000, about a third the rate for whites (1.70 per 1,000). Also the African Americans prevalence of having one or more herpes labialis Numerous studies over the decades have compared lesion within the past 12 months is 50 percent less the health status of blacks and whites in American
74 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem than that for Mexican Americans and non-Hispanic education, HHANES results show that Cuban whites. American and Puerto Rican adults had about twice as many missing teeth as Mexican Americans. Puerto Hispanics Ricans and Cuban Americans also had on average Disparities in oral and general health status between more filled teeth than Mexican Americans. Puerto Hispanic and non-Hispanic populations in the Rican children and adults under 45 years old had United States have been long recognized. Yet the more gingivitis than Cuban Americans and Mexican health profile of Hispanics is incomplete due to insuf- Americans; the highest prevalence of periodontal dis- ficient sampling of subgroups in national surveys, ease was reported among Puerto Ricans compared to inconsistent or inadequate assessment of ethnicity, or the two other Hispanic groups (Ismail and Szpunar ambiguities in reporting of ethnic identity (Hahn 1990). 1992). Recent efforts to improve data collection, A national survey found that employed Hispanic identify subgroups, and provide more baseline data adults were twice as likely to have untreated dental for Hispanics have addressed the situation somewhat, caries as non-Hispanic whites. In this study, gingivi- but much work remains to ensure accurate data for tis and periodontal problems (attachment loss and health planning and research (Delgado and Estrada pockets) were also among the more common prob- 1993). lems among the Hispanic adults studied (Watson and Among preschool Hispanic children early child- Brown 1995). hood caries is a particular concern. Two reports have Analysis of a more recent survey (NHANES III) documented early childhood caries among 12.9 per- that sampled Mexican Americans is particularly cent of Hispanic children examined in San Antonio revealing. After adjusting for age, sex, educational and 37 percent of predominantly Hispanic children attainment, and annual family income, Mexican in San Francisco (Garcia-Godoy et al. 1994, Ramos- American adults are similar to their white non- Gomez 1999). Most recently, national survey data Hispanic counterparts on most oral health indicators. suggest that a higher proportion of Mexican However, among Mexican Americans, individuals in American children ages 12 to 23 months may experi- families with less than $20,000 annual income were ence dental caries than other race/ethnicity groups 1.6 times less likely to have an intact dentition, 3.1 (Kaste et al. 1996b). times more likely to have any untreated decay on the Preliminary data from NHANES III indicate that crowns of their teeth, and 4.2 times more likely to young Mexican American children aged 2 to 4 are have severely decayed teeth (very large cavities or more likely to have experienced dental caries in their only the roots of teeth remaining) than non-Hispanic primary teeth, have on average more decayed and whites (Garcia and Drury 1999). Also, Mexican filled tooth surfaces, and have more untreated disease Americans were less likely to be edentulous regard- than either non-Hispanic white or non-Hispanic less of poverty status than either non-Hispanic black children (Kaste et al. 1996b). Mexican whites or non-Hispanic blacks (Drury et al. 1999). American children aged 2 to 5 years—especially These findings confirm the importance of con- those from lower-income households—were more trolling for sociodemographic factors in reporting on likely than their African American and non-Hispanic oral health status as well as the need to assess other white counterparts to have one or more decayed factors related to health status. As a group, Hispanics primary teeth (Vargas et al. 1998). have lower median incomes, higher poverty rates, Dental caries continues to affect large numbers of more unemployment, and less education than non- school-age children and youth, as only 30 percent of Hispanic whites (Ramirez 1999). However, sociode- Mexican Americans, 32 percent of non-Hispanic mographic factors are just one aspect of the questions whites, and 41 percent of non-Hispanic blacks 12 to raised when attempting to understand differences in 17 years of age were free of caries in their permanent oral health. The effect of financial barriers and nonfi- teeth (USDHHS 1996). However, most of the dental nancial factors such as language, culture, dietary pat- caries in the permanent teeth of non-Hispanic white terns, and behaviors on access, care seeking, and children aged 12 to 17 had been treated or filled (87 health outcomes must also be examined. Variations percent), compared to 63 percent for Mexican in conditions such as diabetes also may contribute to Americans and 60 percent for non-Hispanic blacks. differences in oral health. The only large-scale survey that permits compar- It is estimated that Hispanics will surpass African ison among Hispanic subgroups is the Hispanic Americans as the country’s largest minority group by Health and Nutrition Examination Survey (HHANES 2020 (U.S. Bureau of the Census 2000). Aggregate 1982-84). After controlling for age, sex, income, and statistics obscure substantial variations within
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 75 The Magnitude of the Problem
Hispanic subgroups. More than 20 different coun- Until recent years, vital statistics and other tries of varied cultural, socioeconomic, and political health-related data were virtually nonexistent for the backgrounds are currently included in this category APIA population. Data for this group generally of the U.S. population. Narrowing the gap in oral appeared in the “other” category of national surveys, health between Hispanic and non-Hispanic groups and thus were not helpful in determining specific will require improved data on health status, barriers population-based oral or general health needs. Little to access, and disease factors underlying differences national focus has been given to defining and meas- in oral health in these populations. uring the oral health problems and related health care needs of the APIA population. These needs are Asians, Native Hawaiians, and Other Pacific now highlighted in the 2010 Healthy People Oral Islanders Health Objectives. A few statewide oral health data National data for the oral health of Asian, Native exist for some APIA child populations, but no ethnic Hawaiian, and other Pacific Islander (ANHPI) groups subgroupings can be assessed. Again, this category of that can be generalized to the U.S. population are not the U.S. population is extremely heterogeneous. It is available. Instead the profile of disease and health in estimated that 76 percent is from one of five ethnic this category is only available through studies of spe- origins and that 74 percent in 1990 were foreign cific states and locales. Among all ethnic groups in born. More than 63 percent live in four states: California in 1993 and 1994, Asian and Pacific California, New York, Hawaii, and Texas. Con- Islander American (APIA) children in Head Start had sequently, determining the reasons for variations in the highest prevalence of early childhood caries—20 oral health will require additional data. percent compared to 14 percent for all Head Start children (Pollick et al. 1997). These data are compa- American Indian/Alaska Native Populations rable to other survey findings of 16 to 20 percent and Data on the oral health of American Indians and 29 percent early childhood caries among APIA chil- Alaska Natives (AI/AN) are available through studies dren in Hawaii and California, respectively (Greer conducted by the Indian Health Service (IHS) unpublished, Louie et al. 1990). (Niendorfs 1994). The AI/AN people constitute A California study of 6- to 8-year-olds found dis- about 1 percent of the U.S. population, or an esti- parities in the oral health status of APIA children in mated 2.5 million people in 2000. Little is known or the state when compared to all children nationally. can be easily determined about the general or oral Among the California APIA children, 71 percent had health status of the 1 million AI/AN people not untreated dental caries, with a significant portion of served by the IHS system. For this reason, with the this group requiring urgent dental treatment. By exception of overall death rates obtained from census comparison, NHANES III data indicate that in 1988- data, the statistics described in this section will be 94, 29 percent of children in the United States aged 6 limited to the 1.5 million AI/AN served by the IHS. to 8 years had untreated dental decay. By and large, this group represents AI/AN people liv- There is variation in oral health status among ing on or near reservations. subgroups of ANHPI children. In a recent survey in Preliminary analyses of the IHS-wide Oral Health Hawaii, the prevalence of early childhood caries Status Survey of over 13,000 dental patients in 1999 among APIA children was 16 percent, ranging from a revealed that some conditions have worsened and low of 8 percent among Japanese children to a high some improved since an earlier survey conducted in of 25 percent among Filipino children. The preva- 1991 (IHS 1994, 2000). Across the IHS service pop- lence of untreated dental caries in 6- to 8-year-old ulation there was a statistically significant increase in APIA children was 39 percent, which ranged from a caries among adults over 55 as measured by the low of 16 percent among Japanese children to 40 per- decayed, missing, and filled teeth index. The decayed cent among Native Hawaiians, 48 percent among and filled tooth rate increased from 7.5 to 8.8 teeth, Southeast Asians, and 62 percent among non-Native with no change in the average number of missing Hawaiian Pacific Islanders (Greer 1999). teeth for this age group. Oral cancer incidence and mortality rates for Among AI/AN children across the IHS, there was APIAs are lower than those for white non-Hispanics a significant decline in caries in the permanent den- and African Americans. However, nasopharyngeal tition and a significant increase in caries in the pri- cancer incidence and mortality rates among Chinese mary dentition. Among children aged 2 to 5 years, and Vietnamese populations are many times higher the increase in decayed and filled primary teeth sur- than other groups (Miller et al. 1996), and therefore faces went from 8.6 to 11.4. In general, AI/AN popu- pose a unique health problem for these subgroups. lations have much greater rates of dental caries and
76 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem periodontal disease in all age groups than the gener- of attachment of 6 mm or more for any tooth. Both al U.S. population. AI/AN children aged 2 to 4 years black and white females (6.0 and 6.0 per 100,000) have 5 times the rate of dental decay compared to all have a substantially lower incidence rate of oral and children, and 6- to 8-year-old AI/AN children have pharyngeal cancers compared to black and white about twice the rate of dental caries experience. Rates males, respectively (20.8 and 14.9 per 100,000). A for untreated decay in these age groups are 2 to 3 higher prevalence of females than males have oral- times higher than in the same age groups in the gen- facial pain, including pain from oral sores, jaw joints, eral U.S. population. Periodontal disease in AI/AN face/cheek, and burning mouth syndrome. However, adults is 2.5 times greater than in the general U.S. there are large areas for which information for either population. High prevalence rates of diabetes among sex, even at the descriptive level, is only partial or AI/AN populations are a significant contributing fac- nonexistent. Data gaps regarding craniofacial in- tor to this periodontal disease (IHS 2000). juries, soft tissue pathologies, and salivary gland dys- Substantial unmet dental needs and quality of functions are notable examples. life issues have also been identified in IHS surveys, Most oral diseases and conditions are complex which included studies of representative AI/AN com- and represent the product of interactions between munities with regard to the effect of oral conditions genetic, socioeconomic, behavioral, environmental, on well-being and quality of life (Chen et al. 1997). and general health influences (Chapters 3 and 5). (See Chapter 6 for a general discussion.) One third of Multiple factors may act synergistically to place sub- schoolchildren report missing school because of den- groups of women at higher levels of risk for oral dis- tal pain. Twenty-five percent of schoolchildren avoid eases. For example, the comparative longevity of laughing or smiling, and 20 percent avoid meeting women, compromised physical status over time, and other people because of the way their teeth look. As the combined effects of multiple chronic conditions a consequence of dental pain, almost a quarter of the often with multiple medications, can result in adults are unable to chew hard foods, almost 20 per- increased risk of oral disease (Redford 1993). Many cent report difficulty sleeping, and 15 percent limit women live in poverty, are not insured, and are the their work and leisure activities. Three quarters of sole head of their household. For these women, the elderly experience dental symptoms, and half obtaining needed oral health care may be difficult. In perceive their dental health as poor or very poor and addition, gender-role expectations of women may are unable to chew hard food. Almost half the adults also affect their interaction with dental care providers avoid laughing, smiling, and conversation with oth- and could affect treatment recommendations as well ers because of the way their teeth look. (Redford 1993). Again, the available data allow for obtaining a During the past decade, women’s health has picture only of the AI/AN population residing on emerged as a significant issue in the nation’s health reservations where services, including dental servic- agenda. The scientific community is beginning to es, have been provided by the IHS or contracted to respond to this concern by studying and reporting tribes or urban AI/AN organizations. In 1989, the effects of sex and gender differences on health American Indians, residing in the current reservation and disease management. Although most of the effort states had a median household income of $19,897. has focused upon women, comparisons with men’s Almost one third (31.6 percent) of AI/ANs lived health have begun to elucidate sex- and gender- below the poverty level. For some groups, diabetes specific differences. and high rates of tobacco and alcohol use are preva- Research has demonstrated sex and gender dif- lent and contribute to poor oral health. ferences in the response to kappa opioid analgesics for the control of postoperative pain (Gear et al. 1996). These findings have heightened conjecture Women’s Health about differences in the female and male nervous sys- Analysis of data from NHANES III indicates that tems in response to pain stimuli. There are studies in women have benefited from the trend in general mice that suggest that there are sex-specific respons- improvements in oral health that has been enjoyed es to pain and analgesics (Mogil et al. 1996, 1997). by the U.S. population overall. Many, but not all, sta- Taken together, these findings could help explain tistical indicators show women to have improved why women report certain painful conditions more their oral health status as compared to men than men; for example, temporomandibular joint (NHANES III, Redford 1993). Adult females are less disorders, trigeminal neuralgia, migraine headaches, likely than males at each age group to have severe and burning mouth syndrome (USDHHS 1999). periodontal disease as measured by periodontal loss
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 77 The Magnitude of the Problem
Recent research has also demonstrated sex and ioral and environmental differences—to name a gender differences in taste perception. Women are few—decreases the utility of those data that are avail- more likely than men to be “supertasters” of a bitter able. For example, women are reported to be more compound known as 6-n-propylthyiouracil (PROP) inclined to self-care, to visit the dentist more often, (Bartoshuk et al. 1994). PROP supertasters experi- and to be more likely to report symptoms such as ence more intense tastes (particularly for bitter and pain. However, the effects of these behaviors on their sweet), a greater sensation of oral burning in oral health status cannot be determined fully. Figure response to alcohol, and more intense sensations 4.24 suggests content areas in the study of women’s from fats in food (Bartoshuk et al. 1994, 1996, Tepper oral health. and Nurse 1997). PROP supertasters also have more fungiform papillae on their tongues than medium PROP tasters or those who cannot taste PROP at all. Individuals with Disabilities The Agenda for Research on Women’s Health for No national studies have been conducted to deter- the 21st Century noted that the ability to interpret mine the prevalence of oral and craniofacial diseases oral health in the context of sex and gender was lim- among the various populations with disabilities. ited by large gaps in knowledge. For example, perti- Several local and regional reports, however, provide nent oral health data, even at the descriptive level, are some relevant data in this regard. For example, some partial or nonexistent for many conditions and dis- smaller-scale studies show that the population with eases for either sex. In addition, limited knowledge of mental retardation or other developmental disabili- etiologic factors, natural history of diseases, behav- ties has significantly higher rates of poor oral hygiene
FIGURE 4.24 Content areas in the study of women’s health Oral Influences on Systemic Health Women and the Health Care System Evidence for links between oral infection Treatment decision making and diabetes Over/underutilization of professional services Health policy
Diseases More Common in Women Than Men Systemic Influences on Oral Health TMD, oral-facial pain, Sjögren’s Longevity syndrome, salivary gland Multiple chronic conditions dysfunction, burning mouth, Medication usage alterations in taste, Cognitive impairments pregnancy-associated oral changes Physical confinement Compromised functional status Postmenopausal bone loss HIV Diabetes Oral Diseases Affecting the Most Women Caries Societal Influences on Women’s Health Periodontal diseases Caregiving Status as single head of household Poverty Gender role expectations Underinsurance Concern for aesthetics Access to care Craniofacial trauma Gender Influences on Health Risk Dental care utilization Self-care Eating disorders Unprotected sexual activity
Source: Adapted from Chesney and Ozer 1995 and reprinted in USDHHS 1999.
78 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem and needs for periodontal disease treatment than the ing special health care need. Similarly, children from general population, due, in part, to limitations in less educated households exhibit a higher likelihood individual understanding of and physical ability to of a special health care need. Children in single-par- perform personal prevention practices or to obtain ent families are about 40 percent more likely than needed services. There is a wide range of caries rates children from two-parent households to have special among people with disabilities, but overall their rates health care needs (Newacheck et al. 1998). are higher than those of people without disabilities. Deinstitutionalization has resulted in highlighting Much of the variation stems from where people the problem these individuals have regarding access reside (e.g., in large institutions where services are to dental care as they move from childhood to adult- available versus in the community where services hood. Availability of dental providers trained to serve must be secured from community practitioners). special needs populations and limited third-party Almost two thirds of community-based residential support for the delivery of complex services (see facilities report that inadequate access to dental care Chapter 9) further complicate the issues entailed in is a significant issue (Beck and Hunter 1985, White addressing the needs of this population. et al. 1995, Waldman et al. 1998, Dwyer, Northern Given the wide variability among groups with Wisconsin Center for the Developmentally Disabled disabilities, this review of oral health status and unpublished data, 1996). Parents consistently report needs is quite limited. More in-depth assessment and dental care as one of the top needed services for their analysis of the determinants of oral health status, children with disabilities regardless of age (Haveman access to care, and the role of oral health in the over- et al. 1997). Local studies of independent living cen- all quality of life and life expectancy of individuals ters reported that 24 to 30 percent of adults with with disabilities are needed (see Chapter 10). cerebral palsy, 14 percent with spinal cord injuries, 30 percent with head injuries, and 17 percent who were deaf had dental problems (Arnett 1994). Results UTILIZATION OF PROFESSIONAL from 1999 oral assessments of U.S. Special Olympics CARE: WHAT DO WE KNOW ABOUT athletes (all ages), based on an extremely conserva- THE RELATIONSHIP OF ORAL HEALTH tive assessment protocol (without the use of x-rays, AND USE OF DENTAL SERVICES? mirrors, or explorers), and carried out by the Special With few exceptions, maintenance of oral health Olympics Special Smiles Program in 20 states, indi- through a lifetime requires timely receipt of advice cate that 12.9 percent of the athletes reported some for self-care, preventive therapies, early detection and form of oral pain, 39 percent demonstrated signs of treatment of problems, and restoration of function. gingival infection, and nearly 25 percent had untreat- Chapter 7 describes community-based and profes- ed decay (Special Olympics, Inc., unpublished data). sional interventions that have played a significant Note that this is a population that tends to be from role in the improvement of oral health achieved over higher-income families. the past 50 years; their full promise has not, howev- The oral health problems of individuals with dis- er, been realized. Chapter 8 describes current and abilities are complex. These problems may be due to emerging strategies for personal and provider underlying congenital anomalies as well as to inabil- approaches to maintain and restore oral health, with ity to receive the personal and professional health tooth-conserving approaches being employed more care needed to maintain oral health. There are more and more frequently. As noted earlier, almost every- than 54 million individuals defined as disabled under one experiences oral diseases and conditions over the Americans with Disabilities Act, including almost the course of a lifetime, and, unlike the common a million children under age 6 and 4.5 million chil- cold, most diseases do not resolve over time. dren between 6 and 16 years of age. A greater per- Consequently, receipt of dental services complements centage of males than females and of African self-care as a critical factor in achieving and main- Americans than Hispanics and whites have disabili- taining good oral health. ties (Federal Interagency Forum 1997, Waldman et Although certain counseling and screening serv- al. 1999). Children with disabilities have chronic ices provided by physicians are recommended (U.S. physical, developmental, behavioral, and emotional Preventive Services Task Force 1996), data to indi- limitations, including mental retardation, autism, cate how many persons receive such services or oral- attention deficit hyperactivity disorders, and cerebral health-related recommendations from their physi- palsy. Also, children from families with incomes cian are very limited. There are also no data on physi- below the poverty level are about one third more like- cian-based services for oral and craniofacial condi- ly than children in nonpoor families to have an exist- tions. The data that are available describe utilization
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 79 The Magnitude of the Problem of dental visits. Unfortunately, most of these data are cross-sectional, describing the experience of the pop- TABLE 4.3 ulation in any given year, but providing little detail Percentage of persons 25 years of age and older with a dental about how patterns of care over time contribute to visit within the preceding year, by selected patient character- oral health. Nevertheless, utilization of care is used as istics, selected years a surrogate measure of an individual’s or a popula- 1983a 1989a 1990 1991 1993 tion’s capacity to maintain or improve health status. Totalb,c 53.9 58.9 62.3 58.2 60.8 An understanding of utilization of dental visits and Age differences in such visits among age, racial/ethnic, 25 to 34 years 59.0 60.9 65.1 59.1 60.3 sex, and income groups is important in identifying 35 to 44 years 60.3 65.9 69.1 64.8 66.9 45 to 64 years 54.1 59.9 62.8 59.2 62.0 opportunities for improvement in oral health that 65 years and older 39.3 45.8 49.6 47.2 51.7 would follow from timely receipt of professional care. 65 to 74 years 43.8 50.0 53.5 51.1 56.3 Characteristics of groups with different levels of 75 years and older 31.8 39.0 43.4 41.3 44.9 dental care utilization suggest barriers to care as well Sexc as factors that predispose or enable access to dental Male 51.7 56.2 58.8 55.5 58.2 care. Explanations for variation in utilization are Female 55.9 61.4 65.6 60.8 63.4 alluded to in the following section, and are discussed Poverty statusc,d in further detail in Chapter 10. More studies are Below poverty 30.4 33.3 38.2 33.0 35.9 needed to understand the dimensions of disease and At or above poverty 55.8 62.1 65.4 61.9 64.3 the role of professional care and use of services. Also, Race and Hispanic originc for oral health in particular, the contributions of all White,non-Hispanic 56.6 61.8 64.9 61.5 64.0 Black,non-Hispanic 39.1 43.349.1 44.3 47.3 health professions and the interdisciplinary nature of Hispanice 42.1 48.9 53.8 43.1 46.2 care need to be emphasized. Educationc Less than 12 years 35.1 36.9 41.2 35.2 38.0 12 years 54.8 58.2 61.3 56.7 58.7 Dental Care Utilization 13 years or more 70.9 73.9 75.7 72.2 73.8 Education,race,and Visiting a health care provider at least once per year Hispanic originc and the number of visits made within the past year Fewer than 12 years are used as indicators of an individual’s ability to White,non-Hispanic 36.1 39.1 41.8 38.1 41.2 access professional services. Dental care utilization Black,non-Hispanic 31.7 32.0 37.9 33.0 33.1 statistics are traditionally based on an individual’s Hispanice 33.8 36.5 42.7 28.9 33.0 reporting “at least one dental visit in the past year,” 12 years White,non-Hispanic 56.6 59.8 62.8 58.8 60.4 although there are variations with shorter recall Black,non-Hispanic 40.5 44.8 51.1 43.1 48.2 intervals and different forms of the question. Hispanice 48.7 56.5 59.9 49.5 54.6 Depending on the question and survey method, 13 years or more annual dental care use estimates vary. The 1996 White,non-Hispanic 72.6 75.8 77.3 74.2 75.8 Medical Expenditures Panel Survey (MEPS) esti- Black,non-Hispanic 54.4 57.2 64.4 61.7 61.3 e mates that 43 percent of the U.S. population 2 years Hispanic 58.4 66.2 67.9 61.2 61.8 and older had at least one dental visit that year a Data for 1983 and 1989 are not strictly comparable with data for later years.Data for (MEPS 2000). Responding to a variation of a ques- 1983 and 1989 are based on responses to the question “About how long has it been since you last went to a dentist?”Starting in 1990,data are based on the question tion that had been asked in many previous surveys, “During the past 12 months,how many visits did you make to a dentist?” some 65.1 percent of the U.S. population 2 years and bIncludes all other races not shown separately and unknown poverty status and educa- older reported in 1997 that they had visited a dentist tion level. c in the preceding year (NCHS 1997b), up from 55.0 Age adjusted. dPoverty status is based on family income and family size using Bureau of the Census percent in 1983 (Bloom et al. 1992). The average poverty thresholds. number of visits per person remains at about two per e Persons of Hispanic origin may be of any race. year. Further research is needed to understand rea- Notes:Data are based on household interviews of a sample of the civilian noninstitu- sons for variations in estimates from different survey tionalized population.Denominators exclude persons with unknown dental data. approaches, but differences among persons with dif- Estimates for 1983 and 1989 are based on data for all members of the sample house- hold.Beginning in 1990,estimates are based on one adult member per sample house- ferent characteristics are quite similar regardless of hold.Estimates for 1993 are based on responses during the last half of the year only. survey method. Source:Data from NCHS 1989. Data from the 1997 National Health Interview Survey, reprinted in Healthy People 2010, indicate that the highest percentage reporting at least one
80 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem dental visit was third-grade children (82 percent). Variation by Sex, Race/Ethnicity, Income, Those aged 25 years and older with less than a high and Insurance school education had the lowest rates (41 percent) Dental care utilization varies with sex and race/eth- for annual dental visits as compared to those with at nicity for individuals 25 and older (NCHS 1997a). least some college education (74 percent) (USDHHS Females had slightly higher rates of utilization (67 2000). percent) than males (63 percent). Hispanic individuals had the low- TABLE 4.4 est utilization (53 percent), and Age-adjusted percentage distribution of persons 2 years and older by interval since non-Hispanic whites had the high- last dental visit, by selected characteristics, 1989 est rates (68 percent). Table 4.3 provides an overview of utilization Interval Since Last Dental Visit from 1983 through 1993. A higher 1 Year to 2 Years to percentage of females reported a All Less Than Less Than Less Than 5 Years dental visit than males in each sur- Intervals 1 Year 2 Years 5 Years or More Never vey year. Fewer non-Hispanic All ages 100.0 57.3 9.5 12.3 11.0 4.6 blacks and Hispanics reported a Sex dental visit than non-Hispanic Male 100.0 54.7 9.6 13.4 12.1 4.9 whites in each survey year. Income Female 100.0 59.9 9.4 11.2 10.1 4.4 and education are also key vari- Race ables in utilization. In 1993, White 100.0 59.5 9.1 11.6 10.5 4.4 almost twice as many individuals Black 100.0 43.2 12.3 16.9 15.1 5.8 25 and older living at or above the Other 100.0 51.6 9.7 14.0 10.8 6.7 poverty line had a dental visit than Hispanic origin did those living below the poverty Non-Hispanic 100.0 58.5 9.4 12.0 10.8 4.1 line in 1993 (64.3 versus 35.9 per- Hispanic 100.0 46.0 10.5 14.6 13.0 9.7 cent). Similarly, almost twice as Mexican American 100.0 40.5 8.9 15.3 15.8 13.1 many individuals with 13 years or Other Hispanic 100.0 53.2 12.3 13.7 9.9 5.1 more of education had a visit than Place of residence did those with fewer than 12 years MSAa 100.0 58.4 9.4 11.9 10.1 4.5 of education (73.8 versus 38.0 per- Central city 100.0 54.9 10.1 12.9 10.9 5.1 cent) in that same year. Not central city 100.0 60.6 9.0 11.3 9.6 4.2 Data from the 1989 National a Not MSA 100.0 53.6 9.7 13.6 14.1 5.1 Health Interview Survey showed Geographic region that the overall age-adjusted num- Northeast 100.0 60.7 10.4 10.7 9.0 3.5 ber of visits for blacks was 1.2 vis- Midwest 100.0 61.5 8.3 11.3 10.7 3.5 its compared to 2.2 visits for South 100.0 52.2 10.3 13.9 13.6 5.9 whites (Bloom et al. 1992). West 100.0 57.8 8.6 12.3 9.1 4.9 Table 4.4 shows the percent- Education level age distributions of the interval Less than 9 years 100.0 30.6 9.9 18.4 30.6 5.9 since their most recent dental visit 9 to 11 years 100.0 39.0 10.7 20.3 23.5 1.3 for people aged 2 and older in 12 years 100.0 54.6 10.6 15.0 14.4 0.5 13 years or more 100.0 70.2 8.5 10.3 6.9 0.2 selected demographic and socioe- conomic categories. Individuals Family income who have never visited a dentist Less than $10,000 100.0 42.2 10.9 16.3 20.1 7.0 ranged from a high of 13.1 percent $10,000 to $19,999 100.0 43.9 11.8 17.4 16.1 6.6 $20,000 to $34,999 100.0 58.2 10.5 3.2 10.4 4.6 of Mexican Americans to 5.8 per- $35,000 or more 100.0 72.5 7.8 8.5 5.5 2.9 cent of blacks and 4.4 percent of whites. Eleven percent of the pop- Dental insurance coverage With private dental insurance 100.0 70.4 8.7 9.2 6.6 3.3 ulation had not had a dental visit Without private dental insurance 100.0 50.8 10.7 15.4 14.2 6.0 in 5 years or more. Individuals with fewer than 9 years of educa- a MSA = metropolitan statistical area. tion represented the highest pro- Source:Bloom et al.1992. portion, 30.6 percent, of those reporting no dental visit in 5 years
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 81 The Magnitude of the Problem or more, compared with 6.9 percent of those with 13 tions are also related to dental service utilization. Of years or more of education. A larger proportion of those who reported no physical limitations in activi- individuals without private dental insurance had not ties, 58.5 percent reported a dental visit within the had a dental visit in 5 years or more compared with past year, compared to 46.6 percent of those who those with private dental insurance (14.2 versus 6.6 were unable to carry out their usual activities (Table percent). Hispanic individuals have the lowest rate of 4.5) (Bloom et al. 1992). dental insurance coverage—29.0 percent, compared Whether a person had natural teeth was strongly with 32.4 percent for non-Hispanic blacks and 41.8 associated with dental care utilization (Table 4.5). percent for non-Hispanic whites (U.S. Bureau of the Dentate persons were more than 4 times more likely Census 1997). to report a dental visit within the past year than eden- Professional care is necessary for several critical tulous people: 65.5 versus 14.3 percent. Over half dental disease prevention measures, such as the (55.2 percent) of those who were edentulous reported application of dental sealants. Unfortunately, dental that they had not had a dental visit in 5 years or more. sealants are 3 times less likely to be found on the Recent analyses of data from NHANES III show teeth of Mexican American and African American that adults 18 and older who reported a dental visit children than among white children aged 5 to 17 in the past 12 months were nearly 9 times more like- (Selwitz et al. 1996). Asian and Pacific Islander ly to be dentate and 4.4 times more likely to have a American children in California also demonstrated a complete dentition than adults who did not report low rate of sealant use (Pollick et al. 1997). visiting a dentist within the preceding 12 months. Dentate adults who reported a dental visit in the past 12 months were 3.1 times less likely to have untreat- Variation by Oral Health Status ed coronal decay and 1.5 times less likely to have Utilization of dental care is associated with self- gingivitis than dentate adults who did not report a reported health status, as shown in Table 4.5. Of recent dental visit (T. Drury, NIDCR, personal com- those who reported “excellent” or “very good” munication, 1999). health, 61.4 percent had had a dental visit within the A study comparing individuals who had had a past year, compared with about 45.1 percent of those dental visit in the past 12 months with those who had reporting “fair” or “poor” health. Functional limita- not reported that dentate adults who had a recent visit were less likely to have untreated coronal and root caries, TABLE 4.5 pulpal pathology, and retained Age-adjusted percentage distribution of persons 2 years and older by interval since tooth roots. They also were more last dental visit, by selected health characteristics, 1989 likely to rate the general condition Interval Since Last Dental Visit of their teeth and gums as excel- lent or very good (Drury and 2 Years to Redford 2000). All Less Than 1 Year to Less Than 5 Years Examination of NHANES III Intervals 1 Year 2 Years 5 Years or More Never data by low socioeconomic status Assessed health status (SES) provides an additional per- Excellent or very good 100.0 61.4 9.3 11.2 9.0 4.3 spective. In a recent analysis, SES Good 100.0 51.9 10.1 13.9 12.6 5.8 was measured by a composite Fair or poor 100.0 45.1 10.0 16.6 17.4 5.9 index based on educational attain- Limitation of activity ment and the ratio of annual fami- Unable to carry on usual ly income to the poverty threshold. activity 100.0 46.6 9.8 15.6 16.6 5.1 Limited in amount or kind Among all adults, people with of major activity 100.0 52.3 9.8 14.0 14.4 4.7 lower SES scores were nearly 9 Limited,but not in major times more likely to be edentulous activity 100.0 59.1 8.3 12.8 11.7 4.2 than those with higher SES scores. Not limited in activity 100.0 58.5 9.5 12.0 10.1 4.6 Among the dentate, those with lower SES scores were 6 times Dentition status more likely to have coronal decay Dentate 100.0 65.5 9.6 12.8 10.1 0.5 Edentulous 100.0 14.3 6.4 19.8 55.2 0.4 and nearly 4 times less likely to have visited a dentist in the past 12 Source: Bloom et al.1992. months (Drury et al. 1999).
82 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem
Reasons for Nonutilization 16.4 percent of those in households whose family Reasons for nonutilization of dental services are com- income was less than 150 percent of the poverty level plex. Principal reasons cited by respondents of all reported dental care wants. More than 22 percent of ages (Bloom et al. 1992) are given in Table 4.6. the uninsured reported dental care wants. Insured Slightly less than half of those reporting no dental children with special health care needs were 4 times visit in the past year (46.8 percent) said that they per- more likely to report unmet need for dental care ceived having no dental problem. This perception (23.9 percent versus 6.1 percent) if they were unin- was the predominant response of individuals in all sured than if they were insured, according to a recent demographic categories, except for those 65 and analysis of data from the National Health Interview older, who gave having no teeth as the predominant Survey (Newacheck et al. 2000). reason. Younger individuals were more likely than older to cite “no dental problem.” Blacks were more Outcomes of Appropriate Levels of Access likely to report “no problems” (58.5 percent) as a rea- son for no dental visit, compared to 44.3 percent of and Utilization: An Example whites (Bloom et al. 1992). The effects on health of a system of care with assured Having no teeth (14.3 percent) was the next access and positive expectations of care-seeking and most frequently reported reason for no dental visit. utilization behavior have been demonstrated by the About half of the people 65 and older in the 1989 U.S. Department of Defense. There are currently over survey gave this as their reason for no dental visit— 1.4 million men and women on active duty in the 39.2 percent of blacks compared to 51.2 percent of U.S. military. The population is predominantly male whites. (86 percent). The racial distribution is 68 percent The third most frequently cited reason was the white, 20 percent black, 7 percent Hispanic, 3 per- cost of care, mentioned by 13.7 percent of respon- cent Asian, and 2 percent other groups. Slightly over dents. Whites (14.3 percent) were more likely than 30 percent of active duty personnel are between the blacks (11.4 percent) to cite cost. Other surveys have ages of 20 and 24, and 91 percent are younger than reported substantially higher percentages of individ- 40. In 1997, 59 percent were married. Seventy-six uals indicating cost as a barrier, particularly those in percent had a high school degree, and 19 percent underserved or low-income areas (Bloom et al. were college graduates. 1992). The age group most sensitive to the cost of Free dental care, one of the benefits provided to care was 18- to 34-year-olds, 19.1 percent of whom active duty military personnel, eliminates one of the gave cost as the reason for no dental visit. Finally, a significant barriers that has been identified as small proportion of respondents (4.3 percent) report- limiting access to care for many in the civilian ed fear as a personal barrier to receipt of care. population. In addition, military personnel are required to receive a dental examination annually, even if the individual perceives that he or she has “no Unmet Needs problem.” Dental care is available to most military Unmet health needs can be assessed in many ways. personnel at their duty station, eliminating the need Because oral diseases are common and do not resolve to travel long distances. A comparison of the oral over time in the absence of intervention, the lack of health and utilization of dental care of the military dental visits is used as an indicator of unmet health and civilian populations illustrates the impact of needs. In addition, the National Access to Care elimination of these barriers to care on oral health, Survey documented the extent of dental care that even for persons from demographic groups that are individuals wanted but could not obtain (“wants”) in traditionally underserved. the total population and among various population In 1994 the Tri-Service Comprehensive Oral subgroups (Mueller et al. 1998). About 8.5 percent of Health Survey examined and administered question- the U.S. population wanted, but did not obtain, den- naires to 13,050 active duty military personnel using tal care in 1994 (Table 4.7). In contrast, only 5.6 per- a complex, weighted survey design to examine the cent reported unmet medical or surgical care wants. oral health status, dental treatment needs, dental uti- Adult women aged 19 to 64 reported the greatest lization, and perceived need for care in this popula- level of dental care wants; elderly people 65 and older tion (York et al. 1995). The study found that nearly had the lowest level. Blacks, people in fair or poor all (99.2 percent) active duty military personnel had health or with one or more chronic conditions, and seen a dentist within the past 2 years. Eighty percent people living in the South reported higher levels of of active duty personnel received a dental examina- dental care wants than comparable groups. About tion within the past year, 60 percent had a dental
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 83 The Magnitude of the Problem
TABLE 4.6 Percentage of persons with no dental visit in past year by reason reported, by selected characteristics, 1989 All with No Visits Access No Dental Not Other in Past Year Fear Cost Problem Problem No Teeth Important Reason Age All ages 100.0 4.3 13.7 1.7 46.8 14.3 2.3 8.7 2 to 17 years 100.0 1.3 15.0 1.5 56.8 0.2 1.9 11.9 18 to 34 years 100.0 5.9 19.1 2.4 52.4 0.7 3.2 9.5 35 to 64 years 100.0 5.8 12.8 1.5 43.3 17.8 2.2 8.4 65 years and older 100.0 2.2 4.1 1.1 31.2 49.7 1.1 3.9 Sex Male All ages 100.0 4.0 13.0 1.5 49.1 12.1 2.6 9.3 2 to 17 years 100.0 1.2 14.9 1.3 56.2 *0.2 2.0 12.1 18 to 34 years 100.0 5.5 17.5 2.0 54.8 0.6 3.4 9.7 35 to 64 years 100.0 5.4 11.2 1.5 45.4 16.1 2.8 9.5 65 years and older 100.0 1.7 4.0 1.0 33.6 48.6 1.3 3.5 Female All ages 100.0 4.6 14.3 1.8 44.4 16.6 1.9 8.1 2 to 17 years 100.0 1.5 15.2 1.6 57.4 *0.2 1.8 11.6 18 to 34 years 100.0 6.5 21.0 2.9 49.5 0.8 3.0 9.3 35 to 64 years 100.0 6.2 14.4 1.5 41.1 19.5 1.6 7.3 65 years and older 100.0 2.5 4.2 1.2 22.5 50.6 0.9 4.1 Race White All ages 100.0 4.4 14.3 1.8 44.3 15.7 2.4 9.4 2 to 17 years 100.0 1.3 16.4 1.7 54.0 0.2 2.0 13.3 18 to 34 years 100.0 6.2 20.7 2.6 49.6 0.7 3.4 10.6 35 to 64 years 100.0 5.8 13.0 1.6 41.3 19.0 2.4 9.1 65 years and older 100.0 2.1 3.7 1.1 30.5 51.2 1.1 3.9 Black All ages 100.0 4.0 11.4 1.0 58.5 8.8 1.5 5.1 2 to 17 years 100.0 1.3 10.7 *0.7 68.3 *0.2 1.2 6.6 18 to 34 years 100.0 4.9 13.3 1.5 63.8 *0.7 2.5 4.6 35 to 64 years 100.0 6.0 11.7 0.9 52.8 13.0 1.1 4.9 65 years and older 100.0 3.0 7.0 *1.0 36.6 39.2 *0.9 3.4 Other All ages 100.0 3.7 10.8 1.6 52.1 6.1 2.2 9.2 2 to 17 years 100.0 *1.7 11.4 *0.3 49.8 *0.0 *2.4 12.6 18 to 34 years 100.0 4.6 11.7 *2.5 59.4 *0.3 *2.2 8.8 35 to 64 years 100.0 4.6 10.8 *1.9 51.0 8.2 *2.6 7.7 65 years and older 100.0 *2.8 *4.2 *0.7 31.4 44.9 *0.7 *5.9 Hispanic origin Non-Hispanic All ages 100.0 4.3 13.0 1.7 45.7 15.6 2.2 9.1 2 to 17 years 100.0 1.3 14.4 1.3 56.2 0.2 1.9 12.8 18 to 34 years 100.0 6.0 18.9 2.5 51.6 0.7 3.2 10.1 35 to 64 years 100.0 5.8 12.0 1.5 42.5 18.8 2.2 8.7 65 years and older 100.0 2.1 4.0 1.1 30.9 50.4 1.1 3.9 Hispanic,total All ages 100.0 4.0 19.1 1.8 56.1 3.5 2.6 5.9 2 to 17 years 100.0 1.6 18.4 2.4 59.5 *0.1 2.2 7.3 18 to 34 years 100.0 5.2 20.1 1.5 57.9 *0.2 3.3 5.6 35 to 64 years 100.0 5.3 20.7 1.6 52.2 6.5 2.3 5.2 65 years and older 100.0 *4.6 8.2 *1.4 40.7 31.9 *1.6 *3.4
84 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem
All with No Visits Access No Dental Not Other in Past Year Fear Cost Problem Problem No Teeth Important Reason Hispanic,Mexican American All ages 100.0 3.6 20.7 1.7 56.2 2.4 2.3 5.3 2 to 17 years 100.0 *1.4 19.4 2.6 60.7 *0.1 2.2 5.5 18 to 34 years 100.0 4.7 21.0 *0.9 57.5 *0.1 2.8 4.8 35 to 64 years 100.0 5.2 24.3 *1.4 50.1 4.5 *1.7 6.4 65 years and older 100.0 *4.3 *11.1 *1.4 38.7 30.5 *1.8 *1.8 Hispanic,other All ages 100.0 4.7 16.3 2.0 55.9 5.3 3.1 7.0 2 to 17 years 100.0 *1.8 16.3 *1.9 56.9 *0.2 *2.0 11.3 18 to 34 years 100.0 6.2 18.5 *2.4 58.7 *0.4 4.4 7.0 35 to 64 years 100.0 5.5 16.3 *1.8 54.9 8.9 *3.1 3.8 65 years and older 100.0 *4.9 *5.7 *1.4 42.8 33.2 *1.4 *4.9 Place of residence MSA,totala All ages 100.0 4.4 13.4 1.8 46.6 12.8 2.4 9.0 2 to 17 years 100.0 1.3 14.1 1.4 55.7 0.3 2.0 12.1 18 to 34 years 100.0 5.7 18.5 2.6 51.6 0.5 3.3 9.6 35 to 64 years 100.0 6.1 12.6 1.6 43.1 16.0 2.4 8.7 65 years and older 100.0 2.3 4.2 1.1 31.4 47.6 1.2 4.0 MSA,central citya All ages 100.0 4.4 14.0 1.7 48.0 11.9 2.6 7.8 2 to 17 years 100.0 1.6 14.6 1.4 56.5 *0.2 2.0 10.0 18 to 34 years 100.0 5.3 17.9 2.5 54.2 0.4 3.6 8.4 35 to 64 years 100.0 6.4 14.1 1.3 43.9 14.8 2.5 7.3 65 years and older 100.0 2.5 4.7 1.3 31.5 46.3 1.7 4.2 MSA,not central citya All ages 100.0 4.3 13.0 1.8 45.5 13.5 2.3 9.9 2 to 17 years 100.0 1.2 13.7 1.4 55.1 *0.4 2.0 13.7 18 to 34 years 100.0 6.0 19.0 2.6 49.5 0.6 3.1 10.6 35 to 64 years 100.0 5.8 11.6 1.7 42.6 16.8 2.4 9.6 65 years and older 100.0 2.1 3.9 1.0 31.3 48.5 0.8 4.0 Not MSAa All ages 100.0 4.1 14.4 1.4 47.7 18.8 1.7 8.0 2 to 17 years 100.0 1.3 18.0 1.6 60.0 *0.1 1.5 11.2 18 to 34 years 100.0 6.9 21.1 1.7 55.4 1.2 2.7 9.1 35 to 64 years 100.0 4.9 13.1 1.2 43.8 23.1 1.6 7.7 65 years and older 100.0 2.0 3.9 1.0 30.7 55.2 0.9 3.5 Family incomeb Less than $10,000 All ages 100.0 3.8 19.7 1.7 42.8 22.5 1.4 6.4 2 to 17 years 100.0 *1.1 19.4 2.6 60.0 *0.3 1.9 9.6 18 to 34 years 100.0 5.7 28.8 2.4 51.7 *0.9 1.9 7.2 35 to 64 years 100.0 6.3 25.2 *1.1 35.5 25.1 1.4 5.4 65 years and older 100.0 2.0 6.6 *0.9 27.4 57.4 *0.7 3.9 $10,000 to $19,999 All ages 100.0 4.0 18.8 1.5 47.0 17.4 1.7 6.5 2 to 17 years 100.0 1.4 21.9 1.4 58.8 •0.1 1.3 7.9 18 to 34 years 100.0 6.1 27.8 1.8 53.2 •0.5 2.4 7.9 35 to 64 years 100.0 4.7 19.2 1.5 43.6 21.7 1.6 5.7 65 years and older 100.0 3.0 3.4 1.2 31.4 51.9 1.3 4.3 $20,000 to $34,999 All ages 100.0 4.8 13.7 1.7 51.3 11.5 2.3 11.1 2 to 17 years 100.0 1.6 14.4 0.9 59.7 *0.1 1 .7 13.8 18 to 34 years 100.0 6.4 18.1 2.8 54.7 0.8 3.3 12.3 35 to 64 years 100.0 6.4 12.5 1.4 46.2 18.5 2.0 10.2 65 years and older 100.0 1.8 2.4 *1.3 38.5 47.7 *1.5 4.7 (continues)
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 85 The Magnitude of the Problem
TABLE 4.6 continued All with No Visits Access No Dental Not Other in Past Year Fear Cost Problem Problem No Teeth Important Reason $35,000 or more All ages 100.0 5.9 6.8 2.6 52.3 8.1 4 .1 14.1 2 to 17 years 100.0 1.1 5.8 2.0 56.8 *0.6 3.1 20.2 18 to 34 years 100.0 7.0 9.2 3.6 55.4 *0.6 5.4 13.4 35 to 64 years 100.0 7.8 6.0 2.3 49.7 13.2 4.0 12.9 65 years and older 100.0 *2.8 3.8 *1.6 37.9 41.6 *2.0 4.4 Dental insurance coverage With dental insurance All ages 100.0 6.2 7.2 2.5 53.2 10.1 3.4 15.2 2 to 17 years 100.0 1.2 7.8 1.2 61.4 *0.3 2.4 18.8 18 to 34 years 100.0 8.5 9.5 4.1 55.5 0.8 5.1 16.3 35 to 64 years 100.0 8.0 6.0 2.2 48.8 17.4 3.1 13.7 65 years and older 100.0 2.5 *1.6 *1.1 39.3 44.7 *1.0 5.7 Without dental insurance All ages 100.0 4.0 18.5 1.5 48.7 17.2 2.0 7.0 2 to 17 years 100.0 1.6 20.5 1.7 60.1 *0.2 1.9 9.9 18 to 34 years 100.0 5.5 26.7 1.9 56.3 0.7 2.7 7.6 35 to 64 years 100.0 5.4 18.9 1.3 45.1 19.9 2.1 6.8 65 years and older 100.0 2.3 4.9 1.2 31.9 52.5 1.2 3.9 Insurance status unknown All ages 100.0 1.6 3.9 0.7 23.8 9.3 0.8 2.9 2 to 17 years 100.0 *0.6 4.7 *1.0 25.7 *0.1 *0.6 3.6 18 to 34 years 100.0 2.3 5.1 *0.9 28.2 *0.3 1.1 3.5 35 to 64 years 100.0 1.5 3.4 *0.3 20.8 9.2 *0.7 2.0 65 years and older 100.0 *1.4 *1.6 *0.6 19.8 36.8 *0.6 2.6 Limitation of activity Unable to carry on usual activity All ages 100.0 4.4 15.4 1.7 33.2 31.9 1.1 6.2 2 to 17 years 100.0 *6.0 *27.6 *0.0 36.6 *0.0 *1.5 *20.1 18 to 34 years 100.0 7.4 25.3 *1.9 47.1 *1.9 *1.9 6.1 35 to 64 years 100.0 5.4 18.3 *1.2 34.5 28.9 *1.1 6.6 65 years and older 100.0 *1.7 6.6 2.4 26.0 49.9 *0.7 4.6 Limited in amount or kind of major activity All ages 100.0 4.4 15.2 1.9 34.5 29.7 1.7 7.5 2 to 17 years 100.0 *1.7 18.9 *2.5 58.0 *0.3 *2.0 9.1 18 to 34 years 100.0 6.9 30.2 *3.9 44.3 *0.8 *1.8 10.4 35 to 64 years 100.0 6.1 17.6 1.7 31.2 27.1 2.2 9 .3 65 years and older 100.0 2.4 5.1 *1.2 26.3 54.3 *1.1 3.9 Limited,but not in major activity All ages 100.0 4.4 12.4 0.9 34.3 35.8 1.5 6.3 2 to 17 years 100.0 *1.7 28.0 *2.2 53.0 *0.0 *1.7 *10.8 18 to 34 years 100.0 8.0 29.2 *1.9 50.5 *1.4 *1.7 10.3 35 to 64 years 100.0 6.3 17.5 *0.8 35.3 24.0 *2.0 8.0 65 years and older 100.0 2.6 3.9 *0.6 28.2 54.4 *1.2 3.9 Not limited in activity All ages 100.0 4.3 13.5 1.7 49.6 10.4 2.4 9.2 2 to 17 years 100.0 1.3 14.7 1.4 56.9 0.2 1.9 11.9 18 to 34 years 100.0 5.8 18.2 2.4 52.9 0.6 3.3 9.6 35 to 64 years 100.0 5.8 11.3 1.5 46.1 15.1 2.4 8.6 65 years and older 100.0 2.1 3.4 0.9 34.3 47.3 1.2 3.7
a MSA = metropolitan statistical area. bPersons with unknown income not shown separately. Note: Data are based on household interviews of the civilian noninstitutionalized population. * = Figure does not meet the standard of reliability or precision (more than 30 percent relative standard error and numerator of percent or rate). Source: Bloom et al.1992.
86 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem
prophylaxis, and 29 percent had at TABLE 4.7 least one tooth filled. Estimated number and percentage of people with unmet health care wants, Edentulism is virtually nonex- by selected characteristics, 1994 istent in the active duty military Medical or population. Also, active duty mili- Number of People Dental Care Surgical Care tary personnel have a significantly (in millions) (percentage) (percentage) lower proportion of their decayed, All people 259.2 8.5 5.6 missing, and filled surfaces that are Age and sex untreated; this is primarily due to Children,1 to 18 years 73.5 5.9a 2.9a dramatic improvements in the oral Adult men,19 to 64 years 75.3 9.5 5.8 health of active duty blacks when Adult women,19 to 64 years 79.3 12.1a 9.3a a a compared to their civilian counter- Elderly people,65 years and older 31.1 3.6 2.4 parts. Active duty whites also have Race/ethnicity somewhat better oral health than White 191.4 7.4 4.6 white civilians of a similar age. a a Black 32.2 15.0 10.2 The relative proportion of un- Hispanic 23.9 8.2 6.2 Other 11.7 9.9 8.6 filled surfaces as a component of decayed and filled tooth surfaces Health status in the military and civilian popula- a a Fair or poor 24.6 16.1 11.2 tions is illustrated in Figure 4.25. Good or excellent 233.5 7.7 5.0 Number of chronic conditions None 158.6 7.3 4.6 ORAL HEALTH STATUS IN One or more 100.6 10.4 7.1 CHANGING TIMES Geographical region The burden of oral diseases and Northeast 47.8 6.9 5.8 conditions in the United States is Midwest 65.8 6.9 4.5 extensive and affects persons a South 92.6 11.2 6.1 throughout their life span. Birth West 53.1 7.4 5.9 defects such as cleft lip/palate, Rural/urban status dental caries, and facial trauma are Metropolitan statistical areas 208.2 8.6 5.6 common in the young. Periodontal Nonmetropolitan statistical areas 50.5 8.1 5.9 diseases, autoimmune disorders, Education level of head of household and other chronic disabling condi- High school or less 117.5 9.4 6.8 tions are seen in adults, while Some post-high school 141.2 7.9 4.7 complete tooth loss and oral cavity Family income status and pharyngeal cancers are seen Less than 150 percent of the poverty level 55.7 16.4a 9.1a more often in older Americans. 150 percent of the poverty level or more 174.3 6.3a 4.5 Because the most common oral Health insurance status disease, dental caries, is so wide- Private 166.6 5.9a 4.1 spread in the population, nearly Medicare 36.0 5.6a 3.1a every American has experienced Medicaid 22.2 12.2 8.0 a a oral disease. Uninsured 32.5 22.6 14.9 The effects of oral diseases and Type of private health insurance conditions on quality of life and Health maintenance organization/ well-being are discussed in independent practice association 45.1 5.5a 5.0 a Chapter 6. In sum, conditions Preferred provider organization 30.7 4.6 4.1 such as cleft lip and palate and oral Fee-for-service 73.5 5.3a 3.1a cancer not only involve costly and difficult surgeries and treatments, a The estimate differs from the percentage for the “all people”demographic at the 1 percent confidence level based they also alter facial appearance on a two-tailed t-test of the difference in weighted estimates. Note: The standard error of each percentage is less than 30 percent of the percentage estimate. and impair oral functioning. Pain Source: Mueller et al.1998. Access to dental care in the United States.JADA 1998 April;129(4):429-37.Copyright 1998 by disorders and pain as a conse- Journal of the American Dental Association.Reprinted by permission of ADA Publishing Co.Inc.(2000). quence of dental disease are preva- lent in certain groups and can affect daily living.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 87 The Magnitude of the Problem
The available trend data reveal improvements in to (Chapter 9) complement the statistics needed to dental health for most Americans; however, despite assess oral health in the United States, almost all improvements in dental status, disparities remain. these data come from cross-sectional surveys that do Diseases disproportionately affect some sex, income, not allow for analysis of the outcomes of disease and and racial/ethnic groups, and the magnitude of the related care. differences is striking. All the reasons for these dis- Available state data reveal variations within and parities are not clear. Some of the most common den- among states in patterns of oral health and disease tal diseases, such as dental caries, are preventable among population groups. Having state-specific and (prevention of oral diseases and conditions is pre- local data that augment national data is critical in sented in Chapters 8 and 9). It appears, however, that identifying high-risk populations and areas and in not all individuals are benefiting from interventions addressing health disparities. These data also are vital that involve professional care, as represented by the in program evaluation, planning, and policy deci- data on dental visits. At the same time, as presented sions. Yet state and local data are almost nonexistent. in Chapter 7, about 40 percent of the public does not In recent years, the need for state and local data has receive the benefits of community water fluoridation. intensified as more programs are funded by local The emerging data on the effects of socioeconomic authorities and responsibilities are shifted from status on oral health are beginning to explain some, national to state-based levels. but not all, racial/ethnic differences. For other dis- The nation’s health information system is under- eases, health disparities appear not to be related to going constant change to meet the current and future professional services; a better understanding of the needs for health information. Consequently, many reasons for these differences is needed. factors influence how and what data are collected and This review of available data on oral diseases and analyzed. These factors include emerging technolo- conditions also reveals the lack or limitation of gies, legislation about how data are to be collected, national or state data on oral diseases for many pop- and confidentiality and privacy concerns. ulation subgroups and for many conditions that The need for epidemiologic and surveillance data affect the craniofacial structures. Information on the change as the understanding of specific diseases and variables needed to explain health status differences, conditions evolves and as society’s goals and priori- such as detailed utilization and expenditure data and ties change. The increasing focus on the long-term data on services rendered, is limited as well. Data on benefits of disease prevention and health promotion specific services—self-care, services provided by pro- and the need to close the gap on disparities also fessionals, and services that are community-based— affects how and what data are collected. For example, are needed to understand the dimensions of oral major initiatives such as the Department of Health health. (Some of these services are described in and Human Services’s Healthy People 2010 have pro- Chapters 7 and 8.) Although some data on expendi- vided a framework for data collection and analysis tures for care and health care personnel are available tied to specific objectives and have helped identify needs for new health data systems. The Healthy People initiative now FIGURE 4.25 includes objectives for the nation’s The percentage of unfilled decayed surfaces is higher for civilian males health status as well as for preven- than for males in the U.S. military tive interventions and objectives 50 that would improve infrastructure 45 40 and capacity building to provide 35 the necessary services and moni- 30 toring. 25 This overview of the magni- 20 tude of oral diseases and condi-
and filled surfaces 15 tions in America raises many ques- 10 tions still to be researched. If cer-
Percentage decayed of decayed decayed Percentage 5 tain oral diseases are preventable, 0 why do we have populations with 18-19 20-24 25-29 30-34 35-39 40-44 extensive and untreated disease? Age group Once socioeconomic factors are Black civilian White civilian Black military White military controlled, why do we see differ- Source: York et al. 1995. ences in services received? Why
88 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem are some conditions more prevalent in certain popu- Axéll T, Mornstad H, Sundstrom B. The relation of the lations than in others? How will the rapidly changing clinical picture to the histopathology of snuff dip- and projected demographics of America contribute to per’s lesions in a Swedish population. J Oral Pathol future trends in oral and craniofacial health and dis- 1976 Jul;5(4):229-36. ease? These and many other questions require more Bartoshuk LM, Duffy VB, Miller IJ. PTC/PROP tasting: research, new databases, and an active and trained anatomy, psychophysics, and sex effects. Physiol Behav 1994 Dec;56(6):1165-71. group of researchers. Bartoshuk LM, Duffy VB, Reed D, Williams A. Supertasting earaches and head injury: genetics and pathology alter our taste worlds. Neurosci Biobehav FINDINGS Rev 1996;20(1):79-87. Over the past five decades, major improve- Beck JD, Hunter RJ. Oral health status in the United ments in oral health have been seen nationally for States: problems of special patients. J Dent Educ most Americans. 1985;149:407-25. Despite improvements in oral health status, Bloom B, Gift HC, Jack SS. Dental services and oral profound disparities remain in some population health: United States, 1989. Vital Health Stat 10 1992 groups as classified by sex, income, age, and race/eth- Dec;(183):1-95. nicity. For some diseases and conditions, the magni- Brunelle JA, Bhat M, Lipton JA. Prevalence and distri- butions of selected occlusal characteristics in the US tude of the differences in oral health status among population, 1988-1991. J Dent Res 1996 Feb; population groups is striking. 75(Spec No):706-13. Oral diseases and conditions affect people Burman NT. A case: control study of oro-facial clefts in throughout their life span. Nearly every American Western Australia. Aust Dent J 1985 Dec;30(6): has experienced the most common oral disease, den- 423-9. tal caries. Burt BA, Eklund SA. Dentistry, dental practice, and the Conditions that severely affect the face and community. Philadelphia: W.B. Saunders Co.; 1999. facial expression, such as birth defects, craniofacial Carlsson GE, LeResche L. Epidemiology of temporo- injuries, and neoplastic diseases, are more common mandibular disorders. In: Sessle BJ, Bryant PS, in the very young and in the elderly. Dionne RA, editors. Temporomandibular disorders and related pain conditions. Seattle: IASP Press; Oral-facial pain can greatly reduce quality of 1995. p. 211-26. life and restrict major functions. Pain is a common Centers for Disease Control (CDC). Prevalence of oral symptom for many of the conditions affecting oral- lesions and smokeless tobacco use in Northern facial structures. Plains Indians. MMWR Morb Mortal Wkly Rep 1988 National and state data for many oral and Oct 7;37(39):608-11. craniofacial diseases and conditions and for popula- Chen MS, Andersen RM, Barmes DE, Leclercq MH, tion groups are limited or nonexistent. Available state Lyttle CS. Comparing oral health care systems: A sec- data reveal variations within and among states in pat- ond international collaborative study. Geneva: World terns of health and disease among population groups. Health Organization; 1997. Research is needed to develop better meas- Chesney MA, Ozer EM. Women and health: in search of ures of disease and health, to explain the differences a paradigm. Women’s health: research on gender, among population groups, and to develop interven- behavior, and policy. Hillsdale (NJ): Lawrence Erlbaum Associates; 1995. p. 3-26. tions targeted at eliminating disparities. Council of Economic Advisers. Changing America: indicators of social and economic well-being by race and Hispanic origin. Washington: Council of REFERENCES Economic Advisers, Executive Office of the Albandar JM, Brown LJ, Löe H. Clinical features of President; 1998 1 Sep. Available from: US GPO, early-onset periodontitis. J Am Dent Assoc 1997 Superintendent of Documents, Washington, DC. Oct;128(10):1393-9. Day GL, Blot WJ, Shore RE, Schoenberg JB, Kohler BA, Albandar JM, Brunelle JA, Kingman A. Destructive peri- Greenberg RS, Liff JM, Preston-Martin S, Austin DF, odontal disease in adults 30 years of age and older in McLaughlin JK, et al. Second cancers following oral the United States, 1988-1994. J Periodontol 1999 and pharyngeal cancer: patients’ characteristics and Jan;70(1):13-29. survival patterns. Eur J Cancer B Oral Oncol 1994 American Cancer Society (ACS). Cancer facts and fig- Nov;30B(6):381-6. ures. Atlanta: American Cancer Society; 1999. De Wet FA. The prevention of orofacial sports injuries Arnett H. First round results of the access to health sur- in the adolescent. Int Dent J 1981 Dec;31(4):313-9. vey for selected disabilities and secondary condi- Delgado JL, Estrada L. Improving data collection strate- tions. Boston: Independent Living Centers; 1994. gies. Public Health Rep 1993;108:540-5.
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ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 93
PART THREE
What Is the Relationship Between Oral Health and General Health and Well-being?
The next two chapters establish that oral health is essential to general health and well-being. Chapter 5 examines multiple linkages between oral and general health. The mouth and the face reflect signs and symptoms of health and disease that can serve as an adjunct for diagnosis for some conditions. Diagnostic tests using oral cells and fluids—especially saliva—are available to detect drug abuse, hormonal changes, and specific diseases; and more are being developed. The mouth is also a portal of entry for pathogens and toxins, which can affect the mouth and, if not cleared by the many defense mechanisms that have evolved to protect the oral cavity, may spread to the rest of the body. Recent epidemiologic and experimental animal research provides evidence of possible associations between oral infections—particularly periodontal disease—and diabetes, cardiovascular disease, and adverse pregnancy outcomes, and this evidence is reviewed. The review highlights the need for an aggressive research agenda to better delineate the specific nature of these associations and the underlying mechanisms of action. Chapter 6 looks at the impact of oral health problems on the quality of life and includes examples of the kinds of questionnaires used to measure oral-health-related quality of life. Oral health is highly valued by society and individuals, and the chapter begins with a brief description of the reflections of those values in myth and folklore concerning facial appearance and the meaning of teeth. It then explores dimensions beyond the biological and the physical to examine how oral diseases and disorders can interfere with the functions of daily living, including participation in work or school, and what is known about their psychosocial impacts and economic costs. The deleterious effects of facial disfigurement and tooth loss may be magnified in a society such as ours that celebrates youth and beauty. Self-reported impacts of oral conditions on social functions include limitations in communication, social interactions, and intimacy. Research on the oral-health-related quality of life is needed to permit further exploration of the dimensions of oral health and well-being.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 95
CHAPTER 35
Linkages with General Health
The mouth and face are highly accessible parts of the Physical Signs and Symptoms of Disease body, sensitive to and able to reflect changes and Risk Factors occurring internally. The mouth is the major portal of A number of signs and symptoms of disease, lifestyle entry to the body and is equipped with formidable behaviors, and exposure to toxins can be detected in mechanisms for sensing the environment and or around the craniofacial complex. Pathogens enter- defending against toxins or invading pathogens. In ing the mouth may proliferate locally with oral and the event that the integrity of the oral tissues is pharyngeal signs and symptoms; other pathogens compromised, the mouth can become a source of may enter the bloodstream directly or through lym- disease or pathological processes affecting other parts phatic channels and cause generalized disease. Oral of the body. It can also become a source of contagion signs suspected to be indications of systemic illness by means of contaminated fluids or materials passed may be confirmed by the presence of rash, fever, to others. This chapter explores what the mouth and headache, malaise, enlarged lymph nodes, or lesions face can reveal about general health, describes the elsewhere on the body. role the mouth plays as a portal of entry for infection, Swollen parotid glands are a cardinal sign of and concludes with studies that are associating oral infection with the mumps virus and can also be seen infections with serious systemic diseases and in individuals with Sjögren’s syndrome and HIV. The conditions. salivary glands are also frequently involved in tuber- culosis and histoplasmosis infections. Oral signs of THE MOUTH AND FACE AS A MIRROR infectious mononucleosis, caused by Epstein-Barr OF HEALTH AND DISEASE virus, include sore throat, gingival bleeding, and A physical examination of the mouth and face can multiple pinpoint-sized hemorrhagic spots (pettechi- reveal signs of disease, drug use, domestic physical ae) on the oral mucosa. The oral signs and symptoms abuse, harmful habits or addictions such as smoking, associated with some viral, bacterial, and fungal and general health status. Imaging (e.g., x-ray, MRI, infections are listed in Table 5.1. There can be a large SPECT) of the oral and craniofacial structures may overlap in the clinical appearance of oral manifesta- provide early signs of skeletal changes such as those tions of various diseases with different etiologies, and occurring with osteoporosis and musculoskeletal the clinical diagnosis often involves ancillary proce- disorders, and may also reveal salivary, congenital, dures, which may include laboratory tests, diagnostic neoplastic, and developmental disorders. Oral cells imaging, and biopsy. and fluids, especially saliva, can be tested for a wide Oral tissues may also reflect immune deficiency. range of substances, and oral-based diagnostics are For example, nearly all HIV-infected individuals increasingly being developed and used as a means to develop oral lesions at some time during their illness assess health and disease without the limitations and (Greenberg 1996, Greenspan and Greenspan 1996, difficulties of obtaining blood and urine. Phelan 1997). Other immunosuppressed individuals may have the same lesions (Glick and Garfunkel 1992). However, the presentation and the extent, sev- erity, and management of some of these lesions may reflect nuances due to variation in the underlying
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 97 Linkages with General Health
TABLE 5.1 Diseases and conditions causing lesions of the oral mucosa Condition Usual Location Clinical Features Course Viral Diseases Primary acute herpetic Lip and oral mucosa Labial vesicles that rupture and crust,and intraoral Heals spontaneously in 10 to 14 gingivostomatitis (herpes vesicles that quickly ulcerate;extremely painful; days unless secondarily infected simplex virus type 1,rarely acute gingivitis,fever,malaise,foul odor,and cervi- type 2) cal lymphadenopathy;occurs primarily in infants, children,and young adults Recurrent herpes labialis Mucocutaneous junction of lip, Eruption of groups of vesicles that may coalesce, Lasts about 1 week,but condition perioral skin then rupture and crust;painful to pressure or spicy may be prolonged if secondary foods infection occurs Recurrent intraoral herpes Palate and gingiva Small vesicles that rupture and coalesce;painful Heal spontaneously in about 1 simplex week Chickenpox (varicella-zoster Gingiva and oral mucosa Skin lesions may be accompanied by small vesicles Lesions heal spontaneously within virus) on oral mucosa that rupture to form shallow ulcers; 2 weeks may coalesce to form large bullous lesions that ulcerate;mucosa may have generalized erythema Herpes zoster (reactivation of Cheek,tongue,gingiva,or Unilateral vesicular eruption and ulceration in lin- Gradual healing without scarring; varicella-zoster virus) palate ear pattern following sensory distribution of postherpetic neuralgia is common trigeminal nerve or one of its branches Infectious mononucleosis Oral mucosa Fatigue,sore throat,malaise,low-grade fever,and Oral lesions disappear during con- (Epstein-Barr virus) enlarged cervical lymph nodes;numerous small valescence ulcers usually appear several days before lym- phadenopathy;gingival bleeding and multiple petechiae at junction of hard and soft palates Warts (papillomavirus) Anywhere on skin and oral Single or multiple papillary lesions,with thick, Lesions grow rapidly and spread mucosa white keratinized surfaces containing many point- ed projections;cauliflower lesions covered with normal-colored mucosa or multiple pink or pale bumps (focal epithelial hyperplasia) Herpangina (coxsackievirus Oral mucosa,pharynx,tongue Sudden onset of fever,sore throat,and oropharyn- Incubation period 2 to 9 days;fever A;also possibly geal vesicles,usually in children under 4 years, for 1 to 4 days;recovery uneventful coxsackievirus B and during summer months;diffuse pharyngeal con- echovirus) gestion and vesicles (1 to 2 mm),grayish-white surrounded by red areola;vesicles enlarge and ulcerate Hand,foot,and mouth Oral mucosa,pharynx,palms, Fever,malaise,headache with oropharyngeal vesi- Incubation period 2 to 18 days; disease (type A and soles cles that become painful,shallow ulcers lesions heal spontaneously in 2 to 4 coxsackieviruses) weeks Primary HIV infection Gingiva,palate,and pharynx Acute gingivitis and oropharyngeal ulceration, Followed by HIV seroconversion, associated with febrile illness resembling mononu- asymptomatic HIV infection,and cleosis and including lymphadenopathy usually ultimately by HIV disease
98 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health
Condition Usual Location Clinical Features Course
Bacterial or fungal diseases Acute necrotizing ulcerative Gingiva Painful,bleeding gingiva characterized by necrosis Continued destruction of tissue fol- gingivitis (“trench mouth,” and ulceration of gingival papillae and margins lowed by remission,but may recur Vincent’s infection) plus lymphadenopathy and foul odor Prenatal (congenital) syphilis Palate,jaws,tongue,and teeth Gummatous involvement of palate,jaws,and facial Tooth deformities in permanent bones; Hutchinson’s incisors,mulberry molars, dentition irreversible glossitis,mucous patches,and fissures of corners of mouth Primary syphilis (chancre) Lesion appears where organism Small papule developing rapidly into a large, Healing of chancre in 1 to 2 enters body;may occur on lips, painless ulcer with indurated border; unliteral months,followed by secondary tongue,or tonsillar area lymphadenopathy; chancre and lymph nodes con- syphilis in 6 to 8 weeks taining spirochetes; serologic tests positive by third to fourth week Secondary syphilis Oral mucosa frequently involved Maculopapular lesions of oral mucosa, 5 to 10 Lesions may persist from several with mucous patches,primarily mm in diameter with central ulceration covered weeks to 1 year on palate,also at commissures by grayish membrane; eruptions occurring on of mouth various mucosal surfaces and skin accompanied by fever, malaise, and sore throat Tertiary syphilis Palate and tongue Gummatous infiltration of palate or tongue fol- Gumma may destroy palate,caus- lowed by ulceration and fibrosis; atrophy of ing complete perforation tongue papillae produces characteristic bald tongue and glossitis Gonorrhea Lesions may occur in mouth at Earliest symptoms are burning or itching sensa- Lesions may resolve with appropri- site of inoculation or secondarily tion, dryness, or heat in mouth followed by acute ate antibiotic therapy by hematogenous spread from a pain on eating or speaking; tonsils and orophar- primary focus elsewhere ynx most frequently involved; oral tissues may be diffusely inflamed or ulcerated; saliva develops increased viscosity and fetid odor; submaxillary lymphadenopathy with fever in severe cases Tuberculosis Tongue,tonsillar area,soft A solitary, irregular ulcer covered by a persistent Lesions may persist palate exudate; ulcer has an undermined, firm border Cervicofacial actinomycosis Swellings in region of face,neck, Infection may be associated with an extraction, Acute form may last a few weeks; and floor of mouth jaw fracture, or eruption of molar tooth; in acute chronic form lasts months or form resembles an acute pyogenic abscess, but years; prognosis excellent; actin- contains yellow “sulfur granules”(gram-positive omycetes respond to antibiotics mycelia and their hyphae) (tetracyclines or penicillin) but not antifungal drugs Histoplasmosis Any area in mouth,particularly Numerous small nodules may ulcerate; hoarse- May be fatal tongue,gingiva,or palate ness and dysphagia may occur because of lesions in larynx usually associated with fever and malaise Candidiasis Any area of oral mucosa Pseudomembranous form has white patches that Responds to antifungals are easily wiped off leaving red, bleeding, sore surface; erythematous form is flat and red; rarely, candidal leukoplakia appears as white patch in tongue that does not rub off; angular cheilitis due to Candida involves sore cracks and redness at angle of mouth; Candida seen on KOH prepara- tion in all forms (continues)
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 99 Linkages with General Health
TABLE 5.1 continued Condition Usual Location Clinical Features Course
Dermatologic diseases Mucous membrane Primarily mucous membranes Painful, grayish-white collapsed vesicles or bullae Protracted course with remissions pemphigoid of the oral cavity,but may also with peripheral erythematous zone; gingival and exacerbations; involvement of involve the eyes,urethra,vagi- lesions desquamate, leaving ulcerated area different sites occurs slowly; glu- na,and rectum cocorticoids may temporarily reduce symptoms but do not control the disease Erythema multiforme Primarily the oral mucosa and Intraoral ruptured bullae surrounded by an Onset very rapid; condition may (Stevens-Johnson syndrome) skin of hands and feet inflammatory area; lips may show hemorrhagic last 1 to 2 weeks; may be fatal; crusts; the “iris,”or “target”lesion, on the skin is acute episodes respond to pathognomonic; patient may have severe signs of steroids toxicity Pemphigus vulgaris Oral mucosa and skin Ruptured bullae and ulcerated oral areas; mostly With repeated recurrence of bul- in older adults lae,toxicity may lead to cachexia, infection,and death within 2 years;often controllable with steroids Lichen planus Oral mucosa and skin White striae in mouth; purplish nodules on skin Protracted course,may respond to at sites of friction; occasionally causes oral topical steroids mucosal ulcers and erosive gingivitis Other conditions Recurrent aphthous ulcers Anywhere on nonkeratinized Single or clusters of painful ulcers with surround- Lesions heal in 1 to 2 weeks but oral mucosa (lips,tongue,buc- ing erythematous border; lesions may be 1 to 2 may recur monthly or several cal mucosa,floor of mouth,soft mm in diameter in crops (herpetiform), 1 to 5 times a year;topical steroids give palate,oropharynx) mm (minor), or 5 to 15 mm (major) symptomatic relief; systemic glu- cocorticoids may be needed in severe cases; a tetracycline oral suspension may decrease severity of herpetiform ulcers Behçet’s syndrome Oral mucosa,eyes,genitalia, Multiple aphthous ulcers in mouth; inflammatory Ulcers may persist for several gut,and central nervous system ocular changes; ulcerative lesions on genitalia; weeks and heal without scarring inflammatory bowel disease and CNS disease Traumatic ulcers Anywhere on oral mucosa;den- Localized, discrete ulcerated lesion with red bor- Lesions usually heal in 7 to 10 tures frequently responsible for der; produced by accidental biting of mucosa, days when irritant is removed, ulcers in vestibule penetration by a foreign object, or chronic irrita- unless secondarily infected tion by a denture
Source:Greenspan,in Fauci et al.1998.Harrison’s principles of internal medicine.Reprinted by permission from McGraw-Hill (2000).Copyright 2000 by McGraw-Hill. systemic condition. For example, the linear gingival mented lesion. Addison’s disease causes blotches or erythema and necrotizing ulcerative periodontitis spots of bluish-black or dark brown pigmentation to sometimes seen in HIV infection have been difficult occur early in the disease. Congenital discrete brown to resolve with routine dental curettage and prophy- or black patches (nevi) can appear in any part of the laxis (Glick et al. 1994b). mouth. Pigmentation of the tooth crowns may be The appearance of soft or hard tissue seen in children with cystic fibrosis and porphyria pigmentation is associated with a number of diseases and those exposed to tetracycline during tooth and treatments. Malignant melanoma can appear development. in the mouth as brown or black flat or raised spots. The oral tissues can also reflect nutritional status Kaposi’s sarcoma can appear as a flat or raised pig- and exposure to risk factors such as tobacco. The
100 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health tongue appears smooth in pernicious anemia. Group 1995, Ramos-Gomez et al. 1996) and has been B vitamin deficiency is associated with oral mucositis demonstrated to proceed to esophageal candidiasis, a and ulcers, glossitis, and burning sensations of the sign of overt AIDS (Saah et al. 1992). Both the pseudo- tongue. Scurvy, caused by severe vitamin C deficien- membranous and the erythematous forms of candidi- cy, is associated with gingival swelling, bleeding, asis appear to be important predictors of progression ulceration, and tooth loosening. Lack of vitamin D in of HIV infection (Dodd et al. 1991, Klein et al. 1984, utero or infancy impairs tooth development. Enamel 1992). hypoplasia may result from high levels of fluoride or Like oral candidiasis, oral hairy leukoplakia in from disturbances in calcium and phosphate metab- HIV-positive persons heralds more rapid progression olism, which can occur in hypoparathyroidism, gas- to AIDS (Glick et al. 1994a, Greenspan et al. 1987, troenteritis, and celiac disease. The mouth also can Lifson et al. 1994, Morfeldt-Manson et al. 1989). Oral reflect the effects of tobacco use, perhaps providing hairy leukoplakia is an oral lesion first reported in the only visible evidence of its adverse effects. the early days of the AIDS epidemic (Greenspan D et al. 1984, Greenspan JS et al. 1985). Since its discov- ery, hairy leukoplakia has been found in HIV-negative Oral Manifestations of HIV Infection and persons with other forms of immunosuppression, of Osteoporosis such as organ or bone marrow recipients and those The mouth can serve as an early warning system, on long-term steroid therapy (Epstein et al. 1988, diagnostic of systemic infectious disease and predic- Greenspan et al. 1989, Itin et al. 1988, King et al. tive of its progression, such as with HIV infection. In 1994, Zakrzewska et al. 1995), and less frequently the case where oral cells and tissues have counter- among immunocompetent persons (Eisenberg et al. parts in other parts of the body, oral changes may 1992, Felix et al. 1992). indicate a common pathological process. During rou- In a comprehensive review of periodontal condi- tine oral examinations and perhaps in future screen- tions, Mealey (1996) noted that linear gingival ery- ing tests, radiographic or magnetic resonance imag- thema and necrotizing ulcerative periodontitis may ing of oral bone may be diagnostic of early osteo- be predictive of progression of HIV infection. porotic changes in the skeleton. The following sec- Necrotizing ulcerative periodontitis, a more serious tions provide details. periodontal condition observed in HIV-infected per- sons, is a good predictor of CD4+ cell counts of HIV Infection under 200 per cubic millimeter, and in one study was a strong predictor of rapid progression to death The progressive destruction of the body’s immune (Glick et al. 1994a,b, Winkler and Robertson 1992, system by HIV leads to a number of oral lesions, such Winkler et al. 1988). In addition, the numerous as oral candidiasis and oral hairy leukoplakia, that ulcerative and nonulcerative conditions that affect have been used not only in diagnosis but also in the oral cavity (Aldous and Aldous 1991, Coates et determining specific stages of HIV infection (CDC al. 1996, Cruz et al. 1996, Gandolfo et al. 1991, Itin 1992, 1994, Montaner et al. 1992, Redfield et al. et al. 1993, Mealey 1996) may affect the biologic 1986, Royce et al. 1991, Seage et al. 1997). Oral can- activity of HIV and are affected by its treatments. didiasis is rarely seen in previously healthy young Other oral conditions, unexpected in the oral adults who have not received prior medical therapy cavity, have been noted in the early stages of HIV such as cancer chemotherapy or treatment with other infection. The increased incidence of Kaposi’s sarco- immunosuppressive drugs (Klein et al. 1984). It was ma among young men in New York and California associated with AIDS as early as 1981 in the first was one of the earliest signs of the AIDS epidemic report of the syndrome (CDC 1981a) and was fre- (CDC 1981b). In addition, some conditions create a quently noted among otherwise asymptomatic HIV- problem for differential diagnosis. For example, positive populations (Duffy et al. 1992, Feigal et al. because involvement of the gingiva is common, early 1991). Oral candidiasis may be the first sign of HIV non-Hodgkin’s lymphoma lesions are frequently mis- infection and often occurs as part of the initial phase taken for common periodontal or dental infections of infection—the acute HIV syndrome (Tindall et al. (Epstein and Silverman 1992). 1995). It tends to increase in prevalence with pro- The changing face of the HIV epidemic and gression of HIV infection when CD4 lymphocyte changes in the therapies used to manage complica- counts fall (Glick et al. 1994a, Lifson et al. 1994). It tions are reflected in changes in the oral manifesta- also appears to be the most common oral manifesta- tions, which warrant continued surveillance and tion in pediatric HIV infection (Kline 1996, Leggott research. The increasing resistance of microorganisms
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 101 Linkages with General Health to antibiotics and antifungals is challenging. On the skeletal measures in osteoporotic women and that other hand, the completion of the Candida albicans the height of the edentulous ridge is correlated with genome may yield better treatments for this oppor- total body calcium and mandibular bone mineral tunistic infection. density. Hirai et al. (1993) found that the presence of skeletal osteoporosis strongly affects the reduction of Osteoporosis and Oral Bone Loss the residual ridge in edentulous patients. A small With growing numbers of Americans living longer, case-control study comparing older female patients there have been concomitant increases in the num- with osteoporotic fractures and non-osteoporotic bers affected by age-related chronic degenerative dis- women without fractures found greater periodontal eases. Prominent among these conditions are bone attachment loss in the osteoporotic women than in and joint diseases. It is likely, for example, that some the controls (von Wowern et al. 1994). temporomandibular joint disorders are manifesta- Studies that have controlled for confounding fac- tions of osteoarthritis, rheumatoid arthritis, or tors also have found correlations between oral bone myofascial pain. Paget’s disease, characterized by loss and skeletal bone density. Controlling for pack- enlarged and deformed bone, can be particularly years of smoking, education, body mass, and years painful and debilitating when it affects the cranial since menopause, Krall et al. (1994, 1996) found a and jaw bones. significant positive relationship between number of Osteoporosis, a degenerative disease character- teeth and bone mineral density of the spine and the ized by the loss of bone mineral and associated struc- radius. In a cohort of 70 postmenopausal women, tural changes, has long been suspected as a risk fac- Wactawski-Wende et al. (1996) measured skeletal tor for oral bone loss. In addition, measures of oral bone mineral density at the Ward’s triangle area of the bone loss have been proposed as potential screening femur and compared it with periodontal disease tests for osteoporosis (Jeffcoat 1998). Osteoporosis assessed by attachment loss and the height of alveo- affects over 20 million people in the United States, lar bone measured by radiographs. After adjusting for most of whom are women, and results in nearly 2 age, years since menopause, estrogen use, body mass million fractures per year (National Institute of index, and smoking, the investigators concluded that Arthritis, Musculoskeletal and Skin Diseases 2000). osteopenia (low bone mass) is related to alveolar cres- The disease is more prevalent in white and Asian tal height and tooth loss in postmenopausal women. American women than in black women. Methods used to measure oral and skeletal bone Oral bone loss has been reported to be more loss have varied among investigators and have shown prevalent in women than in men. Studies by Ortman different outcomes. Kribbs (1990) found that et al. (1989) found a higher percentage of women patients in an osteoporotic group had lost more teeth, than men with severe alveolar ridge resorption. This had less mandibular bone, and had a thinner bone finding parallels the findings of Humphries et al. measured at a part of the jaw (cortex at the gonion) (1989), who showed that loss of bone mineral densi- than a comparable non-osteoporotic group. However, ty with age in edentulous adult mandibles was more using periodontal attachment loss as an indicator of significant in women than in men. Also, the associa- mandibular bone loss, they found no differences tion between estrogen status, alveolar bone density, between the osteoporotic and the non-osteoporotic and history of periodontitis in postmenopausal group. Mohajery and Brooks (1992) compared non- women has been studied (Payne et al. 1997). osteoporotic postmenopausal women with women Most of the studies in this area have examined with mild to moderate osteoporosis and found no bone loss in women, and most investigators have correlation between mandibular and skeletal bone reported a correlation between oral and skeletal bone mineral density. This study raises questions about the loss measured in a variety of ways. Studies of non- quantification of mild and moderate osteoporosis. osteoporotic women by Kribbs et al. (1990) showed Defining healthy periodontal tissues as having no that mandibular bone mass is significantly correlated periodontal pockets deeper than 5 millimeters, with skeletal bone mass. Dual photon absorptiometry Hildebolt et al. (1997) studied postmenopausal measurements of jawbone volume in women with women with healthy periodontal tissues and found osteoporosis have shown that reduction in mandibu- no relationship between periodontal attachment lar bone mass is directly related to the reduction in loss and postcranial bone mineral density. How- total skeletal mass density (Kribbs and Chesnut ever, preliminary studies from the oral ancillary study 1984, Kribbs et al. 1983, von Wowern 1985, 1988, of the NIH Women’s Health Initiative report signi- von Wowern et al. 1994). Kribbs et al. (1989) further ficant correlations between mandibular basal showed that mandibular mass is correlated with all bone mineral density and hip bone mineral density
102 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health
(r = 0.74, P < .001) (Jeffcoat et al. in press). In this ulation of bone mineral density in men as well as in study, digital subtraction radiography methods were postmenopausal women needs to be evaluated fur- used for mandibular bone measurements, and dual- ther with reference to oral bone loss, tooth loss, and energy X-ray absorptiometry (DXA) scans were used periodontal disease. Variables such as sex, race, for the hip bone measurements. The authors of this dietary calcium and phosphorus, vitamin D intake, study propose the possibility that high-quality intra- exercise, body mass index, smoking, genetics, med- oral radiographs may be used in the future for screen- ication use, reproductive history, and psychosocial ing osteopenia. factors need to be assessed in depth. In addition, reli- Larger cross-sectional studies, as well as longitu- able and valid criteria and imaging technologies for dinal and mechanism studies, are needed to better assessing osteoporosis and oral bone loss are needed define the relationship between osteoporosis, to better elucidate the full relationship between osteopenia, and oral bone loss, periodontal disease, skeletal and mandibular bone mineral density, peri- and tooth loss. The role of factors involved in the reg- odontal disease, alveolar ridge resorption, and tooth loss. TABLE 5.2 Saliva/oral fluids: sampled analytes and current Oral-fluid-based Diagnostics: FDA-approved tests The Example of Saliva Category Analytes FDA-Approved Tests The diagnostic value of salivary secretions to detect Drugs of abusea Alcohol Cannabinoids systemic diseases has long been recognized (Mandel Amphetamines Cocaine 1990), and oral fluids and tissues (buccal cells) are Barbiturates Cotinine increasingly being used to diagnose a wide range of Benzodiazepines Methamphetamine conditions. Saliva- and oral-based diagnostics use Cocaine Opiates readily available samples and do not require invasive LSD PCP Marijuana Ethanol procedures. Researchers have detected antibodies in Nicotine saliva that are directed against viral pathogens such Opiates as human immunodeficiency virus (Malamud 1997) PCP and hepatitis A virus (O’Farrell et al. 1997) or B virus Antibodiesb HIV HIV antibodies (Richards et al. 1996). Saliva is being used to detect HPV antibodies, drugs, hormones, and environmental tox- HHV-8/KSH ins (Malamud and Tabak 1993) (Table 5.2). The sim- C.parvum plest tests are those that detect the presence or Helicobacter pylori absence of a substance in the saliva, such as various Hormonesc Cortisol Estriol drugs. Greater technical challenges are presented for Progesterone tests that will be used for therapeutic monitoring Testosterone Substance P since accurate levels of a substance and/or its Met-enkephalin metabolites are needed. In these instances the sali- Environmental toxinsd Cadmium va/plasma concentration ratio must be determined Lead experimentally (Haeckel 1993). Tests beyond those Mercury listed in Table 5.2 are currently on the market, but do Therapeuticse Antipyrine not yet have FDA approval. Saliva is also the fluid of Carbamazepine choice to assess the integrity of the mucosal immune Ciprofloxacin system (Mandel 1990). Irinotecan Most recently, oral fluids have been used as a Lithium source of microbial or host DNA. With the advent of Methotrexate Phenytoin polymerase chain reaction methods, the DNA con- Phenobarbital tained within a single cell is sufficient for detection of Theophylline viruses (e.g., Kaposi’s sarcoma-associated herpes virus, Koelle et al. 1997; Epstein-Barr virus, Falk et a Cone et al.1993,1997. bConstantine et al.1997. al. 1997; mumps virus, Afzal et al. 1997) or bacteria c Dabbs 1993,Ellison 1993. (e.g., Helicobacter pylori, Reilly et al. 1997). Similarly, dGonzalez et al.1997,Joselow et al.1968. DNA extracted from sloughed buccal epithelial cells e Wilson 1993. can be used to genotype persons. This has found Source:Constantine et al.1997. application in forensics (Roy et al. 1997) and may be
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 103 Linkages with General Health used for diagnostic purposes in the future (van Schie These microorganisms can induce extensive local- and Wilson 1997). ized infections that compromise general well-being Saliva has the potential of replacing blood, the in and of themselves. However, they also may spread current standard for testing many diseases and to other parts of the body if normal barriers are conditions (e.g., diabetes, infectious disease, breached. The oral mucosa is one such barrier that Parkinson’s disease, alcoholic cirrhosis, Sjögren’s provides critical defense against pathogens and other syndrome, and cystic fibrosis sarcoidosis). Important challenges (Schubert et al. 1999). Salivary secretions goals for the future are the development of new are a second major line of defense. Damage to the diagnostic tests for early disease detection, defining oral mucosa from mechanical trauma, infection, or individual patient risk of adverse response to drugs, salivary dysfunction with resulting derangements in monitoring therapeutic progress, and determin- lubricatory and antimicrobial functions of saliva, as a ing outcomes of treatment. Key issues in the result of chemotherapy, radiation, and medications development of a new generation of saliva diag- causing hyposalivation, allows a portal of entry for nostics include their selectivity, sensitivity, response invading pathogens. time, dynamic range (values of interest), rep- resentative sampling, and, perhaps most important, their reliability or stability as well their ability to Oral Infections and Bacteremia assess multiple substances simultaneously. Oral microorganisms and cytotoxic by-products associated with local infections can enter the blood- stream or lymphatic system and cause damage or Conclusion potentiate an inappropriate immune response else- For the clinician the mouth and face provide ready where in the body. Dissemination of oral bacteria into access to physical signs and symptoms of local and the bloodstream (bacteremia) can occur after most generalized disease and risk factor exposure. These invasive dental procedures, including tooth extrac- signs and symptoms augment other clinical features tions, endodontic therapy, periodontal surgery, and of underlying conditions. Comprehensive care of the scaling and root planing. Even routine oral hygiene patient requires knowledge of these signs and symp- procedures such as daily toothbrushing, subgingival toms, their role in the clinical spectrum of general irrigation, and flossing may cause bacteremia. diseases and conditions, and their appropriate man- However, these distant infections have been seen agement. Oral biomarkers and surrogate measures more often in high-risk patients such as those who are also being explored as means of early diagnosis. are immunocompromised. With further development and refinement, oral- Oral bacteria have several mechanisms by which based diagnostics such as salivary tests can be- they invade mucosal tissues, perhaps contributing come widely used and acceptable tools for individu- to their ability to cause bacteremias. For example, als, health care professionals, researchers, and com- oral bacteria and their products may invade the munity programs. The continued refinement of periodontal tissues directly. Actinobacillus actino- imaging techniques also has the potential of using mycetemcomitans has been found in gingival oral imaging to identify early signs of skeletal bone connective tissue in patients with localized juvenile degeneration. periodontitis (Christersson et al. 1987a,b, Meyer et al. 1991, Riviere et al. 1991). Invasion of tissue by Porphyromonas gingivalis has also been described in THE MOUTH AS A PORTAL OF ENTRY vivo (Saglie et al. 1988) and in vitro (Njoroge et al. FOR INFECTION 1997, Sandros et al. 1993, 1994, Weinberg et al. Chapter 3 provides an overview of the effects of oral 1997). Although oral bacteria can enter the blood microbial infections with viruses, bacteria, and fungi. through injured or ulcerated tissue, bacterial More than 500 bacterial strains have been identified invasion of periodontal tissues represents another in dental biofilm, and more than 150 bacterial strains possible mechanism. have been isolated from dental pulp infections. More In the immunocompetent individual, bacteremia recently, 37 unique and previously unknown strains originating from the oral cavity is usually transient of bacteria were identified in dental plaque (biofilm) and harmless. However, if the individual’s immune (Kroes et al. 1999). Most oral lesions are opportunis- system is compromised, the normally harmless oral tic infections, that is, they are caused by microorgan- bacteria may pose a significant risk. The morbidity isms commonly found in the mouth, but normally and mortality associated with oral foci of infections kept in check by the body’s defense mechanisms. are hard to assess. This is due to the formidable task
104 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health of tracking the source of an infection unless the Oral Infections as a Result of Therapy responsible pathogen is indigenous to a specific anatomic location. Chemotherapy Viridans group streptococci (VGS) have a low degree of virulence but can be associated with mor- Oral mucositis can be a major dose-limiting problem bidity and mortality under certain circumstances. during chemotherapy with some anticancer drugs, Increased pathogenicity of Streptococcus viridans is such as 5-fluorouracil, methotrexate, and doxoru- most prominent in individuals with neutropenia (low bicin. It is estimated that approximately 400,000 blood counts of circulating white blood cells called patients undergoing cancer therapy each year will neutrophils) and has been associated with a toxic- develop oral complications (NIH 1990). Infection of shock-like syndrome (TSLS) or viridans streptococ- ulcerated mucous membranes often occurs after cal shock syndrome (VSSS), as well as with adult res- chemotherapy, especially since patients are usually piratory distress syndrome (ARDS) (Bochud et al. immunocompromised. Bacterial, fungal, and viral 1994). causes of mucositis have been identified (Feld 1997). Although a high degree of morbidity is associat- The mechanism by which cancer-chemotherapy- ed with viridans streptococcal bacteremia, a low inci- induced mucositis occurs is likely associated with the dence of mortality has been reported (Heimdahl et al. rapid rate of turnover of oral epithelial cells. In addi- 1989). Several studies have shown that under tion, other components likely include upregulation adverse circumstances oral flora and oral infections of pro-inflammatory cytokines and metabolic by- are associated with increased incidence of morbidity products of colonizing oral microflora (Sonis 1998). and even mortality (Engelhard et al. 1995, Lucas et Chemotherapy alters the integrity of the mucosa and al. 1998, Martino et al. 1995, Ruescher et al. 1998, contributes to acute and chronic changes in oral tis- Sparrelid et al. 1998, Sriskandan et al. 1995). sue and physiologic processes (Carl 1995). The Reduction of oral foci of infection decreases systemic ulcerated mucosa is susceptible to infection by complications, specifically in severely neutropenic microbial flora that normally inhabit the oral cavity, patients undergoing chemotherapy (Heimdahl et al. as well as by exogenous organisms, and exacerbates 1984). In addition, hospital stays for patients with the existing mucositis. Further, these microflora can oral mucositis undergoing autologous bone marrow disseminate systemically (Pizzo et al. 1993, Rolston transplants were longer than for those without oral and Bodey 1993). Compromised salivary function mucositis (Ruescher et al. 1998). can further elevate risk for systemic infection of oral Other cohorts identified at increased risk for sys- origin. temic complications due to oral bacteria include hos- Both indigenous oral flora and hospital-acquired pitalized patients unable to perform adequate oral pathogens have been associated with bacteremias and hygiene, those receiving saliva-reducing medications, systemic infection (Schubert et al. 1999). Changes in and those taking antibiotics that alter the oral flora. A infection profiles in myelosuppressed (immunosup- positive dental plaque culture for aerobic pathogens pressed) cancer patients tend to occur in cyclic fash- was significantly associated with the development of ion over many years. This evolving epidemiology is hospital-acquired pneumonia and bacteremia in a caused by multiple factors including use of antibi- study of individuals in an intensive care unit (ICU) otics. Gram-positive organisms including viridans (Fourrier et al. 1998). streptococci and enterococci are currently associated In addition, several case reports have been pub- with systemic infection of oral origin in myelosup- lished implicating indigenous oral flora in the devel- pressed cancer patients. In addition, gram-negative opment of brain abscesses (Andersen and Horton pathogens including P. aeruginosa, Neisseria spp., and 1990, Andrews and Farnham 1990, Baker et al. 1999, Escherichia coli remain of concern. Gallagher et al. 1981, Goteiner et al. 1982, Saal et al. Cancer patients undergoing bone marrow radia- 1988). This serious condition is associated with a tion who have chronic periodontal disease may also mortality rate of almost 20 percent and full recovery develop acute periodontal infections with systemic in only slightly more than 50 percent of all patients complications (Peterson et al. 1987). The extensive (Goteiner et al. 1982). These data are based on single ulceration of gingival sulcular epithelium associated case reports and most probably represent rare events. with periodontal disease is not directly observable However, they provide additional examples that clinically, yet may represent a source for disseminat- point to the potential pathogenicity of the normal ed infection by an extensive array of organisms. oral flora during special adverse circumstances. Inflammatory signs may be masked due to the under- lying bone marrow suppression.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 105 Linkages with General Health
Viruses are also associated with clinically impor- can require surgery to excise the dead tissue, which tant oral disease in patients receiving chemotherapy can in turn leave the face badly disfigured as well as (Rolston and Bodey 1993, Pizzo et al. 1993). functionally impaired (Field et al. 2000). The likeli- Infections caused by herpes simplex virus, varicella- hood of ORN is increased with trauma to the bone, zoster virus, and Epstein-Barr virus typically result including that caused by tooth extraction (Murray et from reactivation of a latent virus, whereas al. 1980a, b). The risk is especially marked when the cytomegalovirus infections can result via reactivation trauma occurs near the time of radiation (Epstein et of a latent virus or a newly acquired virus. The sever- al. 1987). Management includes elimination of acute ity of the infection, including fatal outcome, depends or potential dental and periodontal foci of disease, on the degree of immunocompromise. increased patient participation in oral hygiene, use of Many agents and protocols have been investigat- oral topical fluorides for caries prevention, and use of ed to manage or prevent mucositis (Peterson 1999, antiviral, antifungal, or antimicrobial therapy for Schubert et al. 1998). For example, various biologic management of infections associated with mucositis. response modifiers, including transforming growth factor 3 or keratinocyte growth factor, have been Combined Cancer Therapies under recent study in randomized clinical trials. Allopurinol mouthwash and vitamin E have been Rapid developments have occurred in the use of cited as agents that can decrease the severity of blood cell growth factors for treatment of various mucositis, although more extensive testing is neces- conditions, including the anemia of end-stage renal sary. Prostaglandin E2 was not shown to be effective disease, the neutropenia occurring with cancer care, in prophylaxis of oral mucositis following bone mar- and the bone marrow toxicity and mucositis that can row transplant; however, more recent studies indi- follow aggressive chemotherapy or radiation therapy cate possible efficacy when administered via a differ- (Sonis et al. 1997, Williams and Quesenberry 1992). ent dosing protocol. Oral cryotherapy appears to be Sonis et al. (1997) found that topical application of efficacious in reducing severity of oral mucositis transforming growth factor beta (TGF- ) in the ham- caused by 5-fluorouracil and related compounds ster model of oral mucositis significantly reduced (Rocke et al. 1993). basal cell proliferation and reduced the severity of Local application of capsaicin preparations may mucositis associated with 5-fluorouracil treatment. be effective in controlling oral mucositis pain as dis- Other growth factors considered for use in tinguished from tissue injury itself (Berger et al. reducing mucositis include granulocyte-monocyte 1995). Capsaicin and its analogs are the active ingre- colony-stimulating factor and granulocyte colony- dients in chili peppers. Capsaicin’s clinical potential stimulating factor. Bone morphogenetic proteins are derives from the fact that it elevates the threshold for also in development for alleviating the toxicity and pain in areas to which it is applied. mucositis that follow chemotherapy and radiation therapy. Other approaches to reducing mucositis and Radiation Therapy adverse oral effects of chemotherapy and radiation Radiation therapy disrupts cell division in healthy therapy include fractionating the dose of radiation, tissue as well as in tumors and also affects the normal and combining chemotherapy with growth factors or structure and function of craniofacial tissues, includ- with less toxic oncostatic agents. Although the oral ing the oral mucosa, salivary glands, and bone. Oral- mucositis occurring in chemotherapy and in head facial complications are common after radiation ther- and neck radiation patients shares many apy to the head and neck. The most frequent, and characteristics, distinct differences also exist (NIH often the most distressing, complication is mucositis, 1990, Schubert et al. 1998, Wilkes 1998). For but adverse reactions can affect all oral-facial tissues example, in contrast to chemotherapy-associated (Scully and Epstein 1996). lesions, radiation damage is anatomically site- Radiation can cause irreversible damage to the specific; toxicity is localized to irradiated tissue salivary glands, resulting in dramatic increases in volumes. The degree of damage depends on dental caries. Oral mucosal alterations may become treatment-regimen-related factors, including the type portals for invasion by pathogens, which may be life- of radiation used, the total dose administered, the threatening to immunosuppressed or bone-marrow- fractionation, and field size. Thus, research involving suppressed patients. A less common but very serious both cohorts of cancer patients remains essential to adverse consequence is destruction of bone cells and enhancing patient management. bone death, called osteoradionecrosis (ORN). ORN Development of new technologies to prevent can result in infection of the bone and soft tissue and cancer-therapy-induced oral mucositis could
106 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health substantially reduce the risk for oral and systemic mucosal injury, or salivary compromise collectively infections, oral pain, and the number of hospital promote the risk for clinical infection. In addition, days. Improvement in quality of life and reduction in antibiotics and concurrent steroid therapy often alter health costs are also likely and desirable outcomes. oral flora, thereby creating an environment for fungal The new technologies could also provide a set- overgrowth. In high-risk cancer patients, fungal ting in which novel classes of chemotherapeutic infection can cause severe morbidity and even death. drugs, utilized at increased doses, could be imple- mented. These advances in turn could lead to enhanced cancer patient survival and lengthen the Infective Endocarditis duration of disease remission. The purported connection between oral infection and a specific heart disease, infective endocarditis, Pharmaceuticals has a long history. Endocarditis is caused by bacteria A number of medications used to treat systemic dis- that adhere to damaged or otherwise receptive sur- eases can cause oral complications, ranging from faces of the tissue that lines heart valves (the endo- xerostomic effects to alterations in the surface struc- cardium) (Weinstein and Schlesinger 1974). Dental ture of the enamel or mucosa. More than 400 over- and other surgical procedures may predispose sus- the-counter and prescription drugs have xerostomic ceptible patients to infective endocarditis by induc- side effects (Sreebny and Schwartz 1997). These ing bacteremias (Lacassin et al. 1995). However, bac- include tricyclic antidepressants, antihistamines, and teremias from oral infections that occur frequently diuretics. The dimensions and impact of these side during normal daily activities, coincidental even with effects vary depending on the response of the indi- chewing food, toothbrushing, and flossing, con- vidual patient and the duration of medication use. tribute more substantially to the risk of infective Staining of the teeth or mucosa is associated with endocarditis (Bayliss et al. 1983, Dajani et al. 1997, a variety of drugs, including tranquilizers, oral con- Strom et al. 1998). Oral organisms are common etio- traceptives, and antimalarials. The antibiotic tetracy- logic agents of infective endocarditis (Bayliss et al. cline can cause enamel hypoplasia when taken by the 1983). For example, strains of S. sanguis, as well as mother during pregnancy and by children during gram-negative oral bacteria including Haemophilus tooth development. The antimicrobial mouthrinse aphrophilus, A. actinomycetemcomitans, E. corrodens, agent chlorhexidine also can stain the teeth, but this Capnocytophaga spp., and Fusobacterium nucleatum, staining is external and can be removed by dental have been associated with bacterial endocarditis prophylaxis. (Barco 1991, Geraci and Wilson 1982, Kaye 1994, Other drugs have been associated with gingival Moulsdale et al. 1980). overgrowth, including cyclosporin, which has been Infective endocarditis occurs with different incu- used as an immunosuppressant in the United States bation periods, which differ in causative bacteria and since 1984 to prevent rejection of transplanted signs and symptoms. For example, Staphylococcus organs and bone marrow. This drug has also been aureus endocarditis may have a rapid onset and fatal used in other countries for treatment of type 2 dia- course if it affects the left side of the heart. With a betes, rheumatoid arthritis, psoriasis, multiple sclero- more indolent course, patients may often be unaware sis, malaria, sarcoidosis, and several other diseases of infection and may experience fever, night chills, with an immunological basis (Adams and Davies myalgia, and arthralgia for a considerable period of 1984). Other drugs that cause gingival overgrowth time before diagnosis. The infection is often curable include calcium ion channel blocking agents used in if diagnosed and treated early. the treatment of angina pectoris and postmyocardial The classic risk factors for endocarditis include syndrome, such as nifedipine and verapamil (Lucas cardiac valve disorders (valvulopathies) that include et al. 1985), and phenytoin (sodium 5,5-phenylhy- rheumatic and congenital heart disease, complex dantoin), used in the treatment of epilepsy and also cyanotic heart disease in children, and mitral valve for management of other neurological disorders. prolapse with regurgitation. Recent studies indicate Treatment often consists of using an alternate drug, that the use of certain diet drugs (fenfluramine and although this is not always possible. Conservative dexfenfluramine) has induced cardiac valvulopathy, periodontal therapy can reduce the inflammatory which may in some cases be transient. Among at-risk component of enlargement; however, surgery is often persons, bacteremias are more likely to occur in required. Oral candidiasis is typically caused by those with periodontal disease (Silver et al. 1977). opportunistic overgrowth of Candida albicans. Drugs However, the oral pathogens causing periodontitis that cause systemic bone marrow suppression, oral have only rarely been shown to cause endocarditis.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 107 Linkages with General Health
Prevention of infective endocarditis from oral until the seventeenth century, when van Leewenhoek bacteria depends on limiting the entry and dissemi- examined dental plaque using a microscope he nation of bacteria through the bloodstream and lym- had constructed. In 1884, Koch demonstrated that phatic circulation. Antibiotic prophylaxis for dental tuberculosis could be transmitted by airborne procedures that are likely to provoke bacteremia has droplets from the mouth and respiratory tract. Since historically been recommended (Dajani et al. 1997, that time, we have learned that many common respi- Durack 1995). A recent study, however, suggests that ratory infections, such as influenza, the common receiving dental treatment does not significantly cold, pneumonia, and tuberculosis, can be transmit- increase the risk of infective endocarditis, even in ted from oral secretions. Before the development of patients with valvular abnormalities (Strom at al. effective vaccines, orally transmitted diseases such as 1998). Further research is necessary to determine chickenpox, measles, mumps, polio, and diphtheria whether some heart or valvular conditions or certain were a major source of morbidity and mortality in dental procedures, such as surgery or scaling, would childhood. Viral diseases such as hepatitis B, herpes require coverage with pre-procedural antibiotics and labialis, acute herpetic gingivostomatitis, cyto- others would be precluded. megalovirus, and infectious mononucleosis may also originate from oral contact. Disease-causing microorganisms can be spread Oral Infections and Respiratory Disease by direct contact (with saliva or blood from the Pathogens in the oral cavity can also gain access to mouth) or indirect contact (with saliva- or blood- the airway, sometimes with serious consequences. In contaminated surfaces, including hands or lips), adults, bacterial pneumonias are strongly associated droplet infection (from coughing, sneezing, or even with aspiration of bacteria into the lower respiratory normal speech), or by aerosolized organisms. These tract, which is normally sterile. Common respiratory organisms can be inhaled, ingested, or taken in pathogens such as Streptococcus pneumoniae, through mucous membranes in the eyes, nose, or Streptococcus pyogenes, Mycoplasma pneumoniae, and mouth or through breaks in the skin. A number of Haemophilus influenzae can colonize the oropharynx diseases can be spread via oral sexual contact, includ- and the lower airway. In addition, oral bacteria ing gonorrhea, syphilis, trichomoniasis, chlamydia, including A. actinomycetemcomitans (Yuan et al. and mononucleosis. 1992), Actinomyces israelii (Morris and Sewell 1994, As mentioned earlier, the oral mucosa and saliva Zijlstra et al. 1992), Capnocytophaga spp. (Lorenz provide significant defense against disease transmis- and Weiss 1994), Eikenella corrodens (Joshi et al. sion. Epidemiological and animal studies are provid- 1991), Prevotella intermedia, and Streptococcus con- ing evidence, however, that the oral cavity may be the stellatus (Shinzato and Saito 1994) can be aspirated site for transmission of serious systemic infections into the lower airways (Scannapieco 1998, 1999). despite the protective factors in saliva (see Chapter Chronic obstructive pulmonary disease, charac- 2). Infection with HIV provides a case in point (Baba terized by obstruction of airflow due to chronic bron- et al. 1996, Dillon et al. 2000, Pope et al. 1997, chitis or emphysema and by recurrent episodes of Ruprecht et al. 1999, Stahl-Hennig et al. 1999, Baron respiratory infection, has been associated with poor et al. 2000). oral health status (Hayes et al. 1998, Scannapieco et Early in the 1980s, when AIDS was first identi- al. 1998). A positive relationship between periodon- fied in the United States, concern was expressed tal disease and bacterial pneumonia has been shown about casual (i.e., nonsexual) transmission of HIV by Scannapieco and Mylotte (1996). (CDC 1983, 1985). Detailed household studies did Although oral bacteria, including periodontal not demonstrate transmission of HIV, even when pathogens, have the potential for causing respiratory family members shared eating utensils and tooth- infections, the frequency and nature of such infec- brushes with an HIV-affected member (Fischl et al. tions are not known and merit further study. 1987, Rogers et al. 1990, Sande 1986). Similarly, sur- veillance data collected over time showed no evi- dence of casual transmission (Ward and Duchin Oral Transmission of Infections 1997). Besides being a portal of entry for infections, the Only one nonoccupational episode of HIV trans- mouth is an important source of potentially patho- mission has been attributed to blood-contaminated genic organisms and is often the vehicle by which saliva (CDC 1997); this incident involved intimate infection is delivered to the bodies of others. kissing between sexual partners. There have been a Microorganisms were not discovered in the mouth few cases of HIV transmission from performing oral
108 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health sex on a person infected with HIV, and it is also pos- infection can cause acute pharyngitis, but is usually sible to become infected with HIV by receiving oral asymptomatic. The transmission of pharyngeal gon- sex. In the San Francisco Options Study of men who orrhea to sex partners had been thought to be rare. have sex with men identified within 12 months of However, in one study, 17 of 66 men who had sex HIV seroconversion, oral transmission represented with men who had urethral gonorrhea reported 7.8 percent of primary HIV infections (Dillon et al. insertive oral sex as their only risk factor in the past 2000). Rothenberg et al. (1998) reviewed epidemio- 2 months (Lafferty et al. 1997). logic studies and reports of 38 cases of oral transmis- sion of HIV in the literature. They concluded that although oral-genital contact may be less efficient Conclusion than needle-sharing or anal intercourse for the trans- The role of the mouth as a portal of entry for infec- mission of HIV, its increased use by men who have tion presents ever-new challenges for study. Although sex with men (Ostrow and DiFranceisco 1996, oral tissues and fluids normally provide significant Schwarcz et al. 1995) and in crack cocaine smokers barriers and protection against microbial infections, (Faruque et al. 1996a,b) may increase its contribu- at times these infections can not only cause local dis- tion to HIV transmission over time. Several studies ease but, under certain circumstances, can dissemi- provide evidence that when the oral environment is nate to cause infections in other parts of the body. compromised, the mouth can be a potential site of The control of existing oral infections is clearly of transmission of infectious microbes. Data from intrinsic importance and a necessary precaution to Faruque et al. (1996a,b) and Wallace et al. (1996) prevent systemic complications. suggest that there is a positive association between the presence of oral lesions resulting from crack co- caine use, receptive oral intercourse, and HIV trans- ASSOCIATIONS AMONG ORAL mission. A case report has documented the passage of INFECTIONS AND DIABETES, HEART HIV from a partner who is HIV-positive to one who DISEASE/STROKE, AND ADVERSE is HIV-negative in the presence of periodontal disease PREGNANCY OUTCOMES but in the absence of other risk factors (Padian and Recent studies have reported associations between Glass 1997). Because the type, duration, and fre- oral infections—primarily periodontal infections— quency of oral contact in past studies may not have and diabetes, heart disease and stroke, and adverse been specified, the risk could be somewhat higher for pregnancy outcomes, but sufficient evidence does oral transmission of HIV than previously reported. not yet exist to conclude that one leads to the other. The risk might also vary depending on factors such This section characterizes the nature of these associ- as viral load, infectious dose, area of exposure, and ations by describing the quality of the evidence sup- presence or absence of oral lesions. Additional stud- porting the reports. Both observational and experi- ies are needed to evaluate the risk of oral-genital mental studies were accepted as admissible evidence. transmission of HIV; some are under way (J. Table 5.3 presents the hierarchy of evidence used to Greenspan, K. Page-Schafer, personal communica- interpret these associations. Where there are opera- tion, 1999). tive mechanisms proposed that support an associa- Other sexually transmitted diseases (STDs) can tion between oral infectious agents and the systemic occur through oral contact. For example, pharyngeal conditions in question, they are introduced at the infection with Chlamydia trachomatis has been found outset. These are followed by animal studies and then in 3 to 6 percent of men and women attending STD by epidemiologic or population-based studies. The clinics. Most infections are asymptomatic (Holmes et evidence for each association is presented in the table al. 1999). Another common sexually transmitted infection, herpes simplex virus, commonly infects in rank order according to the rigor of the study the pharynx and is seen in 20 percent of patients with design. primary genital herpes. The painless chancre of pri- mary syphilis can be found in the oral cavity; howev- The Periodontal Disease–Diabetes er, there are no data on the prevalence of this site of infection for Treponema pallidum. Among persons Connection with gonorrhea, pharyngeal infection occurs in 3 to 7 There is growing acceptance that diabetes is associat- percent of heterosexual men, 10 to 20 percent of het- ed with increased occurrence and progression of peri- erosexual women, and 10 to 25 percent of men who odontitis—so much so that periodontitis has been have sex with men (Holmes et al. 1999). Gonococcal called the “sixth complication of diabetes” (Löe 1993).
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 109 Linkages with General Health
The risk is independent of whether the diabetes Type 1 Diabetes. Ten reports focused principally on is type 1 or type 2. Type 1 diabetes is the children and adolescents with type 1 diabetes, com- condition in which the pancreas produces little or no paring them with groups of similar ages without dia- insulin. It usually begins in childhood or adoles- betes (Cianciola et al. 1982, de Pommereau et al. cence. In type 2 diabetes, secretion and utilization of 1992, Faulconbridge et al. 1981, Firatli 1997, Firatli insulin are impaired; onset is typically after age 30. et al. 1996, Goteiner et al. 1986, Harrison and Bowen Together, these two types of diabetes affect an esti- 1987, Novaes et al. 1991, Pinson et al. 1995, mated 15.7 million people in the United States and Ringelberg et al. 1977). All but one of the studies represent the seventh leading cause of death (NIDDK (Goteiner et al. 1986) reported greater prevalence, 1999). The goal of diabetic care is to lower blood glu- extent, or severity of at least one measure or index of cose levels to recommended levels. Some investiga- periodontal disease (e.g., gingival inflammation, tors have reported a two-way connection between probing pocket depth, loss of periodontal attach- diabetes and periodontal disease, proposing that not ment, or radiographic evidence of alveolar bone loss) only are diabetic patients more susceptible to peri- among subjects with diabetes, even though these odontal disease, but the presence of periodontal dis- investigations were conducted in a variety of coun- ease affects glycemic control. This section explores tries across several continents. the bidirectional relationship, beginning with the Another set of studies on the relationship effects of diabetes on periodontal disease. between type 1 diabetes and periodontal disease included subjects with and without diabetes between Effects of Diabetes on Periodontitis Prevalence the ages of 15 and 35 (Cohen et al. 1970, Galea et al. and Severity 1986, Guven et al. 1996, Kjellman et al. 1970, Rylander et al. 1987, Sznajder et al. 1978). All six Several reviews have described candidate mecha- studies reported greater prevalence, extent, or sever- nisms to explain why individuals with diabetes may ity of at least one measure or index of periodontal be more susceptible to periodontitis (Grossi and disease. Genco 1998, Manouchehr-Pour and Bissada 1983, A third set of studies conducted in Scandinavia Murrah 1985, Oliver and Tervonen 1994, Salvi et al. looked at the relationship between periodontal dis- 1997, Wilton et al. 1988). These include vascular ease and type 1 diabetes (or diabetes reported as changes, alterations in gingival crevicular fluid, alter- requiring insulin therapy without specification of ations in connective tissue metabolism, altered host diabetes type) in adults between 20 and 70 years old. immunological and inflammatory response, altered Three of the four studies were cross-sectional subgingival microflora, and hereditary patterns. (Glavind et al. 1968, Hugoson et al. 1989, Studies were classified by type of diabetes and age of Thorstensson and Hugoson 1993), and one was a study population (see Table 5.4). treatment follow-up study (Tervonen and
TABLE 5.3 Hierarchy of evidence used in analyzing and interpreting results
Quality of Evidence I: Evidence obtained from at least one properly randomized controlled trial. II-1: Evidence obtained from well-designed controlled trials without randomization. II-2: Evidence obtained from well-designed cohort or case-control analytic studies,preferably from more than one center or research group. II-3: Evidence obtained from multiple time series with or without the intervention.Dramatic results in uncontrolled experiments (such as the results of the introduction of penicillin treatment in the 1940s) could also be regarded as this type of evidence. III: Opinions of respected authorities,based on clinical experience; descriptive studies and case reports; or reports of expert committees. Strength of Recommendation A: There is good evidence to support the recommendation. B: There is fair evidence to support the recommendation. C: There is insufficient evidence to recommend for or against,but recommendations may be made on other grounds. D: There is fair evidence to support the recommendation that the intervention be excluded. E: There is good evidence to support the recommendation that the intervention be excluded.
Source: Adapted from U.S.Preventive Services Task Force 1996.
110 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health
TABLE 5.4 Summary of studies of the association between diabetes and periodontal diseases, classified by strength of evidence, diabetes type, and age group Number of Measure of Subjects Agesb Periodontal Other Study Diabetes a.Diabetes a.Diabetes Disease Status: Diabetes-Related Evidence Country Design Typea b.Control b.Control Diabetes Effectc Variables Considered Leveld Firatli 1997 Turkey Prospective 1 a.44 a.12.2 (mean) Ging:0s Glycemic control II-2 b.20 b.12.3 (mean) Ppd:0s Duration of diabetes Lpa:1s Cohen et al.1970 USA Prospective 1* a.21 a.18,35 Ging:1s None II-2 b.18 b.18,35 Lpa:1r,1s Tervonen and Finland Prospective 1 a.36 a.24,36 Ging:0e Glycemic control II-2 Karjalainen 1997 b.10 b.24,36 Ppd:1r Duration of diabetes Lpa:1e Diabetes complications Novaes et al.1996 Brazil Prospective 2 a.30 a.30,77 Ppd:1s,1r Glycemic control II-2 b.30 b.30,67 Lpa,1s,1r Nelson et al.1990 USA Prospective 2 a.720 a.15,55+ XRBL:1i,1p None II-2 b.1,553 b.15,55+ Taylor et al.1998a USA Prospective 2 a.24 a.15,57 XRBL:1i,1r None II-2 b.338 b.15, 57 Taylor et al.1998b USA Prospective 2 a.21 a.15,49 XRBL:1i,1r Glycemic control II-2 b.338 b.15, 49 Goteiner et al.1986 USA Cross-sectional 1 a.169 a.school ages Ging:0s None III b.80 b.5,18 Lpa:0p,0s PDI:0s Harrison and USA Cross-sectional 1 a.30 a.4,19 Ging:1s Glycemic control III Bowen 1987 b.30 b.4,19 Lpa:1p Novaes et al.1991 Brazil Cross-sectional 1 a.30 a.5,18 Ging:1s None III b.30 b.5, 18 Ppd: 0s XRBL:1s Cianciola et al.1982 USA Cross-sectional 1 a.263 a.<10,>19 Ging:1p Duration of diabetes III b.208 b.<10,>19 Lpa:1p XRBL:1p,1s JPS:1p,1s de Pommereau France Cross-sectional 1 a.85 a.12,18 Ging:1e Glycemic control III et al.1992 b.38 b.12,18 Lpa:0e,0p,0s Duration of diabetes XRBL:0e,0p,0s Ringelberg USA Cross-sectional 1 a.56 a.10,16 Ging:1s None III et al.1977 b.41 b.10,12 MGI:1s Firatli et al.1996 Turkey Cross-sectional 1 a.77 a.12.5 (mean) Ging:0s Duration of diabetes III b.77 b.12.6 (mean) Ppd:1s Lpa:1s Pinson et al.1995 USA Cross-sectional 1 a.26 a.7-18 Ging:1s Glycemic control III b.24 b.7-18 Ppd:0s Duration of diabetes Lpa:0s Faulconbridge England Cross-sectional 1 a.94 a.5,17 Ging:1s Duration of diabetes III et al.1981 b.94 b.5,17 Kjellman et al.1970 Sweden Cross-sectional 1* a.105 a.15,24 Ging:1e Glycemic control III b.52 b.15,24 Ppd:0s Diabetes complications XRBL:0s Guven et al.1996 Turkey Cross-sectional 1 a.10 a.18,27 Ging:1e None III (continues)
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 111 Linkages with General Health
TABLE 5.4 continued Number of Measure of Subjects Agesb Periodontal Other Study Diabetes a.Diabetes a.Diabetes Disease Status: Diabetes-Related Evidence Country Design Typea b.Control b.Control Diabetes Effectc Variables Considered Leveld Rylander et al.1987 Sweden Cross-sectional 1 a.46 a.18,26 Ging:1e,1p Diabetes complications III b.41 b.19,25 Ppd:0e Lpa:1e,1p XRBL:0p Sznajder et al.1978 Argentina Cross-sectional 1* a.20 a.9,29 Ging:1s None III b.26 b.9,29 Lpa:0s Galea et al.1986 Malta Cross-sectional 1* a.82 a.5,29 Ppd:1p Glycemic control III b.unknown b.5,29 Duration of diabetes Diabetes complications Hugoson et al.1989 Sweden Cross-sectional 1 a.154 a.20,70 Ging:1e Duration of diabetes III b.77 b.20,70 Ppd:1e,1p,1s XRBL:1s Glavind et al.1968 Denmark Cross-sectional 1* a.51 a.20,40 Ging:0s Duration of diabetes III b.51 b.20,40 Ppd:0s Diabetes complications Lpa:1s XRBL:1s Thorstensson and Sweden Cross-sectional 1 a.117 a.40,70 Ging:0e Duration of diabetes III Hugoson 1993 b.99 b.40,70 Ppd:1e,1s Onset age XRBL:1s Morton et al.1995 Mauritius Cross-sectional 2 a.24 a.26,76 Ging:1p None III b.24 b.25,73 Ppd:1s Lpa:1s Shlossman et al.1990 USA Cross-sectional 2 a.736 a.5,45+ Lpa:1p None III b.2,483 b.5,45+ XRBL:1p Emrich et al.1991 USA Cross-sectional 2 a.254 a.15,55+ Lpa:1p,1s None III b.1,088 b.15,55+ XRBL:1p,1s Wolf 1977 Finland Cross-sectional 1,2 a.186 a.16,60 Ging:1s Glycemic control III b.156 b.16,60 Lpa:1s Duration of diabetes XRBL:1s Diabetes complications Benveniste USA Cross-sectional 1,2* a.53 a.5,72 Ging:0s None III et al.1967 b.71 b.5,72 Ppd:0p,0s Finestone and USA Cross-sectional 1,2* a.189 a.20,79 PI:1s Glycemic control III Boorujy 1967 b.64 b.20,79 Duration of diabetes Diabetes complications Belting et al.1964 USA Cross-sectional 1,2* a.78 a.20,79 PI:1s Diabetes severity III b.79 b.20, 79 Oliver and Tervonen USA Cross-sectional 1,2 a.114 a.20,64 Ppd:1e,1p None III 1993 b.15,132 b.20,64 Lpa:1e,0p,0s Yavuzyilmaz et al. Turkey Cross-sectional 1,2 a.17 a.25,74 Ppd:1s None III 1996 b.17 b.19,29 Bridges et al.1996 USA Cross-sectional 1,2 a.118 a.24,78 Ging:0s Glycemic control III b.115 b.24,78 Ppd:0s Duration of diabetes Lpa:1s Sandler and Stahl USA Cross-sectional 1,2* a.100 a.20,69 PDR:1e None III 1960 b.3,894 b.20,69 Bacic et al.1988 Yugoslavia Cross-sectional 1,2 a.222 a.<20,60+ Ppd:1e,1p,1s Glycemic control III b.189 b.<20,60+ Duration of diabetes Diabetes complications Hove and Stallard USA Cross-sectional 1,2* a.28 a.20,40+ Ging:0s Duration of diabetes III 1970 b.16 b.20,40+ Ppd:0s Diabetes severity XRBL:0s
112 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health
Number of Measure of Subjects Agesb Periodontal Other Study Diabetes a.Diabetes a.Diabetes Disease Status: Diabetes-Related Evidence Country Design Typea b.Control b.Control Diabetes Effectc Variables Considered Leveld
Mackenzie and USA Cross-sectional 9 a.124 a.32,78 XRBL:0s None III Millard 1963 b.92 b.32,78 Sznajder et al.1978 Argentina Cross-sectional 9 a.63 a.30,49 Ging:1s None III b.39 b.30,50 Lpa:1s Dolan et al.1997 USA Cross-sectional 9 Weighted a.45,75+ Lpa:1e,1p,1s None III a.107 b.45,75+ b.554 Grossi et al.1994 USA Cross-sectional 9 a.1,426 All:25,74; Lpa:1s,1p None III b.69 unknown for diabetes Tervonen and Finland Cross-sectional 9 a.50 a.<30,40+ Ging:1e Glycemic control III Knuuttila 1986 b.53 b.<30,40+ Ppd:1e,1p XRBL:0s Campbell 1972 Australia Cross-sectional 9 a.70 a.17,39 PI:1p,1s None III b.102 b.17,39 Albrecht et al.1988 Hungary Cross-sectional 9 a.1,360 a.15,65+ Ging:1s None III b.625 b.15,65+ PI:0s Szpunar et al. USA Cross-sectional 9 a.474 a.6,65+ PI:1s None III 1989 (NHANES I) b.15,174 b.6,65+ Szpunar et al. USA Cross-sectional 9 a.322 a.15,65+ PI:1s None III 1989 (HHANES) b.8,040 b.12,65+
a Diabetes type:1 = type 1 diabetes mellitus;2 = type 2 diabetes mellitus;1,2 = both type 1 and type 2 diabetes mellitus;9 = diabetes type not specified and not clearly ascertaina- ble from other information in the report;* = diabetes type not specified but ascertained by reviewer from other information in the report. bAges:subjects’ages presented as minimum,maximum reported for those with diabetes and controls unless otherwise specified. c Measure of periodontal disease status.Measures used include Ging = gingivitis or gingival bleeding;Ppd = probing pocket depth;Lpa = loss of periodontal attachment;XRBL = radiographic bone loss;JPS = juvenile periodontal score;MGI = modified gingival index;PI = Russell’s periodontal index;PDR = periodontal disease rate (proportion of teeth affected by periodontal disease).The number following the measure corresponds to greater disease in those with diabetes (1) or no difference between those with diabetes and controls (0). The letter following the number corresponds to the parameter(s) assessed in the study:e = extent;i = incidence;p = prevalence;s = severity;r = progression. dLevels of evidence are delineated in Table 5.3.
Karjalainen 1997). All four studies reported greater Taylor et al. 1998a,b). All seven studies reported prevalence, extent, or severity of at least one measure greater prevalence, extent, or severity of periodontal of periodontal disease. disease among subjects with diabetes for at least one measure of periodontal disease. Three of these stud- Type 2 Diabetes. There are fewer reports on the rela- ies were longitudinal (Nelson et al. 1990, Taylor et al. tionship between type 2 diabetes and periodontal dis- 1998a,b) and showed that the progression of peri- ease, particularly where type 2 diabetes is explicitly odontal disease was greater in diabetes patients than identified or discernible from the ages of subjects. in individuals without diabetes. Seven studies limited to subjects with type 2 diabetes In addition to finding significant differences in included a comparison group without diabetes. Two various measures of periodontal status between sub- of these studies included only adult subjects (Morton jects with and without type 2 diabetes, a number of et al. 1995, Novaes et al. 1996); the remaining five these reports also provide estimates of association were large population-based studies of diabetes and and risk. Using periodontal attachment loss as the periodontal disease in Pima Indians, a group with the measure, Emrich et al. (1991) estimated that people highest known prevalence of type 2 diabetes in the with type 2 diabetes were 2.8 times more likely to world. The Pima Indian studies included subjects have destructive periodontal disease (odds ratio, 2.8; aged 5 years and older (Shlossman et al. 1990) or 15 95 percent CI, 1.9 to 4.1). When they used radi- and older (Emrich et al. 1991, Nelson et al. 1990, ographic bone loss as the measure and controlled for
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 113 Linkages with General Health other important covariates, the estimate rose to 3.4 childhood to older adulthood (Albrecht et al. 1988, (odds ratio, 3.4; 95 percent CI, 2.3 to 5.2). Nelson et Campbell 1972, Szpunar et al. 1989). Szpunar et al. al. (1990) quantified the increased risk of advanced (1989) presented analyses of two separate national periodontal disease in Pima Indians with and without surveys (the National Health and Nutrition type 2 diabetes, finding the prevalence of periodontal Examination Survey, NHANES I, conducted between disease in subjects with diabetes to be 2.6 times 1971 and 1974, and the Hispanic Health and greater (95 percent CI, 1.0 to 6.6) than that of sub- Nutrition Examination Survey, HHANES, conducted jects without diabetes. Taylor et al. (1996), in anoth- between 1982 and 1984). er analysis of data from the Pima Indians, reported All seven studies found subjects with diabetes to that type 2 diabetes was a significant risk factor for have increased prevalence, extent, and severity of more severe alveolar bone loss progression (odds periodontal disease. The statistical significance of the ratio, 4.2; 95 percent CI, 1.8 to 9.9), in addition to diabetes effect was markedly diminished in the final being a significant risk factor for the prevalence of linear regression model used by Szpunar et al. (1989) alveolar bone loss. in analysis of the NHANES I data. Two of the popu- lation-based surveys, Grossi et al. (1994) and Dolan Studies of Individuals with Type 1 or Type 2 Diabetes. et al. (1997), provided epidemiologic estimates of the Twelve reports included analyses in which subjects association of diabetes and attachment loss severity with type 1 and type 2 diabetes were not separated. with odds ratios of 2.3 (95 percent CI, 1.2 to 4.6) and All of these studies were cross-sectional and included 1.9 (95 percent CI, 1.3 to 3.0), respectively, while adults; two studies included children or adolescents controlling for other covariates. as well (Benveniste et al. 1967, Wolf 1977). Nine of the 12 studies reported greater prevalence, extent, or Conclusion. Diabetes is a risk factor for the occur- severity of periodontal disease among the diabetic rence and prevalence of periodontal diseases. subjects for at least one measure or index of peri- Although there is insufficient evidence of a causal odontal disease (Bacic et al. 1988, Belting et al. 1964, association, the findings of greater prevalence, sever- Bridges et al. 1996, Finestone and Boorujy 1967, ity, or extent of at least one manifestation of peri- Hove and Stallard 1970, Oliver and Tervonen 1993, odontal disease in individuals with diabetes is Sandler and Stahl 1960, Yavuzyilmaz et al. 1996, remarkably consistent in the overwhelming majority Wolf 1977). of studies. Furthermore, there are no studies with Hove and Stallard (1970) and Benveniste et al. superior design features in the literature to refute this (1967) did not find significant differences in peri- assessment. The studies were conducted in distinctly odontal disease between subjects with and without different settings, with subjects from different ethnic diabetes. The Hove and Stallard report included 28 populations and of different ages, and with a variety subjects with diabetes and 16 without diabetes and of measures of periodontal status. This inevitable may not have had enough statistical power to detect variation in methodology and study populations lim- clinical differences, although they were able to detect its the possibility that the same biases apply in all the a significantly higher prevalence of gingival vascular studies. There is a need for further research using changes in subjects with diabetes. Benveniste et al. stronger designs that also control for confounding (1967) commented that their results may have been variables such as socioeconomic status. influenced by use of relatives without diabetes as the comparison group and that the subjects with diabetes Glycemic Control were all under reasonably good control with either Several lines of evidence support the plausibility that insulin or dietary regulation. Both factors may have periodontal infections contribute to problems with minimized differences between the groups. glycemic control, thus compromising the health of diabetic patients. It has been reported that the chron- Diabetes Type Not Specified. The final set of reports on ic release of tumor necrosis factor alpha (TNF- ) and the association between diabetes and periodontal dis- other cytokines such as those associated with peri- eases consists of seven cross-sectional studies in odontitis interferes with the action of insulin and which the type of diabetes was not specified and was leads to metabolic alterations (Hotamisligil et al. not easily determined from other information pro- 1993, Flier 1993). Other studies have noted relation- vided. Four of the seven studies included only adults ships between insulin resistance and active inflam- (Dolan et al. 1997, Grossi et al. 1994, Mackenzie and matory connective tissue diseases (Hallgren and Millard 1963, Tervonen and Knuuttila 1986). In the Lundquist 1983, Svenson et al. 1987), other clinical other three studies, subjects ranged in age from diseases (Beck-Nielsen 1992, Beisel 1975), acute
114 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health infection (Drobny et al. 1984, Sammalkorpi 1989), impaired glycemic control is varied in the strength, and periodontal disease (Grossi et al. 1999). Grossi quantity, breadth, and consistency of evidence pre- and Genco (1998) have proposed a model whereby sented. The preliminary evidence, while encourag- periodontal infection contributes to hyperglycemia ing, does not support a clear-cut conclusion that and complicates metabolic control in diabetes. treating periodontal infection can contribute to man- agement of glycemic control in type 1 or type 2 dia- Clinical Studies. The effects of periodontal infection betes. As the table indicates, only studies using sys- on glycemic control have been investigated in a small temic antibiotic treatment affected glycemic control number of clinical studies that looked at metabolic favorably. The results suggest that infections other control at baseline and following various periodontal than periodontitis may be implicated or that inten- treatments (see Table 5.5; Aldridge et al. 1995, sive treatment of periodontal infections with sys- Christgau et al. 1998, Grossi et al. 1996, 1997, Miller temic antibiotics is necessary to affect glycemic con- et al. 1992, Seppala and Ainamo 1994, Seppala et al. trol favorably. Further rigorous controlled studies in 1993, Smith et al. 1996, Westfelt et al. 1996, Williams diverse populations are warranted. and Mahan 1960, Wolf 1977). One report is based on an epidemiological cohort study (Taylor et al. 1996). The randomized controlled trials of Grossi et al. The Oral Infection–Heart Disease and (1997) involving populations with type 2 diabetes Stroke Connection found that use of the systemic antibiotic doxycycline During the past decade, infectious agents have to treat periodontitis patients with diabetes resulted become recognized as causes of systemic diseases, in a transient (3 to 6 months) improvement in without fever or other traditional signs of infection. glycemic control. On the other hand, the two con- Helicobacter pylori is associated with peptic ulcers trolled trials conducted in London by Aldridge et al. and, along with Chlamydia pneumoniae and (1995) involving patients with type 1 diabetes found cytomegalovirus, is now thought to be associated no effect. Taken together, these three studies provide with increased risk for cardiovascular disease as well inconsistent results and are limited in how well they as malignancies (Wu et al. 2000). Studies investigating generalize to broader populations. A small uncon- the relationship between oral and dental infections trolled study of 10 patients by Miller et al. (1992) and the risk for cardiovascular disease suggest that also reported an improvement in glycemic control of there is potential for oral microorganisms, such as diabetic patients whose periodontal disease was periodontopathic bacteria, and their effects to be treated with mechanical therapy and systemic doxy- linked with heart disease. cycline. Five of the above-mentioned studies did not include control groups (Miller et al. 1992, Seppala et al. 1993, Smith et al. 1996, Williams and Mahan Mechanisms of Action 1960, Wolf 1977), and four were not specifically Infectious agents are thought to affect the risk of designed to address the relationship between peri- heart disease through several possible mechanisms. odontal therapy and glycemic control (Grossi et al. Bacteria or viruses originating in tissues such as the 1996, Seppala et al. 1993, Smith et al. 1996, Westfelt lungs or oral mucosa may directly infect blood vessel et al. 1996), although the data collected allowed the walls. Such infection may be largely asymptomatic, investigators to address the issue. One nonrandom- but may cause local vascular inflammation and ized but controlled clinical trial of nonsurgical peri- injury, which would contribute to the development odontal therapy found no significant influence on of lipid-rich plaques and atherosclerosis. Bacteria or medical data for the diabetic patients (Christgau et al. viruses may also interact with white blood cells or 1998). A clear relationship between improvement in platelets, both of which integrate into the developing periodontal health and glycemic control has not been atherosclerotic plaque. Cells of the blood vessel wall shown. The studies seem to suggest that antibiotic and white blood cells and platelets can release treatments may help in glycemic control. A recent prostaglandins (especially PGE2), interleukins (espe- longitudinal study indicates inflammation may be a cially IL-1), thromboxane B2 (TBX2), and tumor precursor to the onset of type 2 diabetes (Schmidt et necrosis factor alpha (TNF- ). Bacterial products in al. 1999). Thus periodontal infection may contribute the blood may also stimulate liver production of to that inflammation. other pro-inflammatory or pro-coagulant molecules such as C-reactive protein and fibrinogen. Microbes Conclusion. The body of literature concerning the may also stimulate expression of tissue factor, which relationship between periodontal infection and would activate coagulation. During the process of
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 115 Linkages with General Health
TABLE 5.5 Effects of periodontal disease and its treatment on glycemic control: clinical and epidemiological evidence
Number of subjects Metabolic Study Diabetes a.Treatment (ages) Follow-up Control Evidence Designa Type b.Control (ages) Time Periodontal Therapy Outcome Effects on Metabolic Control Levelb
Aldridge RCT Type 1 a.16 (16-40) 2 months Experimental group:oral Glycated Periodontal treatment had no I et al.1995, b.15 (16-40) hygiene instruction, scaling, hemoglobin, effect on change in glycated Study 1 adjustment of restoration fructosamine hemoglobin. margins, and reinforcement after 1 month; control group: no treatment Aldridge RCT Type 1 a.12 (20-60) 2 months Experimental group:oral Glycated Periodontal treatment had no I et al.1995, b.10 (20-60) hygiene instruction, scaling hemoglobin effect on change in glycated Study 2 and root planing, extractions, hemoglobin. root canal therapy; control group:no treatment Grossi et RCT Type 2 a.89 (25-65) 12 months Experimental groups received Glycated The three groups receiving I al.1996, b.24 (25-65) either systemic doxycycline or hemoglobin doxycycline and ultrasonic 1997 placebo and ultrasonic bacterial curettage showed bactericidal curettage with significant reductions irrigation using either water, (P < 0.04) in mean glycated chlorhexidine, or povidone- hemoglobin at 3 months. iodine Christgau Treatment Type 1 a.20 (30-66) 2 months Scaling/root planing; Glycated No effect on glycated hemoglobin. II-1 et al.1998 study,non- and type 2 b.20 (30-66) subgingival irrigation with hemoglobin RCT chlorhexidine; oral hygiene Westfelt instruction; and extractions et al.1996 Treatment Type 1 a.20 (45-65) 5 years Baseline oral hygiene Glycated “The mean value of HbA1c II-1 study,non- and type 2 b.20 (45-65) instruction,scaling and root hemoglobin between baseline and 24 months RCT planing followed by periodic was not significantly different from prophylaxis,oral hygiene that between 24 and 60 months.” instruction,localized sub- gingival plaque removal,and surgery at sites with bleeding on probing and a periodontal Smith probing depth of >5 mm et al.1996 Treatment Type 1 a.18 (26-57) 2 months Scaling and root planing with Glycated Found no statistically or clinically II-1 study,non- b. 0 ultrasonics and curets;oral hemoglobin significant change in glycated Taylor RCT hygiene instruction hemoglobin. et al.1996 Historical Type 2 No treatment or 2-4 years Not applicable Glycated Those with severe periodontitis II-2 prospective control subjects hemoglobin were ~6 times more likely to have cohort 49 (severe poor glycemic control at follow-up. periodontitis) 56 (less severe Miller periodontitis) et al.1992 Treatment Type 1 a.10 (not given) 8 weeks Scaling and root planing, Glycated Found decrease in glycated III study,non- b. 0 systemic doxycycline hemoglobin, hemoglobin and glycated albumin RCT glycated in patients with improvement in albumin gingival inflammation (P < 0.01). Patients with no improvement in gingival inflammation had either no change or increase in glycated hemoglobin post treatment.
coagulation, platelets would become trapped in the the lumen of the coronary blood vessels narrows and growing clot or thrombus. Microthrombus formation the blood supply to the heart muscle becomes is one of the key factors in the development of ather- reduced. A frank heart attack or myocardial infarc- osclerotic plaques. As atherosclerotic plaques enlarge, tion results when a larger part of the coronary artery
116 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health
Number of subjects Metabolic Study Diabetes a.Treatment (ages) Follow-up Control Evidence Designa Type b.Control (ages) Time Periodontal Therapy Outcome Effects on Metabolic Control Levelb Seppala Treatment Type 1 a.38 for 1 year; 2 years Scaling and root planing, Medical Reported an improvement of the III et al.1993, study,non- 22 for 2 yearsc periodontal surgery,and history for HBA1 levels of the PIDD and CIDD Seppala and RCT 26 PIDD-1y (48 ± 6) extractions baseline subjects (P < 0.068,t-test). Ainamo 12 CIDD-1y (43 ± 5) control status; 1994 16 PIDD-2y glycosylated 6 CIDD-2y hemoglobin b. 0 A1 and blood glucose for assessing response to treatment Williams Descriptive Not speci- 3-7 Extractions,scaling and Insulin 7 of 9 subjects had “significant” III and Mahan clinical fied a.9 (20-32) months curettage,gingivectomy, requirement; reduction in insulin requirements. 1960 study b. 0 systemic antibiotics diabetes control (not operationally defined) Wolf 1977 Treatment Type 1 and 8-12 Scaling and home care Blood glucose, Compared 23 subjects with III study,non- type 2 a.117 (16-60) months instruction,periodontal surgery, 24-h urinary improved oral infections with 23 RCT b. 0 extractions,endodontic glucose, who had no improvement after treatment,restorations,denture insulin dose treatment for oral infection and replacement or repair inflammation.The subjects with improved oral inflammation and infection tended to demonstrate diabetes control improvement (P < 0.1).However,Wolf states in discussion,“treatment of periodon- tal inflammation and periapical lesions … does little to improve the control of diabetes.” a RCT = randomized controlled trial. b Levels of evidence are delineated in Table 5.3.Note that because this body of literature is small,this review does not distinguish between “well-designed”studies and otherwise in assigning the evidence levels. c PIDD = poorly controlled insulin-dependent diabetes;CIDD = controlled insulin-dependent diabetes. lumen becomes occluded. Failing to receive enough tral event in stopping blood flow. When an experi- blood, the heart muscle dies, resulting in an infarct. mental bacteremia was created with a strain of S. san- guis that carried the collagen-like protein, rabbits Animal Studies showed changes in blood pressure, electrocardio- Bacteria originating in the oral cavity may also con- gram readings, heart rate, and cardiac contractility tribute to platelet clotting or thrombosis, as proposed (Herzberg and Meyer 1996, 1998). Platelets also by Herzberg et al. (1983, 1994). These investigators aggregated in the circulation, resulting in significant have suggested that the association between peri- declines in platelet counts. From the electrocardio- odontal disease and cardiovascular disease may be graphic tracings, rabbit heart muscle also appeared to due in part to the potential for oral bacteria such as have suffered ischemic damage. The investigators S. sanguis and P. gingivalis to induce platelet aggrega- concluded that oral bacteria carrying the collagen- tion. Platelets aggregate in response to these bacteria like protein induced platelet aggregation or clotting as a result of mistaken identity: a protein structure on in the bloodstream. These clots were of sufficient size the surface of certain common strains of S. sanguis to obstruct coronary arteries and produce ischemic and P. gingivalis mimics the platelet-interactive heart damage, an early warning sign of a heart attack regions of collagen molecules (Erickson and or an infarction. Because S. sanguis is present in large Herzberg 1993, Herzberg et al. 1994). Exposure of numbers in dental plaque and is a causative agent in flowing blood to collagen triggers clotting, the cen- infective endocarditis, it is likely that these bacteria
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 117 Linkages with General Health have an opportunity to induce platelet clotting dur- in this study. Periodontal disease was measured at ing human bacteremias from oral sources. Bacteria- baseline, and the incidence of cardiovascular disease induced platelet clotting could contribute to was followed over the next 10 years. When the analy- microthrombosis during the development of athero- sis was restricted to individuals under age 60, the risk sclerotic plaques and occlusive thrombus formation of cardiovascular disease was 2.7 times higher in sub- with occasional myocardial infarction. jects with periodontal disease than in those with lit- tle or no periodontal infection. This association was Population-based Studies seen even after adjusting for other risk factors for Any study investigating the possibility of a unique cardiovascular disease or periodontal disease such as role for oral pathogens as risk factors for cardiovascu- age, sex, cholesterol, weight, high blood pressure, lar disease, including atherosclerosis and the forma- diabetes, and insulin use. The investigators conclud- tion of a blood clot in a coronary artery of the heart, ed that periodontal disease is an important risk fac- which typically precedes myocardial infarction, must tor for cardiovascular disease for individuals under take into consideration such known risk factors as 60 in this group, second only to the presence of smoking, hypertension, obesity, diabetes, genetic sus- long-term diabetes. Further analysis of death due to ceptibility, and elevated cholesterol. Genco (1998) cardiovascular disease is needed in this population to and Beck et al. (1998) have recently reviewed studies complete the study. examining the associations between oral conditions Mattila and coworkers have conducted both (including periodontitis) and atherosclerosis and prospective and retrospective studies. A prospective coronary heart disease, the latter of which affects 12 study (Mattila et al. 1995) showed that new episodes million people in the United States and is the leading of myocardial infarction occurred more frequently in cause of death. These are summarized in Table 5.6. subjects with more extensive “dental” disease. The Of the ten studies cited in the table, six are authors used a measure of dental disease that includ- prospective cohort studies, in which oral health sta- ed a composite index that assessed caries, periodon- tus was established at the outset (baseline) of the titis, pericoronitis, and periapical lesions. The com- study period and the subjects were followed at peri- posite index estimates the combined infectious load odic intervals to a previously defined endpoint, for that contributes to many possible oral infections. example, diagnosis of coronary heart disease or an After combining the prospective study data with data acute myocardial infarction, or death. Beck et al. from an earlier retrospective study (Mattila et al. (1996) combined data from the Veterans 1989) and adjusting for age, triglyceride levels, cho- Administration Dental Longitudinal Study and its lesterol, C-reactive protein, smoking, social class, parent longitudinal study, the Normative Aging diabetes, and hypertension, the investigators found a Study, for a total of 203 cases and 891 noncases, to significant association between dental infections and determine whether periodontal disease, judged by acute myocardial infarction in men under age 50 (P < measuring alveolar crestal bone, is a risk factor for 0.01). A more recent study (Mattila et al. 2000) com- cardiovascular disease. After adjusting for age, blood pared 85 patients with proven coronary heart disease pressure, cholesterol, and body mass index, the and 53 matched controls. This case-control study investigators found that subjects with periodontal showed that dental indices were higher among coro- disease were 1.5 times more likely to develop coro- nary heart disease patients than controls, but the dif- nary heart disease over a 25-year period than controls ferences were not statistically significant. Participants (odds ratio of 1.5). Similarly, after adjusting for age, in the study were older, which the authors believed smoking, and blood pressure, the investigators found was the most likely reason for the results. In the first that veterans with periodontal disease were 1.9 times National Health and Nutrition Examination Survey, more likely to develop fatal coronary heart disease 9,670 subjects were followed for over 14 years. (odds ratio of 1.9). DeStefano et al. (1993) found that there was a 25 per- In a longitudinal study to eliminate the potential cent increased risk of cardiovascular disease in indi- confounding effects of smoking, Genco et al. (1997) viduals with periodontitis compared with those with measured the incidence of periodontal disease and minimal periodontal disease. The strongest associa- cardiovascular disease in 1,372 American Indians of tion was seen in men under 50 (relative risk, 1.7). A the Gila River Indian Reservation. Although diabetes limitation of this study, which the authors acknowl- is prevalent in this population, cigarette smoking is edge, was the lack of baseline data on smoking, a rare in these individuals (a fact confirmed in this major risk factor for both periodontal and cardiovas- study), so it was considered not to be a risk factor for cular disease. Morrison et al. (1999) evaluated a ret- either cardiovascular disease or periodontal disease rospective cohort study using participants in the
118 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health
TABLE 5.6 Summary of studies assessing the association between oral conditions, atherosclerosis, and coronary heart disease
Subjects Association Study (cases/ (odds ratio or Evidence Designa controls) Oral Condition Cardiovascular Outcome Adjustmentsb relative risk) Levelc DeStefano Prospective 1,786/7,974 Russell’s periodontal Coronary heart disease Age,sex,race,education,poverty, 1.72 (1.1-2.68) ll-2 et al.1993 index (admission to hospital or marital status,cholesterol,BMI, (only for men death) diabetes,smoking under age 50) Mattila Prospective 52/162 Dental index (caries, New acute myocardial Smoking,hypertension,age,sex, Yes, P < 0.01 II-2 et al.1995 periodontal disease, infarction or death triglycerides,socioeconomic pulpal infection) status,diabetes,lipids,BMI, previous MI Joshipura Prospective 757/44,119 Periodontal disease New coronary heart Age,BMI,exercise,smoking, 1.67 (1.03-2.71) ll-2 et al.1996 (self-reported), disease alcohol,vitamin C,family history, tooth loss due to MI self-reported periodontal disease Beck Prospective 203/891 Alveolar crestal bone New coronary heart Age,BMI,total cholesterol, 1.5 (1.04-2.14) II-2 et al.1996 loss disease,fatal coronary socioeconomic status,DBP,LDL, 1.9 (1.0-3.43) heart disease,stroke smoking,cholesterol 2.8 (1.45-5.48) Genco Prospective 68/1,304 Alveolar crestal bone New coronary heart Age,sex,smoking,BMI,diabetes, 2.68 (1.35-5.60) II-2 et al.1997 loss disease cholesterol,hypertension Morrison Retrospective 10,000 Severe gingivitis; New coronary heart Age,sex,serum total cholesterol, 1.37 (0.80-2.35) II-2 et al.1999 periodontitis; disease;cerebrovascular smoking,diabetes,hypertension for periodontitis edentulousness deaths 1.90 (1.17-3.10) for edentulousness for fatal CHD Joshipura Prospective 42,151 Number of teeth lost Ischemic stroke Age,smoking,obesity,alcohol, ≤10 teeth 1.75 II-2 et al.1999 exercise,aspirin,family history, (1.03-2.99) profession,hypertension, 11-15 teeth 1.95 hypercholesterolemia (1.07-3.64) 17-24 teeth 1.48 Dental index (caries, (1.02-2.13) Mattila Case-Control 100/102 periodontal disease, Acute myocardial HDL,smoking,C-reactive protein, Yes, P < 0.01 II-2 et al.1989 pulpal infections) infarctions hypertension,age,cholesterol, diabetes,social class Dental index (caries, Grau Case-Control 166/166 periodontal disease, Stroke Diabetes,preexisting vascular Odds ratio 2.6 II-2 et al.1997 periapical infections) disease,socioeconomic status, (1.18-5.70) Dental index (caries, smoking Mattila Case-control 85/53 periodontal disease, New coronary heart Age,sex,smoking,socioeconomic — II-2 et al.2000 pulpal infections) disease class,hypertension,number of teeth,serum lipid levels
aFor the prospective studies,the total number of subjects in the cohort is the sum of the two numbers given,the first number of which represents the subjects followed to the endpoint.For the case-control studies,the first number represents the cases,and the second the controls. bBMI = body mass index;MI = myocardial infarction;LDL = low-density lipoproteins;HDL = high-density lipoproteins. c Levels of evidence are delineated in Table 5.3.
1970-72 National Canada Survey. In the younger dence. This pattern of higher risk observed among cohort, those under age 69, they found that gingivi- younger subjects may, to some extent, reflect the rel- tis, periodontitis, and edentulousness were related to ative instability of risk estimates. However, it is also fatal coronary heart disease in a statistically signifi- possible that periodontal disease, like other co-mor- cant manner. However, in analyzing those over age bid relative risks for coronary heart disease, general- 70, none of these dental conditions was associated ly declines with age (Semenciw et al. 1988). with fatal heart disease. These results were adjusted Wu et al. (1999) found periodontal disease to be for age, sex, serum total cholesterol, smoking status, a potential factor for coronary heart disease and diabetes status, hypertension status, and province of resi- stroke based on an analysis of the first National
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 119 Linkages with General Health
Health and Nutrition Examination Survey and its 21- cular disease or stroke. The methods used to measure year follow-up. In this analysis, periodontitis was or identify periodontal disease ranged widely from found to be a significant risk factor for cerebrovascu- self-report, to composite indices that included dental lar disease, in particular nonhemorrhagic stroke. caries experience, to precise measures of periodonti- Compared with no periodontal disease, relative risk tis severity. Nevertheless, there were consistent find- (95 percent CI) for incident nonhemorrhagic stroke ings of increased odds ratios and significant proba- was 2.11 (1.30 to 3.42) for periodontitis. There was bility (P) values pointing to an association of peri- no significant relationship for gingivitis or edentu- odontal and other oral infections with an increased lousness, which were 1.24 (0.74 to 2.08) and 1.41 risk for cardiovascular disease. Further studies are (0.96 to 2.06), respectively. The increased relative needed to determine whether periodontal disease risk for total cerebrovascular disease and nonhemor- alone or in the presence of other oral infections is an rhagic stroke was not seen for hemorrhagic stroke. independent risk factor for cardiovascular or cere- Similar relative risks for total cerebrovascular disease brovascular disease. Research to elucidate the under- and nonhemorrhagic stroke associated with peri- lying pathological mechanisms is also essential. odontitis were seen in white men and women and Studies must also clarify the potentially confounding African Americans. A conclusive statement about a effects of sex, age, socioeconomic level, and race/ cause-and-effect relationship between periodontitis ethnicity. and the risk of developing cerebrovascular disease, in particular nonhemorrhagic stroke, cannot be made at this time. The consistency of the findings in different Periodontal Disease and Adverse racial groups and the strength of the association war- Pregnancy Outcomes rant further examination of the potentially important Preterm birth and low birth weight are considered association between these two clinical conditions, the leading perinatal problems in the United States which are highly prevalent in the adult population. (Gibbs et al. 1992). Although infant mortality rates In the largest cohort studied, Joshipura et al. have decreased substantially over the past genera- (1996) found that among a group of male health pro- tion, the incidence of low birth weight (just under fessionals who were relatively homogeneous socio- 300,000 cases in 1995) has not shown a comparable economically and who self-reported preexisting peri- decline (Institute of Medicine 1985, USDHHS 1984). odontal disease, those with 10 or fewer teeth were at Over 60 percent of the mortality of infants without increased risk of new coronary heart disease, com- structural or chromosomal congenital defects can be pared with those with 25 or more teeth (relative risk, attributed to low birth weight (Shapiro et al. 1980). 1.67). These results were adjusted for standard car- diovascular disease risk factors. Mechanisms of Action In a case-control study of 166 patients with acute cerebrovascular disease and 166 age- and sex- Periodontal disease may contribute to adverse out- matched controls, Grau et al. (1997) found that comes of pregnancy as a consequence of a chronic “poor dental status” was independently associated oral inflammatory bacterial infection. Toxins or other with cerebrovascular ischemia. These results were products generated by periodontal bacteria in the based on a subgroup of patients and controls who mother may reach the general circulation, cross the completed the dental examination. A modified form placenta, and harm the fetus. In addition, the of the Total Dental Index was used to measure dental response of the maternal immune system to the status. In an 8-year follow-up of 42,151 male health infection elicits the continued release of inflammato- professionals who were free of cardiovascular disease ry mediators, growth factors, and other potent at baseline, Joshipura et al. (1999) reported that cytokines, which may directly or indirectly interfere edentulousness was associated with an increased risk with fetal growth and delivery. of ischemic stroke after adjusting for age, smoking, Evidence of increased rates of amniotic fluid obesity, alcohol, exercise, aspirin, family history of infection, chorioamnion infection, and histologic cardiovascular disease, profession, hypertension, and chorioamnionitis supports an association between hypercholesterolemia. preterm birth, low birth weight, and general infection during pregnancy. It is noteworthy that the largest proportion of such infections occurred during the Conclusion pregnancies of the most premature births (Hillier et None of the studies reviewed to date achieves the al. 1988, 1995). The biological mechanisms involve level of rigor that can unequivocally establish peri- bacteria-induced activation of cell-mediated immuni- odontitis as an independent risk factor for cardiovas- ty leading to cytokine production and the synthesis
120 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health and release of prostaglandins, which may trigger preterm labor; or preterm, premature rupture of preterm labor (Hillier et al. 1988). Elevated levels of membranes. Controls were all normal-birth-weight, prostaglandin as well as cytokines (interleukin-1 (IL- full-term infants. In a case-control study of 124 sub- 1), interleukin-6 (IL-6), and tumor necrosis factor jects, the mean clinical periodontal attachment level alpha (TNF- )) have been found in the amniotic for the mothers of low-birth-weight babies was 3.10 fluid of patients in preterm labor with amniotic fluid + 0.74 (SD) millimeters (mm) per site (93 subjects) infection (Romero et al. 1993), compared with levels versus 2.80 + 0.61 (SD) mm per site (31 subjects) for in patients with preterm labor without infection. mothers of normal-weight infants (P = 0.038 for all cases and controls). For a subset of mothers for Animal Models whom this was the first child, the mean clinical peri- odontal attachment level for those with low-birth- A variety of studies have used the pregnant hamster weight babies was 2.98 + 0.84 (SD) mm per site (46 model. Some investigators have examined the effects subjects) versus 2.56 + 0.54 (SD) mm per site for of lipopolysaccharide, produced by oral gram-neg- controls (20 subjects) at P = 0.041 (Offenbacher et al. ative pathogens, on cytokine production (Collins et 1996). This subset was analyzed separately to avoid al. 1994a). In other studies, hamsters have been the confounding effects of mothers with periodontal infected with P. gingivalis, with or without prior disease who had previously given birth to low-birth- immunization. Collins et al. (1994b) challenged the weight infants but who later had normal-weight animals with nondisseminating, low levels of P. gingi- infants. valis, introduced in a subcutaneous chamber at a Logistic regression models demonstrated that dorsolumbar site. Although the doses were insuffi- severe periodontal disease was associated with a sev- cient to induce fever or wasting, the hamster litters of enfold increase in risk of low birth weight, after con- the infected animals showed a significant reduction trolling for known risk factors such as smoking, race, in fetal weight (24 percent) in comparison with con- alcohol use, age, nutrition, and genitourinary tract trol animals (P < 0.0001). This suppressive effect on infection. This study suggests an association between fetal weight was accompanied by a proportional periodontal disease and prematurity. intrachamber rise in tumor necrosis factor alpha In a subsequent case-control study of 44 sub- (TNF- ) and prostaglandin E2 (PGE ) (P < 0.0001). 2 jects, additional biochemical and microbial parame- Immunization prior to mating did not provide pro- ters of periodontal disease status were studied to tection from a challenge during pregnancy, but rather assess the relationship of current periodontal status potentiated the effects, indicating the potential to current pregnancy outcome (Offenbacher et al. strength of a chronic infection. 1998). Results indicate that PGE levels in gingival In another series of hamster studies, researchers 2 crevicular fluid were significantly higher in mothers observed the effects of experimental periodontitis on of low-birth-weight infants than in controls (131.4 + pregnancy outcomes and amniotic fluid mediators 21.8 (SE) versus 62.6 + 10.3 (SE) nanograms per mil- (Offenbacher et al. 1998). The investigators noted a liliter), respectively (at P = 0.02). Furthermore, with- 20 percent decrease in fetal weight (P = 0.002). in the group of mothers of low-birth-weight infants Periodontal infection in the pregnant hamster also there was a significant inverse association between was associated with a significant rise in intra-amniotic birth weight, gestational age, and gingival crevicular PGE from 3.31 ± 1.1 to 13.5 ± 4.1 micrograms per 2 fluid PGE levels (at P = 0.023 for current births). milliliter (P = 0.03). These data suggest a link be- 2 These data suggest that the level of PGE in gingival tween oral infection and changes in the fetal envi- 2 crevicular fluid, serving as a marker of current peri- ronment. odontal disease activity, varies inversely with birth weight; that is, the higher the PGE2 level, the lower Epidemiologic Studies the birth weights. In this study the periodontal dis- Human case-control studies have demonstrated that ease was more severe in mothers with adverse preg- mothers of low-birth-weight infants born as a result nancy outcomes, as determined by biochemical and of either preterm labor or premature rupture of microbial biomarkers, but the difference in clinical membranes tend to have more severe periodontal dis- attachment levels did not reach statistical signifi- ease than mothers with normal-birth-weight infants cance (P = 0.11). (Offenbacher et al. 1996, 1998). A case was defined Studies also have been reported in other coun- as a mother whose baby weighed less than 2,500 tries. In the United Kingdom a preliminary analysis grams and who had one or more of the following fac- of 167 cases and 323 controls did not show an asso- tors: gestational age of infant of less than 37 weeks; ciation between periodontal disease and pregnancy
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 121 Linkages with General Health outcomes (Davenport et al. 1998); however, the IMPLICATIONS OF THE LINKAGES investigators did not control for confounding factors. This review of oral health linkages with general Dasayanake (1998) conducted a matched case-con- health reveals implications for the clinical practice of trol study with 55 cases in Thailand. Gingivitis was both medicine and dentistry. The recognition of well- associated with a higher risk of having a growth- known and established signs and symptoms of oral restricted infant (odds ratio = 0.3; 95 percent CI, 0.12 diseases may assist in the early diagnosis and prompt to 0.72), controlling for mother’s height, prenatal treatment of some systemic diseases and disorders. care, dental caries status, and the infant’s gender. The presence of these signs also may lead to the insti- Smoking was not controlled for in this study. tution of enhanced disease prevention and health promotion procedures. All health professionals, and Conclusion the public, should be aware of these signs and symp- As a remote gram-negative infection, periodontal dis- toms. Individuals, practitioners, and community pro- ease may have the potential to affect pregnancy out- grams may also benefit from the accelerated develop- come. Not all the obstetric risk factors that result in ment and testing of readily accessible, acceptable, babies being born too soon and too small have been and simple oral-based diagnostics. fully identified (Gibbs et al. 1992, McCormick 1985). A better understanding of the role of the oral cav- Oral infections have been investigated as a potential ity and its components in protecting against infection risk factor for preterm labor or premature rupture of is needed. This information should permit the devel- membranes, which are major obstetric antecedents to opment of interventions to enhance these compo- spontaneous preterm births. Although the findings nents. For example, research is under way investigat- from animal research and case-control studies are ing how to augment some of the natural antimicro- promising, additional work, including longitudinal bial molecules that are present in saliva and how to studies, research on mechanisms, and intervention use oral and nasal vaccination routes to enhance trials, is needed to determine whether periodontitis is immunity. Also, host susceptibility factors contribut- a risk factor and what the mechanisms of action may ing to the dissemination of oral infections to other be for adverse pregnancy outcomes. In the United parts of the body should be investigated, especially in States, longitudinal and intervention studies are populations at high risk for disease and infection. In under way. addition, further studies are needed to elucidate the role of the mouth as a means of transmitting infec- tious microbes. This in turn will allow the develop- Conclusion ment of interventions to prevent transmission and This critical look at the emerging associations among curb the progression of infections once established. oral infections and specific conditions establishes the The associations between oral infections and dia- need for an aggressive research agenda to better betes, heart disease and stroke, and adverse pregnan- understand the specific aspects of these associations cy outcomes warrant a comprehensive and targeted and the underlying mechanisms. Prospective and research effort. If any of these associations prove to intervention studies are under way and should pro- be causal, major changes in care delivery and in the vide additional and stronger evidence of the presence training of health professionals will be needed. and direction of an association. It is essential for such Awareness of the oral complications of medica- studies to include populations at known risk for the tions and other therapies for disease management underlying conditions as well as the general popula- and for health promotion needs to be enhanced tion. Of the conditions reviewed, the relationship of among health care professionals, the public, drug periodontal disease and diabetes has the strongest manufacturers, and the research community. For evidence, demonstrating that the risk of periodontitis some of these therapies, known interventions exist is higher in individuals with diabetes. However, the and should be followed before initiating the therapy effect of periodontitis on glycemic control is less to minimize or modulate its side effects. To prevent clear, a reflection of the difficulty of controlling for the oral complications of other therapies, new the effect of systemic antibiotic treatments used to approaches are needed. Ultimately, and ideally, the manage periodontal disease in diabetic patients in side effects of therapies should be considered in the clinical trials. development of new drugs and biologics.
122 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health
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Rapid infection Craven DE, Makadon H, Goldberg J, Coltin K, Lewin of oral mucosal-associated lymphoid tissue with KS, Epstein AM, et al., The Boston AIDS Survival simian immunodeficiency virus. Science 1999 Aug Score (BASS): a multidimensional AIDS severity 20;285(5431):1261-5. instrument. Am J Public Health 1997 Apr;87(4):567- Strom BL, Abrutyn E, Berlin JA, et al. Dental and cardiac 73. risk factors for infective endocarditis. Arch Intern Semenciw R, Morrison H, Mao Y, Johansen H, Davies Med 1998 Nov 15;129(10):761-9. JW, Wigle D. Major risk factors for cardiovascular Svenson KL, Lundquist G, Wide L, Hallgren R. disease mortality in adults: results from the Nutrition Impaired glucose handling in active rheumatoid Canada Survey. Int J Epidemiol 1988;17:317-24. arthritis: relationship to the secretion of insulin and Seppala B, Ainamo J. A site-by-site follow-up study on counter-regulatory hormones. Metabolism 1987 the effect of controlled versus poorly controlled Oct;36(10):940-3. insulin-dependent diabetes mellitus. J Clin Sznajder N, Carraro JJ, Rugna S, Sereday M. Periodontal Periodontol 1994 Mar;21(3):161-5. findings in diabetic and nondiabetic patients. J Seppala B, Seppala M, Ainamo J. A longitudinal study Periodontol 1978 Sep;49(9):445-8. on insulin-dependent diabetes mellitus and peri- Szpunar SM, Ismail AI, Eklund SA. Diabetes and peri- odontal disease. J Clin Periodontol 1993 Mar;20(3): odontal disease: analyses of NHANES I and 161-5. HHANES. J Dent Res 1989;68(SI):164-438 (abstract Shapiro S, McCormick MC, Starfield BH, Krischer JP, 1605). Bross D. Relevance of correlates of infant deaths for Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman significant morbidity at 1 year of age. Am J Obstet M, Knowler WC, Pettitt DJ. Severe periodontitis and Gynecol 1980 Feb 1;136(3):363-73. risk for poor glycemic control in patients with non- Shinzato T, Saito A. A mechanism of pathogenicity of insulin-dependent diabetes mellitus. J Periodontol “Streptococcus milleri group” in pulmonary infection: 1996 Oct;67(10 Suppl):1085-93. synergy with an anaerobe. J Med Microbiol 1994 Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman Feb;40(2):118-23. M, Knowler WC, Pettitt DJ. Non-insulin dependent Shlossman M, Knowler WC, Pettitt DJ, Genco RJ. Type diabetes mellitus and alveolar bone loss progression 2 diabetes mellitus and periodontal disease. J Am over 2 years. J Periodontol 1998a Jan;69(1):76-83. Dent Assoc 1990 Oct;121(4):532-6. Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman Silver JG, Martin AW, McBride BC. Experimental tran- M. Glycemic control and alveolar bone loss progres- sient bacteraemias in human subjects with varying sion in type 2 diabetes. Ann Periodontol 1998b degrees of plaque accumulation and gingival inflam- Jul;3(1):30-9. mation. J Clin Periodontol 1977 May;4(2):92-9. Tervonen T, Karjalainen K. Periodontal disease related Smith GT, Greenbaum CJ, Johnson BD, Persson GR. to diabetic status. A pilot study of the response to Short-term responses to periodontal therapy in periodontal therapy in type 1 diabetes. J Clin insulin-dependent diabetic patients. J Periodontol Periodontol 1997 Jul;24(7):505-10. 1996 Aug;67(8):794-802. Tervonen T, Knuuttila M. Relation of diabetes control to Sonis ST. Oral mucositis as a biological process: a new periodontal pocketing and alveolar bone level. Oral hypothesis for the development of chemotherapy Surg Oral Med Oral Pathol 1986 Apr;61(4):346-9. induced stomatotoxicity. Oral Oncol 1998;34:39-43. Thorstensson H, Hugoson A. Periodontal disease expe- Sonis ST, Van Vugt AG, Brien JP, Muska AD, Bruskin rience in adult long-duration insulin-dependent dia- AM, Rose A, Haley JD. Transforming growth factor- betics. J Clin Periodontol 1993 May;20(5):352-8. beta 3 mediated modulation of cell cycling and atten- Tindall B, Carr A, Cooper DA. Primary HIV infection: uation of 5-fluorouracil-induced oral mucositis. Oral clinical, immunologic, and serologic aspects. In: Oncol 1997 Jan;33(1):47-54. Sande MA, Volberding PA, editors. The medical man- Sparrelid E, Hägglund H, Remberger M, Ringden O, agement of AIDS. Philadelphia: W.B. Saunders; 1995. Lonnquist B, Ljungman P, Andersson J. Bacteraemia p. 105-29. during the aplastic phase after allogenic bone mar- row transplantation is associated with early death
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U.S. Department of Health and Human Services (USD- Wilson JT. Clinical correlates of drugs in saliva. Ann NY HHS), Center for Research for Mothers and Acad Sci 1993 Sep 30;694:48-61. Children. Public Health Service/National Institutes Wilton JM, Griffiths GS, Curtis MA, Maiden MFJ, Gillet of Health Progress Report. Washington: U.S. IR, Wilson DT, Sterne JA, Johnson NW. Detection of Department of Health and Human Services; 1984. high-risk groups and individuals for periodontal dis- U.S. Preventive Services Task Force. Guide to clinical eases. Systemic predisposition and markers of gener- preventive services. 2nd ed. Washington: US GPO; al health. J Clin Periodontol 1988 Jul;15(6):339-46. 1996. Winkler JR, Robertson PB. Periodontal disease associat- van Schie RC, Wilson ME. Saliva: a convenient source ed with HIV infection. Oral Surg Oral Med Oral of DNA for analysis of bi-allelic polymorphisms of Pathol 1992 Feb;73(2):145-50. Fcg receptor IIA (CD32) and Fcg receptor IIIB Winkler JR, Grassi M, Murray PA. Clinical description (CD16). J Immunol Methods 1997;208:91-101. and etiology of HIV-associated periodontal diseases. von Wowern N. Dual-photon absorptiometry of In: Robertson PB, Greenspan JS, editors. Perspectives mandibles: in vitro test of a new method. Scand J on oral manifestations of AIDS: diagnosis and man- Dent Res 1985 Apr;93(2):169-77. agement of HIV-associated infections. Littleton von Wowern N. Bone mineral content of mandibles: (MA): PSG Publishing; 1988. normal reference values—rate of age-related bone Wolf J. Dental and periodontal conditions in diabetes loss. Calcif Tissue Int 1988 Oct;43(4):193-8. mellitus. A clinical and radiographic study. Proc Finn von Wowern N, Klausen B, Kollerup G. Osteoporosis: a Dent Soc 1977;73 (4-6 Suppl):1-56. risk factor in periodontal disease. J Periodontol 1994 Wu T, Trevisan M, Genco RJ, Dorn JP, Falkner KL, Dec;65(12):1134-8. Sempos CT. Periodontal disease and risk of cere- Wactawski-Wende J, Grossi SG, Trevisan M, Genco RJ, brovascular disease: a prospective study of a repre- Tezal M, Dunford RG, Ho AW, Hausmann E, sentative sample of U.S. adults. Am J Epidemiol Hreshchyshyn MM. The role of osteopenia in oral 1999;149:(11)290, Suppl S Jun 1. bone loss and periodontal disease. J Periodontol Wu TJ, Trevisan M, Genco RJ, Dorn JP, Falkner KL, 1996;67(10 Suppl):1076-84. Sempos CT. Examination of the relation between Wallace JI, Bloch D, Whitmore R, et al. Fellatio is a sig- periodontal health status and cardiovascular risk fac- nificant risk activity for acquiring AIDS in New York tors: serum total and high density lipoprotein, cho- City streetwalking sex workers. Int Conf AIDS lesterol, C-reactive protein, and plasma fibrinogen. 1996;11:381. Am J Epidemiol 2000;151:273-82. Ward JW, Duchin JS. The epidemiology of HIV and Yavuzyilmaz E, Yumak O, Akdoganli T, Yamalik N, Ozer AIDS in the United States. AIDS Clin Rev 1997;45. N, Ersoy F, Yenijay I. The alterations of whole saliva Weinberg A, Belton CM, Park Y, Lamont RJ. Role of constituents in patients with diabetes mellitus. Aust Porphyromonas gingivalis fimbriae invasion of gingi- Dent J 1996 Jun;41(3):193-7. val epithelial cells. Infect Immun 1997 Jan;65(1): Yuan A, Yang PC, Lee LN, Chang DB, Kuo SH, Luh KT. 313-6. Actinobacillus actinomycetemcomitans pneumonia Weinstein L, Schlesinger JJ. Pathoanatomic, pathophys- with chest wall involvement and rib destruction. iologic and clinical correlations in endocarditis (sec- Chest 1992 May;101(5):1450-2. ond of two parts). New Engl J Med 1974;291:832-6, Zakrzewska JM, Aly Z, Speight PM. Oral hairy leuko- 1122-6. plakia in a HIV-negative asthmatic patient on sys- Westfelt E, Rylander H, Blohme G, Jonasson P, Lindhe J. temic steroids. J Oral Pathol Med 1995 Jul;24(6): The effect of periodontal therapy in diabetics. 282-4. Results after 5 years. J Clin Periodontol 1996 Feb; Zijlstra EE, Swart GR, Godfroy FJ, Degener JE. 23(2):92-100. Pericarditis, pneumonia and brain abscess due to a Wilkes JD. Prevention and treatment of oral mucositis combined Actinomyces–Actinobacillus actino- following cancer chemotherapy. Semin Oncol mycetemcomitans infection. J Infect 1992 Jul;25(1): 1998;25:538-51. 83-7. Williams ME, Quesenberry PJ. Hematopoietic growth factors. Hematol Pathol 1992;6(3):105-24. Williams RC Jr, Mahan CJ. Periodontal disease and dia- betes in young adults. JAMA 1960 Feb 20;172:776-8.
132 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL CHAPTER 36
Effects on Well-being and Quality of Life
Fifty years ago the World Health Organization quality of life. In the wake of these developments in (WHO) defined health as the “complete state of general medicine, researchers began to elaborate physical, mental, and social well-being and not mere- multidimensional models of “oral-health-related” ly the absence of infirmity” (WHO 1948). In its defi- quality of life. nition the WHO acknowledged that an individual The efforts to understand these relationships are who is technically “cured” of disease may not neces- particularly relevant given the aging of the popula- sarily be “well” and went on to indicate three dimen- tion. As Gift and Atchison (1995) stated, measuring sions of well-being. Physical well-being assumes the health-related quality of life allows assessment of ability to function normally in activities such as “the trade-off between how long and how well peo- bathing, dressing, eating, and moving around. Mental ple live.” Diseases and disorders that result in dental well-being implies that cognitive faculties are intact and craniofacial defects can thwart that goal, disturb- and that there is no burden of fear, anxiety, stress, ing self-image, self-esteem, and well-being. Oral- depression, or other negative emotions. Social well- facial pain and loss of sensorimotor functions limit being relates to one’s ability to participate in society, food choices and the pleasures of eating, restrict fulfilling roles as family member, friend, worker, or social contact, and inhibit intimacy. citizen or in other ways engaging in interactions with Oral complications of many systemic diseases others. also compromise the quality of life. Problems with The WHO declaration resonated with ongoing speaking, chewing, taste, smell, and swallowing are developments in the social sciences as theoreticians common in neurodegenerative conditions such as recognized the need for multiple indicators in assess- Parkinson’s disease; oral complications of AIDS ing health and treatment outcomes (Bergner et al. include pain, dry mouth, mucosal infections, and 1981, Fries et al. 1982, Hunt et al. 1985, Meenan et Kaposi’s sarcoma; cancer therapy can result in painful al. 1980). These efforts led to definitions of “health- ulcers, mucositis, and rampant dental caries; and related quality of life” (Guyatt et al. 1993) as well as periodontal disease is a complication of diabetes and explanatory models. The model proposed by Wilson osteoporosis. Prescription and nonprescription drugs and Cleary (1995), for example, posits five dimen- often have the side effect of dry mouth. sions by which to measure treatment outcomes: bio- The ability to measure the quality of life has the logical and physiological variables, symptom status, practical value of guiding policymakers, health serv- functional status, general health perceptions, and ice researchers, epidemiologists, program evaluators, overall quality of life. These factors are not inde- and clinicians interested in the effects of interven- pendent but may be reciprocally connected. For tions. The measures can also provide useful informa- example, a diabetic patient with symptoms of depres- tion to patients and family members, third-party pay- sion may experience a rise in serum glucose as a ers, and employers. For example, measures of the result of less vigilant glucose monitoring; the depres- ability to perform activities of daily living may indi- sion may then lead to a deterioration in physical and cate areas where the patient is able and competent, as social activities. Most importantly, measures of bio- well as areas where further therapy may be helpful. logical and physiological factors are often inconsis- This chapter reviews oral-health-related quality tent with patients’ own reports of symptoms, ability of life findings along functional, psychosocial, and to function, general health perceptions, and overall economic dimensions, taking into consideration the
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 133 Effects on Well-being and Quality of Life influence of cultural and spiritual values. The results cultures. The medical model has traditionally of studies in which investigators asked adults how dichotomized body and mind/soul/spirit—science they value their oral health and whether they are sat- and magic. Such a perspective sees the body as rela- isfied with their oral health care are included. The tively objective and value-free, immune to nonso- study of the association between oral health and matic influences. quality of life is a relatively new but rapidly growing That perspective began to change with the pio- field. A variety of questionnaires have been designed neering work of Hans Selye in the 1930s on the to assess oral-health-related quality of life, and the importance of stress in health and disease (McEwen chapter concludes with a discussion of their use in 1999). Research in the intervening half century has surveys and analytic studies, and their potential confirmed the reciprocal connections of the nervous, importance in outcome research. endocrine, and immune systems, not only in relation to stress, but also in terms of the effects of emotions and cognitive processes on health status. THE CULTURAL CONTEXT The model that has emerged as a new paradigm The determination of the health-related quality of life in the study of health and disease incorporates bio- of an individual is implicitly made against a cultural logical with psychological and social factors. This background that includes a set of values, standards, biopsychosocial model is defining agendas for customs, and traditions associated with a particular research in such fields as behavioral medicine and society. psychoneuroimmunology. Social and psychological Decisions about whether to seek care from a den- factors are routinely incorporated into health assess- tist, a physician, or other care provider may be influ- ments, the better to describe the quality of life. Other enced by cultural or ethnic perspectives and under- societies hold views of the body strikingly different standing (Aday and Forthofer 1992, Andersen and from the medical model. In some cultures, individu- Davidson 1997, Davidson and Andersen 1997, als and their care providers conceive of the body as Diehnelt et al. 1990, Kiyak 1993, Lee and Kiyak the union of soul and soma. Illness may occur as a 1992). Different population groups differ in the way result of a “failure in harmony” or “an imbalance of they think about health, and in how they define a forces.” Schools of medicine in China, India, and health problem, determine its seriousness, and other non-Western societies incorporate such princi- decide whether to seek care. In one cultural setting a ples into their teaching and practice (Hufford 1992). painful tooth may be enough to motivate care seek- ing. In another, bleeding, swelling, or fever may be necessary before care is sought. Similarly, decisions Combining Perspectives about whether to comply with a suggested treatment All Americans hold culturally influenced perspec- regimen, whether to engage in self-care, and whether tives on healing and illness (Henderson et al. 1997), to return for a follow-up appointment are also cul- some of which come from more traditional beliefs. turally influenced. Some people accept pain as an inevitable part of ill- The anthropology and ethnography literature is ness, a necessary evil, or even punishment for past rich in references to the ways in which different cul- iniquities or shortcomings and may shun pain-reliev- tures at different times and places have regarded the ing drugs (Zborowski 1952). Many pragmatically human body (Hufford 1992, Kleinman 1979). combine cultural, folk, complementary, and alterna- Cultural beliefs regarding the body, health, and dis- tive healing practices with participation in conven- ease are often embedded in religious or spiritual tional care delivery systems. A recent survey indi- traditions, which in turn may govern how diseases cates that over 50 percent of Americans sought non- and disorders are regarded and treated. A brief des- traditional therapies for a number of ailments cription of Western and non-Western perspectives (Eisenberg et al. 1998). follows. Traditional beliefs are often comforting and satis- fying to individuals (Selikowitz 1994). Certainly, Western culture and science have not always Cultural Models improved the quality of people’s lives (Harris et al. In the medical model typical of Western society the 1993). Dietary changes to refined foods have been body is partitioned into organs and systems, each associated with dental caries (Godson and Williams with identifiable functions. The body is seen as func- 1996, Navia 1994), obesity, and other deleterious tioning well unless disease disrupts it. Diseases in health changes (Selikowitz 1994). The marketing of themselves are understood to be invariable across tobacco products has added to the burden of cancer
134 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life and heart and lung problems worldwide. Migrations Functional Dimensions from traditional community rural life to urban cen- Investigators have reported on the effects of dental ters have been associated with family disruption and and craniofacial diseases on the ability to eat and violence, drug abuse, sexually transmitted diseases, enjoy the full range of dietary choices. The impact of and hypertension in developing countries. less-than-optimal oral health also has been studied in On the other hand, Western science may inform relation to sleep problems, primarily in relation to some cultural groups that certain traditional child- oral-facial pain. rearing practices can be detrimental to oral health (Kolasa 1978, Scheper-Hughes 1990). Early child- Eating hood caries is a form of tooth decay with complex etiologies. Researchers studying high rates of infant Both dental and systemic diseases can profoundly caries among some cultural groups are exploring the affect appetite and the ability to eat, and hence can extent to which traditional means of soothing crying compromise overall health and well-being. Because babies or handling bedtime routines play a role, as chronic illness and medications increase in aging well as investigating prenatal nutrition and transmis- populations, these effects may be particularly evident sion of infection from caregiver to child (Febres et al. among the frail elderly (Ship et al. 1996). 1997, Kelly and Bruerd 1987, Ripa 1988, Tinanoff Undernutrition was observed in 50 percent of geri- and O’Sullivan 1997). atric residents in a U.S. long-term care facility; in People who hold different cultural perspectives many cases, it was linked to eating and swallowing may distance themselves from Western, scientific problems (Keller 1993). worldviews (Lee et al. 1993), a behavior that must be Less severe oral disorders have more subtle addressed in any program of health promotion and effects on functions relating to eating, although the disease prevention. Health professionals who under- high prevalence of those disorders elevates their rela- stand indigenous or local healing practices and con- tive importance among health problems. For exam- cepts are better able to motivate patients and thereby ple, data from the National Health and Nutrition enable them to integrate elements from various heal- Examination Survey III indicate that 33.1 percent of ing systems (Kleinman 1979). people aged 65 and older have no teeth (Marcus et al. America is undergoing major demographic 1996). Furthermore, clinical studies indicate that the changes, with the expectation that at some point masticatory efficiency of replacement teeth is at least before 2050 the white population will no longer 30 to 40 percent lower than that of natural teeth represent the majority (Henderson et al. 1997). As (Idowu et al. 1986). Consistent with these findings, these changes occur, cultural elements that now surveys of elderly populations in the United States reflect minority groups may become more accepted indicate that self-reported chewing problems affect and dominant. However, cultural values are neither significant proportions of people. For example, in static nor omnipotent in shaping people’s lives. California 1 percent of Medicare enrollees were Furthermore, individuals within a culture manifest unable to swallow comfortably, whereas 37 percent of their cultural identity in different ways. Therefore, senior center residents reported trouble biting or both the direction of these changes and their effects chewing foods (Table 6.1). may be hard to predict. A number of studies have indicated that having missing teeth is linked to a qualitatively poorer diet. For example, in studies of U.S. veterans (Chauncey et ORAL-HEALTH-RELATED QUALITY OF al. 1984), Canadians (Brodeur et al. 1993), and Finns LIFE DIMENSIONS (Ranta et al. 1987), people with impaired dentitions Multiple factors act and interact in determining preferred soft, easily chewed foods that were lower in one’s quality of life, as Wilson and Cleary (1995) and fiber and had lower nutrient density than foods eaten others have observed. Thus the idea of assessing by people with intact dentitions. Quality of life clear- quality of life along multiple “dimensions” implies a ly suffers when individuals are forced to limit food departure from a simple linear scale with excellent choices and the foods chosen do not provide optimal quality of life at one end and greatly diminished nutrition. For example, they would be hard put to quality of life at the other. The following sections comply with the healthful diet recommendation of explore several dimensions, beginning with effects “five-a-day” helpings of fiber-rich fruits and vegeta- along functional and psychosocial dimensions and bles. In the elderly, edentulousness and poor oral concluding with a discussion of economic effects on health may contribute to significant weight loss, quality of life.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 135 Effects on Well-being and Quality of Life
used to evaluate the effects of TABLE 6.1 tooth loss and replacement. These Prevalence of self-reported eating dysfunction in surveys of elderly Americans measures capture aspects of eating Dysfunction Attributed to Oral Condition(s) Percentage of Population Group Reporting Dysfunction that are not necessarily reflected in Elderly Persons in Californiaa the clinical measures of chewing Senior Center Residents Medicare Enrollees performance with specific foods Had trouble biting or chewing 37 13 (Demers et al. 1996). Such studies Limited the kinds of foods eaten 23 10 of self-reported chewing ability Unable to swallow comfortably 10 1 confirm several relationships Elderly Persons in Floridab already noted, including the find- Mouth sometimes dry 39 ings that chewing ability declines Noticed an unpleasant taste in mouth 23 as the extent of tooth loss increas- Unable to chew hard things 19 es and that removable dentures do Experienced change in sense of taste 9 not fully compensate for the Difficulty tasting some foods 6 reduction (Hildebrandt et al. 1997, Noticed change in sense of smell 5 Leake 1990, Slade et al. 1996, Elderly Persons in North Carolinac Wayler et al. 1984). In a study of African Americans Whites male veterans with varying levels Difficulty chewing any foods 18 6 of tooth loss, Wayler et al. (1982) Felt sense of taste had worsened 13 3 Uncomfortable eating foods 13 6 reported that levels of taste, smell, Had to avoid eating some foods 10 4 texture, perceived ease of chewing, Felt digestion had worsened 8 <1 and frequency of ingestion were Had to interrupt meals 6 <1 adversely affected only among people with severely compromised a n = 1,842 elderly persons (Atchison and Dolan 1990). dentitions. However, in some stud- b n = 390 dentate persons aged 65 and older living in retirement communities (Gilbert et al.1993). c n = 440 persons aged 70 and older in five North Carolina counties (Hunt et al.1995). ies of prosthodontic treatment, self-reported chewing ability im- proved following treatment, even which may affect overall health (Blaum et al. 1995, in the absence of significant change in clinical meas- Ritchie et al. 2000, Sullivan et al. 1993). ures of chewing performance (van der Bilt et al. 1994). Clinical research has demonstrated a general Impaired eating due to conditions other than reduction in chewing function as the number of tooth loss has been evaluated less frequently. In a missing teeth increases, even when dentures are study of dental patients with intact dentitions, Ernest worn (Carlsson 1984, Feldman et al. 1980, Helkimo (1993) correlated reduced salivary flow with et al. 1978). However, clinical studies in Scandinavia decreased intake of 18 of 22 nutrients. Locker and have observed relatively good chewing performance Slade (1988) found that 6 percent of the Canadians when no more than 12 teeth are missing and the surveyed who reported symptoms of temporo- remaining 20 teeth are distributed fairly equally, mandibular disorders also reported problems with providing good contact between the upper and the eating, talking, or swallowing. These conditions are lower jaw (Agerberg and Carlsson 1975). This find- often associated with limited mouth opening and ing has led some researchers to advocate the concept severe pain, which may be constant or present when- of a “shortened dental arch” as a treatment goal for ever jaw movements are made. The constant dry older adults, that is, retention of at least 20 well-dis- mouth of patients with Sjögren’s syndrome, a disease tributed teeth (Kayser 1981). A consistent finding in which the salivary glands are progressively from research into treatment of tooth loss is that destroyed, is a major source of discomfort that affects removable dentures produce only partial improve- speaking, chewing, and swallowing. ment in chewing performance (Garrett et al. 1996, As part of a Performance Status Scale study of van der Bilt et al. 1994, Witter et al. 1989). Dentures oral and pharyngeal cancer patients, List et al. (1990) anchored by implants result in significantly better reported that only one third of patients achieved a chewing performance than conventional, removable perfect score on a measure of normalcy of diet and dentures (Geertman et al. 1996). only 60 percent on a measurement of eating in pub- Self-reported measures of eating ability, satisfac- lic. Communication skills also suffered; only 55 per- tion with eating, and avoidance of foods are widely cent scored perfectly on understandability of speech.
136 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life
Sleeping recovery by an enemy could be used magically to Sleep problems associated with oral conditions inflict harm on the tooth owner. Remnants of that appear to be most closely related to chronic pain, belief persist in the ritual of the tooth fairy, who res- either directly or indirectly in cases where pain and cues the hidden baby tooth and leaves a reward. The insomnia are exacerbated by depression. In a survey potency of teeth is well recorded in the metaphors of of elderly Floridians, Gilbert et al. (1993) found that language. As Ziolkowski (1976) observed, “if some- 3 percent of the population reported trouble sleeping thing sets our teeth on edge or if someone casts an because of pain or discomfort from dental problems, insult in our teeth, we can gnash our teeth in anger, whereas in a Canadian study Locker and Grushka show our teeth belligerently, grit our teeth resolutely, (1987) reported that 14.2 percent of those with acute take the bit in our teeth, arm ourselves to the teeth, or chronic oral-facial pain (or 5.5 percent of the total and fight tooth and nail in the teeth of great danger population) experienced sleep disturbance related to and, with luck, escape by the skin of our teeth.” pain. Goulet et al. (1995) assessed sleep problems The perception of healthy teeth contrasts sharply not specifically attributed to pain among adults in with that of diseased teeth. The sixteenth-century Quebec. The prevalence of sleep problems was 13 French surgeon Ambroise Paré remarked that percent for persons with no temporomandibular “toothache was the greatest and most eternal of all (jaw) pain. The proportion with sleep disturbance pains . . . the fiery torture of the damned in hell” among persons with jaw pain increased with the (Kunzle 1989); and a preacher of that time saw the severity of the pain, rising from 20 percent for those root of original sin in a rotting tooth, as quoted in with mild pain, to 32 percent for moderate pain, and Kunzle (1989): “We unfortunate humans: We all 59 percent for severe pain. have toothache and suffer ever and always from the teeth with which Adam bit the forbidden apple.” In the nineteenth century, Sir James Frazer reported that Psychosocial Dimensions African tribal kings could not be crowned if they were symbolically emasculated by having a broken The social and psychological dimensions of well- tooth, a theme Freud echoed in declaring that dreams being and quality of life are deeply intertwined in of pulling teeth were symbols of castration everyday life and so are considered together here. (Ziolkowski 1976). Findings are reported for those oral conditions where The link between diseased teeth and weakness, the most research has been conducted: dental dis- impotence, and even moral turpitude and sin has eases (primarily those that affect appearance or been analyzed by scholars exploring the vast legacy involve extensive tooth loss), pain conditions, cran- of dental themes in art and literature. These authors iofacial deformities (primarily clefting syndromes), offer a variety of political, social, psychological, and and oral and pharyngeal cancers. Psychological dis- economic interpretations of diseased versus healthy tress associated with oral health problems has been teeth, attesting to the seriousness with which human- measured through individual questions (e.g., items ity has invested dental pain and tooth loss. assessing worry) and through standardized psycho- Cultures have sanctioned a variety of alterations logical instruments such as the Beck Depression to teeth by shaping and filing, embedding with jew- Inventory (Beck 1967) or the Symptom Checklist 90 els, bleaching, capping, or providing orthodontic (SCL-90) (Derogatis 1983). Overall, the results point treatments to improve occlusion and aesthetics. to a poorer quality of life and a tendency to avoid These procedures have been variously designed to social contact as a result of concerns over facial enhance the status, power, and attractiveness of the appearance. Persistent pain has similar isolating and owner. Cultures have also dictated specific practices depressing effects. to indicate social position, such as the former Japanese custom of dyeing a married woman’s teeth Cultural Significance of Teeth black to denote her marital status. Cultural beliefs and customs are a major influence on Decisions about aesthetic surgery (Kaw 1993), the psychosocial effects of dental disease on individ- the definition of what constitutes a severe malocclu- uals. In a historical essay on the art of pulling teeth, sion, and the need for dental aesthetics (Cons et al. Kunzle (1989) noted that “the tooth has always been 1986) and surgical intervention (Strauss 1985) accorded a special, even magical, role among all peo- depend on social norms. Recently, researchers have ples and at all times, and has stood for power, and its begun to examine the perceived attractiveness of the loss for loss of power.” The practice of hiding or human smile in terms of tooth length, shape, and burying a lost tooth was based on the fear that its color, lip line and plumpness, and tooth exposure
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 137 Effects on Well-being and Quality of Life
(Dunn et al. 1996). Although there are no reliable expressions, particularly smiling, on social relation- studies to document the proportion of people who ships warrant further research. would seek treatment for perceived defects, the The more subtle aspects of social function may growth of practitioner groups and dental supply also be affected by relatively common oral conditions companies that specialize in aesthetic dentistry such as tooth loss. In a study of elderly people with attests to a substantial increase in cosmetic dental tooth loss in the United Kingdom, 30 percent report- treatments. Follow-up studies of patients who have ed difficulty chewing. Although only 5 percent had undergone tooth bleaching indicate high levels of sat- changed their diet, 9 percent felt uncomfortable isfaction with the extent and stability of the color chewing in front of others, and 13 percent reported change (Haywood et al. 1994). embarrassment during social interactions (Smith and Sheiham 1979). Bergendal (1989) acknowledged Dental Problems and Social Function tooth loss in adults to be a serious life event with a more difficult period of readjustment than retire- Given the importance of the mouth and teeth in ver- ment. In a study by Fiske et al. (1998), 25 percent of bal and nonverbal communication, diseases that dis- people without teeth reported that they had avoided rupt their functions are likely to damage self-image close relationships because of fear of rejection when and alter the ability to sustain and build social rela- their toothlessness was discovered. The authors tionships. The social functions of individuals encom- reported that reactions to tooth loss by the elderly pass a variety of roles, from the most intimate in dat- include lowered self-confidence and altered self- ing and mating behaviors, to other interpersonal con- image, bereavement, dislike of appearance, and the tacts, to participation in social or community activi- perception of being more advanced in age. A nation- ties. Dental diseases and disorders can interfere with al study surveying 3,000 homes in Great Britain these social roles at any or all levels (Patrick and regarding the effect of oral health on the quality of Bergner 1990). Whether because of social embarrass- life was performed in 1997-98. Seventy percent of ment or functional problems, people with oral condi- respondents reported that their oral health affected tions may avoid conversation or laughing, smiling, or their quality of life—either positively or negatively. other nonverbal expressions that show their mouth Older people in higher socioeconomic groups, espe- and teeth. cially those who had seen a dentist within the last Two surveys of different segments of the adult year, were more likely to report an enhancing effect population in Ontario, Canada, addressed the issue (McGrath and Bedi 1998). In a study of older of self-consciousness or embarrassment related to Californians, people who viewed themselves as more oral health problems. Both inquired into the frequen- attractive than other people their age were more like- cy of such problems in the prior year. Among persons ly to have a greater number of natural teeth. They over 18 years old in North York, Ontario, 7 percent were also more likely to report less emotional anxiety, reported limiting conversation with others because of to rate their health as excellent or very good, and to oral problems in the prior year, 15 percent reported be less likely to wear full or partial removable den- that they had avoided laughing or smiling because of tures (Matthias et al. 1993). oral problems, and 19 percent reported being embar- Less severe oral conditions may also have rassed at least sometimes by the appearance or health adverse effects on social function. Table 6.2 summa- of their teeth or mouth (Locker and Miller 1994). rizes self-reported levels of impact on personal con- Among persons 50 years of age and older throughout tact and social integration from surveys of numerous the province, 24 percent reported being self-con- population groups within the United States. scious about their appearance at least occasionally Generally, the prevalence of adverse effects ranges because of problems with their teeth, mouth, or den- from 1 to 10 percent, although 20 percent of senior tures, 22 percent reported feeling uncomfortable at center residents in California reported feeling least occasionally, and 13 percent reported that they uncomfortable when eating with others. Avoidance avoided smiling (Locker and Slade 1993). of smiling or conversation tended to be more fre- Recently, investigators have begun to develop quent than limitation of social interaction. However, quantitative tools to assess patterns of facial anima- the largest amount of variation appeared to be among tion, including normal facial expressions, in order to population subgroups, even within studies. For assess functional impairment in these movements example, within the Boston area, Veterans Affairs (Trotman et al. 1998)—and ultimately to address ambulatory care patients in the Veterans Health implications for quality of life. The effects of facial Study had substantially higher prevalence rates of
138 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life adverse effects than community-dwelling, healthy general dental care, including prosthodontic care men enrolled in the Normative Aging Study. (Fiske et al. 1990). The effects on people’s perceived ability to per- form their usual social roles appear to be more subtle Impacts of Oral-Facial Pain (Table 6.2). Depending on the phrasing of questions and the population subgroup surveyed, the preva- Acute pain from dental caries can usually be treated lence of limitation in social roles varied from 0 to 5 effectively or, as in the case of recurrent aphthous percent, although as many as 10 percent of Veterans ulcers (canker sores), will resolve over time. Chronic Affairs patients reported that their daily activities pain in the oral-facial region presents a different situ- were affected because of oral conditions. ation in that the cause may not be removable and There are very few studies of the effects of dental treatment focuses on pain management. Researchers treatment on specific forms of social function. One have compared chronic oral-facial pain to other study of handicapped adults in the United Kingdom types of pain in terms of severity and emotional did, however, report large improvements in five impact. In a study of adult enrollees of a large health aspects of social functioning following provision of maintenance organization, Von Korff et al. (1988)
TABLE 6.2 Reported impacts of oral conditions on social function among U.S. population groups Social Function Dimension(s) Assessed Percentage of Population Group Reporting Effect
Intimacy Elderly Persons in North Carolinaa Perceived effect of mouth on: Good Effect Bad Effect No Effect Sex appeal 75 21 5 Kissing 78 18 4 Romantic relationships 81 17 3 Personal contact/social integration Persons Aged 18 to 61 in Five U.S.Sitesb Avoid conversation 4 Personal contact/social integration Elderly Persons in Californiac Reported impacts due to oral conditions: Senior Center Residents Medicare Enrollees Limiting contact with people 10 1 Feeling uncomfortable eating with others 20 4 Personal contact/social integration Elderly Persons in Floridad Avoid laughing or smiling 6 Avoid conversation 3 Social roles Limit activities 5 Selected Populations in Boston Areae Personal contact/social integration Normative Aging Study Veterans Health Study Women’s Health Project Avoidance of conversation 2 10 7 Social interaction affected 1 9 7 Social roles Daily activities affected 1 10 10 Elderly Persons in North Carolinaf Personal contact/social integration African Americans Whites Avoided smiling 10 3 Unable to enjoy people’s company 5 1 Avoided going out with others 3 0 Less tolerant of others 3 0 Social roles Difficulty doing jobs 1 0 Unable to work 3 0
aStrauss and Hunt 1993. d Gilbert et al.1993. b Gooch et al.1989. eKressin 1997. c Atchison and Dolan 1990. f Hunt et al.1995.
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 139 Effects on Well-being and Quality of Life compared pain in the temporomandibular region to to be some invariant factors in the judgment of facial back pain, headache, chest pain, and abdominal pain beauty and deformity (Stafford et al. 1989), and they on a number of dimensions. The usual intensity of are learned early in life. One U.S. study concluded temporomandibular disorder (TMD) pain (4.3 on a that perceptions of what does and does not constitute 10-point scale) was similar to that of chest pain (4.3) an attractive face are established by age 7 (Cross and and back pain (4.7); abdominal pain and headache Cross 1971). were rated as more intense (5.1 and 5.9, respective- Aristotle also thought that the face, because of its ly). TMD pain and back pain were more persistent position in the uppermost part of the body, pointed to than other pains, with 28 percent of persons with the highest, most spiritual parts of the cosmos. TMD pain (and 29 percent of those with back pain) Something of this mystical belief is preserved in lin- reporting pain on more than half of the days in the guistic traditions that regard what is “higher” and prior 6 months. The daily duration of pain was also “ascending” as nobler than what is “lower” and relatively high for TMD pain, with 27 percent report- “descending,” whether in reference to body parts, ing pain for 9 or more hours per day; this proportion human feelings, or classes and castes in society. was roughly the same as for headache and back pain. But if facial beauty is the mark of truth, moral In this setting, persons with TMD pain sought care superiority, nobility, and the soul, what of the oppo- for their pain at about the same rate as persons with site? Faces judged ugly or disharmonious, or those other pain, with about one quarter having sought marred or scarred by birth defects or injury, have care in the past 6 months and about 60 percent hav- been associated with defects in character, intelli- ing sought care at some time in the past. gence, and morals. There is a long tradition of read- Locker and Grushka (1987) reported that more ing character on the basis of facial and head shapes than 70 percent of persons with all types of acute and according to one or another school of “physiog- chronic pain worried about their dental health. Using nomics.” Some schools likened human faces to ani- scales of the Symptom Checklist 90 (SCL-90), age- mal species, such as cats, monkeys, or horses, and sex-standardized to the population under study, endowing the human with the traits of the animal in persons in the general population who reported TMD question. Others constructed facial geometries that pain had substantially higher levels of anxiety and purported to show which races were nobler, which depression than those without a current pain condi- closer to animal ancestors. During the nineteenth tion (Von Korff et al. 1988). In the same study, items century, Cesare Lombroso, an Italian physician and from the SCL-90 were used to assign an algorithm for criminologist, developed a measuring scheme linking diagnosis of depression. The percentage of persons certain facial types to criminality (Magli 1989). with TMD who met the criteria for a possible diag- Given such a tradition, it is not surprising that nosis of major depression was 11 percent, compared people continue to “judge a book by its cover.” A with 2 percent among those without a current pain large body of research indicates that attractiveness condition and 3 to 5 percent in the general popula- has an important effect on psychological develop- tion. Recent studies suggest that depression in TMD ment and social relationships (Berscheid 1980). patients follows the onset of symptoms and reflects Noteworthy among early social psychological studies uncertainty about the cause(s) and the lack of effec- was the demonstration that physical attractiveness tive treatments. plays a key role in social expectations (Clifford and Walster 1973). Schoolteachers who were asked to evaluate the educational potential of students from Social Responses to Facial Appearance school records and facial photographs judged attrac- Just as cultural considerations color an individual’s tive students to have higher educational potential response to dental disease and tooth loss, so, too, and social ability than unattractive students. This does culture play a major role in the psychosocial finding has been replicated in a variety of school set- impact of craniofacial deformities. More than any tings and grade levels. other body part, the face bears the stamp of individ- The process of attributing positive characteristics ual identity, a fact neurobiology confirms in identify- to physically attractive persons is called the “beauty ing an area of the brain that is dedicated to the recog- is good hypothesis.” The positive impact of attractive nition of faces. appearance has been demonstrated to influence a In ancient Greece the face was seen as the mortal wide range of social activities, from legal proceedings reflection of the gods, and those faces deemed most (Sigall and Ostrove 1975) to psychotherapeutic prog- beautiful were also judged to be morally superior. nosis. This body of research indicates that appear- Although cultures differ in the details, there appear ance affects social expectations not only in educa-
140 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life tional performance, but also in vocational, marital, Cleft Lip/Palate and Malocclusion legal, and health care endeavors. However, the con- Persons with cleft lip/palate have a variety of prob- cept may not apply to all personal attributes. Bennett lems related to appearance, eating, and speech. and Stanton (1993) found that appearance may have Studies of self-concept (Broder and Strauss 1989, little effect on perceptions of intelligence or honesty. Kapp-Simon 1986), psychosocial development Discrimination and stigmatization have histori- (Richman and Eliason 1982, Richman et al. 1988), cally characterized social responses to deformities. and social perception by peers (Schneiderman and People whose appearance is significantly different Harding 1984, Tobiasen 1987), parents and teachers from what society considers “normal” continue to be (Mitchell et al. 1984, Schneiderman and Auer 1984), stigmatized. Examples in literature abound, in fable and the public (Middleton et al. 1986) highlight the and myth, novels, movies, and plays (e.g., Beauty and psychosocial problems of children with cleft the Beast, The Elephant Man, The Hunchback of Notre lip/palate (Broder and Richman 1987). Dame, The Phantom of the Opera, and Scarface). These problems often continue into adolescence, Goffman (1963) provided a theory of stigmatization with appearance and speech remaining problematic useful in understanding social responses to human (Richman et al. 1985), even when the individual has differences and health conditions (Ablon 1981). had comprehensive care (Strauss et al. 1988). Studies Persons seen as deviant experience social devaluation show an association between cleft lip/palate and the associated with prejudices about the causes and con- increased reporting of conduct problems at home sequences of congenital and acquired deformities (Tobiasen and Hiebert 1984) and of behavioral and (Macgregor 1974). learning problems at school (Tobiasen et al. 1987). Ethnographic studies of facial deformities Although children with cleft lip/palate have not been demonstrate marked variation in how birth defects shown to suffer from a negative self-concept (Kapp are explained and treated (Cheng 1990, Meyerson 1979, Richman 1983) or psychological disorders, 1990, Scheper-Hughes 1990, Toliver-Weddington they often become socially inhibited and self-con- 1990). Many cultures have regarded birth defects and scious (Richman and Eliason 1982). the appearance of multiple births as ill omens, with Adolescent girls with cleft lip/palate have higher the infants fated to be abandoned or killed. Even rates of social adjustment problems, particularly today, when it is understood that birth defects may related to appearance (Leonard et al. 1991). Using result from an inherited genetic disorder, decisions psychological projection methods, one study about what that means and what if anything should (Pillemer and Cook 1989) also concluded that chil- be done about it are affected by religious or spiritual dren with facial deformities may have inhibited per- beliefs (Strauss 1988). sonality styles as well as reduced expectations for Progress in dentistry, medicine, and surgery has success in social interactions. Kapp-Simon (1986) raised expectations that deformed or injured persons found that social relationships negatively influence can be treated to enhance their appearance. Although overall self-esteem and that adjustment of adoles- critics have objected to the high value that U.S. soci- cents is associated with the degree of inhibition ety places on attractiveness and youthful appearance, (Kapp-Simon et al. 1992). and on how this emphasis influences opportunity, Many of the earliest studies of the consequences advocates of remediation counter that social values of oral disease examined the impact of developmen- are hard to change and that individuals must adapt to tal disorders such as facial clefts and malocclusion on a society’s norms and stereotypes. Corrective surgery personal contact and social integration. There are few does produce positive assessments from others outcome studies that demonstrate how social, mari- (Berscheid and Gangestad 1982). People in postoper- tal, and occupational status may be affected in adults ative photographs following reconstructive and plas- with facial deformities or cleft lip/palate. In studies tic surgery were seen as kinder, more sexually appeal- dating from the 1970s, persons with cleft lip/palate ing, more likely to be better marriage partners, and achieved greater educational levels than did their more employable and successful than the same indi- fathers, but did not exceed their fathers’ occupation- viduals in preoperative views. al status (McWilliams and Paradise 1973). Persons with cleft lip/palate were less upwardly mobile than their siblings and achieved lower adult incomes (Peter et al. 1975). Although persons with cleft
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 141 Effects on Well-being and Quality of Life lip/palate had higher occupational desires, they had preexisting psychopathology. Persistent pain, as lower income expectations than did controls; adults noted earlier, may also be a contributing factor to felt socially inept and had a tendency to shy away depression. from group activities (Van Demark and Van Demark Gritz et al. (1999) conducted a prospective 1970). Subtle forms of discrimination and stigmati- analysis of changes in quality of life over time with zation were experienced among adults with cleft the aim of identifying which factors might be predic- lip/palate (McWilliams 1970). tive of future improvements or declines. Participants Studies of marital status have indicated that per- were 186 oral and pharyngeal cancer patients, all sons with cleft lip/palate are less likely than nonaf- smokers or recent former smokers, diagnosed with fected peers to date (Peter et al. 1975) or marry primary carcinomas of the oral cavity, pharynx, or (McWilliams and Paradise 1973), and that when they larynx. The patients were tested at baseline, at 1 marry, they marry later (Heller et al. 1981, Peter and month after radiation and/or surgery, and 1 year later Chinsky 1974). Persons with cleft lip/palate were (for a subset of 105 patients available for follow-up). also more likely to remain childless or have fewer Measures used included the Karnofsky Performance children (Peter and Chinsky 1974). Scale, which uses expert judgments of functional per- The evidence concerning anatomical misalign- formance scored from 0 to 100; the Cancer ments of the jaws (e.g., overbite, open bite, crossbite) Rehabilitation Evaluation System Short Form, in is less consistent, with some early studies showing no which patients rate their quality of life along physi- clear relationship between the malocclusion and job cal, psychosocial, marital, sexual, and medical inter- opportunities or social discrimination (Shaw et al. action scales; the previously mentioned Performance 1980a). However, people with severe malocclusions Status Scale for Head and Neck Cancer Patients are likely to be teased and to have difficulty (which includes scales for eating and speaking); and interacting socially. These problems improve the Profile of Mood States, in which patients rate following orthodontic and orthognathic treatment their feelings over the previous week, yielding analy- (Cunningham et al. 1996, Helm et al. 1985, Shaw et ses that enable scaling along six mood states: tension- al. 1980b). anxiety, depression-dejection, anger-hostility, confu- sion-bewilderment, and vigor-activity. Results indi- Oral and Pharyngeal Cancers cated that in spite of functional improvement on some scales over time, there was continued dysfunc- Surgical treatment for oral and pharyngeal cancers tion in speech and eating. Patients also reported can result in functional impairment as well as per- declines in marital and sexual functioning, as well as manent disfigurement. Problems may include the an increase in alcohol use. Interestingly, the best pre- loss of part of the tongue, loss of taste, loss of chew- dictor of quality of life 1 year after treatment was the ing ability, difficulty in speaking, and pain. scores obtained after initial smoking cessation advice Furthermore, in addition to concerns about their was given, while the patients were undergoing treat- function and their future, oral and pharyngeal cancer ment and in recovery. Other predictors were treat- patients must cope with an altered appearance. In a ment type (quality of life was generally poorer for study of patients who were disease-free from 6 radiation patients) and score on the vigor subscale of months to 8 years following surgical tumor removal, the Profile of Mood States. The investigators con- Gamba et al. (1992) reported that those with more cluded that medical follow-up must integrate tailored pronounced disfigurement had greater changes in psychological and behavioral interventions to self-image, a worsened relationship with their part- achieve better quality of life for oral and pharyngeal ner, reduced sexuality, and increased social isolation. cancer patients. A study by Bjordal and Kaasa (1995) also noted that 30 percent of oral and pharyngeal cancer patients were still experiencing psychological distress 7 to 11 Indirect Economic Costs years after treatment. Depression, too, is frequent in The financial impact of oral disease on quality of life cancer patients. Patients with oral and pharyngeal is easiest to quantify in terms of direct per capita cancers are at an even greater risk for depression than costs of oral disease and treatment as well as the costs other cancer patients, due to surgeries that alter their of publicly supported dental care programs. The appearance (Gritz et al. 1999). Because oral and pha- Health Care Financing Administration includes these ryngeal cancers are also frequently associated with costs in its annual total health care expenditure chronic alcohol and tobacco use, depression may be reports. These expenditures are presented in Chapter related to withdrawal from these substances or to 9, and the related data on utilization of care are given
142 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life in Chapter 4. Estimating the indirect costs associated data—used by all states since 1993 on the Behavioral with oral health conditions and treatments, such as Risk Factor Surveillance System (BRFSS) and recent- disability days or lost productivity, is more difficult. ly added to the National Health and Nutrition Several methodologies are used to estimate these Examination Survey (NHANES)—offer the potential costs, although relatively few studies have actually of examining quality of life outcomes in relation to estimated the indirect costs associated with mortality oral health and other disease measures used in these or lost productivity due to dental conditions or treat- surveys (Gift 1996). These productivity-related ments (Reisine and Locker 1995). measures ask about the number of recent days when The annual National Health Interview Survey physical health was not good, mental health was not routinely collects data on disability days associated good, and activities were limited. These measures with selected conditions. As shown in Table 6.3, were found to be valid in use with general popula- there were 3.7 days of restricted activity per 100 tions and among older persons and adults with dis- employed persons 18 years and older reported in the abilities (Moriarty and Zack 1999). Related measures United States in 1996 associated with an acute dental on activity limitations and recent days of pain, condition, as defined by a dental symptom or treat- depression, anxiety, sleeplessness, and vitality are ment visit. Restricted activity days were most preva- also asked by about half of all BRFSS states and— lent among adults aged 18 to 24 years, women, when used with oral disease measures—could help blacks, and individuals with annual incomes of less to identify the impact of oral disease prevention pro- than $10,000. Compared to the 624.0 restricted grams at the state and local levels. activity days per 100 persons per year for all acute In the 1996 National Health Interview Survey, conditions, the 3.7 restricted activity days for dental the percentage of all acute conditions that are med- conditions represent a relatively small loss on an ically attended for all ages is 67.9 percent. “Medically individual basis. They do, however, add up to a siz- attended” is defined as having contacted a physician able number of days lost from work or school every (or other provider) or having a condition that causes year for the population as a whole. a person to cut back on activities for at least half a In addition, Table 6.3 presents the number of bed day. For acute dental conditions, 59.6 percent are days and work-loss days per 100 employed persons medically attended for all ages (NCHS 1996). aged 18 and older. Also, for youths 5 to 17 years of The most dramatic oral diseases by virtue of their age, 3.1 days of school were lost per year. high mortality rates are oral and pharyngeal cancers. An important aspect of identifying the specific The Centers for Disease Control and Prevention esti- health-related quality of life burden of oral disease mated in 1988 that 16.2 years of life were lost per will be to acquire more data on how the overall person dying of cancer of the oral cavity and pharynx health-related quality of life of persons with oral dis- (CDC 1991). This exceeds the average for all cancer ease differs from that of healthy persons, those with sites, which was 15.4 years lost. other diseases and activity limitations, and those with Researchers are beginning to assess costs associ- co-morbid oral and general health problems. The ated with chronic craniofacial conditions such as CDC’s “Healthy Days” measures and population periodontal diseases, pain syndromes, and congeni- tal anomalies. These estimates may also include the costs to care- TABLE 6.3 givers who take time off from Disability days due to all acute conditions and acute dental conditions, work to attend to these needs or United States, 1996 to take children to the dentist. All Acute Conditions Acute Dental Conditions Recent estimates put the lifetime Total Days Days per Total Days Days per costs of multiple surgeries and the (in thousands) 100 Persons (in thousands) 100 Persons other medical, dental, and rehabil- School-loss daysa 152,305 296.9 1,611 3.1b itation therapies typical of the Work-loss daysc 358,377 284.0 2,442 1.9b team approach to the habilitation Bed daysd 717,868 271.7 4,602 1.7b of individuals with cleft lip or Restricted activityd 1,648,932 624.0 9,705 3.7b palate at a minimum of $101,000 (Waitzman et al. 1996). Overall a Youths 5 to 17 years of age. b Figure does not meet NCHS standard of reliability or precision. costs of chronic pain conditions c Currently employed persons 18 years and older. in America are estimated to be d Persons of all ages. $79 billion (Bonica 1990). Given Source: NCHS 1996. the prevalence of headaches and
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 143 Effects on Well-being and Quality of Life temporomandibular disorders, the amount repre- rate oral health as excellent, very good, good, fair, or senting chronic oral-facial pain would certainly be poor, most people rated it as good or above (74 per- in the billions. cent). Interestingly, the relationship between self- rated global oral health and clinical measures used to rate the severity of dental caries or periodontal dis- RATINGS OF ORAL HEALTH ease was weak. The finding of such inconsistency has Researchers use two ways to assess how individuals been confirmed in other studies (Gooch et al. 1989, rate their oral health: global ratings and satisfaction Reisine and Bailit 1980, Rosenberg et al. 1988) and ratings. Global ratings employ a ranking scale, with was noted by Wilson and Cleary (1995). The most excellent health at one end and poor health at the important correlates of self-rated oral health were other. Satisfaction ratings are more akin to oral- worry about teeth and appearance, race, education, health-related quality of life measures insofar as they general health status, and depression scores. ask individuals how satisfied (or dissatisfied) they are with their oral health status in relation to symptoms, physical function, appearance, social function, and Satisfaction Ratings psychological status. According to Jokovic and Locker (1997), “expres- sions of satisfaction and dissatisfaction are important Global Ratings oral health status indicators since they synthesize objective health states, subjective responses, and cul- The dental survey conducted in connection with the turally based values and expectations.” ICS I repre- International Collaborative Survey II (ICS II) asked sented an early effort at assessing satisfaction with younger (35 to 44 years) and older adults (65 to 74 dental status (Arnlijot and WHO 1985). Specifically, years) of various ethnic groups at three sites in the it looked at satisfaction with teeth and gingiva among United States to rate their oral health from 1 (excel- adults and adolescents in metropolitan and non- lent) to 6 (poor). The vast majority of younger and metropolitan areas in 10 countries. With the excep- older white adults rated their oral health as good to tion of Japanese participants, satisfaction with teeth excellent (82 and 80 percent, respectively, in and gingiva among adolescents was fairly high, but Baltimore, and 71 and 68 percent, respectively, in San the percentage of adults satisfied with teeth among Antonio). In contrast, American Indians, Hispanics, participants from all countries was relatively low. A and African Americans were more likely to rate their decade later, ICS II (Chen et al. 1997) again assessed oral health as fair or poor. More detailed analysis whether younger and older adults were satisfied with found a significant relationship between oral health the way their teeth looked. American Indians were ratings and perceived general health, dentate status, the least satisfied with the appearance of their teeth. importance of oral health, income, oral pain, symp- Other community surveys of satisfaction (Barenthin toms, and dental visits (Chen et al. 1997). 1977, Gilbert et al. 1994, Jokovic and Locker 1997, Studies in the United States (Bloom et al. 1992, Murtomaa and Laine 1985, Rosenoer and Sheiham Chen et al. 1997, Gift et al. 1997, Matthias et al. 1995, Van Waas et al. 1994) show that most people 1995) have related global ratings of oral health to are satisfied with the performance and appearance of demographic, clinical, and psychosocial factors. A their teeth. special supplement on oral health in the National Health Interview Survey in 1989 asked participants to rate their oral health as excellent, very good, good, ORAL-HEALTH-RELATED QUALITY OF fair, or poor (Bloom et al. 1992). The majority of peo- LIFE MEASURES ple (67 percent) rated their oral health as excellent or Much of the research on oral health and quality of life very good, 23 percent rated it good, and only 10 per- focuses on the negative impact of craniofacial dis- cent rated it fair or poor. Men, younger people, and eases and disorders, diverting attention from the pos- more frequent users of dental services tended to rate itive effects of good oral health. Although it could be their oral health better than women, older adults, and argued that the benefits are self-evident, few studies less frequent users. African Americans, Hispanics, have investigated how people value oral health. and American Indians were less likely to rate their Strauss and Hunt (1993) found that older adults in oral health positively than were whites in similar geo- North Carolina felt that the presence of teeth graphic locations (Atchison and Gift 1997). enhanced their appearance, ability to eat, and enjoy- A study of Medicare participants in California ment of food, and that teeth also had a positive effect (Matthias et al. 1995) also found that when asked to on comfort, confidence, speech, enjoyment, and
144 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life longevity. More generally, a large multisite study in demiological indices of missing teeth, decayed teeth, the United States found that most adults across eth- and periodontal disease—conditions that are linked nic groups believe in the seriousness of oral disease to a lack of dental care. In several studies, infrequent and the importance of oral health for general health dental visits and problem-motivated dental visits (Davidson et al. 1996, Nakazono et al. 1997). were found to be independently associated with During the last decade, researchers have identi- reduced quality of life in multivariate models (Gilbert fied and described specific effects of oral disease on et al. 1997, Slade and Spencer 1994a). Lower socio- quality of life, and there are now at least 11 ques- economic status was an additional explanatory factor tionnaires designed to measure oral-health-related in five studies (Atchison and Dolan 1990, Gilbert et quality of life (Slade et al. 1998). These range from al. 1997, Gooch et al. 1989, Leao and Sheiham 1995, the three-item Rand Dental Health Index (pain, Locker and Slade 1994). worry, conversation) to the 49-item Oral Health All of the studies in Table 6.4 used cross-section- Impact Profile, which includes items relating to func- al designs to analyze associations with quality of life; tion, pain, physical disability, psychological disabili- it is thus not possible to infer a causal link between ty, social disability, and handicap. quality of life and the factors under study. Other researchers have used generic quality of Information about change in quality of life from life questionnaires (Reisine and Weber 1989) or ana- those questionnaires is available from only two lyzed oral health survey data, statistically summariz- population-based longitudinal studies. In one, a ing clinical measures with self-reported symptoms, study of elderly Floridians, small and statistically perceptions, and behaviors to create scales of oral- nonsignificant changes in the Geriatric Oral Health health-related quality of life (Gift et al. 1997, Gilbert Assessment Index were observed following an oral et al. 1997). An essential requirement for these health promotion program (Dolan 1997). In the sec- analyses is the establishment of theoretical models ond, a 2-year longitudinal study of elderly South that describe and distinguish among quality of life Australians, change in quality of life was measured dimensions. using the Oral Health Impact Profile. The study did Although the questionnaires have been used in not find that regular dental attendees had consistent- population studies, there is increased emphasis on ly better patterns of change than episodic dental the need to incorporate concepts of quality of life attendees (Slade and Spencer 1994b). into outcome research, using the questionnaires in In contrast, some information from experimental longitudinal or intervention studies to examine studies of carefully selected clinical samples indicates changes in quality of life following provision of den- effects of specific dental treatments on quality of life. tal care. Individual items from the questionnaires Using the Sickness Impact Profile in a U.S. study of can be used in describing the impact of oral health 30 patients treated for TMDs, Reisine et al. (1989) status on specific functions. For example, the ques- found significant improvements for rest/sleep, home tions concerning eating dysfunction presented in tasks, work, and leisure following treatment. A ran- Table 6.1 are derived from such questionnaires. domized clinical trial of 63 Canadians treated for Multidimensional indicators also can be used to pro- TMDs compared changes in quality of life, measured duce quantitative scores that indicate the severity of using visual analog scales. The investigators found the impact caused by oral health problems. Because equivalent improvements in quality of life, which there are seldom any reference values or population mirrored improvements in pain ratings, in all three norms to indicate thresholds at which such scores treatment groups (Dao et al. 1994). A German study represent “abnormal” or “severe” impacts on quality by Schliephake et al. (1996) reported improvements of life, the results are more valuable for analytic in quality of life, measured using a 22-item scale, studies examining trends and associations than for among 85 patients following tumor removal and describing impacts of oral health within populations. reconstructive surgery. Surveys in the United States and elsewhere have Two multidimensional scales have been specifi- used multidimensional questionnaires and have cally designed to assess global disability (e.g., disabil- revealed consistent correlations between reduced ity days, pain interference with daily activities) relat- quality of life and poorer clinical oral status and ed to recurrent or chronic pain. Both the Graded reduced access to dental care. Table 6.4 provides an Chronic Pain Scale (Von Korff et al. 1992) and the overview of these studies, their populations, and Multidimensional Pain Inventory (Kerns et al. 1985) descriptions of the assessment tools used. In the have been used to assess disability related to TMDs, studies using varied tools, there are consistent rela- as well as back pain and headache. Although TMD tionships between quality of life and standard epi- patients are generally found to have lower mean levels
ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 145 Effects on Well-being and Quality of Life of disability than patients with other types of pain cepts and methods for determining health-related using these scales, both scales can discriminate the quality of life is a reflection of these advances. People full range of disability in TMDs. For example, the living in societies that enjoy the benefits of this Graded Chronic Pain Scale is an ordinal scale that progress are responding with heightened expecta- assigns persons with pain to hierarchical grades indi- tions: They want to live long and live well, free of cating low-intensity, nondisabling pain (grade I); infirmity, impairment, disability, and handicap; they high-intensity, nondisabling pain (grade II); high- want an optimal quality of life and well-being. In disability, moderately limiting pain (grade III); and terms of oral health, new social norms and cultural high-disability, severely limiting pain (grade IV). In values now dictate that teeth should be retained over a sample of HMO patients with TMDs, 41 percent the lifetime, and oral pain and dysfunction forever were grade I, 43 percent grade II, 11 percent grade III, banished. Quality of life measures applied to oral and 5 percent grade IV (Von Korff et al. 1992). That health outcomes will be used to further those goals. is, about 16 percent of patients seeking care for TMDs were moderately or severely limited by their pain. FINDINGS Examination of efforts to characterize the functional and social implications of oral and craniofacial dis- HEIGHTENED EXPECTATIONS eases reveals the following findings: Advances in public health and biomedical research in Oral health is related to well-being and qual- the late twentieth century have transformed our lives ity of life as measured along functional, psychosocial, remarkably, adding years to the life span, providing and economic dimensions. Diet, nutrition, sleep, cures for many diseases and disorders, and promising psychological status, social interaction, school, and a new era of genetic medicine and bioengineering. work are affected by impaired oral and craniofacial The new field of science aimed at formulating con- health.
TABLE 6.4 Studies of multidimensional quality of life measures Numbers of Population Studied Individuals Assessment Tool Description of Assessment Tool Gooch et al.1989 U.S.insured adults aged 902 female Rand Dental Health Index Three dental questions written to represent 18-61 years 756 male factors contributing to adverse effects of dental disease Atchison and Dolan California Medicare 1,000 female Geriatric Oral Health A series of 12 questions measuring patient-reported 1990 recipients aged 65+ 755 male Assessment Index (GOHAI) oral functional problems Hunt et al.1995 N.C.elderly aged 70+ 440 Oral Health Impact Profile A comprehensive measure of self-reported (OHIP) dysfunction consisting of 49 questions Kressin et al.1996 Male veterans aged 47+ 1,242 male Oral Health-related Quality A brief global assessment of the impact of oral conditions Of Life (OHQOL) consisting of three items Gift et al.1997 U.S.aged 18+ 760 female 1981 Health Resources and Multidimensional concept using data from a large 555 male Services Administration study national sample Gilbert et al.1997 Floridians aged 45+ 491 female Oral Disadvantage Assessment Eight self-reported measures of avoidance in daily 383 male activities due to decrements in oral health Locker and Miller Canadians aged 18+ 299 female Subjective Oral Health Five oral health status indicators based on WHO’s 1994 244 male Status Indicators International Classification of Impairments, Disabilities and Handicaps Locker and Slade Canadians aged 50+ 168 female Oral Health Impact Profile A comprehensive measure of self-reported 1994 144 male (OHIP) dysfunction consisting of 49 questions Slade and Spencer Australians aged 60+ 660 female Oral Health Impact Profile A comprehensive measure of self-reported 1994b 557 male (OHIP) dysfunction consisting of 49 questions Leao and Sheiham Brazilians aged 35-44 303 female Dental Impact on Daily Thirty-six questions that assess the oral health impacts 1995 359 male Living (DIDL) on daily living Coates et al.1996 Australian dental patients 635 (+795 Oral Health Impact Profile A comprehensive measure of self-reported previously (OHIP) dysfunction consisting of 49 questions surveyed)
146 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life