Osteoporosis and Metabolic Bone Diseases

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Endocrine Fellows Series: Osteoporosis and Metabolic Bone Diseases PROGRAM AGENDA - Wednesday, August 1, 2018 7:00 – 7:45 AM Registration and Breakfast 7:45 – 8:00 AM Opening Remarks Michael R McClung, MD Bone Basics 8:00 – 8:20 AM Bone Basics: Structure and Strength Mary Bouxsein, PhD 8:20 – 8:40 AM Bone Basics: Metabolism John P Bilezikian, MD 8:40 – 9:00 AM Building Bone: Childhood and Adolescence Catherine Gordon, MD 9:00 – 9:20 AM Pathophysiology of Osteoporosis in Adults Michael R. McClung, MD 9:20 – 9:40 AM DXA: Principles and Interpretation Susan Greenspan, MD 9:40 – 10:00 AM Break Patient Evaluation 10:00 – 10:20 AM Fracture Risk Assessment and Treatment Guidelines Michael R. McClung, MD 10:20-10:40 AM New Approaches to Skeletal Assessment Mary Bouxsein, PhD 10:40 – 11:00 AM Bone Densitometry in Children Catherine Gordon, MD 11:00 – 11:20 AM Laboratory Evaluation Susan Greenspan, MD 11:20 – 12:00 Abstract Presentations 12:00 - 1:00 PM Lunch Osteoporosis Treatment 1:00 – 1:20 PM Nutrition and Lifestyle Factors Michael R. McClung, MD 1:20 – 1:40 PM Exercise and the Skeleton Mary Bouxsein, PhD 1:40 – 2:10 PM Estrogen and SERMS Susan Greenspan, MD 2:10 – 2:45 PM Bisphosphonates and RANKL Inhibitors Michael R McClung, MD 2:45 – 3:00 PM Break 3:00 – 3:40 PM Parathyroid Hormone Analogues John P Bilezikian, MD 3:40 – 4:00 PM Future Therapies for Osteoporosis Michael R McClung, MD 4:00 –5:00 PM Abstract Presentations PROGRAM AGENDA – Thursday, August 2, 2018 7:00 – 8:00 AM Breakfast Osteoporosis in Other Patients 8:00 – 8:30 AM Osteoporosis in Men John P Bilezikian, MD 8:30 – 9:00 AM Osteoporosis in Children and Adolescents Catherine Gordon, MD 9:00 – 9:30 AM Bone Health in Diabetes and Obesity Michael R McClung, MD 9:30 – 10:00 AM Break 10:00 – 10:30 AM Glucocorticoid-Induced Bone Loss John P Bilezikian, MD 10:30 – 11:00 AM Cancer-treatment Induced Bone Loss Susan Greenspan, MD 11:00 – 11:30 AM Abstract Presentations 11:30 – 12:30 PM Group Picture and Lunch Other Bone Diseases 12:30 – 1:00 PM Hyperparathyroidism John P Bilezikian, MD 1:00 – 1:30 PM Bowed Bones in Children: Rickets and Hypophosphatasia Catherine Gordon, MD 1:30 – 2:00 PM Paget Disease and Osteomalacia Michael R McClung, MD 2:00 – 2:30 PM Hypoparathyroidism John P Bilezikian, MD 2:30 – 3:00 PM Break 3:00 – 3:30 PM Management of Osteoporosis: Current Status Susan Greenspan, MD 3:30 – 4:00 PM Discussion 4:00 – 5:00 PM Abstract Presentations Abstract Presenters: Gauri Behari, MD Zeb Saeed, MD Lisa Cruz-Aviles, MD Nicole Sagalla, MD Kyrmarie Davila, MD Fadwa Sumrein, DO Kristen Gonzales, MD Sikarin Upala, MD Komal Motwani , MD Noor Yazdanie, MD Manav Nayyar, MD Adnin Zaman, MD Mohammed Qureshi, MD .

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Hypophosphatasia Could Explain Some Atypical Femur Fractures
Hypophosphatasia Could Explain Some Atypical Femur Fractures What we know Hypophosphatasia (HPP) is a rare genetic disease that affects the development of bones and teeth in children (Whyte 1985). HPP is caused by the absence or reduced amount of an enzyme called tissue-nonspecific alkaline phosphatase (TAP), also called bone-specific alkaline phosphatase (BSAP). The absence of TAP raises the level of inorganic pyrophosphate (Pi), which prevents calcium and phosphate from creating strong, mineralized bone. Without TAP, bones can become weak. In its severe form, HPP is fatal and happens in 1/100,000 births. Because HPP is genetic, it can appear in adults as well. A recent study has identified a milder, more common form of HPP that occurs in 4 of 1000 adults (Dahir 2018). This form of HPP is usually seen in early middle aged adults who have low bone density and sometimes have stress fractures in the feet or thigh bone. Sometimes these patients lose their baby teeth early, but not always. HPP is diagnosed by measuring blood levels of TAP and vitamin B6. An elevated vitamin B6 level [serum pyridoxal 5-phosphate (PLP)] (Whyte 1985) in a patient with a TAP level ≤40 or in the low end of normal can be diagnosed with HPP. Almost half of the adult patients with HPP in the large study had TAP >40, but in the lower end of the normal range (Dahir 2018). The connection between hypophosphatasia and osteoporosis Some people who have stress fractures get a bone density test and are treated with an osteoporosis medicine if their bone density results are low.
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A Novel Germline Mutation of ADA2 Gene In
International Journal of Molecular Sciences Case Report A Novel Germline Mutation of ADA2 Gene in Two “Discordant” Homozygous Female Twins Affected by Adenosine Deaminase 2 Deficiency: Description of the Bone-Related Phenotype Silvia Vai 1,†, Erika Marin 1,† , Roberta Cosso 2 , Francesco Saettini 3, Sonia Bonanomi 3, Alessandro Cattoni 3, Iacopo Chiodini 1,4 , Luca Persani 1,4 and Alberto Falchetti 1,2,* 1 Department of Endocrine and Metabolic Diseases, IRCCS, Istituto Auxologico Italiano, 20145 Milan, Italy; [email protected] (S.V.); [email protected] (E.M.); [email protected] (I.C.); [email protected] (L.P.) 2 IRCCS, Istituto Auxologico Italiano, San Giuseppe Hospital, 28824 Verbania, Italy; [email protected] 3 Department of Pediatrics, Università degli Studi di Milano-Bicocca, Fondazione MBBM, San Gerardo Hospital, 20100 Monza, Italy; [email protected] (F.S.); [email protected] (S.B.); [email protected] (A.C.) 4 Department of Medical Biotechnologies and Translational Medicine, University of Milan, 20122 Milan, Italy * Correspondence: [email protected] † These authors equally contributed to this paper. Abstract: Adenosine Deaminase 2 Deficiency (DADA2) syndrome is a rare monogenic disorder preva- lently linked to recessive inherited loss of function mutations in the ADA2/CECR1 gene. It consists Citation: Vai, S.; Marin, E.; Cosso, R.; of an immune systemic disease including autoinflammatory vasculopathies, with a frequent onset Saettini, F.; Bonanomi, S.; Cattoni, A.; at
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Overuse Injuries in Sport: a Comprehensive Overview R
Aicale et al. Journal of Orthopaedic Surgery and Research (2018) 13:309 https://doi.org/10.1186/s13018-018-1017-5 REVIEW Open Access Overuse injuries in sport: a comprehensive overview R. Aicale1*, D. Tarantino1 and N. Maffulli1,2 Abstract Background: The absence of a single, identifiable traumatic cause has been traditionally used as a definition for a causative factor of overuse injury. Excessive loading, insufficient recovery, and underpreparedness can increase injury risk by exposing athletes to relatively large changes in load. The musculoskeletal system, if subjected to excessive stress, can suffer from various types of overuse injuries which may affect the bone, muscles, tendons, and ligaments. Methods: We performed a search (up to March 2018) in the PubMed and Scopus electronic databases to identify the available scientific articles about the pathophysiology and the incidence of overuse sport injuries. For the purposes of our review, we used several combinations of the following keywords: overuse, injury, tendon, tendinopathy, stress fracture, stress reaction, and juvenile osteochondritis dissecans. Results: Overuse tendinopathy induces in the tendon pain and swelling with associated decreased tolerance to exercise and various types of tendon degeneration. Poor training technique and a variety of risk factors may predispose athletes to stress reactions that may be interpreted as possible precursors of stress fractures. A frequent cause of pain in adolescents is juvenile osteochondritis dissecans (JOCD), which is characterized by delamination and localized necrosis of the subchondral bone, with or without the involvement of articular cartilage. The purpose of this compressive review is to give an overview of overuse injuries in sport by describing the theoretical foundations of these conditions that may predispose to the development of tendinopathy, stress fractures, stress reactions, and juvenile osteochondritis dissecans and the implication that these pathologies may have in their management.
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Vitamin D and Bone Health
1150 17th Street NW Suite 850 Washington, D.C. 200361 Bone Basics 1 (800) 231-4222 TEL ©National Osteoporosis Foundation 2013 1 (202) 223-2237 FAX www.nof.org Vitamin D and Bone Health Vitamin D plays an important role in protecting your bones. It may also help prevent other conditions including certain cancers. Your body requires vitamin D to absorb calcium. Children need vitamin D to build strong bones, and adults need it to keep bones strong and healthy. When people do not get enough vitamin D, they can lose bone. Studies show that people with low levels of vitamin D have lower bone density or bone mass. They are also more likely to break bones when they are older. Severe vitamin D deficiency is rare in the United States. It can cause a disease known as osteomalacia where the bones become soft. In children, this is known as rickets. These are both different conditions from osteoporosis. NOF Recommendations for Vitamin D The National Osteoporosis Foundation (NOF) recommends that adults under age 50 get 400-800 International Units (IU) of vitamin D every day, and that adults age 50 and older get 800-1,000 IU of vitamin D every day. Some people need more vitamin D. There are two types of vitamin D supplements. They are vitamin D2 and vitamin D3. Previous research suggested that vitamin D3 was a better choice than vitamin D2. However, more recent studies show that vitamin D3 and vitamin D2 are fairly equal for bone health. Vitamin D3 is also called cholecalciferol. Vitamin D2 is also called ergocalciferol.
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Osseous Manifestations of Primary Hyperparathyroidism: Imaging Findings
Hindawi International Journal of Endocrinology Volume 2020, Article ID 3146535, 10 pages https://doi.org/10.1155/2020/3146535 Review Article Osseous Manifestations of Primary Hyperparathyroidism: Imaging Findings Jackson Bennett ,1 James W. Suliburk ,2 and Fanny E. Moroń 3 1School of Medicine, Baylor College of Medicine, Houston, TX, USA 2Department of Surgery, Baylor College of Medicine, Houston, TX, USA 3Department of Radiology, Baylor College of Medicine, Houston, TX, USA Correspondence should be addressed to Fanny E. Morón; [email protected] Received 13 September 2019; Revised 10 December 2019; Accepted 8 January 2020; Published 21 February 2020 Academic Editor: Giorgio Borretta Copyright © 2020 Jackson Bennett et al. -is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Primary hyperparathyroidism is a systemic endocrine disease that has significant effects on bone remodeling through the action of parathyroid hormone on the musculoskeletal system. -ese findings are important as they can aid in distinguishing primary hyperparathyroidism from other forms of metabolic bone diseases and inform physicians regarding disease severity and complications. -is pictorial essay compiles bone-imaging features with the aim of improving the diagnosis of skeletal in- volvement of primary hyperthyroidism. 1. Introduction the symptomatic classical variant in some individuals [2, 4]. Other HPT disease subtypes include secondary and tertiary Hyperparathyroidism (HPT) is an endocrine disorder de- disease, which are primarily seen in patients with chronic fined by a state of inappropriately increased levels of renal disease and posttransplant patients [7].
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Fracture Healing Complications in Patients Presenting with High-Energy Trauma Fractures and Bone Health Intervention Debra L
Scientific Poster #116 Polytrauma OTA 2014 Fracture Healing Complications in Patients Presenting with High-Energy Trauma Fractures and Bone Health Intervention Debra L. Sietsema, PhD1,2; Michael D. Koets, BS3; Clifford B. Jones, MD1,2; 1Orthopaedic Associates of Michigan, Grand Rapids, Michigan, USA; 2Michigan State University, Grand Rapids, Michigan, USA; 3Wayne State University School of Medicine, Detroit, Michigan, USA Purpose: Approximately 5%-10% of fractures will have healing complications of nonunion or malunion. Altered bone metabolism is one of many contributing factors to abnormal bone healing. Trauma patients may have many of the risk factors for osteoporosis which when combined with a high-impact injury can lead to poor fracture healing. The purpose of this study was to determine fracture healing complications following high-energy trauma in those who have had bone health follow-up. Methods: From 2011 through 2012, 522 consecutive adults with high-energy trauma frac- tures received treatment in a Level I trauma center, were seen in an outpatient clinic for bone health, and retrospectively evaluated. 96 patients were excluded due to insufficient chart data, resulting in 426 patients in the study. Patients had a full workup consisting of mechanism of traumatic fracture(s), radiologic determination of healing, health and medi- cation history, physical examination, bone health laboratory values drawn inpatient, and dual x-ray absorptiometry (DXA) outpatient when physically feasible. Vitamin D 50,000 IU was given following trauma presentation prior to initial laboratory draw and continued maintenance dose was dependent on laboratory results. Individualized bone health life- style behavioral counseling, treatment and prescription were provided as indicated.
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Nephrology II BONE METABOLISM and DISEASE in CHRONIC KIDNEY DISEASE
Nephrology II BONE METABOLISM AND DISEASE IN CHRONIC KIDNEY DISEASE Sarah R. Tomasello, Pharm.D., BCPS Reviewed by Joanna Q. Hudson, Pharm.D., BCPS; and Lisa C. Hutchison, Pharm.D., MPH, BCPS aluminum toxicity. Adynamic bone disease is referred to as Learning Objectives low turnover disease with normal mineralization. This disorder may be caused by excessive suppression of PTH 1. Analyze the alterations in phosphorus, calcium, vitamin through the use of vitamin D agents, calcimimetics, or D, and parathyroid hormone regulation that occur in phosphate binders. In addition to bone effects, alterations in patients with chronic kidney disease (CKD). calcium, phosphorus, vitamin D and PTH cause other 2. Classify the type of bone disease that occurs in patients deleterious consequences in patients with CKD. Of these, with CKD based on the evaluation of biochemical extra-skeletal calcification and increased left ventricular markers. mass have been documented and directly correlated to an 3. Construct a therapeutic plan individualized for the stage increase in cardiovascular morbidity and mortality. The goal of CKD to monitor bone metabolism and the effects of of treatment in patients with CKD and abnormalities of bone treatment. metabolism is to normalize mineral metabolism, prevent 4. Assess the role of various treatment options such as bone disease, and prevent extraskeletal manifestations of the phosphorus restriction, phosphate binders, calcium altered biochemical processes. supplements, vitamin D agents, and calcimimetics In 2003, a non-profit international organization, Kidney based on the pathophysiology of the disease state. Disease: Improving Global Outcomes, was created. Their 5. Devise a therapeutic plan for a specific patient with mission is to improve care and outcomes for patients with alterations of phosphorus, calcium, vitamin D, and CKD worldwide by promoting, coordinating, collaborating, intact parathyroid hormone concentrations.
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Osteoporosis/Bone Health in Adults As a National Public Health Priority
Position Statement Osteoporosis/Bone Health in Adults as a National Public Health Priority This Position Statement was developed as an educational tool based on the opinion of the authors. It is not a product of a systematic review. Readers are encouraged to consider the information presented and reach their own conclusions. Osteoporosis is a widespread metabolic bone disease characterized by decreased bone mass and poor bone quality. It leads to an increased frequency of fractures of the hip, spine, and wrist. Osteoporosis is a global public health problem currently affecting more than 200 million people worldwide. In the United States alone, 10 million people have osteoporosis, and 18 million more are at risk of developing the disease. Another 34 million Americans are at risk of osteopenia, or low bone mass, which can lead to fractures and other complications. Low bone mass is a growing global health burden, and likely reflects only a small part of the true burden of osteoporosis, given that bone mineral density (BMD) does not indicate other important components of bone strength. Fragility fractures have a morbidity and mortality related to them that may be avoided more effectively if information is provided in clinical and public health prevention and management programs.14 Eighty percent of people who suffer osteoporosis are females.1 Although more commonly seen in females, osteoporosis in males remains underdiagnosed and underreported.8 The lifetime risk for fracture may be rising in certain populations, specifically Hispanic females. According to the 2004 Surgeon General's Report on Bone Health and Osteoporosis, the prevalence of osteoporosis in Hispanic females is similar to that found in Caucasian females.
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Osteomalacia and Vitamin D Status: a Clinical Update 2020
Henry Ford Health System Henry Ford Health System Scholarly Commons Endocrinology Articles Endocrinology and Metabolism 1-1-2021 Osteomalacia and Vitamin D Status: A Clinical Update 2020 Salvatore Minisola Luciano Colangelo Jessica Pepe Daniele Diacinti Cristiana Cipriani See next page for additional authors Follow this and additional works at: https://scholarlycommons.henryford.com/endocrinology_articles Authors Salvatore Minisola, Luciano Colangelo, Jessica Pepe, Daniele Diacinti, Cristiana Cipriani, and Sudhaker D. Rao SPECIAL ISSUE Osteomalacia and Vitamin D Status: A Clinical Update 2020 Salvatore Minisola,1 Luciano Colangelo,1 Jessica Pepe,1 Daniele Diacinti,1 Cristiana Cipriani,1 and Sudhaker D Rao2 1Department of Clinical, Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy 2Bone and Mineral Research Laboratory, Division of Endocrinology, Diabetes & Bore and Mineral Disorders, Henry Ford Hospital, Detroit, MI, USA ABSTRACT Historically, rickets and osteomalacia have been synonymous with vitamin D deﬁciency dating back to the 17th century. The term osteomalacia, which literally means soft bone, was traditionally applied to characteristic radiologically or histologically documented skeletal disease and not just to clinical or biochemical abnormalities. Osteomalacia results from impaired mineralization of bone that can manifest in several types, which differ from one another by the relationships of osteoid (ie, unmineralized bone matrix) thickness both with osteoid surface and mineral apposition rate. Osteomalacia related to vitamin D deﬁciency evolves in three stages. The initial stage is characterized by normal serum levels of calcium and phosphate and elevated alkaline phosphatase, PTH, and 1,25-dihydroxyvitamin D [1,25(OH)2D]—the latter a consequence of increased PTH. In the second stage, serum calcium and often phosphate levels usually decline, and both serum PTH and alkaline phosphatase values increase further.
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Metabolic Bone Disease in Lizards: Prevalence and Potential for Monitoring Bone Health
Metabolic Bone Disease In Lizards: Prevalence And Potential For Monitoring Bone Health Deborah A. McWilliams* and Steve Leeson University of Guelph, Guelph, ON, Canada A consensus that metabolic bone disease (MBD) is the nutritional pathology (NP) most likely to occur in captive lizards was apparent in a study at the Ontario Veterinary College Teaching Hospital (OVCTH) and in two surveys on NP in accredited zoos in Canada and the United States. The prevalence, pathogensis and diagnosis of MBD relative to the OVCTH and zoological research is discussed. A proposed study to investigate the multifactorial nature of MBD in lizards in zoo populations and veterinary clinics is presented. This study includes researching a qualitative ultrasound (QUS) method to diagnose MBD in lizards and correlate that methodology to dietary and environmental factors in MBD. Key words: nutritional pathology; osteopathy; reptiles INTRODUCTION A retrospective study at the Ontario Veterinary College Teaching Hospital (OVCTH) from 1992 to 1996 (inclusive) indicates 84.4% of lizard clients are diagnosed with metabolic bone disease (MBD) [McWilliams, 1998]. Metabolic bone disease is an osteopathy that results in an impairment of the remodelling, growth and health of bone. The pervasiveness of MBD in captive lizards also appeared in the results of two surveys on nutritional pathology (NP) in accredited zoos (68.8% response rate) in Canada and the United States (US) [McWilliams, 2000]. Metabolic bone disease in reptiles has been studied for at least four decades [Truit, 1962; Reichenbach-Klinke and Elkan, 1965]. Ultraviolet (UV) light, for example, is thought to be essential to reptilian health, yet many captive reptiles develop MBD despite exposure to UV light [Dickinson and Fa, 1997].
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Sports Injuries in Children Continued
Me d i c i n eT o d a y PEER REVIEWED ARTICLE POINTS: 2 CPD/1 PDP Sports injuries in childre n The number of children with sports injuries seen in sports medicine practices is increasing. The usual outcome is full recovery, but the consequence of a missed diagnosis of a more serious condition may be significant for the child. The important issue of encouraging children to be injuries seen in sports medicine practices appears more active in an effort to improve their overall to be actually increasing.1 , 2 health is a complex public health problem.1 , 2 Fortunately, many of the sports injuries that Childhood sports participation in Australia has occur in children are self-limited and full recovery unfortunately declined over the past few decades. is the usual outcome. However, more serious con- Some 86% of children aged 5 to 14 years were ditions may occasionally occur and the conse- active in sport in 1985, but by 2003, the level of quence of a missed diagnosis, especially during the participation had fallen to 54% for girls and 69% rapid pubertal growth phase, may be significant for boys.1 During this time period, the number of for the child. overweight and obese children has been increas- Pain in a child should not be dismissed as ‘grow- TOM CROSS ing. At the other end of the spectrum, more active ing pains’. If an informed systematic approach FACSP, MBBS, DCH children are training more intensively and for is followed, the clinical assessment of a child will longer periods of time in one or several sports.
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A Study of the Association Between Serum Bone-Specific Alkaline Phosphatase and Serum Phosphorus Concentration Or Dietary Phosphorus Intake
J Nutr Sci Vitaminol, 58, 442–445, 2012 Note A Study of the Association between Serum Bone-Specific Alkaline Phosphatase and Serum Phosphorus Concentration or Dietary Phosphorus Intake Mayu HARAIKAWA1, Rieko TANABE1, Natsuko SOGABE2, Aoi SUGIMOTO1, Yuka KAWAMURA1, Toshimi MICHIGAMI3, Takayuki HOSOI4 and Masae GOSEKI-SONE1,* 1 Department of Food and Nutrition, Faculty of Human Sciences and Design, Japan Women’s University, Bunkyo-ku, Tokyo 112–8681, Japan 2 Department of Health and Nutrition Sciences, Faculty of Human Health, Komazawa Women’s University, Tokyo 206–8511, Japan 3 Research Institute, Osaka Medical Center for Maternal and Child Health, Osaka 594–1101, Japan 4 Department of Clinical Research and Development, National Center for Geriatrics and Gerontology, Aichi 474–8511, Japan (Received March 27, 2012) Summary Alkaline phosphatase (ALP) hydrolyzes a variety of monophosphate esters into phosphoric acid and alcohol at a high optimum pH (pH 8–10). Human ALPs are clas- sified into four types: tissue-non specific (TNSALP, liver/bone/kidney), intestinal, placen- tal, and germ cell types. Based on studies of hypophosphatasia (HPP), which is a systemic bone disease caused by the presence of either one or two pathologic mutations in ALPL that encodes TNSALP, TNSALP was suggested to be indispensable for skeletal mineralization. In this study, we explored the possibility that dietary nutrients contribute to regulate serum bone-specific ALP (BAP) activity. Serum biochemical parameters, such as serum ALP, BAP, osteocalcin, and fibroblast growth factor 23 (FGF23), were measured in healthy young sub- jects (n5193). Dietary nutrient intakes were measured based on 3-d food records before the day of blood examinations.
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