INVITED ARTICLE AGING AND INFECTIOUS DISEASES Thomas T. Yoshikawa, Section Editor Infectious Complications of Dental and Periodontal Diseases in the Elderly Population Kenneth Shay Geriatrics and Extended Care Service Line, Veterans Integrated Services Network 11, Geriatric Research Education and Clinical Center and Dental Service, Ann Arbor Downloaded from https://academic.oup.com/cid/article/34/9/1215/463157 by guest on 02 October 2021 Veterans Affairs Healthcare System, and University of Michigan School of Dentistry, Ann Arbor Retention of teeth into advanced age makes caries and periodontitis lifelong concerns. Dental caries occurs when acidic metabolites of oral streptococci dissolve enamel and dentin. Dissolution progresses to cavitation and, if untreated, to bacterial invasion of dental pulp, whereby oral bacteria access the bloodstream. Oral organisms have been linked to infections of the endocardium, meninges, mediastinum, vertebrae, hepatobiliary system, and prosthetic joints. Periodontitis is a pathogen- specific, lytic inflammatory reaction to dental plaque that degrades the tooth attachment. Periodontal disease is more severe and less readily controlled in people with diabetes; impaired glycemic control may exacerbate host response. Aspiration of oropharyngeal (including periodontal) pathogens is the dominant cause of nursing home–acquired pneumonia; factors reflecting poor oral health strongly correlate with increased risk of developing aspiration pneumonia. Bloodborne peri- odontopathic organisms may play a role in atherosclerosis. Daily oral hygiene practice and receipt of regular dental care are cost-effective means for minimizing morbidity of oral infections and their nonoral sequelae. More than 300 individual cultivable species of microbes have growing importance in the elderly population. In 1957, nearly been identified in the human mouth [1], with an estimated 1014 70% of the US population aged 175 years had no natural teeth. individual microscopic organisms occupying the mouth and or- Due to water and dentifrice fluoridation, preventive dental be- opharynx at a time [2]. The most prevalent oral infectious dis- haviors, and an expanded dental profession, !35% of Americans eases, caries and periodontal disease, are historically the province aged 175 years now are missing all teeth [9]. This extends the of dentists for diagnosis and treatment. However, the effect of likelihood of risk for dental and periodontal disease into a time these oral diseases often extends systemically, particularly in older in life often marked by impaired self-care. This article will discuss adults. Hematogenous seeding from an oral source is a dominant the pathophysiology and, particularly, the systemic consequences cause of bacterial endocarditis [3] and is implicated in late pros- of these 2 oral infections in elderly people. thetic joint infection (LPJI) [4]. Periodontal disease impairs gly- cemic control in people with diabetes [5], and poorly controlled MICROECOLOGIC NICHES OF THE MOUTH diabetes may exacerbate periodontal disease [6]. Aspiration of oropharyngeal secretions is the predominant cause of nosocomial The mouth offers multiple microbiologic environments, several pneumonia in elderly persons [7]. Periodontopathic bacteria in of which involve the teeth. Tooth surfaces most apparent in the bloodstream have been linked to atherosclerosis, coronary the mouth are covered by enamel, an acellular material that is artery disease, and stroke [8]. ∼95% calcium hydroxyphosphate (hydroxyapatite) microcrys- This review focuses on caries and periodontal disease and their tals and 5% organic material [10]. Biting surfaces of teeth are marked by grooves and fissures that shelter bacterial colonies, Received 5 October 2001; revised 18 December 2001; electronically published 2 April although these irregularities in aged teeth have commonly been 2002. obliterated through years of chewing or dental restoration. The Reprints or correspondence: Dr. Kenneth Shay, Geriatrics and Extended Care Service Line, Veterans Integrated Services Network 11, PO Box 134002, Ann Arbor, MI 48113-4002 sides of teeth that contact one another represent a second mi- ([email protected]). croenvironment. This contact area, which is surrounded by Clinical Infectious Diseases 2002;34:1215–23 ᮊ 2002 by the Infectious Diseases Society of America. All rights reserved. tooth structure and gingiva, is sheltered from food debris and 1058-4838/2002/3409-0009$03.00 oral hygiene and shelters adherent bacteria. AGING AND INFECTIOUS DISEASES • CID 2002:34 (1 May) • 1215 Near the gingiva, the tooth surface abruptly changes from DENTAL CARIES: PATHOGENESIS acellular enamel into cementum, which is cellular tissue that AND LOCAL SEQUELAE is nearly 30% organic [11]. Initially, after a tooth’s eruption, the cemento-enamel junction is covered by gingiva; accumu- Dental caries is initiated by the nonhemolytic viridans strep- lated disease, trauma, and maturation expose it. In time, tooth- tococci [2], termed “mutans streptococci,” most commonly brushing and professional cleanings remove cementum and Streptococcus mutans and Streptococcus sobrinus. These organ- expose underlying dentin. Dentin is also ∼30% organic and isms are not present in newborns but appear as primary den- cellular. The tooth surface adjacent to the gingiva is a distinct tition erupts. DNA analysis confirms that transmission occurs microenvironment constantly bathed in plasma ultrafiltrate usually from mother to child, probably through shared food (“sulcular fluid”) seeping out of the sulcus between the gingiva implements [19]. The organisms thrive on sucrose, which they and the tooth. In the absence of gingival or periodontal disease, convert into organic acids and sticky polysugar (dextrans), the tooth-gingiva attachment is 1–3 mm from where the tooth which adheres the organisms to tooth surfaces [20]. Oral sites emerges from soft tissue (figure 1). The sulcular or subgingival that are not regularly disturbed, such as fissures and contact Downloaded from https://academic.oup.com/cid/article/34/9/1215/463157 by guest on 02 October 2021 microenvironment offers a continuum of conditions: the sulcus areas, thereby become susceptible to dental decay. entrance supports aerobic organisms; regions at increasing Tooth structure is in chemical equilibrium with saliva under depth are associated first with facultative species, then with neutral pH. Increasing acidity to pH 5.4 by exposing plaque to anaerobic species, that build adherent multispecies colonies sugar causes a net efflux of calcium and phosphorus from the (plaque) on the tooth [12]. enamel into saliva [21]. Initially, crystals of surface hydroxyapatite Another ecologic niche, saliva, is partially removed (and re- dissolve, leaving behind an organic matrix of the sparse inter- newed) continuously. Saliva is a variable and complex solution crystalline material. When neutrality is reestablished through sal- of water, glycoprotein, and organic and inorganic ions. Under ivary dilution and buffering, hydroxyapatite reforms on the ma- normal circumstances, saliva protects the oral cavity and its trix. However, an undisturbed plaque colony limits the effects contents [13]. Through chemical buffer systems (predomi- of saliva, even as colonies maintain a low pH at the underlying nantly bicarbonate), saliva maintains oral pH at nearly neutral tooth surface. When dissolution has proceeded to the point that values. Long-chain glycoproteins, enzymes, statins, and im- the matrix collapses, a cavity forms. When cavitation extends munoglobulins temper microbial growth. Calcium and phos- through the enamel to the dentin, the caries process shifts as phate in solution maintain equilibrium between the soluble proteolytic organisms, particularly Lactobacillus species, exploit tooth structure and saliva [14]. Diminished salivary flow and the more organic substrate [20]. modified saliva composition allow oral pH to decrease, dis- Older people frequently have dentin exposed near the gin- turbing the equilibrium between tooth structure and oral fluids, giva, and root caries initiates there. Root caries is started by and permitting uninhibited microbial growth [15]. Flow from mutans streptococci, and there is early involvement of prote- parotid [16], submandibular [17], and minor salivary glands olytic Actinomyces species, including Actinomyces viscosus, Ac- remains largely unaffected in healthy persons, regardless of age. tinomyces odontolyticus, and Actinomyces naeslundii. Root caries It has been reported that a reduced flow rate can potentially is relatively uncommon before the age of 30 years, but it rapidly accompany use of the majority of medications commonly pre- increases in incidence in the succeeding decades of life. In scribed for older people [15]; saliva composition and flow are contrast, the attack rate of enamel caries remains stable commonly deleteriously altered in elderly individuals [18]. throughout a person’s life [22]. Figure 1. Schematic representation (not to scale) of selected dental and periodontal structures in healthy persons 1216 • CID 2002:34 (1 May) • AGING AND INFECTIOUS DISEASES Without dental treatment, natural progression of caries fol- Bacterial endocarditis is the most common of these condi- lows 1 of 2 paths. In younger people, tooth pulp begins to be tions. Approximately 27% of cultured cases of bacterial en- affected when caries invades dentin [23]. Dental pulp consists docarditis are caused by mutans streptococci [30]. A link be- of capillaries, nerves,