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
Veterans Affairs Healthcare System, and University of Michigan School of Dentistry, Ann Arbor

More than 300 individual cultivable species of microbes have

been identified in the human mouth [1], with an estimated 1014
individual microscopic organisms occupying the mouth and oropharynx at a time [2]. The most prevalent oral infectious diseases, caries and periodontal disease, are historically the province
of dentists for diagnosis and treatment. However, the effect of
these oral diseases often extends systemically, particularly in older
adults. Hematogenous seeding from an oral source is a dominant
cause of bacterial endocarditis [3] and is implicated in late prosthetic joint infection (LPJI) [4]. Periodontal disease impairs glycemic control in people with diabetes [5], and poorly controlled
diabetes may exacerbate periodontal disease [6]. Aspiration of
oropharyngeal secretions is the predominant cause of nosocomial
pneumonia in elderly persons [7]. Periodontopathic bacteria in
the bloodstream have been linked to atherosclerosis, coronary
artery disease, and stroke [8].
This review focuses on caries and periodontal disease and their
Received 5 October 2001; revised 18 December 2001; electronically published 2 April
2002.
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
(kenneth.shay@med.va.gov).
Clinical Infectious Diseases 2002; 34:121523
 2002 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2002/3409-0009$03.00

growing importance in the elderly population. In 1957, nearly

70% of the US population aged 175 years had no natural teeth.
Due to water and dentifrice fluoridation, preventive dental behaviors, and an expanded dental profession, !35% of Americans
aged 175 years now are missing all teeth [9]. This extends the
likelihood of risk for dental and periodontal disease into a time
in life often marked by impaired self-care. This article will discuss
the pathophysiology and, particularly, the systemic consequences
of these 2 oral infections in elderly people.

MICROECOLOGIC NICHES OF THE MOUTH

The mouth offers multiple microbiologic environments, several
of which involve the teeth. Tooth surfaces most apparent in
the mouth are covered by enamel, an acellular material that is
95% calcium hydroxyphosphate (hydroxyapatite) microcrystals and 5% organic material [10]. Biting surfaces of teeth are
marked by grooves and fissures that shelter bacterial colonies,
although these irregularities in aged teeth have commonly been
obliterated through years of chewing or dental restoration. The
sides of teeth that contact one another represent a second microenvironment. This contact area, which is surrounded by
tooth structure and gingiva, is sheltered from food debris and
oral hygiene and shelters adherent bacteria.
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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 pathogenspecific, 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 homeacquired pneumonia; factors
reflecting poor oral health strongly correlate with increased risk of developing aspiration pneumonia. Bloodborne periodontopathic 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.

Figure 1.

DENTAL CARIES: PATHOGENESIS

AND LOCAL SEQUELAE
Dental caries is initiated by the nonhemolytic viridans streptococci [2], termed mutans streptococci, most commonly
Streptococcus mutans and Streptococcus sobrinus. These organisms are not present in newborns but appear as primary dentition erupts. DNA analysis confirms that transmission occurs
usually from mother to child, probably through shared food
implements [19]. The organisms thrive on sucrose, which they
convert into organic acids and sticky polysugar (dextrans),
which adheres the organisms to tooth surfaces [20]. Oral sites
that are not regularly disturbed, such as fissures and contact
areas, thereby become susceptible to dental decay.
Tooth structure is in chemical equilibrium with saliva under
neutral pH. Increasing acidity to pH 5.4 by exposing plaque to
sugar causes a net efflux of calcium and phosphorus from the
enamel into saliva [21]. Initially, crystals of surface hydroxyapatite
dissolve, leaving behind an organic matrix of the sparse intercrystalline material. When neutrality is reestablished through salivary dilution and buffering, hydroxyapatite reforms on the matrix. However, an undisturbed plaque colony limits the effects
of saliva, even as colonies maintain a low pH at the underlying
tooth surface. When dissolution has proceeded to the point that
the matrix collapses, a cavity forms. When cavitation extends
through the enamel to the dentin, the caries process shifts as
proteolytic organisms, particularly Lactobacillus species, exploit
the more organic substrate [20].
Older people frequently have dentin exposed near the gingiva, and root caries initiates there. Root caries is started by
mutans streptococci, and there is early involvement of proteolytic Actinomyces species, including Actinomyces viscosus, Actinomyces odontolyticus, and Actinomyces naeslundii. Root caries
is relatively uncommon before the age of 30 years, but it rapidly
increases in incidence in the succeeding decades of life. In
contrast, the attack rate of enamel caries remains stable
throughout a persons life [22].

Schematic representation (not to scale) of selected dental and periodontal structures in healthy persons

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Near the gingiva, the tooth surface abruptly changes from

acellular enamel into cementum, which is cellular tissue that
is nearly 30% organic [11]. Initially, after a tooths eruption,
the cemento-enamel junction is covered by gingiva; accumulated disease, trauma, and maturation expose it. In time, toothbrushing and professional cleanings remove cementum and
expose underlying dentin. Dentin is also 30% organic and
cellular. The tooth surface adjacent to the gingiva is a distinct
microenvironment constantly bathed in plasma ultrafiltrate
(sulcular fluid) seeping out of the sulcus between the gingiva
and the tooth. In the absence of gingival or periodontal disease,
the tooth-gingiva attachment is 13 mm from where the tooth
emerges from soft tissue (figure 1). The sulcular or subgingival
microenvironment offers a continuum of conditions: the sulcus
entrance supports aerobic organisms; regions at increasing
depth are associated first with facultative species, then with
anaerobic species, that build adherent multispecies colonies
(plaque) on the tooth [12].
Another ecologic niche, saliva, is partially removed (and renewed) continuously. Saliva is a variable and complex solution
of water, glycoprotein, and organic and inorganic ions. Under
normal circumstances, saliva protects the oral cavity and its
contents [13]. Through chemical buffer systems (predominantly bicarbonate), saliva maintains oral pH at nearly neutral
values. Long-chain glycoproteins, enzymes, statins, and immunoglobulins temper microbial growth. Calcium and phosphate in solution maintain equilibrium between the soluble
tooth structure and saliva [14]. Diminished salivary flow and
modified saliva composition allow oral pH to decrease, disturbing the equilibrium between tooth structure and oral fluids,
and permitting uninhibited microbial growth [15]. Flow from
parotid [16], submandibular [17], and minor salivary glands
remains largely unaffected in healthy persons, regardless of age.
It has been reported that a reduced flow rate can potentially
accompany use of the majority of medications commonly prescribed for older people [15]; saliva composition and flow are
commonly deleteriously altered in elderly individuals [18].

DENTAL CARIES: METASTATIC SEQUELAE

Hematogenous spread of oral pathogens becomes a potential
result of untreated dental decay once bacteria enters the pulp
chamber. Navazesh and Mulligan [29] reviewed 15 years worth
of medical literature to identify reports linking oral pathogens
with systemic disease in adults aged 150 years and reported
that oral streptococci had been linked to mediastinal abscesses,
meningitis, vertebral osteomyelitis, hepatobiliary disease, and
bacterial endocarditis.

Bacterial endocarditis is the most common of these conditions. Approximately 27% of cultured cases of bacterial endocarditis are caused by mutans streptococci [30]. A link between these strictly oral organisms and endocardial disease, and
the somewhat less clear association with dental treatment, has
resulted in published regimens for antibiotic prophylaxis for
certain at-risk patients before they undergo many dental procedures (table 1) [31]. The highest-risk groups of patients are
those with prosthetic heart valves and acquired valvular dysfunction, both of which occur predominantly in aged people.
Without results from a prospective, blinded clinical trial (which
has not been performed for ethical reasons), it is unknown
whether the prescribed regimen is appropriate or effective, but
it is a standard of practice that is unwise to ignore. Nevertheless,
Wahl [30] has focused on potential long-term effects of indiscriminate antibiotic use to argue for conducting such a trial.
Staphylococcus aureus and Staphylococcus epidermidis are
found both in patients with dental infection (particularly abscess) and in those with infected joint prostheses. These organisms, which usually have a nonoral source, together account
for nearly two-thirds of cases of LPJI of the hip [32]. Nearly
250,000 hip prostheses are placed in the United States annually,
mostly in people aged 165 years [33]. Temporal associations
between dental infection and LPJI historically resulted in widespread acceptance among orthopedists of the need for administration of antibiotics to arthroplasty patients before they undergo dental treatment [34]. More-recent deliberations, done
in light of better data, more-sophisticated analysis of risks and
benefits [35], and growing concerns about the long-term consequences of widespread antibiotic use have resulted in published recommendations by a panel of dentists, orthopedists,
and infectious disease doctors to limit such coverage to recipients of total hip replacements who are at high risk, and then
only for specific dental procedures (table 2) [36].

PERIODONTAL DISEASE PATHOGENESIS

Two distinct types of disease of the periodontium are of interest
in older humans. Nonspecific gingivitis is a reversible inflammation of the gums adjacent to the teeth that is caused by
presence of bacterial plaque (figure 2) [12]. Improved oral hygiene resolves the condition, although, in older people, inflammation forms faster in response to plaque and resolves more
slowly when plaque is removed [37]. Adult periodontitis occurs
when an inflammatory reaction to gingival pathogens extends
into the epithelial attachment between the tooth and the bone
and into the bone itself (figure 3).
As the plaque colonies that cause gingivitis mature, they
become depleted in gram-positive organisms and cocci, and
they begin to favor obligate anaerobes over facultative species
[30]. Clinically, tissues become red and edematous and gums
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Without dental treatment, natural progression of caries follows 1 of 2 paths. In younger people, tooth pulp begins to be
affected when caries invades dentin [23]. Dental pulp consists
of capillaries, nerves, and connective tissue surrounded by osteoblast-like cells (odontoblasts) that secrete the precalcified
matrix that will become additional dentin. Odontoblasts have
thin cellular processes extending the thickness of dentin. When
tooth structure is lost as a result of caries, odontoblastic processes, now less insulated from the mouth, expand and contract
more readily in response to oral environmental shifts (e.g., hot,
cold, sweets, air), and sensory nerves in the pulps odontoblastic
layer transmit the sensation of pain [24]. As caries progresses,
bacteria irritate the cellular processes and trigger an inflammatory reaction in pulp. In the closed space of the pulp chamber, an increase in tissue pressure causes severe pain (toothache)
and, ultimately, pulp necrosis. Commonly, oral debris occluding
the cavity forces the inflammatory process to extend out to the
root apex. From there, infection spreads through bone and into
soft tissue.
It is more common for untreated caries in older people to
have a self-limiting course. Odontoblasts, as described above,
add dentin onto the walls of the pulp chamber to the extent
that diminished chamber size in advanced age is perceptible
on dental radiographs [25]. Analogous processes reduce the
number and diameter of dentinal tubules [26]. As a result, acute
dental pain is an uncommon complaint in older people [27].
Greater tooth destruction occurs before the dental pulp is affected, because the dentin is thicker. Loss of tooth structure
reduces shelter for bacterial colonies, and natural salivary defenses are able to arrest the process.
The microorganisms associated with dental abscess and cellulitis are generally not the microorganisms associated with
caries but are anaerobic species from deep within the gingival
sulcus that thrive in debris-filled pulp chambers. Infections are
most commonly combinations of 3 obligate anaerobes (such
as Peptostreptococcus species, Porphyromonas gingivalis, Prevotella intermedia, and Prevotella melaninogenica) and Fusobacterium nucleatum. Less commonly identified are the facultative
anaerobes Streptococcus milleri, Streptococcus sanguis, and Actinomyces species [28].

Table 1. Recommendations for antibiotic prophylaxis for bacterial endocarditis in patients scheduled to undergo dental
procedures.

Table 1.

Cardiac conditions for which prophylaxis is recommended

Other notes

High risk

(Continued.)

Poor dental hygiene and periodontal or periapical infections produce bacteremia even in the absence of dental procedures, so people at risk
should establish and maintain the best possible oral health

Prosthetic heart valves

Previous diagnosis of endocarditis

Antiseptic mouth rinse applied immediately before dental procedures may

reduce magnitude and incidence of bacteremia; agents include 0.12%
chlorhexidine gluconate and 10% povidone-iodine

Complex cyanotic congential heart disease

Surgically constructed pulmonary shunts or conduits

For patients already taking antibiotics, an agent different from the one
currently being used should be selected from among those listed
above

Moderate risk
Patent ductus arteriosus
Ventricular septal defect

Status after cardiovascular procedures

Primum atrial septal defect

There is no evidence that coronary artery bypass graft introduces a risk

for endocarditis

Aortic coarctation
Bicuspid aortic valve
Acquired valvular dysfunction (e.g., rheumatic heart disease or collagen
vascular disease, such as lupus erythematosus)

Noncoronary vascular grafts may merit antibiotic prophylaxis for the

first 6 months after implantation [31]
NOTE.

Hypertropic cardiomyopathy

Dental procedures before which prophylaxis is recommended

Interligamentary injections
Placement of orthodontic bands, but not brackets
Subgingival periodontal procedures (e.g., scaling or root planing)
Periodontal probing
Tooth extraction
Periodontal surgery
Periapical surgery
Placement of medicated fibers into a periodontal pocket
Dental prophylaxis (unless no bleeding is anticipated)
Dental implant placement and reimplantation of avulsed teeth
Dental procedures before which prophylaxis is not recommended
Suture removal
Restorative dental procedures with or without use of a retraction cord
Intraoral injection of local anesthetic, if not intraligamentary
Endodontic procedures, if not extended beyond the root apex
Impressions
Dental radiography
Placement of a rubber dam
Fluoride treatment
Adjustment of an orthodontic appliance
Recommended regimens
Standard recommendation: amoxicillin, 2.0 g given 1 h before the
procedure
Regimen for patients unable to take medications orally: ampicillin sodium,
2.0 g given im or iv before the procedure
Possible regimens for patients allergic to penicillins
Clindamycin, 600 mg given 1 h before the procedure
Cephalexin or cefadroxil, 1.0 g given 1 h before the procedure
Azithromycin or clarithromycin, 2.0 g 1 h before the procedure
(continued)

bleed upon brushing; the flow of sulcular fluid increases and

becomes enriched in lymphocytes and phagocytes [38]. Histologic findings include vasculitis and lymphocytic infiltration
of the gingiva and the junctional epithelium (i.e., the sulcus
base tissue) [12]. Gingivitis can remain in the state described
for months and years and will not progress to periodontitis,
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unless changes in local conditions or generalized host susceptibility occur [39]. When the host/pathogen balance tips, the
lymphocytic nature of the gingivitis inflammatory infiltrate
changes to a plasma cell lesion as pathogens evade neutrophils
and elaborate proteolytic collagenase and hyaluronidase [38]
that degrade junctional epithelium. The specific pathogens that
are most commonly implicated are P. gingivalis and Bacteroides
forsythus [1], which are transmitted both vertically and horizontallythat is, between parents and children [1] and between
spouses [40], respectively.
In response to the invasion of the junctional epithelium, an
antibody reaction is initiated and may successfully limit disease.
But, if the antibody response is inadequate, deeper bacterial
penetration results in monocytic activation with elaboration of
cytokines and other inflammatory mediators. Fibroblasts and
macrophages in turn secrete matrix metalloproteinases that destroy collagen, glycosaminoglycans, and bone [39]. The process
is painless, although the host may note a disagreeable taste or
odor. Bony support of the tooth is lost as the sulcus base
migrates toward the end of the tooth root. Initially, the height
of gingiva on the tooth is unchanged, resulting in deepening
of the sulcus (now termed the periodontal pocket). The
pockets bacterial population becomes dominantly anaerobic
[28].
Clinical and epidemiologic evidence indicates that the preceding description applies, in most cases, to relatively brief
(duration, days to weeks) disease episodes, followed by much
longer periods during which host defenses dominate [41]. Over
years and decades, measurable loss of osseous support around
teeth occurs; in the most extreme case, affected teeth are exfoliated. More than 95% of dentate adults older than 50 years
of age show clear evidence of this process (hence the use of
growing long in the tooth as a metaphor for aging), although
only 20% such adults at any given point in time will show
signs consistent with active periodontal destruction [42].

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Mitral valve prolapse with regurgitation evidenced by audible clicks and

murmurs or Doppler-demonstrated mitral insufficiency (this includes
myxomatous mitral valve degeneration and exercise-induced mitral
insufficiency in men aged 145 years)

Data are from [31].

Table 2. Recommendations for antibiotic prophylaxis for prosthetic joint infection in patients scheduled to undergo dental
procedures.
Patients at elevated risk for prosthetic joint infection
Patients whose joint prostheses have been implanted within the previous
2 years
Patients with rheumatoid arthritis
Patients who are immunosuppressed due to pharmacotherapy
or immunocompromised due to disease
People with type 1 diabetes
Patients receiving corticosteroid therapy
Patients who have previously experienced a prosthetic joint infection
Dental procedures for which prophylaxis is recommended
Interligamentary injections
Placement of orthodontic bands, but not brackets
Subgingival periodontal procedures (e.g., scaling or root planing)
Periodontal probing
Tooth extraction
Periodontal surgery
Placement of medicated fibers into a periodontal pocket
Dental prophylaxis (unless no bleeding is anticipated)
Dental implant placement and reimplantation of avulsed teeth
Dental procedures for which prophylaxis is not recommended
Suture removal
Restorative dental procedures with or without use of retraction cord
Intraoral injection of local anesthetic, if not intraligamentary
Endodontic procedures if not extended beyond the root apex

ORAL CONDITIONS OF PERIODONTAL

DISEASE AND ASPIRATION PNEUMONIA

Impressions
Dental radiography
Placement of a rubber dam
Fluoride treatment
Adjustment of orthodontic appliance
Recommended regimens
Standard recommendation: amoxicillin, 2.0 g given 1 h before the procedure; cephalexin or cefadroxil, 1.0 g given 1 h before the procedure; or
clindamycin, 600 mg given 1 h before the procedure
Other notes
Late prosthetic joint infection has not been reported as a consequence of
dental management in the absence of dental infection; therefore, dental
and periodontal infection in a patient with a prosthetic joint should be
treated immediately and definitively
Antiseptic mouth rinse applied immediately before dental procedures may
reduce magnitude and incidence of bacteremia; agents include 0.12%
chlorhexidine gluconate and 10% povidone-iodine
Presence of other osseous implants, such as plates, screws, and pins, do
not dictate the need for antibiotic prophylaxis before dental procedures
NOTE.

Data are from [36].

PERIODONTAL DISEASE AND DIABETES

Dental clinicians have long observed that periodontal disease is
worse in people with diabetes [43], to the extent that periodontitis
has been considered a sixth addition to the 5 complications of
diabetes (i.e., peripheral neuropathy, retinal degeneration, renal
insufficiency, atherosclerosis, and microangiopathy) [44]. Diabetes is a strong risk factor for bone loss caused by periodontitis
[45]. Poor control of diabetes is correlated with markers of periodontal disease activity [4648]. The dominant periodontal pathogens are the same for persons with and persons without diabetes

The leading cause of death among nursing home patients and

the second mostcommon cause for hospitalization in this population is nursing homeacquired pneumonia [57]. Unlike
community-acquired pneumonia, which is largely caused by
viral and pneumococcal pathogens [58], nosocomial pneumonia, in general, and nursing homeacquired pneumonia,
specifically, is almost entirely caused by anaerobic gram-negative bacilli [59]. Reports have established the propensity of
severely ill people to experience oropharyngeal colonization
with gram-negative rods [60], which, in turn, have been demonstrated to populate the dental plaque of patients in intensive
care units [61] and nursing homes [62]. Finegold [63] specified
several prominent periodontal pathogens (including Bacteroides
and Fusobacterium species) among anaerobic bacteria that are
most important as causes of aspiration pneumonia. A longterm prospective study of 1350 elderly veterans residing in a
Department of Veterans Affairs (VA) nursing home found significant correlations between nursing homeacquired pneumonia and swallowing dysfunction, dependence in feeding, xerostomia, and presence of S. aureus, the periodontal pathogen
P. gingivalis, and the decay organism S. sobrinus [6466]. A
consistent picture emerges that conditions of poor oral hygiene,
plaque accretion, and compromised host defense that accompany periodontal breakdown also provide conditions favorable
for proliferation and subsequent aspiration of orally incubated
pulmonary pathogens [67, 68].
Clinically, the critical question is whether control of periAGING AND INFECTIOUS DISEASES CID 2002:34 (1 May) 1219

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Periapical surgery

[49, 50]. Studies have also focused on whether periodontitis, as

an infectious disease, impairs glycemic control in people with
diabetes. At least 1 investigation contradicted this theory of causation [51], although others have supported it [52, 53]. Improving periodontal health to improve glycemic control has also
been studied, but, to date, studies have failed to demonstrate
causation [54].
Explanations for the interaction between periodontitis and
diabetes are still hypothetical. Salvi et al. [55] documented that
the type 2 diabetic inflammatory response includes exaggerated
secretion of several inflammatory mediators, notably IL-1b,
prostaglandin E2 (PGE2), and TNF-a, in response to the presence of gram-negative cell-wall lipopolysaccharides, with consequent extensive tissue lysis. A second hypothesis is that advanced glycation end products formed in response to
hyperglycemia, elevated serum low-density lipoprotein levels,
and elevated triglyceride levels alter the macrophage phenotype
involved in periodontal lesions. Increased inflammatory tissue
destruction and alveolar bone loss result from that phenotypes
excessive cytokine production [56].

Figure 2. Schematic representation (not to scale) of selected dental and periodontal structures involved in gingivitis. Refer to figure 1 for a
description of unmarked anatomic structures.

CONCERNS ABOUT POSSIBLE

HEMATOGENOUS EFFECTS OF PERIODONTAL
PATHOGENS
The edematous state of the diseased periodontal pocket and
the robust pathogenic bacterial population thriving within
readily lead to periodontopathic bacteria entering the bloodstream. Cobe [70] reported that gentle toothbrushing and even
chewing caused cultivable anaerobic and aerobic bacteremia in
patients with and patients without periodontal disease. Increased gingival inflammation correlates with increasing incidence and severity of bacteremia after toothbrushing [71]. Periodontal pathogens are among the organisms implicated in both
bacterial endocarditis and LPJI [31, 35].
Mattila et al. [72] and Syrjanen et al. [73] independently
noted correlations between cardiovascular disease, cerebrovascular disease, and indices of oral health reflecting both caries
and periodontal disease activity. Relationships remained sig-

nificant for men, even after adjusting for age, blood lipid level,
body-mass index, smoking, and socioeconomic factors. DeStefano et al. [74] demonstrated that, among National Health
and Nutrition Examination Survey (NHANES) II participants,
there was a doubling of risk for coronary heart disease for those
with periodontal disease and tooth loss, even after controlling
for the patients sex, smoking, and socioeconomic factors. Joshipura et al. [75] noted significant multifactorial correlations
between periodontal disease and subsequent cardiovascular disease in 151,000 health care professionals observed prospectively.
Loesche et al. [76] reported significant correlations between
periodontal disease, lack of periodontal care, and cerebrovascular disease in 1350 elderly veterans. Beck et al. [77] found
significant correlations between bone loss and coronary artery
disease, fatal coronary artery disease, and cerebrovascular accident in the 1147 veterans of the VA Normative Aging Study/
Dental Longitudinal Study, even after adjusting for age, smoking, diet, and other obvious potential confounding variables.
Herzberg and Meyer [78] and Loesche and Lopatin [67] have
suggested that cell-wall lipopolysaccharides of bloodborne periodontopathic bacteria activate conversion of fibrinogen to fibrin,
triggering thrombus formation. Haraszthy et al. [79] examined
atherosclerotic plaques recovered from endarterectomies and
identified cellular remnants (in 42% of specimens) and DNA
fragments (in 72% of specimens) from P. gingivalis, Prevotella
intermedia, B. forsythus, and Actinobacillus actinomycetemcomi-

Figure 3. Schematic representation (not to scale) of selected dental and periodontal structures involved in adult periodontitis. Refer to figure 1
for a description of unmarked anatomic structures.
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odontal disease would reduce the incidence of pneumonia.

Yoneyama et al. [69] reported that Japanese nursing home residents subjected to daily and weekly oral hygiene interventions
experienced fewer bouts of pneumonia, fewer fevers, and fewer
hospitalizations than did control subjects. The findings are intriguing and merit independent confirmation and possibly consideration for broader implementation.

CLINICAL RECOMMENDATIONS
Oral bacteria are unquestionably related to disease outside the
oral cavity, particularly in older people. Hematogenous metastasis of caries-derived and periodontally derived infectious organisms causes serious cardiac and orthopedic disease. Aspiration of pathogens that colonize the oropharynx significantly
contributes to geriatric mortality, morbidity, and health care
expense. The total area of the inflamed epithelial lining of periodontal pockets in a person with a full dentition may exceed
25 cm2 [41]. A bleeding cutaneous wound of this dimension
should receive immediate medical and nursing attention. But a
combination of factors has allowed much of the mainstream
medical system, the caregiving population, and elderly persons
themselves to passively accept or simply ignore oral disease in
advanced age. These factors include the historic schism between
dentistry and medicine, the expense of dental care in the face of
the relative scarcity of third-party dental coverage among older
Americans, peoples resignation to the dental deterioration associated with advancing age, the aversion of most adults to having
their teeth brushed by someone else, the aversion of most people
to cleaning another persons mouth, and many adults aversion
to dental treatment because of unpleasant memories.
Caries and periodontal diseases are preventable through
widely known measures: use of a toothbrush and fluoridated
dentifrice at least twice daily, some means for cleaning between
teeth and at the gumline, receipt of regular dental examinations
with professional cleaning, and limited intake of refined sugar.
People with decreased saliva production as a side effect of medication are at increased risk for dental decay and should prob-

ably apply concentrated sodium fluoride gel daily and schedule

more frequent dental visits. People who have had missing teeth
replaced by dental appliances may need to become adept with
1 or more of a variety of specialized dental brushes to clean
nonanatomic surfaces. Someone who has experienced advanced
bone loss due to periodontal disease will need to devote extra
effort to clean exposed root surfaces. In older persons, the
preceding 3 factors, plus othersfinances, motivation, social
settingmay impede the efficacy of preventive dentistry.
Daily provision of oral hygiene is more than a matter of
grooming. Effective toothbrush use requires a level of manual
dexterity, tactile acuity, and visual ability that has likely diminished in an older person who requires assistance with other
care. Frail elderly persons are understandably encouraged to
participate in their own daily hygiene routines as much as
possible. But a caregiver must recognize when minimal standards of oral cleanliness are not being maintained. Sadly, nurse
aides are themselves seldom aware of the importance of and
techniques for maintaining oral health, either for themselves
or for those under their care, and they are rarely sanctioned
for failing to provide oral care; therefore, they consider the
chore to be among the lowest priorities in their overcrowded
daily routines [83].
In response to the endemically unclean mouths among dependent elderly individuals, some chemotherapeutic approaches for sanitizing the oral cavity have been used. Unfortunately, the agents introduced to date have limited efficacy
against caries and periodontal disease unless combined with
traditional daily oral hygiene. The topical antiseptic agent chlorhexidine gluconate is available as 0.12% mint-flavored oral
rinse. Twice-daily 60-s rinses reduce the counts of gingivitis
pathogens and, to a lesser extent, cariogenic organisms; gingival
inflammation is reduced as well [84]. Yoneyama et al. [69] used
a 10% povidone-iodine solution swabbed onto the palate and
oropharynx in conjunction with toothbrushing to reduce the
pathogenicity of oropharyngeal aspirates.
If poor oral health did not lead to serious disease, unclean
mouths would merely be an aesthetic concern. But uncontrolled
dental and periodontal diseases lead to serious morbidity, mortality, and considerable avoidable health care costs. Sadly, the
avoidable but undeniable status quo of poor oral hygiene
among frail elderly persons will remain unchanged until the
public demands a higher standard of oral care for their dependent forebears, or until those who control distribution of
health care resources realize that the added expense of daily
oral care is lower than the cost of ignoring it.

References
1. Haffajee AD, Socransky SS. Microbial etiological agents of destructive
periodontal diseases 1994. Periodontology 2000 1994; 5:78111.
2. Liljemark WF, Bloomquist CG. Normal microbial flora of the human

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tans. Beck et al. [77] and Offenbacher et al. [80] proposed an

alternative model for the periodontitis/vascular disease connection that was related to the aforementioned mechanism described
by Salvi et al. [55], which involved injury to the endothelium
caused by inflammatory mediators, such as C-reactive protein,
IL-1b, PGE2, and TNF-a, elaborated by bloodborne periodontopathic bacteria.
To date, no intervention studies have been published that
indicate that there are positive cardiovascular effects resulting
from periodontal therapy. Hujoel et al. [81] expressed concern
that reports linking periodontal and vascular diseases might
inspire a return to the practice of premature full-mouth extractions that occurred early in the 20th century, when the
focal infection theory of oral disease metastatic to other sites
was accepted as a cause for inflammatory conditions [82]. Hujoel et al. [81] reviewed studies correlating periodontal and
vascular diseases and concluded it was, at present, imprudent
to recommend extraction of periodontally involved teeth for
patients solely to improve cardiovascular or cerebrovascular
status.

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