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Periodontal Disease and Systemic Health -- What You
and Your Patients Need to Know Joan Otomo-Corgel, DDS, MPH, Robert L. Merin, DDS, MS
For many years, most dentists have recognized the importance of dental
health to the general health of their patients. Since the surgeon general’s
report on oral health in America1 was issued by the U.S.
Department of Health and Human Services, the medical profession, the news
media, and the public have become more aware of this association. Recent
research findings point to possible associations between chronic oral
infections such as periodontitis and systemic health problems such as
diabetes, heart and lung diseases, stroke, and low birth weight premature
births. This article will review the evidence for some of these associations
and explore factors that may underlie oral-systemic disease connections. Within the oral cavity dwells a dynamic microbiologic ecosystem of approximately
6 billion microbes living in a delicate balance that can be altered by the
health of the host and the integrity of its defenses. The periodontium, as
well as other body surfaces, carry an enormous microbial load, yet underlying
tissues and blood are relatively sterile. Protective barriers prevent easy
penetration of bacteria. Skin and mucous membranes, immunologic defenses, and
high oxidation reduction potentials with oxygen levels of host cells provide
barriers from bacterial penetration and invasion. If the host is
immunosuppressed, immunodeficient, hypoxic, or injured, the potentials for
microbial penetration increase.2 In recent years, evidence points
to the health of the host as playing an intimate role in the maintenance of
periodontal stability. Therefore, both patient and clinician should recognize
health status and its influence on periodontal diseases or inversely,
periodontal diseases and risk to health. As a result of exposure of the periodontium to complex dental plaques
consisting of more than 400 bacterial species, periodontal disease occurs.3
Periodontitis is generally a chronic infection that results in the
inflammatory destruction of the periodontal ligament and alveolar bone. This
destruction occurs due to toxic bacterial byproducts (lipopolysaccharides,
peptidoglycans, hydrolytic enzymes); a mounted host response (cytokines,
interleukins, and prostaglandins); and systemic reaction via serum
antibodies.4 It is, therefore, reasonable to hypothesize that
periodontal infections may influence overall health and the course of some
systemic diseases.5 Cardiovascular Disease Orally derived bacteremia infecting damaged heart valves is currently
the strongest association between dental plaque/periodontal inflammation and
systemic disease.6 It is well-accepted that dental and other
surgical procedures predispose susceptible patients to infectious
endocarditis or infections in the mural endocardium.7 Periodontal
bacteria and/or their byproducts may also gain access to the circulation by
direct invasion of periodontal tissues.8,9 Bacteremia from oral
origin appears to be directly related to the severity of periodontal
inflammation.10 There are two forms of infectious endocarditis, acute and subacute. Clinical
manifestations and implicated microflora frequently differ. Acute infectious
endocarditis presents with abrupt onset of fever, cutaneous and oral
petechia, and focal dermal gangrene. The clinical course is rapid, less than
six weeks. Intravascular coagulation may occur, which increases the risk for
emboli and metastatic infection in any body organ.11 Death occurs
unless antibiotic therapy is instituted. Subacute infectious endocarditis may persist for months. During its
chronic course, patients present with low-grade fever, fatigue, myalgias,
arthralgias, and anemia. Antimicrobial therapy at early stages will cure the
disease, but it is fatal without intervention. Oral streptococci, i.e., Streptococcus
viridans and S. sanguis, have been isolated from subacute infectious
endocarditis patients. Strains of S. sanguis adhere to thrombotic
vegetations on heart valves and may cause in vivo thrombus formation.12
Note that infectious endocarditis can also be caused by other
periodontal pathogens: Hemophilu species, Actinobacillus
actinomycetemcomitans, Eikenella corrodens, Capnocytophaga species, and Fusobacterium
nucleatum. Clinical therapy, therefore, should focus primarily on
minimizing gingival inflammation in at-risk patients. The current American
Heart Association guidelines recommend antibiotic prophylaxis in procedures
that induce bleeding. Frequent periodontal maintenance, preventive home care,
and necessary periodontal interventions need to be performed because
maintenance of periodontal health is imperative in this patient population. Patients with heart valvular disease, heart valve replacement, or a
history of infectious endocarditis are at high risk for infectious
endocarditis, congestive heart failure, or significant arrhythmias. Clinicians
treating the periodontium should consult with the patient’s cardiologist. It
is equally important that the dental team advise the physician regarding the
periodontal/dental disease status. Is there an association between cardiovascular disease,
atherosclerosis, and periodontal disease? Several studies indicate possible
relationships with chronic periodontal/oral infection and atherosclerosis,
myocardial infarction, and cerebrovascular disease.13-16 Severe
periodontal disease, including advanced alveolar bone loss in multiple sites
with edema, suppuration, and/or swelling may be a risk factor for
cardiovascular disease (Figure 1). Correlations with gingivitis and
periodontal disease are not evident. Some researchers, for example, Hujoel
and colleagues, could not find convincing evidence of a causal association
between periodontal disease and coronary heart disease.17 Further
research is needed to evaluate this association. Periodontal infections may directly effect atheroma formation as seen
in Porphyromonas gingivalis studies, which found P. gingivalis in
carotid and coronary atheromas,18 invading endothelial cells,19
and inducing platelet aggregation. Another mechanism that may associate
periodontal infections and infections in general with atherosclerosis is via
indirect or host-mediated responses, i.e. ,production of C-reactive proteins
and fibrinogen, which are independent risk factors for coronary disease.20
This inflammatory response characteristic of periodontal disease, marked by
high levels of inflammatory mediators, may exacerbate the process of atherogenesis.5
Recent studies indicate a possible association of stroke or
cerebrovascular ischemia with dental infection (odds ratio, 2.6).21
Also, the Normative Aging Study and the Dental Longitudinal Study of the
Department of Veterans Affairs found that incidence odds ratios for bone loss
and total cardiovascular disease, fatal cardiovascular disease, and stroke
were 1.5, 2.2, and 2.8 respectively.15 Patients with periodontal disease who are at risk for atherosclerosis
should have thorough periodontal examinations and medical review. Comprehensive
periodontal therapy should be provided with meticulous preventive care and
maintenance therapy. Patients need to be informed about possible periodontal
disease relationships to cardiovascular diseases (Table 1). Also,
patients with pre-existing cardiovascular disease should have open
communication with medical care providers for consultation regarding both
periodontal/dental and medical concerns. Respiratory Disease Chronic obstructive pulmonary disease was the fourth leading cause of
death (100,000 lives), and pneumonia/influenza caused 84,000 deaths in the
United States in 1996.22 There is increasing evidence that oral
bacteria, especially periodontal pathogens, may alter the course of
respiratory infections. Also, it is known that the lower airway can be
contaminated by microorganisms through aspiration of oropharyngeal contents,
inhalation of infectious aerosols, hematogenous spread, or spread from
contiguous sites.23 Oral pathogens may serve as a reservoir for
these respiratory infections and influence the bacterial flora of the lower
bronchi. There are documented studies that show poor oral hygiene in patients
hospitalized , institutionalized,24 or admitted to intensive care
units.25,26 Potential respiratory pathogens may become established in the oral
flora of patients with periodontal disease. Patients treated with antibiotics
appear to have greater numbers of potential respiratory pathogens adherent to
bacteria in subgingival plaque. High-risk pneumonia patients may be more
prone to oral colonization by respiratory pathogens following mucosal
modification due to prolonged exposure to dental plaque. Also, many at-risk
patients have compromised swallowing reflexes, which leads to easier
aspiration. Bacterial pneumonia, chronic bronchitis, emphysema, and chronic
obstructive pulmonary disease may be adversely affected by oral microflora. Antibiotic-resistant
strains of bacteria are emerging, and oropharyngeal flora and secretions are
directly responsible for potential respiratory infection. Aspiration of oral
bacteria may be responsible for exacerbation of chronic obstructive pulmonary
disease.27 Recommendations for the dental clinician include: 1. Reducing levels of periodontopathic flora by maintaining good home
care and frequent periodontal maintenance. 2. Rinsing with chlorhexidine prior to dental/periodontal therapy 3. Performing required periodontal therapies to stabilize the
periodontium 4. Due to xerostomia in this population from mouthbreathing/obstruction
and medications, close monitoring of dental caries is recommended, as well as
fluoride therapy at home. 5. Consultation with the patient’s physician for periodontal/dental or
medical concerns. Adverse Pregnancy Outcomes Preterm low birth weight is a significant cause of perinatal morbidity
and mortality. Despite attempts to reduce recognized risk factors for preterm
low birth weight, including low socio-economic status, poor prenatal care, a
mother older than 34 or younger than 17, alcohol abuse, smoking,
hypertension, genitourinary tract infections, diabetes, multiple pregnancies,
and African American ancestry,27 minimal alteration in the number
of preterm low-birth-weight infants occurred. Recent studies suggests that infection may increase the likelihood of
preterm low birth weight. Genitourinary or other infections, possibly
periodontal, may adversely affect pregnancy outcomes.28,29
Prostaglandin E2, and tumor necrosis factor a are normal biologically active
molecules during childbirth. They may be raised to high levels with infection
and induce premature labor. In a case-control study, preterm low-birth-weight
infants had mothers with significantly more periodontal attachment loss than
the control group with normal-weight infants at birth.30 In light of the possible link between periodontal infection and
adverse pregnancy outcomes, the dental/periodontal clinician will need to
educate the pregnant patient on the latest research and the implications. The
incidence of pregnancy gingivitis (30 percent to 75 percent) is high. This
may be due to alterations in the composition of subgingival plaque, altered
immunoresponse, and increases in sex hormone concentrations during pregnancy.31
More frequent periodontal maintenance visits in order to maintain periodontal
health during pregnancy is paramount.32 The second trimester is
the safest time to treat the pregnant patient because most organ systems have
been formed. The third trimester is also safe, however, the clinician should
be aware of the pressure of the gravid uterus on the inferior vena cava
creating a risk for postural hypotension. In light of the new research,
however, it is apparent that the patient should have closer monitoring and
management of periodontium and oral infections. Conclusion In this new millennium, dental practitioners are obligated to care for
the patient’s total health. They are able to see the links and potential
risks of periodontal and other oral infections to systemic health. Future
research will help dentistry unravel the complex interactions between host
susceptibility, immune response, genetic associations, behavioral components,
and disease control. Dentists must not only treat localized oral infections,
but manage risk that varies with each individual patient. Author Joan Otomo-Corgel, DDS, MPH, FACD, is chair of postdoctoral research
at the Greater Los Angeles VA Health Care System, Department of Dentistry; an
adjunct assistant professor at the UCLA School of Dentistry; and faculty at
the West Los Angeles City College Dental Hygiene Department. She has a
private practice limited to periodontics, implantology, and oral medicine in
Los Angeles.. References 1. U.S. Department of Health and Human Services, Oral Health in
America: A Report of the Surgeon General (Executive Summary), 2000 2. Loesche WJ, Periodontal disease as a risk factor for heart disease.
Compendium 15:976-92, 1994. 3. Moore WEC, Moore LVH, The bacteria of periodontal disease. Periodontal
2000 5:66-77, 1994. 4. Ebersole JL, Systemic humoral immune response in periodontal
disease. Crit Rev Oral Bio Med 1:283-331, 1990. 5. Scannapieco FA, Periodontal disease as a potential risk factor for
systemic disease: AAP Position Paper. J Periodontol 69:841-50, 1998. 6. Kaye D, Infective endocarditis In, Isselbacker KJ, Braunwald E, et
al, eds, Harrison’s Principles of Internal Medicine, 13th ed. McGraw-Hill,
New York, 1994, pp 520-6. 7. La Cassin R, Hoen B, et al. Procedures associated with infective
endocarditis in adults -- a case control study. Eur Heart J 16:1698-974,
1995. 8. Meyer DH, Sreenivasan PK, Fives-Tayor PM, Evidence for invasion of
a human oral cell line by Actinobacillus actinomycetemcomitans. Infect
Immuno 59:2719-26, 1991. 9. Riviere GR, Weisz KS, et al, Pathogen-related oral spirochetes from
dental plaque are invasive. Infect Immuno 59:3377-80, 1991. 10. Silver JG, Martin AW, McBride BC, Experimental transient
bacteremias in human subjects with varying degrees of plaque accumulation and
gingival inflammation. J Clin Periodontol 4:92-99, 1977. 11. Karchmer AW, Infective endocarditis. In, Dale DC, Federman DD,
eds. Scientific American Medicine. Scientific American, Inc, New York,
1999. 12. Herzberg MC, Meyer MW, Effects of oral flora on platelets:
possible consequences in cardiovascular disease. J Periodontol 67:1138-42,
1996. 13. Matilla KJ, Valtonen VV, et al, Dental infection and the risk of
new coronary events: prospective study of patients with documented coronary
artery disease. Clin Infect Dis 20:588-92, 1995. 14. DeStefano F, Anda RF, et al, Dental disease and risk of coronary
heart disease and mortality. Bbr Med J 306:688-91, 1993. 15. Beck JD, Garcia RI, et al, Periodontal disease and cardiovascular
disease. J Periodontol 67:1123-37, 1996. 16. Joshipura KJ, Rimm EB, et al, Poor oral health and coronary heart
disease. J Dent Res 75:1631-6, 1996. 17. Hujoel PP, Drangsholt M, et al, Periodontal disease and coronary
heart disease risk. J Am Med Assoc 284:1406-10, 2000. 18. Haraszthy VI, Sambon JJ, et al, Identification of pathogens in
atheromatous plaques. J Dent Res 77:273, 1998. 19. Deshpande RG, Kahn MB Genco CA, Invasion of aortic and heart
endothelial cells by Porphyromonas gingivalis. Infect Immun 66:5337-43,
1998. 20. Genco, RJ, Offenbacher S, et al, Cardiovascular diseases and oral
infections. In, Rose LF, Genco, et al, eds. Periodontal Medicine. BC
Decker Inc, St Louis, 2000:, pp 63-82. 21. Grau AJ, Bugle F, et al, Association between acute cerebrovascular
ischemia and chronic and recurrent infection. Stroke 28:1724-9, 1997. 22. Petty TL, Weinmann GG, Building a national strategy for the
prevention and management of and research in chronic obstructive pulmonary
disease. J Am Med Assoc 277:246-53, 1997. 23. Scannapieco FA, Relationships between periodontal and respiratory
diseases. In, Rose LF, Genco, RJ, et al, eds, Periodontal Medicine. BC
Decker Inc, St Louis, 2000, pp 83-97. 24. Potter RT, Rotman F, et al, The bacteriology of the lower
respiratory tract. Bronchoscopic study of 100 clinical cases. Am Rev
Respir Dis 97:1051-61, 1968. 25. Fourrier F, Duvivier B, et al, Colonization of dental plaque: a
source of nosocomial infections in intensive care unit patients. Crit Care
Med 26:301-8, 1998. 26. Russell SL, Boyland RJ, et al. Respiratory pathogen colonization
of the dental plaque of institutionalized elders. Spec Care Dent 19:1-7,
1999. 27. Murphy TF, Sethi S, Bacterial infection in chronic obstructive
pulmonary disease. Am Rev Respir Dis 146:1067-83, 1992. 28. Offenbacher S, Katz VL, et al, Periodontal infection as a risk
factor for preterm low birth weight. J Periodontol 67:1103-13, 1996. 29. McDonald HM, O’Loughlin JA, et al, Vaginal infections and preterm
labor. Br J Obstet Gynecol 98:427-35, 1991. 30. Gibbs RS, Romero R, et al, A review of premature birth and
subclinical infections. Am J Obstet Gynecol 166:1515-28, 1992. 31. Collins JG, Smith MA, et al, Effects of 32. Otomo-Corgel J, Steinberg BJ, Periodontal medicine and the female
patient. In, Rose LF, Genco RF, et al, eds, Periodontal Medicine. BC
Decker Inc, St Louis, 2000, pp 151-65. 33. Grau A, Buggle F, et al. Association between acute cerebrovascular
ischemia and chronic and recurrent infection. Stroke 28:1724-9, 1997. 34. Committee on Research, Science, and Therapy of the American
Academy of Peridontology. Periodontal disease as a potential risk factor for
systemic diseases J Periodontol 69:841-850, 1998 To request a printed copy of this article, please contact/Joan
Otomo-Corgel, DDS, 1127 Wilshire Blvd., Suite 1110, Los Angeles, CA
90017-4002. Legend
Figure 1. Example of a case with chronic
periodontal and oral infections.
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