Abstract
Advanced forms of periodontal disease are associated with the overgrowth of a limited number of gram-negative anaerobic species in plaques found in periodontal pockets. Double-blind clinical trials of metronidazole and doxycycline, combined with debriding of the tooth surfaces, have significantly reduced the need for periodontal surgery. Epidemiologic studies have indicated that untreated periodontal disease could be a risk factor for preterm delivery of low birth weight infants, coronary heart disease, and cerebral vascular accidents. This is because gram-negative anaerobic species implicated in periodontal disease, eg, Bacteroides forsythus, Porphyromonas gingivalis, and Treponema denticola, could introduce lipopolysaccharides, heat-shock proteins, and proinflammatory cytokines into the blood stream. If periodontal disease is a risk factor for cardiovascular disease, then it is a modifiable risk factor, as periodontal disease is treatable.
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Offenbacher S, Katz VL, Fertik GS, et al.: Periodontal infection as a risk factor for preterm low birth weight. J Periodontol 1996, 67:1103–1113. This paper provides data that indicates that a mother’s severe periodontal disease is an important risk indicator for preterm birth of low birth weight infants. Mothers with a certain level of periodontal disease were 7.5 times more likely to have a preterm birth than mothers without periodontal disease.
Mattila KJ, Nieminen MS, Valtonen VV, et al.: Association between dental health and acute myocardial infarction. BMJ 1989, 298:779–781.
Mattila KJ, Valtonen VV, Nieminen M, Huttunen JK: Dental infection and the risk of new coronary events: prospective study of patients with documented coronary artery disease. Clin Infect Dis 1995, 20:588–592.
DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM: Dental disease and risk of coronary heart disease and mortality. BMJ 1993, 306:688–691.
Beck JD, Garcia RI, Heiss G, et al.: Periodontal disease and cardiovascular disease. J Periodontol 1996, 67:1123–1137. Young healthy US veterans who had bone loss around the teeth as observed in dental radiographs were significantly more likely to subsequently develop coronary heart disease or stroke compared with individuals without bone loss.
Loesche WJ, Terpenning MS, Kerr C, et al.: The relationship between dental disease and coronary heart disease in elderly United States veterans. J Am Dent Assoc 1998, 129:301–311. In older US veterans, many missing teeth, gingivitis, and a positive BANA test were significantly associated with a diagnosis of coronary heart disease.
Syrjänen J, Peltola J, Valtonen V, et al.: Dental infections in association with cerebral infarction in young and middleaged men. J Intern Med 1989, 225:179–184.
Grau AJ, Buggle F, Ziegler C, et al.: Association between acute cerebral vascular ischemia and chronic and recurrent infection. Stroke 1997, 28:1714–1729.
Loesche WJ, Schork MA, Terpenning MS, et al.: The relationship between dental disease and cerebral vascular accident in elderly United States veterans. Ann Periodontol 1998, 3:161–174.
Valtonen VV: Infection as a risk factor for infarction and atherosclerosis. Ann Med 1991, 23:539–543.
Syrjänen J: Vascular diseases and oral infections. J Clin Periodontol 1990, 17:497–500.
Loesche WJ, Giordano JR: Treatment paradigms in periodontal disease. Compend Contin Edu Dent 1997, 18:221–232. A review of three double-blind studies that showed the clinical efficacy of 1 week of systemic metronidazole in periodontal disease. The nonspecific and specific treatment paradigms are discussed in the context of the antimicrobial management of periodontal disease.
Loesche WJ, Giordano J, Soehren S, et al.: The non-surgical treatment of periodontal patients. Oral Med Oral Surg Oral Path 1996, 81:533–543. This clinical trial shows that a combination of either metronidazole or doxycycline, when combined with scaling and root planing of the teeth and the use of locally delivered antimicrobials to the periodontal pocket, can reduce periodontal surgical needs by about 90%.
Ofman JJ, Etchason J, Fullerton S, et al.: Management strategies for Helicobacter pylori-seropositive patients with dyspepsia: clinical and economic consequences. Ann Intern Med 1997, 126:280–291.
Moore WEC, Moore LVH: The bacteria of periodontal diseases. Periodontol 2000 1994, 5:66–77.
Zambon JJ, Sunday GJ, Smutko JS: Molecular genetic analysis of Actinobacillus actinomycetemcomitans epidemiology. J Periodontol 1990, 61:75–80.
Lindhe J: Treatment of localized juvenile periodontitis. In Host Parasite Interactions in Periodontal Disease. Edited by Genco RJ, Mergenhagen SE. Washington, DC: ASM Publications; 1982:382–394.
Grossi SG, Genco RJ, Marthei EE, et al.: Assessment of risk for periodontal disease. II Risk indicators for alveolar bone loss. J Periodontol 1995, 66:23–29.
Socransky SS, Haffejee A, et al.: Microbial complexes in subgingival plaque. J Clin Periodontol 1998, 25:134–144. The most extensive bacterial survey of the plaque flora yet reported. DNA probes of 40 species were used to examine a plaque sample taken from each tooth in the mouth. Only P. gingivalis, B. forsythus, and T. denticola could be associated with bleeding and increased pocket depth.
Papapanou PN, Baelum V, Luan WM, et al.: Subgingival microbiota in adult Chinese: prevalence and relation to periodontal disease progression. J Periodontol 1997, 68:651–666.
Loesche WJ, Lopatin DE, Giordano J, et al.: Comparison of the benzoyl-DL-arginine-naphthylamide (BANA) test, DNA probes, and immunological reagents for ability to detect anaerobic periodontal infections due to Porphyromonas gingivalis, Treponema denticola, and Bacteroides forsythus. J Clin Microbiol 1992, 30:427–433.
Loesche WJ, Kazor CE, Taylor GW: The optimization of the BANA test as a screening instrument for gingivitis among subjects seeking dental treatment. J Clin Periodontol 1997, 24:718–726.
Matthews DC, McCulloch CA: Evaluating patient perceptions as short-term outcomes of periodontal treatment: a comparison of surgical and non-surgical therapy. J Periodontol 1993, 64:1029–1039.
Kornman KS, Loesche WJ: The subgingival microbial flora during pregnancy. J Periodontol Res 1980, 5:111–122.
Offenbacher S, Jared HL, O’Reilly, et al.: Potential pathological mechanisms of periodontitis-associated pregnancy complications. Ann Periodontol 1998, 3:233–250. Additional study implicating periodontal disease as a risk factor for preterm birth of low birth weight infants. DNA probes were used to show significant increases in T. denticola, P. gingivalis, B. forsythus, and A. actinomycetemcomitans in plaques taken from mothers with preterm births.
Loesche WJ: Periodontal disease as a risk factor for heart disease. Compend Contin Edu Dent 1995, 15:976–991.
Matilla K, Rasi V, Nieminen M, et al.: von Willebrand factor antigen and dental infections. Thrombosis Res 1989, 56:325–329.
Kweider M, Lowe GDO, Murray GD, et al.: Dental disease, fibrinogen and white cell count; links with myocardial infarction? Scott Med J 1993, 38:73–74.
Ebersole JL, Machen RL, Steffen MJ, et al.: Systemic acute-phase reactants, C-reactive protein and haptoglobin in adult periodontitis. Clin Exp Immunol 1997, 107:347–352. Individuals with periodontal disease have significant increases in Creactive protein and haptoglobulin, with the serum levels increasing as a function of the number of periodontally involved teeth. Treatment with nonsteroidal anti-inflammatory drugs reduced both the periodontal inflammation and the C-reactive protein.
Gillum RF, Ingram DD, Makuc DM: White blood cell count, coronary heart disease and death: the NHANES I epidemiologic follow up study. Am Heart J 1993, 125:855–863.
Ridker PM, Cushman M, Stampfer MJ, et al.: Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997, 336:973–979.
Haraszthy VI, Zambon JJ, Trevisan MN, et al.: Identification of pathogens in atheromatous plaques [abstract]. J Dent Res 1998, 77:273.
Herzberg MC, MacFarlane GD, Gong K, et al.: The platelet interactivity phenotype of Streptococcus sanguis influences the course of experimental endocarditis. Infect Immunol 1992, 60:4809–4818.
Herzberg MC, MacFarland GD, Liu P-X, etal.: The platelet as an inflammatory cell in periodontal disease: interactions with Porphyromonas gingivalis. In Molecular Basis for Pathogenesis and Molecular Targeting in Periodontal Disease. Edited by Genco RJ, Mergenhagen S, McGhee J, et al. Washington, DC: American Society for Microbiology; 1994:247–255.
Young RA, Elliott TJ: Stress proteins, infection, and immune surveillance. Cell 1989, 59:5–8.
Xu Q, Wick G: The role of heat shock proteins in protection and pathophysiology of the arterial wall. Mol Med Today 1996, 2:372–379. A review article describing the role of hsp in the pathophysiology of cardiovascular disease.
Schett G, Metzler B, Kleindienst R, et al.: Salivary anti-hsp65 antibodies as a diagnostic marker for gingivitis and a possible link to atherosclerosis. Int Arch Allergy Immunol 1997, 114:246–250.
Brown LJ, Brunelle JA, Kingman A: Periodontal status in the United States, 1988–91: prevalence, extent and demographic variation. J Dent Res 1996, 75:672–683.
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Loesche, W.J. Anaerobic periodontal infections as risk factors for medical diseases. Curr Infect Dis Rep 1, 33–38 (1999). https://doi.org/10.1007/s11908-999-0007-5
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DOI: https://doi.org/10.1007/s11908-999-0007-5