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Advances in Dental Research, Vol 7, 163-174, Copyright © 1993 by International & American Associations for Dental Research
ARTICLES |
G. Dahlen
University of Goteborg, Faculty of Odontology, Department of Oral Microbiology, Sweden.
Periodontal disease is the clinical result of a complex interaction between the host and plaque bacteria. Although a specificity to some degree is found for Actinobacillus actinomycetemcomitans in localized juvenile periodontitis (LJP), it has been difficult to obtain evidence for a specific etiological role of the bacteria associated with periodontal disease in adults. What we see is the net result of host-parasite interactions which in an unpredictable moment accumulate and exceed the threshold of tissue integrity. This hypothesis is concomitant with the view of periodontal disease as a polymicrobial infection, predominantly anaerobic, which occurs commonly in the oral cavity or elsewhere in the body. Some micro-organisms (risk markers) occur more frequently than others and may significantly determine the outcome of this host-parasite interaction. Microbiological sampling and analysis seem to be of limited value in risk assessment; however, they can be used as tools in diagnosis in LJP patients and acute infections, and in treatment decision and therapy control in "refractory" patients. Suspected pathogens (risk markers) are Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and some species of spirochetes, while the roles of Prevotella intermedia, Bacteroidesforsythus, Fusobacterium nucleatum, Campylobacter rectus, and Peptostreptococcus micros are more uncertain. The presence of periodontopathogens as well as enterics, Staphylococcus aureus and Candida especially, should be considered in patients with systemic individual disorders--e.g., diabetes mellitus, neutropenia, agranulocytosis, and AIDS--or with implants.
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