Bacteria as risk markers for periodontitis
This paper selectively reviewed bacteria as risk markers for periodontitis. The identification of bacteria as risk factors, in contrast to bacteria as risk indicators, requires longitudinal clinical studies. Cross-sectional data is used to identify bacterial risk indicators, so these studies do not have the ability to determine whether a disease marker occurred before the onset of disease. Bacteria implicated as risk indicators for destructive periodontal disease are P. gingivalis (Pg.), P. intermedia (Pi),A. actinomycetemcomitans (A.a), E. corrodens (E. c.), F. nucleatum (F. n.), G. forsythus (G.f), C. rectus (Cr.), and spirochetes or Treponema species. In the laboratory, five bacterial pathogens (Pg.,A.a., P.i., F.n., and E.c.) were found in subgingival plaque taken from 3,052 molar sites (886 subjects) with early periodontitis.
As the concentration for a bacterial pathogen increased in site, there was a progressively higher mean probing depth associated with it. Odds ratios were 3.6 (P.g.), 2.5 (A.a.), 2.1 (Fi.), 2.3 (E.c.), and 1.4 (F.n.) of finding these bacterial pathogens at greater than 5 mm probing depth (these were higher as probing depths increased).The presence of P.i. and Pg. at levels greater than 2% of the bacterial cell count were associated with a greater likelihood of attachment loss (odds ratios 2, 3,1, and 9, respectively).A strong association between P.g. and probing depth was reported by Wikstrom et al. (if found at one site, probability of finding a different site was 80-90%). In another study, A.a., Pg., and C.r. each demonstrated a strong association with bone loss (becoming stronger with combinations). Data from cross-sectional studies does not allow the use of bacterial combinations to predict periodontal disease progression (only possible in longitudinal studies).The prevalence pathogen in subjects was lowest for P.g. (32%), and highest for E.c. (49%). Site-based 10.3% P.g. to 18.7% E.c. periodontal pathogens were detected in an adult population on a rigorous three-month maintenance program for over two years (P.i., 50%; P.g., 37%). A recent study by Papapanou revealed that Cr., F.n., E.c., and P.i. were detected in 50% of the subjects (A.a., 25%, and P.g., 14%).A.a., Pi., and P.g. showed an age-related distribution, with Ala. found more frequently in younger individuals, while P.g. and P.i. were found more frequently with increasing age. Even though these species inhabit the subgingival environment, they are not always associated with advanced disease. This suggests that a susceptible host is required for disease progression. Loesche has suggested that a bacterial succession may exist in subgingival plaque. P i. and P.g. (and other black pigmented G(-)) may be replaced by a higher proportion of spirochetes as periodontal disease progresses. It was found that species with identical phenotypes can be separated into different clones, each of which exhibited different pathogenicity. Some authors found that A.a., P. i., and P.g. were associated with progressive periodontitis, but bacteria alone could not predict which individual would lose attachment. Haffajee reported that a higher subgingival temperature, the presence of existing disease, and lower levels of protective bacterial species increased the risk of progressive periodontitis. In relation to behavioral patterns, poor oral hygiene and infrequent dental visits will result in more plaque and can lead to higher protease levels produced by bacteria. Tobacco smoke adversity affects PMNS phagocytic function. Data suggests that there is a strong association between a PMN defect and refractory periodontitis, and that tobacco smoke contributes to this. A model for progressive periodontitis was developed based on bacterial, environmental, and host markers (microorganisms are prominent).
In conclusion, periodontitis should be regarded as a disease limited to a segment of the population with a primary bacterial etiology but to which the normal balance between the microorganisms and the host is disturbed in the same way. [c.c.]
Wolff, L., G. Dahlen, and G. Aeppli, J Periodont, 65:498, 1994