Clinical, microbiological and immunological features of subjects with destructive periodontal diseases

Abstract

76 subjects with prior evidence of destructive periodontal diseases were monitored clinically and immunologically every 2 months for up to 5 years. Clinical parameters measured included bleeding on probing, gingival redness, plaque accumulation, suppuration, pocket depth and attachment level. Blood samples were taken by venipuncture and serum antibody levels to a series of 18 subgingival species determined. 33 of these subjects showed evidence of active disease during the monitoring period, based on changes in attachment level measurements assessed using the tolerance method of analysis. Mean attachment loss in these 33 subjects varied from 1.4 mm to 9.0 (median value 3.4 mm) and subjects whose mean attachment level was above the median showed a higher % of pockets greater than 3 mm and more suppuration. Severity of gingival inflammation related poorly to mean attachment loss. Subgingival plaque samples were taken from the active site(s) and from control sites of equal pocket depth and attachment loss in the same active disease subjects, prior to therapy, for predominant cultivable microbiota studies. 50 randomly selected isolates were identified from each sample. Predominant cultivable species in 170 pretreatment active and inactive sites combined (8500 isolates) were enumerated. The most frequently detected species were F. nucleatum (112 sites) and S. intermedius (106 sites), although the predominant species in the samples from each subject differed. The distribution of putative pathogens differed among subjects. For example, A. actinomycetemcomitans was found in 21 samples in 11 subjects and B. forsythus was found in 18 samples from 10 individuals. Antibody response patterns to the 18 subgingival species also varied among subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Th1 Immune Response Promotes Severe Bone Resorption Caused by Porphyromonas gingivalis

“…The pathogen Porphyromonas gingivalis has been associated with active disease in both systems. [1][2][3][4][5][6] In periodontal disease, an epithelial barrier separates the microbial biofilm from host tissues, whereas in periapical periodontitis; there is direct tissue invasion and parenteral contact of bacteria with the host immune system. Remarkably, actual microbial invasion of bone rarely occurs in periapical periodontitis, suggesting that the local immune response contains the infection but at the same time mediates bone resorption.…”

T-Cell Expression Cloning ofPorphyromonas gingivalisGenes Coding for T Helper-Biased Immune Responses during Infection

“…P. gingivalis is more frequently isolated, and is present in elevated levels, in subgingival pockets from patients with periodontitis compared to gingivitis or periodontally healthy subjects. Its numbers are further increased at sites of active tissue destruction and are reduced in successfully treated sites but commonly remain high in sites with disease recurrence (6,15,43). Implantation of P. gingivalis leads to periodontal disease initiation in monkeys (16) and in mice (4,35).…”

Prevotella intermedia Stimulates Expansion of Vβ-Specific CD4 + T Cells

“…Studies have shown that P. intermedia is associated with periodontal breakdown in type I diabetics (40) and is frequently encountered in periodontal lesions or abscesses associated with destructive disease (5,7,9,10,25,33,35,36,39). Thus, these studies provide strong clinical support for a role for P. intermedia in the development of periodontal diseases.…”