New BGI classifications create categories with distinct biologic phenotypes. The increased titers of C. rectus IgG among 68.5% of the BGI-G subjects and elevated P. gingivalis titers among BGI-DL/MB and BGI-DL/SB subjects (63.8% and 75.7%, respectively) are strongly supportive of the microbial specificity of pathogenesis for BGI categories.

While PD and AL are each associated with increased GCF IL-1beta, patients with severe disease show higher IL-1beta GCF levels in shallow sites, suggesting that high GCF IL-1beta expression is in part a host trait, and not strictly a function of clinical parameters.

These findings supported results relating chronic oral infections and the inflammation of periodontitis as contributors to and/or triggers for systemic inflammatory responses. Finally, similarities in the clinical and microbiological parameters of gingival inflammation and periodontitis between humans and non-human primates was extended to identification of changes in serum APP in the non-human primates that appeared to be in direct response to the induction of progressing periodontitis. These systemic changes provide additional evidence for the biological plausibility of periodontal infections contributing to various systemic diseases.

Highly significant correlations between salivary betaG activity and mean probing depth (MPD), mean gingival index (MGI), and the number of sites with probing depth > or = 5 mm were found. When subjects were divided into tertiles based on their MPD and MGI, elevated salivary betaG activity was detected in subjects in the 2 upper tertiles. Logistic regression modeling was used to determine which of the clinical or laboratory parameters were able to identify patients with at least 4 sites with PD > or = 5 mm. Salivary betaG activity > or = 100 produced an odds ratio (OR) of 3.77. In comparison, current and former smokers had an OR of 3.15 and 2.29, respectively. CONLCUSIONS: The results suggest that a significant association exists between periodontal clinical parameters and salivary betaG activity. Due to the non-invasive and simple nature of saliva collection, this association should be studied to determine its usefulness as a screening test for periodontitis, and a means of monitoring the response to treatment.

Extracts of in vitro-cultured human dental plaque contain factors toxic to mammalian cells. Previous studies demonstrated that those toxic factors most readily released from cultured plaque had very low molecular weights and were heat stable. Studies reported here demonstrate that metabolic end products including short-chain fatty acids were present in fractions containing the low-molecular-weight, heat-stable factors. The salts of two of these acids, butyrate and propionate, inhibited proliferation of both mouse L929 cells and human gingival fibroblasts. Furthermore, when tested at concentrations present in plaque extracts, the inhibitory effects of butyrate and propionate accounted for essentially all the inhibitory potential of the extracts. These findings, taken together with those of other groups, suggest that butyrate and propionate, end products of dental plaque metabolism, may have an etiological role in periodontal disease.