No abstract

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.

Targeting bacterial virulence factors such as proteases for immunization may hold the key to hmiting or preventing loss of attachment and alveolar bone in periodontal disease. This study examined the chnical, microbiological, and immunological responses following active immunization with a purified Porphyromonas gingivalis cysteine protease (porphypain‐2) in the nonhuman primate (Nhp) Macaca fascicularis. One group of Nhp was immunized with porphypain‐2 antigen while control Nhp received placebo injections. AU Nhp were subjected to experimental gingivitis followed by hgature‐induced periodontitis in a split‐mouth design. An enzyme‐hnked immunosorbent assay demonstrated that immunization elicited a significantly elevated and specific IgG antibody response to both whole cell P. gingivalis (36‐fold) and to porphypain‐2 (194‐fold). Checkerboard hybridization DNA analysis of subgingival plaque from ligated sextants demonstrated that 25% more Gram‐negative anaerobic species became significantly elevated from basehne and at earlier timepoints in the control group than in the immunized group. Immunization with this protease did not suppress the emergence of P. gingivalis. Chnical indices showed few changes related to immunization. Alveolar bone density changes demonstrated a highly significant loss in ligated sextants compared to non‐ligated sextants within the control group (P < 0.001), and a smaller but significant difference within the immunized group (P = 0.043). Comparison of ligated sextants only demonstrated more bone loss in the control group versus the immunized group (−13.07±9.51 versus −9.41±6.18; computerassisted densitometric image analysis units ± SD); the difference approached, but did not reach, significance. The results suggest that porphypain‐2 may contribute to the pathogenic potential of the subgingival plaque microbiota in the Nhp model of hgature‐induced periodontitis, and that active immunization with porphypain‐2 appeared capable of altering this pathogenic response. J Periodontol 1998;69:686–697.

This report describes our findings regarding the potential contribution of periodontitis to atherosclerotic processes using a nonhuman primate model. The goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemic translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis; and (iii) the relationship of periodontitis to serum lipids/lipoproteins. Increases in serum endotoxin (e.g. LPS) during ligature-induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactants and chemokines (e.g. CRP, alpha 1-antitrypsin, haptoglobin, fibrinogen, IL-8). A number of these host factors were significantly increased during gingivitis and/or periodontitis. Finally, we observed specific changes in serum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins (apoA-I) during periodontitis, which were exacerbated by exposure of the animals to a diet with elevated fat content. Thus, we have described systemic manifestations of periodontitis that include detection of bacterial products, inflammatory biomarkers, and dyslipoproteinemia consistent with an increased atherogenic risk.