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Accumulating evidence indicates that epithelia are not merely mechanical barriers but also important elements of the innate immune system. The present study was performed to examine cytokine responses of oral epithelial cells after infection with the periodontal pathogen Porphyromonas gingivalis. The KB-cell line and primary cultures of periodontal pocket epithelium were infected with P. gingivalis for assessment of bacterial invasion by an antibiotic protection assay, and examination of expression of interleukin-1 beta, interleukin-6, interleukin-8, and tumor necrosis factor-alpha by in situ hybridization and immunohistochemistry. We observed that P. gingivalis induces a strong cytokine response, positively correlated with the adhesive/invasive potential of the infecting strain, in both KB cells and primary cultures. These findings indicate that the epithelial cells of the periodontal pocket are an integral part of the immune system, eliciting cytokine responses to a bacterial challenge. In this context, the adhesive/invasive phenotype of P. gingivalis appears to contribute to pathogenicity.

Objective: We used epidemiologic data of clinical periodontal status from two population-based samples in two countries, United States and Germany, to examine 1) the impact of age on the relative contribution of recession and pocketing on the distribution of clinical attachment loss, and 2) whether it is feasible to define age-dependent thresholds for severe periodontitis. 2012. NHANES used a full-mouth examination protocol to collect data on recession (R), pocket depth (PD) and clinical attachment loss (CAL) for six sites/tooth on a maximum of 28 teeth; SHIP-Trend used a half-mouth examination at four sites/tooth. In both samples, percentile distributions of mean CAL/person were generated for each 5-year age interval. Age-dependent thresholds defining the upper quintile of mean CAL were calculated for both samples. The topographic intraoral distribution of CAL and the relative contribution of R and PD on CAL was assessed.Results: Mean CAL increased linearly with age in both samples and was higher in SHIP-Trend than NHANES across the age spectrum. In contrast, mean PD was constant across age groups in both populations. R contributed increasingly to CAL with age, especially after 45 to 49 years. Upper quintile mean CAL thresholds in NHANES were < 3 mm for ages up to 39 years, and under 3.58 mm in all other age groups. Corresponding values in SHIP-Trend were also < 3 mm in ages up to 39 years but increased linearly with age up to 7.21 mm for ages ≥75 years.Conclusions: Despite substantial differences in the overall severity of attachment loss between the two samples, common patterns of CAL and of the relative contribution of R and PD to CAL with increasing age were identified. Although periodontitis severity may vary in different populations, empirical evidence-driven definitions

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Porphyromonas gingivalis FDC381 replication and persistence within KB epithelial cells in vitro were studied by means of an antibiotic protection assay and electron microscopy. Intracellular counts decreased during the first 24 h; showed a threefold increase during the second day, indicating intracellular multiplication; and after 8 days declined to levels approximating 40% of the initial invasion. The ability of P. gingivalis to persist and multiply within epithelial cells may constitute a pathogenic mechanism in periodontal disease.

The aim of the present study was to elucidate events related to receptor function, signal transmission and cytoskeletal rearrangements concurrent with Porphyromonas gingivalis invasion of oral epithelial cells in vitro. Porphyromonas gingivalis strain FDC 381 and the KB cell line (ATCC CCL 17) were used in a previously described antibiotic protection assay. The involvement of a receptor-mediated endocytosis pathway in the internalization process was demonstrated after treatment of the epithelial cells with monodansylcadaverine and ouabain, substances that inhibit formation of coated pits, resulting in reduction in the number of invading P. gingivalis: Treatment of the epithelial cells with the protein kinase (PK) inhibitor staurosporine and the tyrosine-specific PK inhibitor genistein was also found to significantly decrease the number of invading bacteria, suggesting involvement of tyrosine phosphorylation in signal transduction during invasion. This was further supported by the identification of a 43 kD protein acting as a substrate for tyrosine phosphorylation subsequent to the microbial-host cell interaction. Tyrosine phosphorylation of the 43 kD protein was strongly reduced by treatment with PK inhibitors. The decrease in invasion observed after treatment of epithelial cells with colchicine and nocodazole, inhibitors of microtubuli polymerization, suggested that the bacterial-receptor interaction and the phosphotyrosine-dependent intracellular signalling trigger an internalization process involving rearrangements of cytoskeletal microtubuli.

The role of periodontal infections as a putative risk factor for atherosclerotic vascular disease (ASVD) has been reported in the literature over the past decade. This review provides insights into biologically plausible pathways that can potentially mediate such an association, and discusses recent findings from epidemiological studies and intervention trials. Accumulating epidemiological evidence suggests that clinical, microbiological and serological markers of periodontal infection are associated with subclinical and manifest ASVD. Early evidence from intervention studies suggests that the control of periodontal infections may result in improved levels of markers of systemic inflammation and measures of endothelial dysfunction. The extent to which the control of periodontal infections results in lower incidence of ASVD events is logistically difficult to assess and has not been addressed in any study so far.

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