The purpose of this study was to evaluate the tissue levels of matrix metalloproteinase (MMP)-1, -2, -3 and their distributions in inflamed human dental pulps and periapical lesions. Samples were subjected to enzyme-linked immunosorbent assay and/or immunohistochemistry by using specific antibodies to MMP-1, -2, and -3. Results from enzyme-linked immunosorbent assay were analyzed by using the Mann-Whitney U test and presented as p values. The concentrations of MMP-1 in all experimental groups were significantly higher than in the control (p < 0.05). The acute pulpitis and control groups were significant different in terms of their MMP-2 levels (p < 0.05). The concentration of MMP-3 in acute pulpitis was significantly higher than the control and chronic pulpitis groups (p < 0.05). Immunohistochemically, MMP-1 and MMP-3 were localized in the infiltrating neutrophils, macrophages, and extracellular matrix of the acute pulpitis group. These results suggest that MMPs play an important role in the pulp tissue destruction of acute, inflamed pulp.

The objective of this study was to investigate the expression of surface markers on T lymphocytes and the Th1/Th2 immune response in pulpal inflammation associated with specific bacteria. Pulpal inflammation was experimentally induced in rat mandibular incisors by drilling, without coolant, to open pulp chambers. Streptococcus mutans (S. mutans group), Porphyromonas endodontalis (P. endodontalis group), and a sterile cotton pellet only (control group) were inoculated in the canal. The expression of CD25 and CD54 on CD4+, and CD8+ lymphocytes in pulp tissues was determined by using a flow cytometer. The levels of interleukin (IL)-2, interferon (IFN)-gamma, and IL-4 were measured by ELISA. Flow-cytometric analysis showed that the mean ratio of CD4+:CD8+ was 0.96 in the control group, 0.99 in the S. mutans group, and 0.52 in the P. endodontalis group. An increase in CD25 and CD54 expression on CD4+ T lymphocytes was related to the bacterial infection (p < 0.05) and accompanied an increase in IL-2 concentration. The higher concentration of IFN-gamma than IL-4 in the P. endodontalis group suggested a Th1 reaction in the early stage of pulpal inflammation induced by P. endodontalis.

The purpose of this study was to examine whether the sonicated extract of Enterococcus faecalis (SEF) alters the cell cycle transition of lymphocytes and thus regulates the fate of the arrested cells. Human lymphocytes were activated by phytohemagglutinin in the presence or absence of SEF, and cell cycle was assessed by flow cytometry. Seventy-two hours after activation with phytohemagglutinin, cells were activated from G0/G1 to S (6.1%) and G2/M (3.8%) phases of the cell cycle. In contrast, pretreatment with SEF resulted in 90.5% of cells remaining in G0/G1, and cell cycle progression to the S and G2/M phases was consequently inhibited. Caspase assay demonstrated that SEF-treated cells exhibited significantly increased apoptosis (56.7%) compared with phytohemagglutinin alone (28.1%). We propose that if this irreversible cell cycle arrest induced by E. faecalis occurs in vivo, it may result in local immunosuppression and contribute to the pathogenesis of endodontic failure. Our findings that E. faecalis can inhibit lymphocyte responses may be of particular relevance to the pathogenesis of endodontic failure. Although the immunologic mechanism involved in the pathogenesis of persistent periapical lesion is not clearly defined, it is reasonable to predict that the altered immune reaction may be linked to the immunosuppressive potential of E. faecalis or other oral bacteria.

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