Abstract

Background Although periodontitis is a kind of infectious disease, studies indicate that regulation of host own inflammatory reaction may be a key pathway to prevent periodontal damage that caused by host immune reaction. Caspase-3 is a member of caspase family and is involved in cell apoptosis. Many studies suggest that the expression of active caspase-3 may be one of the apoptosis key markers. Cell death through apoptosis pathway can prevent the damage cause by cell necrosis, including release of cytokines and cytotoxins. The imbalance between apoptosis and inflammation may be a mechanism of periodontal pathogenesis. Objective The aim of this study was to investigate active caspase-3 expression in periodontal tissue from healthy sites and inflammatory sites, to find out if there is different apoptotic activity in periodontal healthy and inflammatory sites. Material and Methods Eighteen inflammatory tissues were obtained from chronic periodontitis patients, 8 relatively healthy tissues were also obtained from these patients to act as control sites of periodontal diseased patients, and 7 gingival tissues from non periodontitis individuals were included in this study. Tissue samples were paraffin fixed and cut into sections, and examined microscopically after immunohistochemical staining -LSAB method. Result The stained area of active caspase-3 was different(P=0.0001) among groups of those three groups of healthy contol, patient control, and inflammatory group . The stained intensity also was statistically significant different between patient control group and the other two groups(P<0.0001). The expression stained power of active caspase-3 in patient control group is significantly higher than the other two groups(P<0.0001). Conclusion The statistically less expression of active caspase-3 in tissues of inflammatory group and the abundant expression of active caspase-3 in tissues of patient control group suggest that apoptostic activity may be reduced in highly inflamed periodontal tissue but highly expressed in relatively healthy periodontal tissue of periodontitis patients. This result highly suggest that there is some relationship between inflammation and apoptosis in periodontal tissue. However, further studies with a larger sample size are needed to clarify this relationship in periodontal disease.

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