Method: The immersion-fixed, decalcified, cryoprotected and frozen-sectioned free-floating consecutive sections of human healthy and inflamed PDL with third human molars were incubated in TrkA (a marker for ERM), Bcl-2 and Bax antibodies using the immunohistochemical quantitative avidin-biotin peroxidase complex method.
Result: In healthy and inflamed ERM, Bax was not identified. In ERM of healthy PDL, Bcl-2 was detected with higher staining intensity (1568.45±123.29 DU, n=10) at acellular cementum region, whereas staining intensity of Bcl-2 in healthy ERM at cellular cementum region (apical area) was significant weaker (1365.82 ± 155.74 DU, n=10). In comparison to expression of Bcl-2 in healthy ERM of apical PDL, a higher Bcl-2 staining was detected in inflamed ERM (1433,69+-136,81 DU n=16) at apical PDL.
Conclusion: From our results could be concluded that healthy ERM located at acellular cementum region may be regulated by Bcl-2 with a stronger anti-apoptotic signal than in cellular cementum region. The higher anti-apoptotic regulation of inflamed ERM by Bcl-2 at cellular cementum region enables the proliferation and/or differentiation of ERM which may be involved in the formation apical cystes and odontogenous tumors.