Abstract
Gingival overgrowth is a known side effect of drugs such as phenytoin, cyclosporin A, and amlodipine (AML). Several recent reports have shown that gingival overgrowth induced by AML is caused by gingival inflammation as well as by a decrease in apoptosis and an increase in proliferation, which is mediated by the cell cycle, in gingival fibroblasts (GFs). It has also been reported that both phenytoin- and cyclosporin A-induced gingival overgrowth are caused by tumour necrosis factor (TNF)-α, which is an inflammatory cytokine and a cellular apoptosis inducer. However, few reports have investigated the relationship between AML-induced gingival overgrowth and TNF-α. Therefore, in this study, we evaluated the effect of AML on the cell cycle, apoptotic ability, viability, and total cell number of human GFs (hGFs) in the presence of TNF-α. Cultured quiescent hGFs were stimulated by TNF-α (100 ng/mL) ±AML (1 or 10 μM) or AML alone (1 or 10 μM) and then assessed for their cell cycle phase distribution as well as for the number of apoptotic, viable, and total cells. The results showed that AML treatment significantly suppressed TNF-α-induced apoptosis in hGFs and significantly increased the viability and total number of hGFs in the presence of TNF-α. Thus, these results may be related to the cause of AML-induced gingival overgrowth.
