The role of inflammation and apoptosis in cyclosporine A-induced gingival overgrowth

Bosn J Basic Med Sci. 2013 Feb;13(1):14-20. doi: 10.17305/bjbms.2013.2407.

Abstract

Cyclosporin A(CsA) - induced gingival overgrowth(GO) is a current problem of tissue-specific mechanism which is still incompletely explained. The apoptotic process has been of particular interest like a new concept in the etiology of this unwanted effect. The aim of our study was to detect the level of apoptosis, expression bcl-2 and p53, associated with the different doses of CsA. in gingival stroma. A cohort of 84 kidney transplant recipients was divided into four subgroups based on average daily dose of therapeutically applied CsA (Neoral®), (100 mg, 125 mg, 150 mg and 175 mg). The control group consisted of 21 patients, clinically diagnosed with periodontitis, who were not subjected to any medicamentous treatment causing gingival overgrowth. The following indexes were analyzed: plaque index (PI), index of gingival inflammation (GI) according to Loe-Silnes, and gingival overgrowth index (GOI) according to MacGaw et al. The tissue samples were subjected to a semiquantitative analysis to detect apoptotical cells and immunohistochemically stained to detect the expression of the bcl-2 and p53 proteins. The difference in percentage of apoptotic cells between the group taking 175 mg and other subgroups, as well as the control group was statistically significant (p<0.05). There was a significant difference in percentage of expression bcl-2 between the 175 mg group compared to the other three subgroups and the control (p=0.001). However, a statistically significant positive correlation between the medicament dose, p53, apoptosis, and bcl-2 was registered (p<0.05). Inflammation plays the most important role in the induction of apoptosis and proliferation in gingival tissues.

MeSH terms

  • Apoptosis / drug effects*
  • Cyclosporine / adverse effects*
  • Gingival Overgrowth / chemically induced*
  • Humans
  • Immunosuppressive Agents / adverse effects*
  • Inflammation / complications*
  • Proto-Oncogene Proteins c-bcl-2 / analysis
  • Tumor Suppressor Protein p53 / analysis

Substances

  • Immunosuppressive Agents
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • Cyclosporine