El-Firt E.Y.Ghalwash D.M.Departement of Oral Medicine and PeriodontologyFaculty of Oral and Dental MedicineCairo UniversityCairoEgypt; Departement of Oral Medicine and PeriodontologyFaculty of DentistryOctober University for Modern Sciences and Arts6th OctoberEgypt2020-01-252020-01-25201110978135https://t.ly/p8LDbScopusKi-67 is a well-recognized nuclear proliferation marker. Considering that an unusual cell proliferation may have a role in the pathogenesis of gingival overgrowth with different etiologies. The study involved 4 patients with cyclosporine induced gingival overgrowth (CGO), 6 patients with phenytoin induced GO (PGO) and 5 patients with hereditary gingival fibromatosis (HGF). Healthy tissue samples without clinical signs of periodontal inflammation were also included as control samples. Immunohistochemistry against the proliferation antigen Ki-67 was performed and optical density measured and compared in both epithelium and connective tissue. Ki-67 was expressed both in the epithelium and corium of the four studied groups. The expression patterns of Ki-67 were significantly higher (p<0.00) in CGO, while no significant difference between HGF and PGO groups was detected and both showed lower values than CGO. Control group showed the significantly lowest mean of Ki-67 level and the expression was mainly in the basal layer of epithelium. In conclusion; increased cell division may have a role in the pathogenesis of gingival overgrowth induced by cyclosporine and phenytoin or inherited as HGF as reflected by increased expression of Ki-67.EnglishCyclosporineGingival hyperplasia/pathogenesisHereditary gingival fibromatosisKi-67PhenytoinArticle