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The Relationship between Proliferating Cell Nuclear Antigen Expression and Histomorphometrical Alterations in Cyclosporin A-Induced Gingival Overgrowth in Rats
1 Faculty of Dentistry, Department of Periodontology, Ondokuzmayis University, Samsun, 55139,Turkey Correspondence: Address correspondence to: Dr. Burcu Ozkan Cetinkaya, Faculty of Dentistry, Department of Periodontology, Ondokuzmayis University, 55139 Samsun, Turkey; e-mail:ozkandt{at}hotmail.com The aim of this study was to investigate the relationship between Proliferating Cell Nuclear Antigen (PCNA) expression and histomorphometrical alterations in cyclosporin A (CsA)-induced gingival overgrowth with or without microbial dental plaque accumulation. Forty male Wistar rats were equally divided into 4 groups; Group I (control); Group II (CsA); Group III (ligature); Group IV (ligature and CsA). After 8 weeks of experimental period, rats were subsequently decapitated and mandibular molars were dissected. Gingival overgrowth was determined by measuring depth of the gingival sulcus, then the mandible were decalcified and serial sections were obtained for histomorphometric and immunohistochemical analysis. Histomorphometric analysis included the measurement of epithelial thickness; immunohistochemical analysis included the assessment of PCNA expression in the oral and sulcular epithelium of buccal and lingual gingiva. Epithelial thickness and PCNA expression were significantly increased in buccal oral epithelium of Group II (p < 0.05) and in all regions in Group IV (p < 0.05) compared to control group. Also gingival overgrowth was more prominent in Group IV in comparison to Group II. These results indicate that CsA-induced gingival alterations are closely accociated with increased epithelial proliferative activity, and dental plaque accumulation seems not to be an essential but to be an aggrevating factor for the progression of the lesion.
Key Words: Cyclosporine A gingival overgrowth PCNA rats Abbreviations: CsA, Cyclosporine A PCNA, Proliferating cell nuclear antigen
Toxicologic Pathology, Vol. 34, No. 2,
180-186 (2006) This article has been cited by other articles:
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