Local Inflammation Exacerbates Cyclosporine A-Induced Gingival Overgrowth in Rats
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Local Inflammation Exacerbates Cyclosporine A-Induced Gingival Overgrowth in Rats Jianbin Guo,1 Wenyu Wang,2 Liyan Yao,1 and Fuhua Yan1,3
Abstract—Gingival overgrowth (GO) is a common side effect of long-term cyclosporine A (CsA) treatment. The risk factors appraised include drug interactions with calcium channel blockers, age, cyclosporine dose, dental bacterial plaque, duration of treatment, and genetic predisposition. The relationship and mechanism between GO and local inflammation caused by dental bacterial plaque have not been clearly defined. This research was carried out to investigate the histomorphometrical alterations and serum levels of transforming growth factor β1 (TGF-β1) in CsA-induced GO with or without local inflammation. Thirty-four male Sprague-Dawley rats were divided into 4 groups: Group I (control); Group II (ligation); Group III (CsA); Group IV (ligation and CsA). After 9 weeks the rats were sacrificed. The morphological examination was made and the histological changes with hematoxylin and eosin (HE) staining were observed. TGF-β1 levels in serum were detected by Enzyme-linked immunosorbent assay (ELISA). We report here that obvious GO are found in Group III and Group IV after CsA treatment, especially those rats with existed gingivitis presented an aggravation of GO. TGF-β1 levels in CsA-exposed groups were significantly higher than untreated groups, but ligation did not affect TGF-β1 level. These findings suggest that CsA-induced GO can be exacerbated by local inflammation. TGF-β1 may be a key factor for the development of GO. KEY WORDS: cyclosporin A; gingival overgrowth; inflammation; transforming growth factor β1.
and neurotoxicity, hypertension and gingival overgrowth (GO) [2, 3]. Of particular interest to the periodontologist is the problem of GO,, occurring in a range of 25–81% of the patients associated with CsA [4]. GO, characterized by epithelial hyperplasia, interstitial fibrosis, and focal inflammatory cell infiltration [5], is a severe pathology that interferes with normal oral functions such as speech and mastication, causing profound psychological problems. Although there are numerous studies focusing on the cellular and molecular relations between CsA and GO, the exact mechanisms underlying the pathogenesis of CsA-induced GO still remains unclear. Many risk factors have been suggested including age, sex, genetic pre-disposition, duration of therapy, gingival inflammation and concomitant medication, such as calcium channel blockers [6–10]. Dental plaque is composed of an aggregation of micro organisms deposited on the tooth surfaces and it is able to begin inflammatory changes in the gingival
INTRODUCTION Cyclosporin A (CsA), a lipophilic, hydrophobic, cyclic endecapeptide, is used successfully as an immunosuppressive agent to prevent rejection of transplanted organs and to treat various autoimmune diseases [1]. Unfortunately, this drug is associated with several side effects including chronic nephrotoxicity, hepatotoxicity
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School and Hospital of Stomatology, Fujian Medical University
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