2017年6月
A novel gingival overgrowth mouse model induced by the combination of CsA and ligature-induced inflammation
JOURNAL OF IMMUNOLOGICAL METHODS
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- 巻
- 445
- 号
- 開始ページ
- 31
- 終了ページ
- 36
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.jim.2017.03.003
- 出版者・発行元
- ELSEVIER SCIENCE BV
Drug-induced gingival overgrowth (DIGO) is a side effect of the enlargement of gingival tissue by phenytoin, nifedipine, and cyclosporine A (CsA). Gingival inflammation has been identified as a key factor that initiates DIGO. However, a sufficient animal model for clarifying the role of inflammation in DIGO has not yet been generated. We herein describe a novel CsA-induced gingival overgrowth mouse model to evaluate the role of inflammation. A ligature was placed around the second molar in maxillae for 7 days to induce gingival inflammation, and CsA (50 mg/kg/day) was administered to mice during each experimental period. The severity of gingival overgrowth and mRNA expression of inflammatory cytokines in gingiva were assessed by the gingival overgrowth degree, histological analyses, and RT-PCR. The administration of CsA for 28 days in combination with ligation significantly increased the gingival overgrowth degree and expanded the connective tissue area. Increases in the gingival overgrowth degree continued in a time-dependent manner until 21 days. Furthermore, the cessation of CsA reduced gingival overgrowth. Thin ligatures (7-0 size) induced weaker tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6 mRNA expression and less gingival overgrowth than thick ligatures (5-0 ligature). Moreover, the administration of an antibiotic cocktail, which suppressed the expression of these inflammatory cytokines in gingiva, attenuated gingival overgrowth induced by ligatures and CsA. These results suggest that inflammation in gingival tissue plays a role in initiating CsA-induced gingival overgrowth. This gingival overgrowth mouse model has potential for elucidating the etiology of DIGO from the view point of gingival inflammation. (C) 2017 Elsevier B.V. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.jim.2017.03.003
- ISSN : 0022-1759
- eISSN : 1872-7905
- PubMed ID : 28274836
- Web of Science ID : WOS:000401205600005