Cyclosporine A-induced gingival overgrowth: a comprehensive review.
Cyclosporine A-induced gingival overgrowth: a comprehensive review.
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DOI：
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发表时间：
1999-11
影响因子：
1.9
通讯作者：
Boltchi Fe;T. Rees;Iacopino Am
中科院分区：
文献类型：
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作者：
Boltchi Fe;T. Rees;Iacopino Am
环孢菌素 A 是一种极其有效的免疫抑制剂，也与各种不良反应有关，包括牙龈过度生长。尽管进行了大量的临床和实验室研究，但环孢素 A 在充当选择性免疫抑制剂的同时引起牙龈结缔组织反应的细胞分子机制仍然知之甚少。近年来，细胞和分子生物学技术已经阐明了控制结缔组织稳态的多种生长因子。已知在伤口修复和结缔组织稳态中起主要作用的两种生长因子是血小板源性生长因子和转化生长因子-β1。这些因子的牙龈水平增加可能是促进过度生长的牙龈组织中成纤维细胞增殖和细胞外基质成分的成纤维细胞产生的原因。最近显示这些因子的表达在这些组织中上调。这些最近的研究结果可能为理解环孢素 A 诱导的牙龈过度生长的分子机制提供基础。
Cyclosporine A, an extremely effective immunosuppressant, is also associated with various untoward effects, including gingival overgrowth. Despite intense clinical and laboratory investigation, the cellular-molecular mechanism through which cyclosporine A simultaneously acts as a selective immunosuppressant while it elicits a connective tissue reaction in the gingiva remains poorly understood. In recent years, cellular and molecular biologic techniques have elucidated a variety of growth factors that control connective tissue homeostasis. Two growth factors known to be major elements in wound repair and connective tissue homeostasis are platelet-derived growth factor and transforming growth factor-beta 1. Increased gingival levels of these factors may be responsible for promoting fibroblastic proliferation and fibroblastic production of extracellular matrix constituents in overgrown gingival tissues. Expression of these factors has recently been shown to be upregulated in these tissues. The results of these recent studies may provide a foundation for understanding the molecular mechanism involved in the pathogenesis of cyclosporine A-induced gingival overgrowth.