Vescovi P, Meleti M, Manfredi M, Bonanini M
Sezione di Odontostomatologia, Dipartimento di Scienze Otorino-Odonto Oftalmologiche e Cervico Facciali, Università degli Studi di Parma, Parma, Italy.
Minerva Stomatol. 2003 May;52(5):219-29.
Several studies, during the last 20 years, tried to explain the pathogenetic mechanisms of the cyclosporine (CS) induced gingival overgrowth (and in general, of the drugs induced gingival overgrowth), but they are still poorly understood. The relationship between the drug and the different pharmacokinetic variables (dosage, duration of therapy, plasmatic and salivary Cs concentration) is still on discussion. It is accepted that a threshold concentration is necessary, in the gingival tissues, to begin or to enhance the morphostructural changes of the gums, but the total Cs weight, from the beginning of the therapy to the time of clinical examinations, has to be evaluated. The pharmacokinetic variables are associated with many other factors (first of all the oral hygiene score) that are probably connected with the developing of the gingival lesions. Gingival inflammation could be very important in the pathogenesis of gingival overgrowth. It has been shown by several cross-sectional studies a strong association between plaque and gingival lesions, but it is not yet clear if plaque accumulation is a causal factor or a consequence of the morphological gums changes. It would seem that the morphological alterations, in drug-induced gingival overgrowth, could be started by the plaque induced inflammation, and this would lead to an hyperemic and edematous gingival tissue. Oral hygiene (professional and at home) is more difficult and represents an irritation factor that makes the pathological cycle to go on. Other factors, probably connected with the cyclosporine induced gingival overgrowth, are represented by age, gender, genetic predisposition, alterations of gingival connective homeostasis and metabolism, inflammatory alterations, interactions with the growth factors and protective or synergic effects of other drugs.
在过去20年里，有多项研究试图解释环孢素（CS）诱导牙龈增生（以及一般而言药物诱导牙龈增生）的发病机制，但目前仍了解甚少。药物与不同药代动力学变量（剂量、治疗持续时间、血浆和唾液中环孢素浓度）之间的关系仍在讨论中。人们公认，牙龈组织中需要达到一定阈值浓度才能开始或加剧牙龈的形态结构变化，但必须评估从治疗开始到临床检查时的环孢素总量。药代动力学变量与许多其他因素（首先是口腔卫生评分）相关，这些因素可能与牙龈病变的发展有关。牙龈炎症在牙龈增生的发病机制中可能非常重要。多项横断面研究表明菌斑与牙龈病变之间存在密切关联，但尚不清楚菌斑堆积是形态学牙龈变化的因果因素还是结果。在药物性牙龈增生中，似乎形态学改变可能由菌斑诱导的炎症引发，进而导致牙龈组织充血和水肿。口腔卫生（专业的和居家的）更难维持，并且是促使病理循环持续的刺激因素。其他可能与环孢素诱导牙龈增生相关的因素包括年龄、性别、遗传易感性、牙龈结缔组织内稳态和代谢的改变、炎症改变、与生长因子的相互作用以及其他药物的保护或协同作用。
