Treatment of drug-induced gingival enlargement: aesthetic and functional considerations
Treatment of drug-induced gingival enlargement: aesthetic and functional considerations
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DOI：
10.1034/j.1600-0757.2001.027001131.x
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发表时间：
2001-01-01
影响因子：
18.6
通讯作者：
Takei, HH
中科院分区：
文献类型：
--
作者：
Camargo, PM;Melnick, PR;Takei, HH
牙龈肿大是与服用几种药物相关的副作用之一。这些药物基本上可分为三类：抗惊厥药、钙通道阻滞剂和免疫抑制剂环孢菌素。据了解，与抗惊厥药苯妥英相关的牙龈肿大已发生数年，影响约 50% 的服用该药的患者 (6,13,20)。最近，据报道，牙龈肿大的发生与钙通道阻滞剂的使用之间存在关联，钙通道阻滞剂是一组用于治疗高血压、不稳定心绞痛和其他心血管疾病的药物。与牙龈肿大相关的最常见的钙通道阻滞剂是硝苯地平 (2, 8, 18)，但使用维拉帕米 (16, 17, 21)、非洛地平 (15)、尼群地平 (3)、地尔硫卓 (4, 5, 7) 和氨氯地平 (26) 也存在类似问题。在所有钙通道阻滞剂中，硝苯地平引起牙龈肿大的发生率最高。环孢素是一种有效的免疫抑制剂，用于避免移植器官排斥并治疗多种被认为具有自身免疫成分的疾病，也被广泛报道可引起牙龈肥大 (7)。上述任何药物引起牙龈肥大的机制尚不清楚，并且每种药物可能不同。有人提出，牙龈成纤维细胞会产生无活性形式的胶原酶，它会造成胶原蛋白产生和降解的不平衡，从而影响牙龈组织的体积 (14)。其他提出的药物引起牙龈肿大的机制包括对菌斑的反应改变 (9) 和成纤维细胞亚群对药物的过敏 (27)。
Gingival enlargement is one of the side effects associated with the administration of several drugs. These drugs can be basically divided into three groups: anticonvulsants, calcium-channel blockers and the immunossupressant cyclosporin. Gingival enlargement associated with the anticonvulsant phenytoin has been known to occur for several years and affects approximately 50% of the patients taking the drug (6, 13, 20). More recently, an association between the development of gingival enlargement and the administration of calciumchannel blockers, a group of drugs used as therapy for hypertension, unstable angina pectoris and other cardiovascular disorders, has been reported. The most common calcium-channel blocker associated with the development of gingival enlargement is nifedipine (2, 8, 18), but similar problems have been associated with the administration of verapamil (16, 17, 21), felodipine (15), nitrendipine (3), diltiazem (4, 5, 7) and amlodipine (26). Among all calcium-channel blockers, the prevalence of gingival enlargement is highest with nifedipine. Cyclosporin, a potent immunosupressant used to avert transplanted organ rejection and to treat several diseases thought to have an autoimmune component, has also been extensively reported to induce gingival enlargement (7). The mechanism by which any of the above-mentioned drugs induces gingival enlargement is not well understood and may be distinct for each drug. The production of an inactive form of collagenase by gingival fibroblasts has been suggested, and it affects the volume of the gingival tissues by creating an imbalance in the production and degradation of collagen (14). Other proposed mechanisms for drug-induced gingival enlargement include an altered response to bacterial plaque (9) and hypersensitivity presented by subpopulations of fibroblasts to the drug (27).