Effects of chlorpromazine on alveolar bone loss in experimental periodontal disease in rats
Effects of chlorpromazine on alveolar bone loss in experimental periodontal disease in rats
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DOI：
10.1034/j.1600-0722.2000.00766.x
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发表时间：
2000-04-01
影响因子：
1.9
通讯作者：
Ribeiro, RD
中科院分区：
文献类型：
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作者：
de Lima, V;Bezerra, MM;Ribeiro, RD
氯丙嗪(CPZ)是吩噻嗪类化合物，具有抗炎、抑制肿瘤神经症因子-α(TNF-α)合成和骨吸收的作用。肿瘤坏死因子-α促进牙周炎的炎症改变和骨吸收。我们研究了环丙沙星对实验性牙周炎的影响。Wistar大鼠在右侧第二上磨牙颈部进行结扎术。牙槽骨丢失的评估方法是牙尖和牙槽骨之间沿每个磨牙根轴的距离之和，减去对侧牙槽骨的距离。牙周组织病理学分析的基础是细胞流入、破骨细胞数量、牙槽骨和牙骨质完整性。诱导牙周炎后6h、1d、7d、11d取外周血进行白细胞总数和分类计数。两组均在牙周炎发生前1h及每日给药至第11天。CPZ 1 mg/kg、3 mg/kg和9 mg/kg对牙槽骨骨丢失的抑制率分别为46%、55.4%和76.5%。组织学分析显示，细胞内流和破骨细胞数量显著减少，牙槽突和牙骨质得以保留。CPZ可逆转白细胞升高，但不能减轻体重。总而言之，CPZ减少实验性牙周炎的骨丢失可能是通过阻断肿瘤坏死因子-α。
Chlorpromazine (CPZ), a phenothiazine derivative, possesses anti-inflammatory properties, inhibition of tumor neurosis factor-alpha (TNF-alpha) synthesis and bone resorption. TNF-alpha promotes inflammatory changes and bone resorption in periodontitis. We have studied the effect of CPZ in experimental periodontitis. Wistar rats were subjected to a ligature placement around the cervix of the right second upper molars. Alveolar bone loss was evaluated by the sum of the distances between the cusp tip and the alveolar bone along the axis of each molar root, which was subtracted from the contralateral side. Histopathological analysis of the periodontium was based on cell influx, osteoclast number, and alveolar bone and cementum integrity. Animals were weighed daily and total and differential peripheral white blood cell counts were performed 6 h and 1, 7 and 11 d after periodontitis induction. Groups were treated with CPZ 1 h before and daily up to the 11th d of periodontitis. Alveolar bone loss was inhibited 46%, 55.4%, and 76.5% by CPZ at 1, 3 and 9 mg/kg, respectively. Histological analysis showed a significant reduction of cell influx and osteoclast number, as well as preservation of the alveolar process and cementum. CPZ reversed leukocytosis but not weight loss. In conclusion, CPZ reduces bone loss in experimental periodontitis, probably via TNF-alpha blockade.