Coimbra L S, Steffens J P, Muscará M N, Rossa C, Spolidorio L C
Department of Physiology and Pathology, Faculdade de Odontologia de Araraquara, UNESP-Universidade Estadual Paulista, Araraquara, SP, Brazil.
J Periodontal Res. 2014 Dec;49(6):729-35. doi: 10.1111/jre.12155. Epub 2013 Dec 28.
After activation, platelets express mediators that modulate inflammation. We hypothesized that drug-induced platelet inactivation may interfere in the inflammatory process in experimental periodontal disease by suppressing the release of biological mediators to the injury site.
To evaluate the effects of antiplatelet drugs on experimental periodontal disease, 60 rats were randomly assigned to six groups (n = 10) and ligatures were placed around lower first molars in three groups. The other three groups were not subjected to the induction of periodontal disease and were used as negative controls. During the experimental period, animals were given aspirin (30 mg/kg) or clopidogrel (75 mg/kg) intragastrically once daily for 3 d. On day 3, they were killed and gingival tissue were used to evaluate myeloperoxidase activity and the expression of the chemokine CXCL4. Hemi-mandibles were used for microscopic evaluation.
Clopidogrel significantly reduced the inflammatory infiltrate and increased the amount of collagen fibers. Histometric analysis showed that clopidogrel impaired alveolar bone loss. Expression of CXCL4 was significantly increased (p < 0.001) in rats subjected to periodontal disease. Systemic administration of aspirin and clopidogrel induced a significant decrease ( p < 0.05) in the expression of CXCL4. Treatment with antiplatelet drugs resulted in a significant reduction of myeloperoxidase activity when compared to saline-treated animals with periodontal disease.
Clopidogrel but not aspirin showed the ability of preventing bone loss in experimental periodontitis.
血小板激活后会表达调节炎症的介质。我们推测药物诱导的血小板失活可能通过抑制生物介质向损伤部位的释放来干扰实验性牙周炎的炎症过程。
为评估抗血小板药物对实验性牙周炎的影响，将60只大鼠随机分为6组（每组n = 10），其中3组在右下第一磨牙周围放置结扎线。另外3组未诱导牙周炎，用作阴性对照。在实验期间，动物每天经胃内给予阿司匹林（30 mg/kg）或氯吡格雷（75 mg/kg），持续3天。在第3天，将它们处死，取牙龈组织评估髓过氧化物酶活性和趋化因子CXCL4的表达。半侧下颌骨用于显微镜评估。
氯吡格雷显著减少了炎症浸润并增加了胶原纤维的数量。组织计量学分析表明氯吡格雷减轻了牙槽骨吸收。在患有牙周炎的大鼠中，CXCL4的表达显著增加（p < 0.001）。全身给予阿司匹林和氯吡格雷可使CXCL4的表达显著降低（p < 0.05）。与用生理盐水处理的牙周炎动物相比，抗血小板药物治疗导致髓过氧化物酶活性显著降低。
氯吡格雷而非阿司匹林显示出预防实验性牙周炎骨吸收的能力。
