Department of Physiology and Pathology, Faculdade de Odontologia de Araraquara, UNESP-Univ Estadual Paulista, Araraquara, Brazil.
J Clin Periodontol. 2014 Mar;41(3):295-302. doi: 10.1111/jcpe.12203. Epub 2014 Jan 16.
We hypothesized that platelet inactivation induced by drugs might interfere with periodontal repair in experimental periodontitis by suppressing the release of biological mediators from platelets at the site of injury.
Sixty rats were randomly assigned to six groups (n = 10) and ligatures were placed around lower first molars of three groups. The other three groups were used as negative controls. Ligatures were removed after 10 days of periodontitis induction and all groups were submitted to treatment with aspirin (Asp) (30 mg/kg), clopidogrel (Clop) (75 mg/kg) or NaCl 0.9% intra-gastrically once daily for 3 days. Periodontal tissue was assessed by the measurement of CXCL12, CXCL4, CCL5 and platelet-derived growth factor (PDGF) by enzyme-linked immunosorbent assay; histomorphometrical analysis of polymorphonuclear (PMN) infiltration, attachment loss, bone loss and osteoclast numbers and quantification of blood vessels by imunnohistochemistry.
During periodontal repair and treatment with NaCl 0.9%, CCL5 was decreased and CXCL12 increased when compared with negative control groups. Asp and Clop did not affect CCL5 expression, decreased CXCL12 but only Clop decreased CXCL4 and PDGF content compared with saline-treated animals. Clop increased blood vessel number, reduced PMN count and decreased attachment and bone loss, also decreased osteoclast number in animals submitted or not to periodontal repair.
Systemic administration of Clop for 3 days improved the repair process associated with experimental periodontal disease, suggesting that it may have therapeutic value under situations where tissues undergo a transition from inflammation to repair.
我们假设药物引起的血小板失活可能通过抑制损伤部位血小板释放生物介质来干扰实验性牙周炎的牙周修复。
60 只大鼠随机分为 6 组（n = 10），3 组结扎下颌第一磨牙。另外 3 组作为阴性对照。牙周炎诱导 10 天后去除结扎线，所有组均给予阿司匹林（Asp）（30mg/kg）、氯吡格雷（Clop）（75mg/kg）或 0.9%NaCl 灌胃，每日 1 次，连续 3 天。通过酶联免疫吸附试验测定 CXCL12、CXCL4、CCL5 和血小板衍生生长因子（PDGF）；多形核（PMN）浸润、附着丧失、骨丧失和破骨细胞数量的组织形态计量学分析以及免疫组织化学定量血管。
在牙周修复和 0.9%NaCl 治疗期间，与阴性对照组相比，CCL5 减少，CXCL12 增加。Asp 和 Clop 不影响 CCL5 表达，降低 CXCL12，但仅 Clop 降低 CXCL4 和 PDGF 含量与生理盐水处理的动物相比。Clop 增加血管数量，减少 PMN 计数，减少附着和骨丧失，并减少牙周炎修复或不修复动物的破骨细胞数量。
3 天的 Clop 全身给药改善了与实验性牙周病相关的修复过程，表明在组织从炎症向修复过渡的情况下，它可能具有治疗价值。
