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Leukotriene inhibition in hamster periodontitis. A histochemical and morphometric study

机译:仓鼠牙周炎中白三烯的抑制作用。组织化学和形态计量学研究

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摘要

The effects of leukotriene (LT) inhibition on gingival and adjacent bone compartments were assessed by using phenidone (100 mg/kg/d) and ketoconazole (50 mg/kg/d) given for 4 weeks to periodontitis-affected hamsters. In the gingiva the two agents significantly decreased PMNL recruitment and migration and increased the vascular lumen. At the bone level, they reduced significantly preosteoclast and osteoclast numbers but did not affect osteoclast activity. Phenidone had no action on periodontitis induced inhibition of bone formation; in contrast ketoconazole enhanced formation. As both phenidone and ketoconazole are unspecific LT inhibitors it cannot be ascertained that the effects observed were actually due to LT inhibition. However, phenidone and ketoconazole induced changes different from indomethacin used in previous studies to inhibit the cyclooxygenase pathway. These discrepancies suggest that LT inhibition occurred in the present study and that they participate in gingival inflammation and osteoclastic destruction during hamster periodontitis.
机译:通过使用苯甲酮(100 mg / kg / d)和酮康唑(50 mg / kg / d)4周给受牙周炎影响的仓鼠服用,评估白三烯(LT)对牙龈和相邻骨腔的影响。在牙龈中,这两种药物显着降低了PMNL的募集和迁移,并增加了血管腔。在骨骼水平上,它们显着降低了破骨细胞和破骨细胞的数量,但不影响破骨细胞的活性。苯乙酮对牙周炎引起的骨形成抑制没有作用。相反,酮康唑可增强形成。由于苯乙酮和酮康唑都是非特异性的LT抑制剂,因此无法确定观察到的作用实际上是由于LT抑制所致。然而,吩酮和酮康唑诱导的变化不同于先前的研究中使用的消炎痛抑制环氧合酶途径的变化。这些差异表明在本研究中发生了LT抑制作用,并且它们参与了仓鼠牙周炎期间的牙龈发炎和破骨细胞破坏。

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