白三烯抑制在仓鼠牙周炎中的作用。组织化学和形态计量学研究。
Leukotriene inhibition in hamster periodontitis. A histochemical and morphometric study.
机构信息
Laboratoire de Biologie et Biomatériaux du Milieu Buccal et Osseux Groupe Physiopathologie Osseuse Faculté de Chirurgie Dentaire Université Paris-V, 1 rue Maurice Arnoux Montrouge 92120 France.
出版信息
Mediators Inflamm. 1992;1(5):335-9. doi: 10.1155/S0962935192000504.
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.
用 phenidone（100mg/kg/d）和 ketoconazole（50mg/kg/d）对牙周炎仓鼠进行 4 周处理，评估白三烯（LT）抑制对牙龈和相邻骨间隙的影响。在牙龈中，这两种药物可显著减少 PMNL 的募集和迁移，并增加血管腔。在骨水平，它们显著减少了破前骨细胞和破骨细胞的数量，但不影响破骨细胞的活性。Phenidone 对牙周炎引起的骨形成抑制没有作用；相反，酮康唑增强了形成。由于 phenidone 和 ketoconazole 都是非特异性的 LT 抑制剂，因此不能确定观察到的效果实际上是由于 LT 抑制所致。然而，phenidone 和 ketoconazole 诱导的变化与以前用于抑制环氧化酶途径的 indomethacin 不同。这些差异表明，在本研究中发生了 LT 抑制，它们参与了仓鼠牙周炎期间的牙龈炎症和破骨细胞破坏。
Zotero 插件