Baroukh B, Saffar J S
Laboratoire de Physiopathologie Osseuse, Université Paris-V, Faculté de Chirurgie Dentaire, Montrouge, France.
Arch Oral Biol. 1990;35 Suppl:189S-192S. doi: 10.1016/0003-9969(90)90155-4.
The purpose of these experiments was to assess the role of the lipoxygenation products of arachidonic acid in hamster periodontitis. Phenidone and ketoconazole were used as inhibitors of leukotriene synthesis. In an established periodontitis, both drugs administered for 30 days induced a statistically significant decrease in PMNLs in the infiltrated connective tissue and around bacterial plaque within periodontal pockets. These changes were associated with a significant decrease in osteoclastic bone resorption. The results suggest that leukotrienes, and particularly leukotriene B4, are involved during hamster periodontitis and are responsible for PMNL infiltration of the periodontal pocket. The effects on bone are probably the consequence of the reduced inflammation resulting from the decrease in PMNL chemotaxis.
这些实验的目的是评估花生四烯酸的脂氧化产物在仓鼠牙周炎中的作用。苯茚二酮和酮康唑被用作白三烯合成的抑制剂。在已建立的牙周炎模型中，两种药物连续给药30天，均可使浸润结缔组织和牙周袋内菌斑周围的中性粒细胞数量出现统计学意义上的显著下降。这些变化与破骨细胞骨吸收的显著减少相关。结果表明，白三烯，尤其是白三烯B4，在仓鼠牙周炎发病过程中发挥作用，并导致中性粒细胞浸润至牙周袋。对骨骼的影响可能是由于中性粒细胞趋化性降低导致炎症减轻的结果。
