Saffar J L, Lasfargues J J
Arch Oral Biol. 1984;29(7):555-8. doi: 10.1016/0003-9969(84)90077-3.
The action on bone remodelling of indomethacin, a potent inhibitor of prostaglandin (PG) synthesis, was determined in hamster periodontitis and compared to that of calcitonin. The two treatments reduced the extent of bone resorption considerably but not significantly (NS). The reversal phase, the intermediate step between resorption and formation, was decreased by 33 per cent (NS) by indomethacin and 75 per cent by calcitonin (p less than 0.02). Bone formation was increased by 270 per cent with indomethacin (p less than 0.05) and by 400 per cent with calcitonin (p less than 0.03), compared with untreated animals. This exceeded the extent of bone formation activity in control animals. These data strongly suggest that PG are involved in the mechanism of bone destruction in hamster periodontitis and that PG are potent in vivo uncouplers of bone remodelling as they participate both in an increase in bone resorption and a decrease in bone formation. A partial decrease in reversal lacunae indicates that other factors, also acting as uncouplers, probably take part in the mechanism of bone destruction.
在仓鼠牙周炎模型中,研究了强效前列腺素(PG)合成抑制剂吲哚美辛对骨重塑的作用,并与降钙素进行了比较。两种治疗方法均显著降低了骨吸收程度,但差异无统计学意义(NS)。吲哚美辛使吸收与形成之间的中间步骤——逆转期减少了33%(无统计学意义),而降钙素使其减少了75%(p<0.02)。与未治疗的动物相比,吲哚美辛使骨形成增加了270%(p<0.05),降钙素使其增加了400%(p<0.03)。这超过了对照动物的骨形成活动程度。这些数据有力地表明,PG参与了仓鼠牙周炎的骨破坏机制,并且PG在体内是骨重塑的有效解偶联剂,因为它们既参与骨吸收的增加,也参与骨形成的减少。逆转腔隙的部分减少表明,其他同样作为解偶联剂的因素可能参与了骨破坏机制。