Abstract
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 < 0.02). Bone formation was increased by 270 per cent with indomethacin ( p < 0.05) and by 400 per cent with calcitonin ( p < 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.
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