Abstract
Background: One of the most important factors in the fracture healing is the intracellular production of prostaglandins by osteoblast cells. Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their effects through inhibition of prostaglandin synthesis. NSAIDs are widely used in orthopedic practices and their effect on bone healing is not fully understood yet.
Objectives: The current study aimed at examining the effects of indomethacin and meloxicam on tibia fracture union in rats.MethodsThe current study was conducted on 60 male rats. Mid-shaft tibia fracture was induced in rats using bone-breaker device. The animals were randomly divided into 3 groups; a control group that received distilled water and 2 other groups that received indomethacin and meloxicam respectively for 28 days. At the end of weeks 1, 2, 4, 8 and 12, four rats were randomly sacrificed from each group, and histological evaluation, measurement of the calcium, phosphorus, and alkaline phosphatase plasma levels, as well as radiographic examinations were performed on them.
Results: After 4 weeks, a thin layer of woven bone was observed in the vast spaces of the bone marrow in the fracture area in the control group. In the meloxicam group in the week 4, the formation of immature blades of bone was observed, which were less organized and more irregular. In the indomethacin group in the week 4, new bone formation was less immature and more areas of cartilage were still observed. In the radiographic evaluations, delayed union in indomethacin and meloxicam groups was observed, which was more significant in the indomethacin group.
Conclusions: Indomethacin and meloxicam had impact on the process of bone repair and delayed union in both groups of drugs. This delayed union was more significant in non-selective NSAIDs (COX-I and = II inhibitors) rather than selective NSAIDs (COX-II inhibitor).