Abstract
To determine if Cyclooxygenase -2 (COX-2) functions in fracture healing, 10 dogs were treated with COX-2-selective nonsteroidal anti-inflammatory drugs (Celecoxib) to reduce and stop COX-2-dependent prostaglandin production. Radiographic testing evaluation determined that fracture healing was not affected in dogs treated with a low dose of COX-2-selective NSAIDs (celecoxib) and delayed union was observed in dogs treated with a high dose of COX-2selective NSAIDs (celecoxib). Celecoxib dose of 5 mg/kg/day did not affect fracture callus formed in the study group and did not cause a significant increase in the proportion of delayed unions, however, at a dose of 10 mg/kg/day it reduced the rate of fracture callus formation and significantly increased the proportion of delayed unions for dogs in the group.
Highlights
Considerable evidence has shown that conventional nonspecific, non-steroidal, anti-inflammatory drugs, such as ibuprofen, ketoprofen, ketorolac and indomethacin, have an inhibitory effect on fracturehealing as well as other forms of postoperative bone repair (Allen et al, 1980; Huo et al, 1991)
The results of this study show that Celecoxib at a dose of 5mg/kg daily enhanced healing of stable transverse femoral fractures created and fixed with intramedullary pins, but at a dose of 10mg/kg daily it retarded fracture healing
This observation is supported by report that inhibition of cyclooxygenase-2 enzyme impairs fracture healing and that the effects are dependent on the dose (Gerstenfeld, et al, 2007)
Summary
Considerable evidence has shown that conventional nonspecific, non-steroidal, anti-inflammatory drugs, such as ibuprofen, ketoprofen, ketorolac and indomethacin, have an inhibitory effect on fracturehealing as well as other forms of postoperative bone repair (Allen et al, 1980; Huo et al, 1991). Non steroidal, anti-inflammatory drugs (NSAIDs) could be expected to have significant consequences in divergent clinical situations where bone formation or remodelling is a contributory factor. NSAIDs are used clinically to prevent ectopic bone formation known a heterotrophic ossification (e.g. after total hip arthroplasty or trauma). The efficacy of NSAIDs in the avoidance of heterotrophic ossification has been documented in controlled clinical trials, but the inherent risk on bone fracture healing processes and loosening of implants need further studies (Goodman et al, 2003)
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