COX inhibitors and their effects on bone healing

Prostaglandins (PGs) are released as part of the inflammatory response. They are synthesised from arachidonic acid by the cyclooxygenase enzymes, COX-1 and -2. NSAIDS inhibit COX activity and have become the primary means of alleviating chronic pain associated with rheumatoid and osteoarthritis. They are also widely used as analgesics in the treatment of acute postsurgical and traumatic pain. PGs are known to play important functions in bone repair and normal bone homeostasis. Animal studies suggest that, whilst both nonspecific and specific inhibitors of COXs impair fracture healing, some studies have suggested that this impairment is due to COX-2. Although these data raise concerns about the use of COX-2-specific inhibitors as anti-inflammatory or analgesic drugs in patients undergoing orthopaedic procedures, clinical reports have been largely inconclusive concerning the effects of NSAIDs on bone healing. Since animal data suggest that the effects of COX-2 inhibitors are both dose-dependent and reversible, in the absence of scientifically sound clinical evidence it is suggested that physicians consider short-term administration or use of other drugs in the management of these patients.