Effect of Non-Steroidal Anti-Inflammatory Drugs on Bone Healing.docVIP

Pharmaceuticals 2010, 3, 1668-1693; doi:10.3390/ph3051668 OPEN ACCESS pharmaceuticals ISSN 1424-8247 /journal/pharmaceuticals Review Effect of Non-Steroidal Anti-Inflammatory Drugs on Bone Healing Jessica Cottrell and J. Patrick O’Connor * Department of Biochemistry Molecular Biology, University of Medicine and Dentistry of New Jersey—New Jersey Medical School, Newark, NJ 07013, USA * Author to whom correspondence should be addressed; E-Mail: oconnojp@; Tel.: +1-973-972-5011; Fax: +1-973-972-5594. Received: 9 April 2010; in revised form: 5 May 2010 / Accepted: 24 May 2010 / Published: 25 May 2010 Abstract: Nonspecific and COX-2 selective nonsteroidal anti-inflammatory drugs (NSAIDs) function by inhibiting the cyclooxygenase isoenzymes and effectively reduce pain and inflammation attributed to acute or chronic musculoskeletal pathologies. However, use of NSAIDs as an analgesic is thought to negatively contribute to bone healing. This review strived to provide a thorough unbiased analysis of the current research conducted on animals and humans regarding NSAIDs and their effect on bone healing. Specifically, this review discusses the role of animal models, dosing regiments, and outcome parameters when examining discrepancies about NSAIDS and their effects on bone regeneration. The role of COX-2 in bone regeneration needs to be better defined in order to further elucidate the impact of NSAIDs on bone healing. Keywords: NSAIDs; bone healing; COX-2; COX-1; fracture 1. Prostaglandins, Cyclooxygenases, and Bone Metabolism Vertebrate bone is in a constant state of flux between destruction of old tissue and synthesis of new in a process often referred to as bone remodeling. An imbalance in bone remodeling can lead to osteoporosis or osteopetrosis [1]. Prostaglandins synthesized from arachidonic acid via cyclooxygenase activity mediate bone destructio