Treating Skeletal Pain: Limitations of Conventional Anti-inflammatory Drugs, and Anti-neurotrophic Factor as a Possible Alternative

Cory J. Xian; Xin-Fu Zhou


Nat Clin Pract Rheumatol. 2009;5(2):92-98. 

In This Article

Summary and Introduction


Inflammatory and injury-induced skeletal pain are common conditions, and both conventional nonselective NSAIDs and the newer cyclo-oxygenase-2-specific inhibitors are widely used as post-traumatic and post-surgical analgesics. However, new research suggests that these drugs, particularly the cyclo-oxygenase-2 inhibitors, have a negative effect on the healing process in fractured bone and within orthopedic surgical sites, thus highlighting a need to develop new approaches for managing skeletal pain. Various experimental studies have revealed that locally upregulated neurotrophic factors, especially nerve growth factor, have a major role in mediating injury-induced or inflammatory pain. Nerve growth factor inhibitors, therefore, might be an effective alternative modality for post-traumatic and post-surgical analgesia, without impairing bone healing.


Chronic pain is a leading cause of morbidity worldwide, with a prevalence of 50% in Europe—a figure that is likely to rise in elderly patients with chronic disorders, such as rheumatoid arthritis or osteoarthritis.[1] Nonselective NSAIDs, which inhibit cyclo-oxygenase (COX)-1 and COX-2, and the newer COX-2-specific inhibitors are commonly used in the management of post-traumatic or post-operative skeletal pain. However, studies have demonstrated a strong association between these agents and impaired bone healing, highlighting the need for new approaches to skeletal pain management. Data from the past few years indicate that neurotrophins—growth factors that are required for the survival, development and maintenance of neuronal cells—might be involved in the pathophysiology of injury-induced or inflammatory skeletal pain. This Review discusses the inhibitory effects of NSAIDs (particularly COX-2-specific agents) on bone healing, and the potential role of neurotrophic factors as mediators of skeletal pain and as targets for the treatment of skeletal pain.


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