The role of joint innervation in the pathogenesis of arthritis.
Recently, an expanding body of knowledge has documented the nature and functions of receptors in joint tissues and their potential importance in preserving the smooth normal functioning of the motor-skeletal system and in amplifying the inflammatory response to joint injuries and diseases. This review summarizes the current knowledge of the anatomical and physiological substrates of these mechanisms. The distribution, morphologic and functional characteristics of joint receptors have been well described. In the past decade there has been a new appreciation of the major role played by sensory neurons in promoting regional inflammatory responses, and many of the specific neuronal mechanisms and molecules that mediate these reflexes have been identified. This knowledge promises to significantly improve the selectivity and effectiveness of pharmacologic approaches to pain, trauma and regional inflammatory disorders. Other investigations have revealed important contributions of joint receptors to motor function. These refer not to proprioception or the sense of limb position in space, but rather to a more sophisticated tailoring of muscle activity to increase joint stability and to protect joint structures from damaging loads. Whether a loss of these reflexes may play a role in the pathogenesis of osteoarthritis remains controversial. However, there is a growing consensus that a loss of these reflexes may contribute to the morbidity associated with disruption of the anterior cruciate ligament. Synovial joints are sites of major interactions between the musculoskeletal and the nervous systems. Understanding the mechanisms that activate and control these interactions will certainly offer the opportunity to develop new, more effective treatments for patients with joint disorders.
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McCaig Center for Joint Injury and Arthritis Research, Department of Surgery, University of Calgary, Alberta.
D000818:Animals; D001168:Arthritis / Q000503:physiopathology*; D006614:Hindlimb / Q000294:innervation; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D007596:Joints / Q000294:innervation*; D009474:Neurons / Q000502:physiology; D009479:Neuropeptides / Q000502:physiology; D010003:Osteoarthritis / Q000503:physiopathology
D009479:Neuropeptides