Pathophysiology of joint pain.
Irrespective of the underlying mechanisms, joint pain usually originates in activation of nociceptors, or free nerve endings. Nociceptive signals release a large number of neuromediators, such as substance P and the calcitonin gene-related peptide. Complex neuronal activation occurs, which involves not only local sensitization of joint nociceptors but also modifications in central pain pathways. Additional complexity results from the ability of numerous environmental, psychological, and constitutional factors to influence joint pain.
Rheumatology Department A and Pain Clinic, Cochin Teaching Hospital, Paris, France.
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Guilbaud
D000818:Animals; D018771:Arthralgia / Q000175:diagnosis / Q000209:etiology; D006801:Humans; D007592:Joint Diseases / Q000150:complications / Q000503:physiopathology*; D007596:Joints / Q000294:innervation* / Q000503:physiopathology; D009619:Nociceptors / Q000503:physiopathology; D010147:Pain Measurement; D010148:Intractable Pain / Q000209:etiology / Q000503:physiopathology; D011379:Prognosis; D012684:Sensory Thresholds