Neurogenic acceleration of osteoarthritis.
The nervous system has a variety of mechanisms whereby it can potentially initiate or accelerate joint disease. Whether these potential mechanisms are clinically significant factors in the etiology of osteoarthritis remains uncertain. However, 11 papers published in the past year provide further support for the view that these mechanisms are important in the pathogenesis of the disease.
Vilensky
J A
JA
Department of Anatomy, Indiana University School of Medicine, Fort Wayne 46805, USA.
Cook
J A
JA
D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D015740:Calcitonin Gene-Related Peptide / Q000502:physiology; D002211:Capsaicin / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000503:physiopathology; D004594:Electrophysiology; D006801:Humans; D009420:Nervous System / Q000503:physiopathology*; D009479:Neuropeptides / Q000502:physiology; D010003:Osteoarthritis / Q000150:complications / Q000209:etiology* / Q000503:physiopathology*; D011434:Proprioception / Q000502:physiology; D013373:Substance P / Q000502:physiology
D009479:Neuropeptides; D013373:Substance P; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin