Innervation of the joint and role of neuropeptides

Rheumatoid arthritis is considered to represent a disease of the synovial membrane, osteoarthritis of the hyaline articular cartilage, and osteoporosis of the bone. It can be questioned to what extent this is true and to what extent these diseases could be considered to be due to extra-articular, extra-skeletal pathology related to the neuroendocrine system. Pain is the main symptom in arthritis. This is related to prostaglandin-mediated sensitization of the primary afferent nociceptive nerves. Accordingly, nonsteroidal anti-inflammatory drugs are used in symptomatic treatment, occasionally together with opioids and tricyclic antidepressants. The midline symmetry and involvement of the richly innervated, small peripheral joints in rheumatoid arthritis have raised speculation about the role of neurogenic inflammation and neuropeptides in its pathogenesis. In contrast to the free nerve endings, the role of the proprioceptive sensors is to provide information of our actual motor performance (the afferent copy of our movements) compared to the efferent motor program, which is activated by our will to move. These include proprioceptors in the skin (e.g., Meissner corpuscles), muscles (annulospiral and flower-spray endings of the muscle spindles), Golgi tendon organs, and Ruffini end organs and Pacinian corpuscles in the superficial and deep layers of the joint capsule. Elderly people may have slow reflexes, lax joints, joint incongruity, and loss of muscle power; obesity, alcohol and medicinal use, and joint pain can be combined with poor/nonexisting capacity for repair and remodeling of the musculoskeletal tissues. Impaired biomechanics contributes to increased joint tenderness, accumulation of minor trauma (secondary osteoarthritis), and falls (osteoporotic fractures). More attention needs to be paid to aging of proprioception, not only to the terminal disease target.