Mechanisms and Mediators That Drive Arthritis Pain

Abstract

There are over 100 different types of arthritis and each can differ greatly in their aetiology and pathophysiology; however, one characteristic that is common to all arthritic conditions is joint pain. Musculoskeletal pain is the leading cause of disability in the world, and the number one reason arthritis patients visit their primary care physician. Despite the prevalence and burden of arthritis pain, current analgesics lack sufficient efficacy and are plagued by multiple adverse side effects. In this review, we outline the current landscape of research concerning joint pain, drawing from both preclinical and clinical studies. Specifically, this review is a discussion of the different neurophysiological processes that occur during joint disease and how inflammatory and neuropathic aspects contribute to the development of arthritis pain.

Joint problems arising from lack of repair mechanisms: can cannabinoids help?

“…However, chondrocytes isolated from OA patients are very diverse, ranging from normal (healthy) cells to those with severe changes in both morphology and metabolism, which must be considered in human tissue studies. Chondrocytes maintain cartilage homeostasis and regulate the stability between anabolic and catabolic processes (Krustev et al ., ). Cartilage degeneration can arise from ageing, trauma, low‐grade local or systemic inflammation, metabolic syndromes, obesity and genetic predispositions (Buckwalter and Mankin, ).…”

Mangiferin: Possible uses in the prevention and treatment of mixed osteoarthritic pain

“…Further, demyelination of the ipsilateral saphenous nerve was confirmed by an increase in the G‐ratio, asserting MIA‐induced peripheral neuropathy compared with saline control animals (McDougall et al, ), suggesting that neuronal damage occurs in OA, probably in relation to the neuroinflammatory environment. It is accepted that low‐level inflammation contributes to degenerative changes that affect the entire joint leading to the development of peripheral sensitization and nociceptive pain (Krustev, Rioux, & McDougall, ; Moilanen et al, ; Robinson et al, ; Schuelert & McDougall, ). The contribution of spinal glial cell to chronic pain behavior, in particular distal allodynia, has also been reported in this OA model (Sagar et al, ).…”

Mechanisms Underlying Bone and Joint Pain

“…fibroblasts, chondrocytes), blood, and local and migrating inflammatory cells [57, 47, 58, 59]. These factors may promote disease progression and pathology in disease states such as arthritis or cancer-induced bone pain.…”