Pain in osteoarthritis: A review of literature

Abstract

There is a vast body of evidence to suggest that osteoarthritis is a heterogenous condition that involves not only the articular cartilage but also an adaptive response of the bone and the synovium to a variety of environmental, genetic and biomechanical stresses. 5-11 There is also growing evidence pointing towards long term potentiation as the most likely mechanism for the transition of acute nociception to a chronic pain (CP) state. The complexity and plasticity of the nociceptive system not only serve survival needs but also provide research opportunities for pharmacologic modulation of human suffering resulting from osteoarthritis.

The role of extra-cellular adenosine receptors in modulating pain progression during osteoarthritis (OA): A systematic review of the literature

“…Conventional wisdom argues that OA is a weight-bearing disease resulting in progressive and cumulative destruction of articular cartilage which leads to pain [17,20,22]. This progressive and destructive process consists of early cartilage fibrillation with developments to fissuring, ulceration, subchondral sclerosis, joint-space narrowing, and eventual full-thickness loss of hyaline cartilage [4,8,[23][24][25].…”

“…Although these treatments can be beneficial [10] in treating the symptoms of pain associated with the early stages of OA, the quality of these treatment modalities is largely unpredictable and can develop adverse side effects [19]. These treatments have been shown to be less effective during the late worsening stages of OA [20]. To date, there are no currently known treatments which block the progression of OA, nor the pain associated with this disease [21].…”

The Therapeutic Effect of rhMK on Osteoarthritis in Mice, Induced by Destabilization of the Medial Meniscus

“…56,57) Another possible reason is that the rhMK promoted the retrieval of pathologic changed nervous system that was involved in the OA chronic pain. 2,3,5) Because beyond the bioactivity on cartilage, the neurotrophic and neurite outgrowth activities of MK have also been widely reported 22,23) . In addition, the study on Midkine knockout mice showed that the midkine (−/−) mice has a regenerative delay of the axonal damage after freezing injury of the sciatic nerve.…”

“…2) More researches [2][3][4]35) indicate that OA occurrence and development is a long-term process with that the long-lasting knee injury or un-rational mechanical force induced dysfunction of the joint, which leading to the turn-over of the cartilage and bone and even the pathologic remodeling of vascular and peripheral nerve system of the joint, and this will further backward deteriorating the function of the joint over again. Once these pathological changes surpass a certain threshold, the OA is irreversible without any intervention.…”

“…1) Pain is the main clinical symptom of OA, which is also the foremost reason cause the disability. Pain in OA, like other pain, is a complex integration of sensory, affective and cognitive processes, 2) however, being different from the normal physiological pain which plays important role for the body defense of tissue injury, 2,3) the pain in OA is a pathophysiological state (neuropathic pain) 3,4) involving the sensitization of the peripheral and central nervous system induced by the destruction of the homeostasis and low grade chronic inflammation inside the joint. 2,3,5) Until now, the therapeutic drug for pain of OA is mainly focused on non-steroidal anti-inflammatory drugs (NSAIDs), steroids and opioid analgesics, which only attenuated the pain of partial OA patients, even with severe side effects.…”