The Role of Peripheral Nociceptive Neurons in the Pathophysiology of Osteoarthritis Pain

Abstract

Knee osteoarthritis is characterized by progressive damage and remodeling of all tissues in the knee joint. Pain is the main symptom associated with knee osteoarthritis. Recent clinical and pre-clinical studies shed light on the mechanisms that drive the pain associated with joint destruction. In this narrative review, we describe current knowledge regarding the changes in the peripheral and central nervous system that occur during the progression of osteoarthritis and discuss how therapeutic interventions may provide pain relief.

Pain and structural alterations in knee joints in patients with haemophilia

“…Analysing central components of pain processing by other methods, for example conditioned pain modulation have to be performed in further studies to clarify the role of central sensitization in PwH. 35 The results of the orthopaedic examinations revealed, as expected, a more impaired joint status in PwH (Table 3).…”

“…Therefore, one can consider if PPT is suitable to assess central alterations in PwH. Analysing central components of pain processing by other methods, for example conditioned pain modulation have to be performed in further studies to clarify the role of central sensitization in PwH …”

Effects of carrageenan induced synovitis on joint damage and pain in a rat model of knee osteoarthritis

“…The mechanisms that drive OA pain are likely to include peripheral and central sensitisation, and recent data in rats 44e46 and humans 47,48 using NGF-blocking pharmaceutical agents emphasise the key contribution of peripheral sensitisation. Peripheral sensitisation in OA has been associated with synovitis 49 . Further research would be needed to define the underlying mechanism of carrageenan-induced pain in rat OA knees, and how these might overlap with mechanisms of augmented joint damage.…”

Emerging Targets for the Management of Osteoarthritis Pain

“…Chronic pain associated with OA can be generated, modified, and maintained at different levels along the neuraxis, all of which may provide opportunity for pharmacological intervention [5, 6]. There is ample clinical evidence to indicate that ongoing peripheral input from the affected joint drives OA pain.…”