Osteoarthritis (OA) is the most common form of arthritis, with the hand, knee and hip being the most prevalent joints affected. Pain is the primary clinical symptoms of knee OA and knee OA itself is a leading cause of disability among older adults worldwide. Yet there are limited management options for the symptoms of knee OA, and no proven therapies that can alter its progression. An improved understanding of pain etiology in knee OA is critical to improving OA outcomes by identifying rational therapeutic targets.
While there are data to support the importance of structural pathology as contributing to pain in knee OA, such structural lesions do not fully account for the pain experience in OA. Whereas knee OA pain is typically activity-related earlier in the course of disease, pain can be come chronic later in the disease course, suggesting the possibility of altered neurobiological pathways playing a role in OA pain. Peripheral and central sensitization, which reflect alterations in the ascending nociceptive signals in the peripheral and central nervous systems, respectively, and inadequate descending inhibition can lead to heightened pain sensitivity.
Sensitization can be assessed in clinical studies with pressure pain threshold and temporal summation, and assessment of conditioned pain modulation provides insights into efficiency of the descending inhibitory pathways. Conditioned pain modulation has been demonstrated to be abnormal in patients awaiting joint replacement surgery, and to improve post-replacement, raising in the intriguing possibility that certain abnormalities of pain processing can be altered by removing the pathologic tissue. In terms of sensitization, pressure pain threshold is lower (i.e., more pain sensitive and/or sensitized) in subjects with knee OA than in healthy controls around the knee and other anatomic sites on both the ipsilateral and contralateral sides. Lower pressure pain threshold and temporal summation are also associated with higher likelihood of pain presence and severity both at the knee and distant to the knee, but have no clear relation to radiographic severity or duration of disease. However, synovitis and effusion, which are inflammatory lesions in knee OA, are associated with both pressure pain threshold and temporal summation. In contrast, bone marrow lesions, which are largely mechanically-driven lesions in knee OA, are not associated with these measures of sensitization. These results suggest that certain features of knee OA may result in sensitization, and offer a potential avenue for targeted therapy to reduce the occurrence of sensitization, and thereby reduce pain severity in knee OA.
Disclosure of Interest None declared