Seminar

Osteoarthritis (OA) is one of the most prevalent causes of chronic pain and disability worldwide, yet currently available therapies remain largely symptomatic and do not effectively prevent disease progression. Increasing evidence indicates that the endocannabinoid system (ECS) represents a promising therapeutic target in OA, particularly through modulation of cannabinoid receptor type 2 (CB2). This lecture will summarize recent experimental findings concerning the analgesic and disease-modifying properties of cannabinoids in OA.

 

Special attention will be devoted to the selective CB2 agonist JWH-133 and its effects on pain behavior, cartilage metabolism, and subchondral bone remodeling. Experimental studies in rat models of chemically induced OA demonstrated that repeated administration of JWH-133 produced sustained antinociceptive effects, improved weight bearing, and reduced cartilage degradation. Chronic CB2 activation was associated with decreased expression of matrix metalloproteinases (MMPs) and proinflammatory mediators, suggesting a protective role in joint tissue preservation. In vitro studies on human chondrocytes further showed that CB2 stimulation enhances cell proliferation and migration while reducing cytotoxicity, indicating a potential role in cartilage regeneration and delayed disease progression.The lecture will also address the interplay between the ECS and cartilage-degrading processes during OA progression, emphasizing the potential of cannabinoid-based therapies to simultaneously modulate pain signaling and joint degeneration.

 

In addition, the lecture will address the neurobiological consequences of chronic OA pain, including its impact on mood, cognition, and hippocampal plasticity. Altered hippocampal neurogenesis observed in chronic pain models may contribute to the development of depressive symptoms and cognitive impairment frequently accompanying OA.