Synovitis is a key contributor to the development of OA, and early modulation of the synovial environment may help limit downstream cartilage damage. This study compared the clinical and biochemical effects of intra-articular triamcinolone acetonide (TA) and autologous conditioned serum (ACS) in an equine model of IL-1β–induced synovitis. Six healthy adult horses were used in a crossover design involving five groups: PBS (negative control), IL-1β (positive control), IL-1β + ACS, IL-1β + TA, and an exploratory ACS-alone group administered post hoc to isolate its effects without IL-1β interference. Both TA and ACS mitigated inflammation through distinct profiles. TA was superior in reducing joint heat, swelling, and effusion. Conversely, IL-1β + ACS provided greater lameness improvement at 24, 36, and 72 h compared to IL-1β. ACS demonstrated potential chondroprotective advantages, as it did not increase synovial glycosaminoglycan (GAG) concentrations, which were highest in the IL-1β + TA group. ACS treatment resulted in significantly higher synovial total nucleated cell counts and total protein, driven primarily by monocyte enrichment. This cellular profile suggests that ACS may support the restoration of joint homeostasis. While TA remains highly effective for visual inflammatory signs, ACS offers a promising biological alternative for modulating the synovial environment and protecting cartilage during acute synovitis.
Alvarez et al. (2026) studied this question.