Concurrent joint contact in anterior cruciate ligament injury induces cartilage micro-injury and subchondral bone sclerosis, resulting in knee osteoarthritis.

OBJECTIVE

Anterior cruciate ligament (ACL) injury initiates post-traumatic osteoarthritis (PTOA) via two distinct processes: initial direct contact injury of the cartilage surface during ACL injury, and secondary joint instability due to the ACL deficiency. Using the well-established Compression-induced ACL-rupture and a novel Non-Compression ACL-rupture mice model, we aimed to reveal the individual effects of cartilage compression and joint instability on PTOA progression.

DESIGN

Twelve-week-old C57BL/6J males (n = 118) were divided to three experimental groups: Compression ACL-rupture, Non-Compression ACL-rupture, and Intact. Following ACL injury, we performed joint laxity testing and microscopic analysis of the articular cartilage surface at 0 days, in vivo optical imaging of matrix-metalloproteinase (MMP) activity at 3 and 7 days, and histological and microCT analysis at 0, 7, 14, and 28 days.

RESULTS

The Compression ACL-R group exhibited a significant increase in cartilage roughness immediately after injury compared with the Non-Compression group (p = 0.047). At 7 days, the Compression group increased MMP-induced fluorescence intensity slightly but showed no significant differences, and MMP-13 positive cell ratio of chondrocytes compared with the Non-Compression group (p < 0.001, 95% confidence interval = [-18.328, -7.154]). Moreover, histological cartilage degeneration was observable in the Compression group at the same time point. Sclerosis of the tibial subchondral bone in the Compression group was more significantly developed than in the Non-Compression group at 28 days (p = 0.027).

CONCLUSIONS

Joint contact during ACL rupture caused initial micro-damage on the cartilage surface and initiated early MMP activity, which could accelerate subchondral bone sclerosis compared to ACL injury without concurrent joint contact.