Stepwise loss of shoulder stabilizers induces humeral head migration and progression of cuff tear arthropathy in a rat model.

BACKGROUND

Cuff tear arthropathy (CTA) is a distinctive form of shoulder osteoarthritis characterized by superior migration of the humeral head, cartilage degeneration, synovitis, and subchondral bone collapse. Although deficiencies of the rotator cuff (RC), superior capsule, and long head of the biceps (LHB) tendon are clinically implicated in CTA, the relative contribution of each structure and the quantitative relationship between humeral head migration and joint degeneration remain unclear.

METHODS

Adult male Sprague-Dawley rats were assigned to 4 experimental models: resection of the supraspinatus and infraspinatus tendons alone (RC), RC with additional LHB resection, RC with additional resection of the superior capsule, and a modified CTA model incorporating both procedures (modified cuff tear arthropathy [mCTA]). Superior migration of the humeral head was quantified histologically. Articular cartilage degeneration was assessed using the Murine Shoulder Arthritis Score. Inflammatory cytokines and catabolic enzymes were evaluated by immunohistochemistry. Osteoclast number, the receptor activator of nuclear factor-κB ligand/osteoprotegerin ratio, and the bone volume (BV) fraction (BV/tissue volume ratio) were analyzed, and correlations with humeral head migration were examined.

RESULTS

RC alone induced approximately 500 μm of superior humeral head migration, accounting for nearly half of the total displacement observed in the mCTA model (approximately 1,100 μm). Additional capsule resection caused greater migration than LHB tendon resection, whereas concomitant resection of both was required to reproduce the full mCTA phenotype. The Murine Shoulder Arthritis Score and expression of inflammatory cytokines and catabolic enzymes in cartilage and synovium increased stepwise with sequential tissue disruption and showed strong correlations with the degree of humeral head migration. In the subchondral bone, osteoclast number and the receptor activator of nuclear factor-κB ligand/osteoprotegerin ratio increased, whereas the BV/tissue volume ratio decreased in association with humeral head migration, indicating a shift toward resorption-dominant bone remodeling.

CONCLUSIONS

These findings demonstrate that, in this rat model of RC disease, superior migration of the humeral head progresses sequentially with cumulative loss of shoulder stabilizers and is closely linked to multitissue joint degeneration. The superior capsule plays a more prominent role than the LHB tendon in restraining humeral head migration, although both contribute to full CTA development. Subchondral bone appears particularly sensitive to altered mechanical loading. Sequential disruption of the RC, superior capsule, and LHB tendon induces stepwise humeral head migration that strongly correlates with inflammation and degeneration across cartilage, synovium, and subchondral bone. These results suggest that preservation or restoration of shoulder stability, potentially including RC repair, may help suppress CTA progression.