The pathology of frozen shoulder. A Dupuytren-like disease

TLDR

Frozen shoulder shows a Dupuytren‑like pathology with thick collagenous bands, no inflammation, and a contracture that limits external rotation and both active and passive motion. In 50 patients with primary frozen shoulder, the coracohumeral ligament and rotator interval were excised and the specimens were histologically and immunocytochemically examined for collagen, inflammatory cells, fibroblasts, and myofibroblasts. The analysis revealed active fibroblastic proliferation with myofibroblast differentiation and deposition of thick nodular collagen bands.

Abstract

Of 935 consecutive patients referred with shoulder pain, 50 fitted the criteria for primary frozen shoulder. Twelve patients who failed to improve after conservative treatment and manipulation had excision of the coracohumeral ligament and the rotator interval of the capsule. The specimens were examined histologically, using special stains for collagen. Immunocytochemistry was performed with monoclonal antibodies against leucocyte common antigen (LCA, CD45) and a macrophage/synovial antigen (PGMI, CD68) to assess the inflammatory component, and vimentin and smooth-muscle actin to evaluate fibroblasts and myofibroblasts. Our histological and immunocytochemical findings show that the pathological process is active fibroblastic proliferation, accompanied by some transformation to a smooth muscle phenotype (myofibroblasts). The fibroblasts lay down collagen which appears as a thick nodular band or fleshy mass. These appearances are very similar to those in Dupuytren's disease of the hand, with no inflammation and no synovial involvement. The contracture acts as a check-rein against external rotation, causing loss of both active and passive movement.