We treated 22 patients with a diagnosis of primary frozen shoulder resistant to conservative treatment by manipulation under anaesthetic and arthroscopic release of the rotator interval, at a mean time from onset of 15 months (3 to 36). Biopsies were taken from this site and histological and immunocytochemical analysis was performed to identify the types of cell present. The tissue was characterised by the presence of fibroblasts, proliferating fibroblasts and chronic inflammatory cells. The infiltrate of chronic inflammatory cells was predominantly made up of mast cells, with T cells, B cells and macrophages also present.

The pathology of frozen shoulder includes a chronic inflammatory response with fibroblastic proliferation which may be immunomodulated.

We have studied cellular and vascular changes in different stages of full thickness tears of the rotator cuff. We examined biopsies from the supraspinatus tendon in 40 patients with chronic rotator cuff tears who were undergoing surgery and compared them with biopsies from four uninjured subscapularis tendons. Morphological and immunocytochemical methods using monoclonal antibodies directed against leucocytes, macrophages, mast cells, proliferative and vascular markers were used.

Histological changes indicative of repair and inflammation were most evident in small sized rotator cuff tears with increased fibroblast cellularity and intimal hyperplasia, together with increased expression of leucocyte and vascular markers. These reparative and inflammatory changes diminished as the size of the rotator cuff tear increased. Marked oedema and degeneration was seen in large and massive tears, which more often showed chondroid metaplasia and amyloid deposition. There was no association between the age of the patient and the duration of symptoms. In contrast, large and massive tears showed no increase in the number of inflammatory cells and blood vessels.

Small sized rotator cuff tears retained the greatest potential to heal, showing increased fibroblast cellularity, blood vessel proliferation and the presence of a significant inflammatory component. Tissue from large and massive tears is of such a degenerative nature that it may be a significant cause of re-rupture after surgical repair and could make healing improbable in this group.

Age-related localised deposition of amyloid in connective tissue has been found in degenerative articular and periarticular tissue. Biopsies of the supraspinatus tendon of 28 patients undergoing repair of the rotator cuff were analysed histologically for the presence of localised deposition of amyloid. There was a long history of impingement in 20 patients, and eight patients had suffered an acute traumatic tear with no preceding symptoms. Localised deposition of amyloid identified by Congo Red staining was detected in 16 samples (57%). Amyloid was present in 14 (70%) of the degenerative tears, but in only two (25%) of the acute tears. Immunohistochemical staining showed that the amyloid deposits were positive for P component, but negative for κ and λ light chains, prealbumin, and β2 microglobulin. Critical electrolyte staining revealed highly-sulphated glycosaminoglycans at sites of deposition of amyloid. The presence of localised deposition of amyloid in tears of the rotator cuff is likely to represent irreversible structural changes. These findings support the theory that impingement and tears are due to intrinsic degenerative changes within the tendons of the rotator cuff.