Pathology of the torn rotator cuff tendon
T. J. W. Matthews,
G. C. Hand,
J. L. Rees,
N. A. Athanasou,
A. J. Carr
From Nuffield Othopaedic Centre, Oxford, England
J Bone Joint Surg Br, Apr 2006; 88-B 489 - 495.
Reduction in potential for repair as tear size increases
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.
Full thickness tears of the rotator cuff are among the most frequently encountered causes of pain and dysfunction in the shoulder. 1 Since shoulder complaints are the third most frequent cause (after knee and spine) of musculoskeletal symptoms in the community, rotator cuff disease represents a significant health economic issue. 2 Cadaver studies in the elderly estimate the prevalence of full thickness tears to be from 5% to 30%. 3,4 MRI and ultrasound studies have demonstrated that the prevalence of asymptomatic full thickness tears is from 15% to 23% 5,6 overall, 4% to 13% in subjects under the age of 59 years and 28% to 51% in subjects between 60 and 80 years of age.
The pathogenesis of rotator cuff tears remains unclear, but is considered to be a combination of extrinsic impingement from structures surrounding the cuff and intrinsic degeneration from changes within the tendon itself.
Recent pathological and genetic studies have emphasised the importance of intrinsic factors, 7-11 but little information regarding the process of tendon degeneration is available. Kannus and Jozsa 12 demonstrated characteristic histopathological changes in tendons that rupture spontaneously. Degenerative changes were evident in 865 of 891 cases (97%) and included features of hypoxic degenerative tendinopathy, mucoid degeneration, tendolipomatosis and calcifying tendinopathy, either individually or in combination. They concluded that hypoperfusion is a central aspect of tendon failure. Nirschl 13 also described changes in the rotator cuff tendon, such as disorganisation and fragmentation of collagen architecture and infiltration of fibroblasts and vascular tissue. Hashimoto et al 9 described different patterns of degenerative change in partial and full thickness rotator cuff tears. However, they observed no correlation between the pattern of degenerative change and the size or extent of the rotator cuff tear.