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Pathophysiology of Adhesive Capsulitis

At this time there is no accepted complete understanding of the pathophysiological basis for the development of adhesive capsulitis. Harryman and Lazarus  credit Reidel’s report in the early German literature as the first to propose that a pathologic process originating in the glenohumeral capsule was responsible for shoulder stiffness. Neviaser  subsequently described the histologic findings of perivascular infiltration, capsular fibrosis, and capsular thickening associated with the clinical development of adhesive capsulitis.

These findings were later confirmed by Lundberg , who noted capsular changes including an increase in the density of collagen and a glycosaminoglycan pattern similar to that found in repair tissue. Omari and Bunker  studied biopsies of rotator interval tissue in patients with frozen shoulder and described a dense matrix of Type 3 collagen populated with fibroblasts and myoblasts.

Some authors have hypothesized that autoimmune processes might be involved in the development of adhesive capsulitis. Studies showing reduced levels of IgA as well as an increased incidence of the immunohistocompatability antigen HLA-B27 initially suggested this relationship; however, subsequent reports have failed to establish an autoimmune etiology or identify an immunologic test to diagnose this condition. The possibility of a relationship between Dupuytrens contracture and adhesive capsulitis has intrigued investigators for many years.

Many of the histologic characteristics of Dupuytrens disease have been observed in capsuloligamentous biopsies obtained from patients with adhesive capsulitis. Investigators have suggested these two conditions may share a common biochemical pathway that leads to contracture.

More recently, investigations into the activity of polypeptide growth factors and matrix metalloproteinases have suggested a possible contribution to the development of adhesive capsulitis through their effects upon the activation and migration of fibroblasts and their alteration of normal collagen matrix remodeling.

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