The pathology of frozen shoulder

G. C. R. Hand,
N. A. Athanasou,
T. Matthews,
A. J. Carr

From Nuffield Department of Othopaedic Surgery, Oxford, England

J Bone Joint Surg Br. 2007 Jul;89(7):928-32.

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.

Primary frozen shoulder is a common, severely debilitating condition with a prevalence of between 2% and 5%.1-3 It is frequently difficult to manage. The diagnosis is made on clinical grounds. A set of diagnostic criteria were initially described by Codman in 19344 and still hold true today. They include pain in the shoulder which comes on slowly and is felt at the insertion of the deltoid, inability to sleep on the affected side, atrophy of the spinati, and little in the way of local tenderness. There is restriction of both active and passive movement, with painful and restricted elevation and external rotation. The pain is ‘very trying’, but the patient is able to continue with daily habits and routines. Radiographs of the shoulder appear normal. Stiffness may also occur after fracture or in association with joint diseases such as osteoarthritis (OA); this is referred to as a secondary frozen shoulder.

The pathology of frozen shoulder remains unclear, with information usually derived only from recalcitrant cases. Arthroscopy and open exploration of the frozen shoulder have increased our understanding of both the macroscopic and microscopic appearances. The pathology affects the glenohumeral capsular tissue and is particularly localised to the coracohumeral ligament in the rotator interval. 5-9 Analysis of this tissue has shown inflammatory changes,10,11 fibrosis12 and proliferative myelofibrosis.13 This process may be cytokine mediated.14,15 The aim of our study was to identify the cell type or types involved in the pathology of frozen shoulder, using new and previously unused immunocytochemical techniques and antibodies, in the hope that this may lead to earlier and more effective treatment of this often debilitating condition.