Abstract
The aetiology and pathophysiology of frozen shoulder is poorly understood. The macroscopic pathological finding is dense fibrosis of the glenohumeral capsule and ligaments. Cellular histological studies reveal active proliferation of fibroblasts and their transformation to myofibroblasts, resulting in a dense matrix of disorganised collagen, causing capsular contracture. To further elucidate these pathological changes we arthroscopically examined 45 consecutive frozen shoulders immediately prior to performing arthroscopic release.
The distinctive finding in all cases was new blood vessel formation or angiogenesis in the synovium and capsule. There were five distinct angiogenic patterns: 1.vascular synovial proliferation at the base of the anchor of the long head of biceps tendon (most common); 2.petechial haemorrhagic spots widely spread across the synovium, in the rotator interval and even on the labral surface; 3.capillary loops and spirals, appearing like “lava flow”; 4.dense red vascular synovitis; 5.spectacular capillary whorls, similar in appearance to glomeruli (least common). High quality arthroscopic digital images will illustrate these findings.
The vascular changes seen in the shoulder joint in frozen shoulder are pathognomonic and similar to those seen in the formation of hypertrophic and keloid scarring of the skin, diabetic retinopathy, a variety of auto-immune disorders and tumours, rheumatoid arthritis and many other disease processes. The ability to therapeutically inhibit angiogenesis via inhibition of cytokines or adhesion molecules in these diseases suggests a possible role for these developing non-surgical treatments in frozen shoulder.
Correspondence should be addressed to BESS c/o BOA, 35-43 Lincoln’s Inn Fields, London WC2A 3PE