Can magnetic resonance imaging distinguish clinical stages of frozen shoulder? A state-of-the-art review.

Background: Frozen shoulder (FS) is a common disorder causing shoulder pain and limited motion. Magnetic resonance imaging (MRI) is expected to help diagnose FS and realize the disease stage if stage-specific features are present. We aimed to survey stage-related MRI findings of FS in the literature. Methods: MEDLINE, SCOPUS, and Google Scholar databases were searched with search terms "frozen shoulder" or "adhesive capsulitis" combined with "magnetic resonance imaging." Studies that discussed MRI findings in relation to FS stages were retrieved. The course of FS was divided into stages 1 to 4 according to Hannafin and Chiaia. Results: Two of the noncontrast-enhanced MRI findings were stage-related. T2 signal hyperintensity of the joint capsule was more frequent in stages 1 and 2. The axillary capsule thickness was greater in stages 1 and 2. However, these findings were also seen in the later stages to a lesser degree. Effusion around the long head of biceps, subcoracoid fat obliteration, and coracohumeral ligament thickening were common in FS but their relation to the stages was not evident. Signal enhancement on contrast-enhanced MRI was not consistently linked to stages. Conclusion: T2 signal hyperintensity and axillary capsule thickening are characteristic of the early stages of FS, although MRI alone cannot completely define the disease stage.

Frozen shoulder. An overview of pathology and biology with hopes to novel drug therapies.

Frozen shoulder (FS) is a common disorder characterized by spontaneous onset of shoulder pain accompanied by progressive loss of range-of-motions. The cause of FS is still unclear, and radical therapy has not been established. With the final aim of preventing or curing FS at an earlier stage, we reviewed the pathological and biological features of this disease. Many studies indicate that the main pathology of FS is inflammation initially and fibrosis later. There are inflammatory cytokines, immune cells, fibrotic growth factors, and type-III collagen in the synovium and the joint capsule. The immune cell landscape switches from the macrophages to T cells. Activated fibroblasts seem to regulate the inflammatory and fibrotic processes. The imbalance between matrix metalloproteinases and tissue inhibitors of metalloproteases might promote fibrosis. Additionally, advanced glycation end-products are noted in the FS synovium. Diabetes mellitus and hypothyroidism are closely related to the development of FS. In terms of nonsurgical treatment, oral or intra-articular glucocorticoids are the only drugs that provide early benefit. Some other anti-inflammatory or antifibrotic drugs may potentially control the FS, but have not been proven effective in the clinical setting. Future studies should be targeted to develop steroid-sparing agents that inhibit biological events in FS.