BackgroundPrimary frozen shoulder (FS) is a painful contracture of the glenohumeral joint that arises spontaneously without an obvious preceding event. Investigation of the intra-articular and periarticular pathology would contribute to the treatment of primary FS.Review of literatureMany studies indicate that the main pathology is an inflammatory contracture of the shoulder joint capsule. This is associated with an increased amount of collagen, fibrotic growth factors such as transforming growth factor-beta, and inflammatory cytokines such as tumor necrosis factor-alpha and interleukins. Immune system cells such as B-lymphocytes, T-lymphocytes and macrophages are also noted. Active fibroblastic proliferation similar to that of Dupuytren’s contracture is documented. Presence of inflammation in the FS synovium is supported by the synovial enhancement with dynamic magnetic resonance study in the clinical setting.ConclusionPrimary FS shows fibrosis of the joint capsule, associated with preceding synovitis. The initiator of synovitis, however, still remains unclear. Future studies should be directed to give light to the pathogenesis of inflammation to better treat or prevent primary FS.

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Microvessel density (MVD) is an excellent predictive biomarker regarding tumor stage and survival in esophageal squamous cell carcinomas (ESCCs). However, it is obscure when tissues initiate angiogenesis in the malignant transformation of human esophageal squamous epithelium. To investigate the onset of angiogenesis in the multistep progressive process of ESCCs, immunohistochemical staining for CD31, CD105, and vascular endothelial growth factor receptor 2 (VEGFR-2) was performed in normal epithelium, Lugol-unstained lesions with non-dysplastic epithelium (LULs-NDE), low-grade dysplasia (LGD), and high-grade dysplasia (HGD) samples. There were significant differences in the mean MVD for CD31 and CD105 between LULs-NDE and LGD (p less than 0.001, p less than 0.001), and between LGD and HGD (p less than 0.001, p=0.006), respectively. Furthermore, a significant difference in MVD for CD105 was seen in normal controls and LULs-NDE (p=0.002), while thick vessels (less than 10m m) stained with anti-CD105 were not present in normal controls and LULs-NDE despite the presence of these thickened vessels in dysplasia. Our results suggest that CD105 is an efficient marker protein to determine MVD, suggesting that the angiogenic switch occurs at the earliest stage of dysplastic transformation in ESCC.

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