Bilateral anterior dislocation of the shoulder: review of seventy cases and proposal of a new etiological-mechanical classification.

BACKGROUND: Although anterior shoulder dislocation is common in everyday practice in Emergency Departments, bilateral presentation is a rare entity. OBJECTIVES: The aim of this article is to report two additional cases of this rare injury and to introduce a new mechanism that can produce it. We made an exhaustive review of the literature and found 68 cases in printed publications. Also, we analyzed the mechanism of injury and the presence of predisposing factors, and propose a new etiological-mechanical classification. CASE REPORT: One case occurred after a trivial fall, and the other was produced by a mechanism not previously reported: the patient pushed strongly forward, expecting a resistance and finding none, his arms kept the forward movement and the shoulders dislocated. DISCUSSION: This lesion has a bimodal distribution, affecting mainly men (70%) with a mean age of 33.5 years, whereas in women, the average age is 57 years. The most common cause is trauma (50%), followed by muscle contractions (37%) due to seizures of different causes (epileptic, hypoglycemia, toxic, or hypoxic) or electrocution. In 15.7% of the cases, the diagnosis of bilateral anterior dislocation was not acute (<3 weeks), and in virtually all of these cases it was not traumatic. CONCLUSION: The bilateral anterior shoulder dislocation may not be as rare as previously thought and must be taken into account in emergency services. The authors propose a new etiological-mechanical classification. Also, the importance of radiologic diagnosis must be highlighted.

Synoviocyte-derived CXCL12 is displayed on endothelium and induces angiogenesis in rheumatoid arthritis.

CXCL12 (stromal cell-derived factor-1) is a potent CXC chemokine that is constitutively expressed by stromal resident cells. Although it is considered a homeostatic rather than an inflammatory chemokine, CXCL12 has been immunodetected in different inflammatory diseases, but also in normal tissues, ant its potential functions and regulation in inflammation are not well known. In this study, we examined the cellular sources of CXCL12 gene expression and the mechanism and effects of its interactions with endothelial cells in rheumatoid arthritis synovium. We show that CXCL12 mRNA was not overexpressed nor induced in cultured rheumatoid synoviocytes, but it specifically accumulated in the rheumatoid hyperplastic lining layer and endothelium. CXCL12 gene expression was restricted to fibroblast-like synoviocytes, whereas endothelial cells did not express CXCL12 mRNA, but displayed the protein on heparitinase-sensitive factors. CXCL12 colocalized with the angiogenesis marker alpha(v)beta(3) integrin in rheumatoid endothelium and induced angiogenesis in s.c. Matrigel plugs in mice. The angiogenic activity of rheumatoid synovial fluid in vivo was abrogated by specific immunodepletion of CXCL12. Our results indicate that synoviocyte-derived CXCL12 accumulates and it is immobilized on heparan sulfate molecules of endothelial cells, where it can promote angiogenesis and inflammatory cell infiltration, supporting a multifaceted function for this chemokine in the pathogenesis of rheumatoid arthritis.