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Introduction: Posterior hip impingement is a recently-identified cause of hip pain. The purpose of this study is to characterise posterior femoroacetabular and ischiofemoral impingement and identify its predisposing morphologic traits. Methods: Two hundred and six cadaveric hips were randomly selected and taken through controlled motion in two pure axes associated with posterior hip impingement: external rotation (through the mechanical axis) and adduction (coronal plane). The range of motion and location of impingement was noted for each specimen. Morphologic traits including femoral/acetabular version, and true neck-shaft angle (TNSA) were also measured. Results: External rotation impingement occurred between the femoral neck and acetabulum in 83.0% of hips, and between the lesser trochanter and ischial tuberosity in 17.0%. Adduction impingement occurred between the lesser trochanter and ischial tuberosity in 78.6% of hips, and between the femoral neck and acetabulum in 21.4%. Multiple regression revealed that increased femoral/acetabular version predicted earlier external rotation and adduction impingement. Unstandardised betas ranging from −0.39 to −0.64 reflect that each degree of increased femoral/acetabular version individually accounts for a loss of external rotation or adduction of approximately half a degree before impingement (p < 0.001 for each). Increased TNSA was associated with earlier adduction impingement only (unstandardised beta −0.35, p = 0.005). Discussion: Relative femoral/acetabular anteversion was associated with earlier posterior hip impingement. Coxa valga was associated with earlier adduction impingement, but protective against external rotation impingement. These findings highlight the importance of monitoring correction during femoral/acetabular osteotomies, as overcorrection of retroversion may predispose to earlier posterior impingement. [ABSTRACT FROM AUTHOR]

B1a B-cells are concentrated in peritoneal and pleural cavities, are producers of 'natural auto-antibodies', and have been implicated in autoimmune responses. Their numbers are increased in humans and mice with systemic autoimmune diseases, but their role in the immune pathology is not known. Asbestos causes pulmonary, pleural, and peritoneal pathologies by accessing these tissues after inhalation. Amphibole asbestos has been shown to elicit immune dysfunction, including chronic inflammation, fibrosis, and autoantibody production. This study tested the hypothesis that asbestos affects immune dysfunction by activating B1a B-cells to traffic to secondary lymphatic tissue. C57Bl/6 mice were exposed to amphibole asbestos (Libby 6-Mix) either endotracheally or intraperitoneally, and the B1a B-cells in pleural or peritoneal compartments were tested by multi-parameter flow cytometry. Adoptive transfer of peritoneal lymphocytes from CD45.1 transgenic to wild-type mice was used to track the migration. The percentage and numbers of B1a B-cells in pleural and peritoneal cavities decreased 3-6 days following exposure. During that time, asbestos exposure led to a decrease in cells expressing alpha-4 ( α4) integrin and MHC II antigen. Peritoneal cells treated in vitro showed decreased α4 integrin with no change in CD5, IgM, or MHC II antigen. Therefore, B1a cells (IgM+, CD5+, MHC II+) traffic from the peritoneal cavity following loss of α4 integrin expression. Following adoptive transfer into the peritoneum of asbestos-exposed mice, CD45.1+ B1a cells were detected in the spleen and mesenteric lymph nodes after 3 days, peaking at 6 days. Interestingly, the percentage of splenic suppressor B-cells (IgM+, CD5+, CD11b+, CD1d+) decreased following amphibole exposure, demonstrating that the B1a cells did not contribute to an increased pool of suppressive B-cells. These results show that B1a B-cells respond to asbestos exposure by trafficking to secondary lymphatic tissue where they may affect ultimate immune dysfunction. [ABSTRACT FROM AUTHOR]