Association of Idiopathic Cam Morphology With Femoral and Acetabular Version: Analysis of 986 Cadaveric Hips.

Background: Studies have correlated symptomatic femoroacetabular impingement (FAI) with femoral retroversion and cam lesions. Purpose: To investigate any association between femoral and acetabular versions with cam deformity in a largely asymptomatic population. Study Design: Descriptive laboratory study. Methods: A total of 986 cadaveric hips were selected from a historical osteologic collection. Each hip was assessed to determine the femoral and acetabular versions, anterior offset, and alpha angle. Cam morphology was defined as an alpha angle >60°. Multiple regression analysis was performed to determine the relationship between age, femoral version, acetabular version, and either alpha angle or anterior femoral offset. Results: The mean alpha angle and anterior offset for the sample population were 48.1°± 10.4° and 0.77 ± 0.17 cm, respectively, with cam morphology in 149 of the 986 (15.1%) specimens. No significant difference was observed between hips with and without cam morphology with respect to the femoral (10.8°± 10° vs 10.3°± 9.6°; P = .58) or acetabular versions (17.4°± 6° vs 18.2°± 6.3°; P = .14). Multiple regression analysis did not demonstrate an association between the femoral or acetabular versions and the alpha angle, and it showed a small association between the increasing femoral and acetabular versions and a decreased anterior femoral offset (both P < .01). Conclusion: In a large random sample of cadaveric hips, cam morphology was not associated with femoral or acetabular retroversion. Combined with the existing literature, these findings suggest that retroversion is not associated with cam development. Clinical Relevance: This study provides insight into the development of cam morphology, which may eventually aid in the evaluation and treatment of FAI.

Subtle Slipped Capital Femoral Epiphysis Is not Associated With Idiopathic Cam Morphology.

BACKGROUND: The etiology of idiopathic cam morphology remains unclear. One theory suggests that subtle slipped capital femoral epiphysis (SCFE) leads to proximal femoral changes resulting in cam morphology. The purpose of this study was to evaluate the association between subtle SCFE and cam morphology in a large osteological collection. METHODS: We examined 962 cadaveric hips to measure 2 markers of cam morphology, alpha angle and anterior femoral head-neck offset (AHNO), and a validated, objective marker of subtle SCFE deformity (calcar ridge line offset). When the femur is viewed medially, the calcar ridge line extends from the lesser trochanter proximally along the postero-inferior femoral neck and points toward the fovea. In SCFE-like deformity, the fovea deviates posteriorly from this projected line. Pearson correlations were performed to evaluate for possible association of calcar ridge line offset with alpha angle and AHNO. In addition, a multiple regression analysis was performed to determine the influence of age, alpha angle, and AHNO on calcar ridge line offset. RESULTS: There was no clinically relevant association between the calcar ridge line offset and alpha angle (r=-0.02, P=0.58) or AHNO (r=0.08, P=0.012). Furthermore, specimens whose calcar ridge line deviated 1 SD above the mean (more SCFE-like deformity) had a smaller alpha angle (46.6±9.1 vs. 48.3±10.6, P=0.046) and greater AHNO (0.83±0.19 vs. 0.77±0.16, P<0.001), both reflecting less cam-like morphology. On regression analysis, increasing age and increasing AHNO (decreased cam morphology) predicted increased calcar ridge line offset, though the model accounted for only 1.2% of the variance. CONCLUSIONS: Subtle SCFE-like deformity, as objectively measured from the calcar ridge line, was not predictive of more cam-like morphology, and in fact mild opposite associations were found. Further study is needed to identify other potential etiologies of idiopathic cam morphology. CLINICAL RELEVANCE: We present evidence from a large, well-documented osteological collection indicating that subtle SCFE is not associated with idiopathic cam morphology.

Hip morphology predicts posterior hip impingement in a cadaveric model.

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.

Activation and trafficking of peritoneal B1a B-cells in response to amphibole asbestos.

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.