Background and purpose

It is controversial whether the transverse acetabular ligament (TAL) is a reliable guide for determining the cup orientation during total hip arthroplasty (THA). We investigated the variations in TAL anatomy and the TAL-guided cup orientation.

Methods

80 hips with osteoarthritis secondary to hip dysplasia (OA) and 80 hips with osteonecrosis of the femoral head (ON) were examined. We compared the anatomical anteversion of TAL and the TAL-guided cup orientation in relation to both disease and gender using 3D reconstruction of computed tomography (CT) images.

Results

Mean TAL anteversion was 11° (SD 10, range –12 to 35). The OA group (least-square mean 16°, 95% confidence interval (CI): 14–18) had larger anteversion than the ON group (least-square mean 6.2°, CI: 3.8 – 7.5). Females (least-square mean 20°, CI: 17–23) had larger anteversion than males (least-square mean 7.0°, CI: 4.6–9.3) in the OA group, while there were no differences between the sexes in the ON group. When TAL was used for anteversion guidance with the radiographic cup inclination fixed at 40°, 39% of OA hips and 9% of ON hips had more than 10° variance from the target anteversion, which was 15°.

Interpretation

In ON hips, TAL is a good guide for determining cup orientation during THA, although it is not a reliable guide in hips with OA secondary to dysplasia. This is because TAL orientation has large individual variation and is influenced by disease and gender.

We investigated whether the vertical-center-anterior (VCA) angle measured on the false-profile view of the hip represents true anterior coverage by computer simulation using three-dimensional (3-D) computed tomography (CT) in 100 hips without osteoarthritic changes. True anterior coverage angle on the sagittal plane was measured in the pelvic coordinate system. Two types of VCA angle were measured on the digital reconstructed radiographs: the anterior point of the VCA angle was defined as the foremost aspect of the acetabulum, denoted VCA-1, whereas the anterior edge of the dense shadow of the subchondral bone of the acetabulum was defined as VCA-2. In the normal hips, VCA-1 was consistent with anterior coverage angle (r = 0.88, Spearman rank test), whereas VCA-2 underestimated the anterior coverage (r = 0.72). In the dysplastic hips, VCA-2 did not always indicate true anterior coverage (r = 0.64), whereas VCA-1 overestimated the anterior coverage (r = 0.002). Although VCA-1 in normal hips shows true anterior coverage, the VCA angle does not indicate true anterior coverage in dysplastic hips, and VCA angle measurement in dysplastic hips should be used carefully.

Level of Evidence: Level IV, diagnostic study. See Guidelines for Authors for a complete description of levels of evidence.

In revision surgery with proximal femoral bone loss, progressive bone atrophy due to stress shielding remains a concern. We compared 2-year radiological results between two types of cementless long titanium stems with different configurations and surface coatings. Of 17 hips implanted with a wholly hydroxyapatite-coated stem, 12 (71%) exhibited stress shielding of the second degree or higher according to Engh’s criteria, and the mean relative bone mass index decreased from 22.1% pre-operatively to 14.6% at 2 years post-operatively. In 23 hips implanted with a sand-blasted, conically shaped stem, no hip showed stress shielding of the second degree or higher. The mean relative bone mass index increased from 21.6% to 31.4%. These results indicate that the configuration and surface coating of the stem have a significant influence on proximal bone remodelling after revision surgery.

Although MRI is useful for predicting progression of osteonecrosis (ON) of the femoral head or femoral condyle, predicting outcome of atraumatic osteonecrosis of the humeral head using MRI has not been previously examined. We asked whether the prognosis was related to the extent and location of necrotic lesions on MRI. We investigated 46 radiographically noncollapsed humeral heads in 27 patients, 24 steroid-related and three alcohol-related, using MRI and serial radiographs. The minimum followup was 24 months (mean, 84.9 months; range, 24–166 months). The necrotic lesion was typically located at the medial and superior aspect of the humeral head. The necrotic angle, which expressed the extent of the necrotic lesion, was measured on midoblique-coronal plane (range; 0°–134.7°) and on midoblique-sagittal plane (range; 0°–150.6°). Of the 46 lesions, 34 were less than 90° and did not collapse, whereas 11 of the other 12 lesions of more than 90° (92%) collapsed within 4 years. Of these 11 collapsed lesions, four of less than 100° did not progress, followed by reparative reaction on plain radiographs, whereas the other seven of more than 100° progressed to osteoarthritis. The extent of a necrotic lesion on MRI is useful to predict collapse of the humeral head.

Level of Evidence: Level IV, prognostic study. See the Guidelines for Authors for a complete description of levels of evidence.

In response to ionizing radiation (IR), the tumor suppressor p53 is stabilized and promotes either cell cycle arrest or apoptosis. Chk2 activated by IR contributes to this stabilization, possibly by direct phosphorylation. Like p53, Chk2 is mutated in patients with Li-Fraumeni syndrome. Since the ataxia telangiectasia mutated (ATM) gene is required for IR-induced activation of Chk2, it has been assumed that ATM and Chk2 act in a linear pathway leading to p53 activation. To clarify the role of Chk2 in tumorigenesis, we generated gene-targeted Chk2-deficient mice. Unlike ATM−/− and p53−/− mice, Chk2−/− mice do not spontaneously develop tumors, although Chk2 does suppress 7,12-dimethylbenzanthracene-induced skin tumors. Tissues from Chk2−/− mice, including those from the thymus, central nervous system, fibroblasts, epidermis, and hair follicles, show significant defects in IR-induced apoptosis or impaired G1/S arrest. Quantitative comparison of the G1/S checkpoint, apoptosis, and expression of p53 proteins in Chk2−/− versus ATM−/− thymocytes suggested that Chk2 can regulate p53-dependent apoptosis in an ATM-independent manner. IR-induced apoptosis was restored in Chk2−/− thymocytes by reintroduction of the wild-type Chk2 gene but not by a Chk2 gene in which the sites phosphorylated by ATM and ataxia telangiectasia and rad3+ related (ATR) were mutated to alanine. ATR may thus selectively contribute to p53-mediated apoptosis. These data indicate that distinct pathways regulate the activation of p53 leading to cell cycle arrest or apoptosis.

The intracellular region (RAMIC) of the mouse Notch1 receptor interacts with RBP-J/CBF-1, which binds to the DNA sequence CGTGGGAA and suppresses differentiation by transcriptional activation of genes regulated by RBP-J. Epstein-Barr virus nuclear antigen 2 (EBNA2) is essential for immortalization of human B cells by the virus. EBNA2 is a pleiotropic activator of viral and cellular genes and is targeted to DNA at least in part by interacting with RBP-J. We found that EBNA2 and the Notch1 RAMIC compete for binding to RBP-J, indicating that their interaction sites on RBP-J overlap at least partially. EBNA2 and Notch1 RAMIC transactivated the same set of viral and host promoters, i.e., the EBNA2 response element of the Epstein-Barr virus TP1 and the HES-1 promoter. Furthermore, EBNA2 functionally replaced the Notch1 RAMIC by suppressing differentiation of C2C12 myoblast progenitor cells.