The aim of this study was to assess the influence of bone mineral density and hip geometry on the fragility fracture of femoral neck and trochanteric region. There were 95 menopausal females of age ≥ 50 years with fragility fracture of hip, including 55 cases of femoral neck fracture and 40 cases of trochanteric fracture. Another 63 non-fractured females with normal bone mineral density (BMD) were chosen as control. BMD, hip axis length, neck-shaft angle and structural parameters including cross surface area, cortical thickness and buckling ratio were detected and compared. Compared with control group, the patients with femoral neck fracture or trochanteric fractures had significantly lower BMD of femoral neck, as well as lower cross surface area and cortical thickness and higher buckling ratio in femoral neck and trochanteric region. There were no significant differences of BMD and structural parameters in the femoral neck fracture group and intertrochanteric fracture group. Hip axis length and neck-shaft angle were not significantly different among three groups. The significant changes of BMD and proximal femur geometry were present in the fragility fracture of femoral neck and trochanteric region. The different types of hip fractures cannot be explained by these changes.

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The Pavlik harness and the Tübingen hip flexion splint (Tübingen hip flexion splint) are two effective options for the early management of patients younger than 6 months of age with developmental dysplasia of the hip (DDH). The main objective of this study was to evaluate the clinical and radiological outcomes of patients younger than 6 months of age with type IIb to IV DDH managed by Pavlik harness or Tübingen hip flexion splint. The Pavlik harness and Tübingen hip flexion splint groups were comparable regarding the affected side (P = 0.09), Graf grade (P = 0.635), and age at initial treatment (P = 0.77). Overall, failure rates were 12 and 33% in Pavlik harness (4/33 hips) and Tübingen hip flexion splint groups (14/43 hips), respectively (P = 0.038). No cases of avascular necrosis (AVN) were found in either group. In the Tübingen hip flexion splint group, the failure rate was significantly higher in bilateral cases (66.6%; P = 0.004), in severe forms (Graf grade IV hips; P ≤ 0.0001), and in patients with lower age at initial treatment (67.7 ± 39.3 days; P = 0.005). The average follow-up time was 30.35 ± 3.58 months (range: 24–36). At the last follow-up visit, no statistically significant differences were found between the Pavlik harness and Tübingen hip flexion splint groups regarding the acetabular index (t = 0.632; P = 0.53) or center-edge angle (Z = −0.303; P = 0.762). Our study showed that both the brace treatments for DDH in children younger than 6 months of age were effective and well tolerated. However, Tübingen hip flexion splint should not be used in patients with severe forms of DDH (Graf grade IV hips).

MicroRNA (miR)-335-5P has the ability to regulate chondrogenic differentiation and promote chondrogenesis in mouse mesenchymal stem cells. It is also abnormally elevated in human osteoarthritic chondrocytes. However, the biological function of miR-335-5P in osteoarthritis (OA) is not well understood. The present study investigated the mechanism of miR-335-5P in the pathogenesis of OA. To investigate the effect of miR-335-5P on the pathogenesis of OA in vitro, a miR-335-5P mimic and inhibitor were transfected into chondrocytes. Cell Counting kit-8 assay and flow cytometry were used to observe the effects of miR-335-5P on chondrocyte apoptosis and the expression of cartilage-specific genes, such as aggrecan, collagen II, matrix metalloproteinase 13 and collagen X, were detected by reverse transcription-quantitative PCR and western blot analysis. Moreover, the current study assessed whether HMG-box transcription factor 1 (HBP1) is a novel target of miR-335-5P with dual luciferase reporter assays. Finally, a rescue experiment was used to prove the regulation between miR-335-5P and HBP1. The results revealed that HBP1 was a novel target of miR-335-5P, and that miR-335-5P mediated the apoptosis of chondrocytes and changes in cartilage-specific genes via targeting HBP1. Overall, the present study revealed that miR-335-5P mediated the development of OA by targeting the HBP1 gene and promoting chondrocyte apoptosis. These data suggested that miR-335-5P may be used to develop novel early-stage diagnostic and therapeutic strategies for OA.