Background The clinical outcome of a new fixation device (femoral neck system, FNS) for femoral neck fractures remains unclear. The main purpose of this study was to evaluate two different internal fixation methods for the treatment of femoral neck fractures in patients aged under 60 years. Methods We retrospectively studied patients who underwent internal fixation surgery in our hospital for femoral neck fractures between January 2017 and January 2020. Cannulated compression screws (CCS) and FNS groups were divided according to different internal fixation methods. General data (such as sex, age, body mass index, type of fracture) of all patienFemoral neck shorteningts were collected, and joint function was evaluated using the Harris Hip Score (HHS) before and 1 year after surgery. We recorded related surgical complications, including femoral head necrosis, nonunion, and femoral neck shortening. Results There were no significant differences in age, sex, or body mass index between the two groups. There was no statistical difference in HHSs between the two groups before surgery. Patients who underwent FNS treatment had longer surgery time (79.75 ± 26.35 min vs. 64.58 ± 18.56 min, p = 0.031) and more blood loss (69.45 ± 50.47 mL vs. 23.71 ± 28.13 mL, p < 0.001). The degree of femoral neck shortening in the FNS group was significantly lower than that in the CCS group (10.0% vs 37.5%, p = 0.036). Regarding postoperative complications, there was no statistical difference in the incidence of femoral head necrosis and fracture nonunion between the two groups. Conclusion Patients younger than 60 with femoral neck fractures can obtain satisfactory clinical results with CCS or FNS treatment. FNS has excellent biomechanical properties and shows significantly higher overall construct stability.

Abstract. Low oxygen availability is known to activate the hypoxia-inducible factor-1α (HIF-1α) pathway, which is involved in the impairment of fracture healing. However, the role of low oxygen in fracture healing remains to be fully elucidated. In the present study, rats were divided into two groups and treated with CoCl 2 or saline, respectively. Rats with tibial fractures were sacrificed at 14, 28 and 42 days subsequent to fracture. Autoradiography was performed to measure healing of the bone tissue. In addition, the effects of cobalt chloride (CoCl 2 ) on the expression of two major angiogenic mediators, HIF-1α and vascular endothelial growth factor (VEGF), as well as the osteoblast markers runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP) and osteocalcin (OC) were determined at mRNA and protein levels by reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry. Systemic administration of CoCl 2 (15 mg/ kg/day intraperitoneally) significantly promoted fracture healing and mechanical strength. The present study demonstrated that in rats treated with CoCl 2 , the expression of HIF-1α, VEGF, Runx2, ALP and OC was significantly increased at mRNA and protein levels, and that CoCl 2 treatment enhances fracture repair in vivo. IntroductionTraumatic fractures are the most common type of injury in daily life. In the majority of clinical cases, the most simple fractures heal with minimal intervention; however, in severe fractures and in certain patient populations, including diabetics and patients with splintered fractures, impaired fracture healing and bone defects occur (1,2). In spite of numerous advances in every discipline of medicine, patients with complex bone injuries of the upper and lower extremities and are required to undergo prolonged reconstructive procedures for retrieval of their limb functions (2,3).It has been reported that the hypoxia-inducible factor (HIF) pathway is the central pathway for sensing and responding to alterations in local oxygen levels in a wide variety of organisms (4). Activation of the HIF-1α pathway can act as a critical mediator of neoangiogenesis, which is required for skeletal regeneration; thus, it is suggested that the application of HIF activators may be used as therapies to improve bone healing (4). An increasing number of studies suggested that hypoxia may be a powerful stimulus for bone cells via the mediation of angiogenesis [vascular endothelial growth factor (VEGF)], cellular metabolism (glucose transporter) and the recruitment of mesenchymal cells (MSCs) to areas of matrix damage (5-7). A more thorough understanding of hypoxia in bone healing will lead to the elucidation of cellular and molecular mechanisms that may aid in the development of protective therapies. CoCl 2 , a mimic of hypoxia, directly enhances HIF-1α stabilization and downstream target genes by inhibiting prolyl hydroxylase enzymes (8). An improved understanding of the alterations in gene expression that occur during fracture he...

Background/Aims: Hypoxia has been reported to regulate osteoblastic differentiation of bone cells and cartilage development. However, information concerning the molecular mechanisms remains largely unknown. Methods: The expression of miR-429 was evaluated by quantitative real-time PCR analysis. To test whether miR-429 directly regulate the expression level of ZFPM2 at transcription level, dual-luciferase reporter gene assay was performed. Western blotting was performed to detect osteogenesis related protein expression. The cell proliferation, apoptosis, alkaline phosphatase activity and matrix mineralization were performed to assess the functions of miR-429 in vitro and in vivo the effects of miR-429 on fracture healing. Results: Expression of miR-429 was increased in MC3T3-E1 cells treated with 200 μM CoCl₂ by qRT-PCR, and overexpression of miR-429 promoted cell differentiation, and enhanced alkaline phosphatase activity and matrix mineralization. Luciferase reporter assays suggested that miR-429 directly targets the 3'UTR of ZFPM2. In addition, knockdown of ZFPM2 could phenocopy the effects of miR-429 expression. Furthermore, overexpression of ZFPM2 in miR-429-expressing MC3T3-E1 cells suppressed cell differentiation. Conclusions: Our results provide valuable insight into the potential role of hypoxia in regulation of osteoblastic cell differentiation.

Background: Degenerative disorders of the lumbar spine decrease the mobility and quality of life of elderly patients. Lumbar fusion surgery is the primary method of treating degenerative lumbar spine disorders; however, the surgical stress response associated with major surgery has been linked to pathophysiological changes in the elderly, resulting in undesirable postoperative morbidity, complications, pain, fatigue, and extended convalescence. In the present study, we aimed to determine whether enhanced recovery after surgery significantly improved satisfaction and outcomes in elderly patients (> 65 years old) with short-level lumbar fusion. Methods: The study enrolled lumbar disc herniation or lumbar spinal stenosis patients if they were over the age of 65 years old underwent lumbar fusion at one or two levels. Data including demographic, comorbidity, and surgical information were collected from electronic medical records. Enhanced recovery after surgery interventions was categorized as preoperative, intraoperative, and postoperative. We also evaluated primary outcome, surgical complication, length of stay, postoperative pain scores, and 30-day readmission rates.