Predicting fracture classification and prognosis with hounsfield units and femoral cortical index: A simple and cost-effective approach.

BACKGROUND: The relationship between bone density and fracture has been widely studied and recognized, and the role of cortical bone in proximal femoral fractures has also been increasingly studied. However, both the determination of bone mineral density (BMD) and the determination of cortical mass are expensive and cumbersome. The purpose of this study is to investigate whether two readily available indicators, Hounsfield Units (HUs) and femoral cortical index (FCI), can be used to predict hip fracture classification and prognosis. METHODS: A retrospective study was conducted on 110 patients with hip fragility fractures. Cortical index was calculated on fractured and contralateral femur FCI, with HUs calculated on the proximal femur. The correlation of the FCI and HU with diabetes, hypertension, and related indicators, such as albumin, creatinine, and urea nitrogen levels, were also analyzed in the study. RESULTS: Both the Evans classification of intertrochanteric fractures and the Garden and Pauwels classifications of femoral neck fractures showed that as the severity of the fracture increased, the HUs and FCI decreased. Age and albumin level also had a negative correlation with HUs and FCI. There was also a significant correlation between HUs and FCI. CONCLUSIONS: The HUs and FCI, which can be easily and quickly obtained, can be used to predict the classification and prognosis of hip fractures.

PPARδ agonist protects against osteoarthritis by activating AKT/mTOR signaling pathway-mediated autophagy.

Osteoarthritis (OA) is the most prevalent degenerative joint disease, and PPARs are involved in its pathogenesis; however, the specific mechanisms by which changes in PPARδ impact the OA pathogenesis yet to be discovered. The purpose of this study was to ascertain how PPARδ affects the onset and development of OA. In vitro, we found that PPARδ activation ameliorated apoptosis and extracellular matrix (ECM) degradation in OA chondrocytes stimulated by IL-1ß. In addition, PPARδ activation may modulate AKT/mTOR signaling to partially regulate chondrocyte autophagy and apoptosis. In vivo, injection of PPARδ agonist into the articular cavity improved ECM degradation, apoptosis and autophagy in rats OA models generated by destabilization medial meniscus (DMM), eventually delayed degeneration of articular cartilage. Thus, targeting PPARδ for OA treatment may be a possibility.

Oleic and linoleic acids promote chondrocyte apoptosis by inhibiting autophagy via downregulation of SIRT1/FOXO1 signaling.

Osteoarthritis (OA) is a complex joint disease that currently has no cure. OA involves metabolic disorders in chondrocytes and an imbalance between autophagy and apoptosis. As a common risk factor for OA, obesity induces changes in the fatty acid composition of synovial fluid, thereby disturbing chondrocyte homeostasis. However, whether unsaturated fatty acids affect the development of OA by regulating chondrocyte autophagy remains unclear. This study aimed to determine the effects of oleic and linoleic acids on chondrocyte autophagy and related mechanisms. Based on the mass spectrometry results, the levels of multiple unsaturated fatty acids, including oleic and linoleic acids, in the synovial fluid of patients with OA and obesity were significantly higher than those in patients with OA only. Moreover, we found that FOXO1 and SIRT1 were downregulated after oleic and linoleic acids treatment of chondrocytes, which inhibited chondrocyte autophagy. Importantly, the upregulation of SIRT1 and FOXO1 expression not only increased the level of autophagy but also improved the expression of chondrocyte extracellular matrix proteins. Furthermore, upregulated SIRT1 and FOXO1 expression alleviated the destruction of the articular cartilage in an OA rat model. Our results suggest that SIRT1/FOXO1 signaling can alleviate oleic acid- and linoleic acid-induced cartilage degradation both in vitro and in vivo and that the SIRT1/FOXO1 pathway may serve as an effective treatment target for inhibiting OA progression.

Accurate reduction of medial arch fracture fragments in intertrochanteric fractures: A novel technical note.

Intramedullary fixation is currently used to stabilize intertrochanteric fractures. Surgical reduction of the medial arch cortex is crucial to achieve stabilization of the internal fixation system, however, it is challenging to perform. To ensure anatomical reduction, we developed a novel surgical technique to assist in achieving accurate and convenient reduction. In this technique, right-angle forceps were used to pry and reset medial arch cortex fragments via a mini-helical blade incision. Noteworthily, all patients who underwent this technique achieved anatomical reduction with reduced operation times and bleeding. Our article illustrates intraoperative reduction techniques and summarizes tips and tricks that may be beneficial and educative for orthopedists.

Forkhead box O3 attenuates osteoarthritis by suppressing ferroptosis through inactivation of NF-κB/MAPK signaling.

Background: Ferroptosis is a nonapoptotic cell death process that is characterized by lipid peroxidation and intracellular iron accumulation. As osteoarthritis (OA) progresses, inflammation or iron overload induces ferroptosis of chondrocytes. However, the genes that play a vital role in this process are still poorly studied. Methods: Ferroptosis was elicited in the ATDC5 chondrocyte cell line and primary chondrocytes by administration of the proinflammatory cytokines, interleukin (IL)-1ß and tumor necrosis factor (TNF)-α, which play key roles in OA. The effect of FOXO3 expression on apoptosis, extracellular matrix (ECM) metabolism, and ferroptosis in ATDC5 cells and primary chondrocytes was verified by western blot, Immunohistochemistry (IMHC), immunofluorescence (IF) and measuring Malondialdehyde (MDA) and Glutathione (GSH) levels. The signal cascades that modulated FOXO3-mediated ferroptosis were identified by using chemical agonists/antagonists and lentivirus. In vivo experiments were performed following destabilization of medial meniscus surgery on 8-week-old C57BL/6 mice and included micro-computed tomography measurements. Results: In vitro administration of IL-1ß and TNF-α, to ATDC5 cells or primary chondrocytes induced ferroptosis. In addition, the ferroptosis agonist, erastin, and the ferroptosis inhibitor, ferrostatin-1, downregulated or upregulated the protein expression of forkhead box O3 (FOXO3), respectively. This, suggested, for the first time, that FOXO3 may regulate ferroptosis in articular cartilage. Our results further suggested that FOXO3 regulated ECM metabolism via the ferroptosis mechanism in ATDC5 cells and primary chondrocytes. Moreover, a role for the NF-κB/mitogen-activated protein kinase (MAPK) signaling cascade in regulating FOXO3 and ferroptosis was demonstrated. In vivo experiments confirmed the rescue effect of intra-articular injection of a FOXO3-overexpressing lentivirus against erastin-aggravated OA. Conclusions: The results of our study show that the activation of ferroptosis promotes chondrocyte death and disrupts the ECM both in vivo and in vitro. In addition, FOXO3 can reduce OA progression by inhibiting ferroptosis through the NF-κB/MAPK signaling pathway. The Translational potential of this article: This study highlights the important role of chondrocyte ferroptosis regulated by FOXO3 through the NF-κB/MAPK signaling in the progression of OA. The inhibition of chondrocyte ferroptosis by activating FOXO3 is expected to be a new target for the treatment of OA.

CircFOXO3 protects against osteoarthritis by targeting its parental gene FOXO3 and activating PI3K/AKT-mediated autophagy.

Osteoarthritis (OA) is a degenerative joint disorder causing pain and functional disability. Emerging evidence reveals that circular RNAs (circRNAs) play essential roles in OA progression and development. This study aimed to investigate the role of a novel circRNA factor, circFOXO3, in the progression of OA and elucidate its underlying molecular mechanism. The function of circFOXO3 in OA and interaction between circFOXO3 and its downstream mRNA target, forkhead box O3 (FOXO3), were evaluated by western blot (WB), immunofluorescence (IF), RNA immunoprecipitation, reverse transcription-quantitative PCR (RT-qPCR), and fluorescence in situ hybridization (FISH). Upregulation of circFOXO3 and autophagic flux were detected both in vivo and in vitro by WB, transmission electron microscopy (TEM), IF, and immunohistochemistry (IHC). A mouse model of OA was also used to confirm the role of circFOXO3 in OA pathogenesis in vivo. Decreased expression of circFOXO3 in OA cartilage tissues was directly associated with excessive apoptosis and imbalance between anabolic and catabolic factors of the extracellular matrix (ECM). Mechanistically, circFOXO3 functioned in cartilage by targeting its parental gene FOXO3 and activating autophagy. Intra-articular injection of lentivirus-circFOXO3 alleviated OA in the mouse model. In conclusion, our results reveal the key role played by circFOXO3 in OA progression; circFOXO3 overexpression may alleviate apoptosis of chondrocytes and promote anabolism of the ECM via activation of FOXO3 and autophagy, providing a potentially effective novel therapeutic strategy for OA.

Factors Associated With the Accuracy of Depth Gauge Measurements.

Background: It is important to select appropriate screws in orthopedic surgeries, as excessively long or too short a screw may results failure of the surgeries. This study explored factors that affect the accuracy of measurements in terms of the experience of the surgeons, passage of drilled holes and different depth gauges. Methods: Holes were drilled into fresh porcine femurs with skin in three passages, straight drilling through the metaphysis, straight drilling through the diaphysis, and angled drilling through the diaphysis. Surgeons with different surgical experiences measured the holes with the same depth gauge and using a vernier caliper as gold standard. The length of selected screws, and the time each surgeon spent were recorded. The measurement accuracy was compared based on the experiences of the surgeons and the passage of drilled holes. Further, parameters of depth gauges and 12-mm cortical bone screws from five different manufacturers were measured. Results: A total of 13 surgeons participated in 585 measurements in this study, and each surgeon completed 45 measurements. For the surgeons in the senior, intermediate, and junior groups, the average time spent in measurements was 689, 833, and 785 s with an accuracy of 57.0, 42.2, and 31.5%, respectively. The accuracy and measurement efficiency were significantly different among the groups of surgeons (P < 0.001). The accuracy of measurements was 45.1% for straight metaphyseal drilling, 43.6% for straight diaphyseal drilling, and 33.3% for angled diaphyseal drilling (P = 0.036). Parameters of depth gauges and screws varied among different manufacturers. Conclusion: Both observer factor and objective factors could affect the accuracy of depth gauge measurement. Increased surgeon's experience was associated with improvements in the accuracy rate and measurement efficiency of drilled holes based on the depth gauge. The accuracy rate varied with hole passages, being the lowest for angled drilled holes.