Angiogenesis and osteogenesis are coupled. However, the cellular and molecular regulation of these processes remains to be further investigated. Both tissues have recently been recognized as endocrine organs, which has stimulated research interest in the screening and functional identification of novel paracrine factors from both tissues. This review aims to elaborate on the novelty and significance of endocrine regulatory loops between bone and the vasculature. In addition, research progress related to the bone vasculature, vessel-related skeletal diseases, pathological conditions, and angiogenesis-targeted therapeutic strategies are also summarized. With respect to future perspectives, new techniques such as single-cell sequencing, which can be used to show the cellular diversity and plasticity of both tissues, are facilitating progress in this field. Moreover, extracellular vesicle-mediated nuclear acid communication deserves further investigation. In conclusion, a deeper understanding of the cellular and molecular regulation of angiogenesis and osteogenesis coupling may offer an opportunity to identify new therapeutic targets.

Background: The prognostic nutritional index (PNI) has been proposed as a useful prognostic tool in multiple populations. However, its prognostic value has not been fully evaluated in the hip fracture population. We aimed to assess the relationship between PNI and postoperative complications as well as 2-year all-cause mortality in the hip fracture population. Materials and Methods: We included patients aged 45 or older who underwent surgery for hip fracture between 2000 and 2022. The baseline serum albumin and total lymphocyte count were used to calculate PNI with the following formula: 10×serum albumin level (g/dl)+0.005×total lymphocyte count (per mm³). Patients were classified into low, medium, and high categories based on tertiles of PNI (≤43.23, 43.23–47.35, and >47.35, respectively). Logistic regression and Cox proportional hazards models were used to calculate the odds ratio (OR) for postoperative compilations and the hazard ratio (HR) for mortality, adjusting for potential confounders. Results: Of 3351 hip patients, 236 (7.04%) developed postoperative complications, and 305 (9.10%) died during the 2-year follow-up. Compared to the low-category patients, the medium-category and high-category patients showed lower odds of postoperative complications (ORs 0.69, 95% CI 0.48–0.98; and 0.61, 95% CI 0.40–0.93, respectively), and lower hazards of 2-year mortality (HRs 0.66, 95% CI 0.49–0.88; and 0.61, 95% CI 0.42–0.88, respectively). These associations were robust across a series of analyses, including subgroup analyses and dose–response sensitivity analyses. Conclusion: PNI is an independent predictor of postoperative complications and 2-year all-cause mortality in hip fracture patients. PNI can be used to identify patients who may be at high risk of a poor prognosis.

Displaced femoral neck fractures in young adults are most likely to result from high energy trauma that causes a vertically-oriented shearing injury through the femoral neck. The optimal strategy for treatment of displaced femoral neck fractures remains an unsolved challenge in orthopedic surgery. our group has previously designed a medial anatomical buttress plate (MABP) based on the analysis of the computed tomography (CT) data of anatomical structures derived from a large sample population. In this study, finite element analyses (FEA) were carried out to compare the outcomes of the combination of our MABP with cannulated screws to those of the combination of tubular plate with cannulated screws, and to those of using cannulated screws alone. MABP resulted in a more stable fixation as compared to the other two approaches, with respect to the femur and the stress distributions, stress peaks, and Z axis displacements. The FEA encouraged us that addition of a medial buttress plate not only achieved superior medial buttress stability but also achieves superior performance because it perfectly fits with the existing anatomic structure of medial femoral neck. The results from our study may provide references for clinical decision making in dealing with such patients.

Current surgical interventions for the femoral neck fracture are using either cannulated screws (CCS) or a single large screw at a fixed angle with a side-plate (i.e., a sliding hip screw, AKA dynamic hip screw, DHS). Despite these interventions, the need for reoperation remains high (10.0–48.8%) and largely unchanged over the past 30 years. Femoral neck fracture is associated with substantial morbidity, mortality, and costs. In this study, our group designed a plate that combines the strength of both CCS and sliding hip screw, through providing three dynamic screws at a fixed angle with a side-plate, namely the slide compression anatomic place-femoral neck (SCAP-FN). Finite element analyses (FEA) were carried out to compare the outcomes of the combination of our SCAP-FN plate with DHS+DS (derotational screw) and to those of using cannulated screws alone. SCAP-FN produces more stable fixation with respect to the femur and the stress distributions, stress peaks, and rotational angles. The FEA encouraged us that in the following biomechanical experiment, SCAP-FN may remain the strengths of both CCS and DHS+DS and show a better performance in resisting shearing and rotational forces, therefore achieving the best stability in terms of smallest displacement and rotational angle.

Systematic bone and muscle loss is a complex metabolic disease, which is frequently linked to gut dysfunction, yet its etiology and treatment remain elusive. While probiotics show promise in managing diseases through microbiome modulation, their therapeutic impact on gut dysfunction-induced bone and muscle loss remains to be elucidated. Employing dextran sulfate sodium (DSS)-induced gut dysfunction model and wide-spectrum antibiotics (ABX)-treated mice model, our study revealed that gut dysfunction instigates muscle and bone loss, accompanied by microbial imbalances. Importantly, Bifidobacterium animalis subsp. lactis A6 (B. lactis A6) administration significantly ameliorated muscle and bone loss by modulating gut microbiota composition and enhancing butyrate-producing bacteria. This intervention effectively restored depleted butyrate levels in serum, muscle, and bone tissues caused by gut dysfunction. Furthermore, butyrate supplementation mitigated musculoskeletal loss by repairing the damaged intestinal barrier and enriching beneficial butyrate-producing bacteria. Importantly, butyrate inhibited the NF-κB pathway activation, and reduced the secretion of corresponding inflammatory factors in T cells. Our study highlights the critical role of dysbiosis in gut dysfunction-induced musculoskeletal loss and underscores the therapeutic potential of B. lactis A6. These discoveries offer new microbiome directions for translational and clinical research, providing promising strategies for preventing and managing musculoskeletal diseases.

Degenerative musculoskeletal diseases (DMDs), including osteoporosis, osteoarthritis, degenerative disc disease, and sarcopenia, present major challenges in the aging population. Patients with DMDs present with pain, functional decline, and reduced exercise tolerance, which result in long‐term or permanent deficits in their ability to perform daily activities. Current strategies for dealing with this cluster of diseases focus on relieving pain, but they have a limited capacity to repair function or regenerate tissue. Cell‐based therapies have attracted considerable attention in recent years owing to their unique mechanisms of action and remarkable effects on regeneration. In this review, current experimental attempts to use cell‐based therapies for DMDs are highlighted, and the modes of action of different cell types and their derivatives, such as exosomes, are generalized. In addition, the latest findings from state‐of‐the‐art clinical trials are reviewed, approaches to improve the efficiency of cell‐based therapies are summarized, and unresolved questions and potential future research directions for the translation of cell‐based therapies are identified.