Studies have shown that high-energy focused extracorporeal shock wave therapy (HF-ESWT) has a certain therapeutic effect on glucocorticoid-induced osteonecrosis of the femoral head (ONFH). This study aimed to observe the efficacy and safety of HF-ESWT as a precautionary measure to reduce the probability of glucocorticoid-induced ONFH. A prospective randomized controlled trial was designed to evaluate whether HF-ESWT (Group A) can significantly prevent the incidence of glucocorticoid-induced ONFH relative to a control group without shockwave intervention (Group B). MRI was used to assess whether all participants experienced ONFH at 3, 6, and 12 months after the intervention. Continuous scoring was used to evaluate the intervention results: the 10-cm visual analog scale (VAS) was used to evaluate pain, and the hip Harris score (HHS) was used to evaluate the function of the hip joint. Any adverse events were recorded. 153 patients (89 females and 64 males) who had been allocated to group A (75 patients) or Group B (78 patients) were included in the final analysis. The patients were 45.0 ​± ​13.0 years old. There were significant differences between the two groups in MRI diagnosis of ONFH patients (2 cases in Group A, 9 cases in Group B; p ​= ​0.034). Significant differences between groups were found in bilateral hip function measured using the HHS at 6 months (Left p ​= ​0.026; Right p ​= ​0.033) and 12 months (Left p ​= ​0.018; Right p ​= ​0.038). However, there was no difference in the functional results measured at 3 months and the VAS at any points. This study confirms that HF-ESWT can be successfully used to reduce the probability of glucocorticoid-induced ONFH. Pain and hip dysfunction are common clinical manifestations when ONFH is unavoidable. Therefore, HF-ESWT can be recommended for the prevention and intervention of ONFH high-risk populations receiving high-dose glucocorticoid therapy. The effective prevention of HF-ESWT on ONFH after high-dose glucocorticoid application demonstrated its transformation potential as a preventive method in the clinical prevention of glucocorticoid-induced ONFH.

Background. Multiple reports have demonstrated the therapeutic potential of extracorporeal shock wave (ESWT) in osteonecrosis of the femoral head (ONFH). However, few studies reported the changes in hip articular cartilage after the intervention. This study aimed to investigate the effect of ESWT on femoral head cartilage using a novel technique, quantitative T2‐mapping magnetic resonance imaging. Methods. A total of 143 eligible patients with unilateral early‐stage ONFH were randomized into the ESWT group and control group. Seventy‐three patients in the ESWT group received two sessions of ESWT with oral drug treatment, while seventy patients in the control group received oral drug treatment only. The visual analog pain scale (VAS) and Harris hip score (HHS) at 3‐month, 6‐month, and 12‐month follow‐up were used as the clinical evaluation index. The radiological evaluation index used the T2 mapping values, necrotic size, and China‐Japan Friendship Hospital (CJFH) classification. Results. A total of 143 patients (62 females and 81 males) were finally included, and the characteristics before treatment were comparable between the two groups. At the last follow‐up (12 months), the T2 values and ΔT2 changes in the ESWT group were all smaller than those in the control group (p = 0.042; p = 0.039), while the CJFH classification of ONFH and necrotic lesion size were not statistically significant. At 3 months and 6 months, the VAS in the ESWT group was lower than that in the control group (p = 0.021; p = 0.046) and the HHS in the ESWT group was higher (p = 0.028; p = 0.039). However, there were no significant differences in the VAS and HHS at 12 months between the ESWT and control groups. Conclusions. The results of the current study indicated that, based on drug treatment, ESWT is an effective treatment method for nontraumatic ONFH, which could result in significant pain relief and function restoration. Furthermore, it could delay the injury of femoral head cartilage during the progression of ONFH.

With advances in materials science and biology, there have been continuing innovations in the field of artificial joint prostheses. Cementless prostheses have the advantages of long service life, easy revision, and good initial stability and are widely used in artificial joint replacement. Coatings are the key to cementless prostheses and are at the heart of their excellent functionality. This article mainly studies the clinical application of hydroxyapatite (HA) coating, standard porous coating represented by Porocoat coating, and new high-porosity coating represented by Gription coating. The clinical application and biological functionalization of different artificial joint prosthesis surface coatings are clarified, and it provides a reference for the clinical selection and development of different prosthesis surface coating materials.

Background: Traumatic brain injury (TBI) is a leading cause of death and long‐term disability worldwide. Secondary cerebral oedema, driven by neuroinflammation and blood–brain barrier (BBB) disruption, critically determines poor outcomes, yet effective targeted therapies remain absent. This study aimed to identify immune cell subsets associated with post‐TBI cerebral oedema and to explore their functional contributions in preclinical models. Methods: We integrated single‐cell transcriptomic datasets from a mouse TBI model (GSE175430) and human intracerebral haemorrhage (ICH) perihaematomal oedema samples (GSE266873) with our previously published temporal bulk RNA‐seq profiling data. Through cross‐species comparative analysis, Mfuzz clustering, AUCell scoring and gene set enrichment analysis (GSEA), Acp5 was identified as an oedema‐associated signature gene, and its macrophage‐enriched expression pattern was supported by single‐cell profiling and immunofluorescence colocalisation. Using the controlled cortical impact (CCI) model, we validated Acp5 expression dynamics across injury severities. Pharmacological inhibition (AubipyOMe) and genetic knockout of Acp5 were employed to assess brain oedema, neuroinflammation, neurological function and long‐term cognitive recovery. Results: A previously unrecognised population of ACP5‐positive monocytes/macrophages infiltrated the brain parenchyma within 1–3 days post‐injury, coinciding with peak oedema severity and neurological deficits. Inhibiting ACP5 significantly reduced brain water content, BBB leakage and proinflammatory cytokines, while improving sensorimotor function. Mechanistically, ACP5‐positive macrophages were associated with CSF2‐related JAK/STAT and NF‐κB signalling. Genetic Acp5 ablation attenuated acute macrophage infiltration and neuroinflammation, and was associated with improved long‐term behavioural outcomes. Conclusions: ACP5‐positive macrophages represent an injury‐associated myeloid population that contributes to neuroinflammatory and oedema‐related phenotypes after experimental TBI. Pharmacological and genetic findings provide preclinical evidence supporting further investigation of ACP5 and CSF2‐related signalling in secondary TBI injury.