特発性大腿骨頭壊死症

OBJECTIVE: To investigate the biomechanical characteristics of the CT-based lateral classification of Japanese Investigation Committee (JIC) type C1 osteonecrosis of the femoral head (ONFH) under different necrotic extents using finite element analysis, and to evaluate the validity of the CT-based lateral classification for assessing the risk of femoral head collapse. METHODS: A finite element model of the hip joint was established based on CT data from a healthy 35-year-old male volunteer. According to the JIC C1 classification criteria, three necrotic extents were defined in the coronal plane: M1 (30%), M2 (50%), and M3 (70%). According to the sagittal location of the necrotic lesion, the femoral head was equally divided into anterior, middle, and posterior regions, and five types of the CT-based lateral classification were defined: type 1, involvement of the anterior region only; type 2, involvement of the anterior and middle regions; type 3, involvement of the anterior, middle, and posterior regions; type 4, involvement of the middle and posterior regions; and type 5, involvement of the posterior region only. A total of 15 finite element models were constructed by combining the three necrotic extents with the five CT-based lateral classification types. Bilateral standing loading was simulated, and the maximum von Mises stress and maximum displacement of the femoral head surface and necrotic region were recorded. RESULTS: Stress concentration was mainly located in the superolateral region of the femoral head directly above the necrotic lesion, consistent with previous studies. Within the same CT-based lateral classification type, increases in necrotic extent from M1 to M3 were associated with significant increases in the maximum von Mises stress and maximum displacement of the femoral head surface, as well as the maximum displacement of the necrotic region. No significant difference was found in the maximum von Mises stress in the necrotic region among M1, M2, and M3 groups ( P>0.05). Except for the differences in the maximum von Mises stress on the femoral head surface between groups M2 and M3, and the differences in the maximum displacement in the necrosis region between groups M1 and M2 ( P>0.05), there were significant differences in the maximum von Mises stress on the femoral head surface, the maximum displacement on the femoral head surface, and the maximum displacement in the necrosis region between other groups ( P<0.05). At the same necrotic extent, the maximum von Mises stress and maximum displacement on the femoral head surface and in the necrosis region were significantly higher in type 3 than in other types; followed by type 2>type 1>type 4>type 5. Among them, there was no significant difference in the maximum von Mises stress on the femoral head surface between types 1 and 4, types 2 and 3, and the maximum displacement on the femoral head surface between types 1 and 2, types 2 and 3, types 4 and 5, as well as the maximum von Mises stress in the necrosis region between types 4 and 5, and the maximum displacement in the necrosis region between types 1 and 2, types 4 and 5, types 2 and 3, and types 4 and 5 ( P>0.05); all other comparisons between different types showed significant differences ( P<0.05). CONCLUSION: Both the location and extent of osteonecrosis affect the biomechanical stability of the femoral head, with lesion location, particularly involvement of the anterior weight-bearing region, exerting a greater influence on stress distribution. The CT-based lateral classification can effectively distinguish biomechanical differences associated with different necrotic locations and may provide a useful reference for evaluating the risk of femoral head collapse and guiding individualized treatment in patients with JIC type C1 ONFH.

BACKGROUND: Avascular necrosis of the femoral head, a known long-term complication following traumatic posterior hip dislocation, can result in femoral head collapse, osteochondral defects, and eventual posttraumatic osteoarthritis. This condition is especially problematic in young, active patients for whom total hip arthroplasty survivorship is a concern. Biologic treatments are therefore preferable to delay or avoid total hip arthroplasty. CASE REPORT: A 16-year-old male developed progressive left hip pain after a posterior dislocation sustained while playing football. The hip was emergently reduced. Imaging (x-ray, computed tomography, and magnetic resonance imaging [MRI]) showed a small depressed cortical fracture on the anterior and superior femoral head. Conservative treatment included protected weight-bearing for 6 weeks, knee immobilization to restrict hip flexion, physical therapy, and a home exercise program. However, symptoms worsened after 5 months of conservative care. Repeat MRI demonstrated avascular necrosis with associated cartilage loss, hip effusion, and femoroacetabular impingement (a cam deformity). Given the patient's young age, persistent symptoms, functional limitations, and radiographic findings, the decision was made to perform surgical intervention. Surgical hip dislocation via an anterolateral approach with a small trochanteric osteotomy (modified Hardinge approach) was used to expose the femoral head while maintaining the remaining blood supply. Fresh femoral head osteochondral allograft transplantation was performed, along with femoral neck osteoplasty to address the cam deformity. CONCLUSION: Osteochondral allograft transplantation is an effective technique to treat osteochondral defects of the femoral head in the setting of avascular necrosis following traumatic hip dislocation. This surgical option restores hip function and may delay or prevent total hip arthroplasty in young, active patients.

UNLABELLED: The classical "vascular occlusion" model does not fully account for osteonecrosis of the femoral head (ONFH). Femoral head collapse may progress despite restored perfusion, and ischemia alone cannot adequately explain steroid-associated ONFH. We propose that ONFH involves disruption of bone-vascular-immune homeostasis, with macrophage immunometabolic reprogramming in response to hypoxic and lipotoxic stress acting as a potential driver of inflammatory repair failure. Among the metabolic mechanisms implicated in ONFH, the strongest disease-specific evidence supports roles for hypoxia, oxidative stress, disordered lipid metabolism, macrophage imbalance, and ferroptosis-associated injury. By contrast, macrophage-specific glycolytic reprogramming, remodeling of the tricarboxylic acid (TCA) cycle, epigenetic fixation, osteomac dysfunction, and cuproptosis remain less well established. Regulated cell death pathways, particularly ferroptosis and pyroptosis, may exacerbate local tissue injury by releasing damage-associated molecular patterns (DAMPs) and inflammatory mediators that disrupt type H vessel-osteogenesis coupling and shift repair toward fibrosis. Establishing causal relationships rather than correlative associations will require lineage-tracing experiments, spatial validation, metabolic flux analyses, and genetic loss-of-function studies in ONFH models. THE TRANSLATIONAL POTENTIAL OF THIS ARTICLE: Viewing ONFH as an immunometabolic disorder identifies experimentally tractable targets beyond conventional anti-inflammatory strategies, including SLC7A11/GPX4-dependent ferroptosis defense, NLRP3 inflammasome signaling, and HIF-1α-associated macrophage metabolic adaptation. Extracellular vesicle- or biomaterial-based delivery systems designed for prolonged local retention should currently be considered experimental platforms for assessing lesion-specific target engagement in early-stage ONFH. Their clinical relevance must be established through ONFH-specific studies evaluating efficacy, safety, biodistribution, manufacturability, and long-term structural outcomes.

Legg-Calvé-Perthes disease (LCPD) is an idiopathic paediatric osteonecrosis characterized by avascular injury to the femoral head, resulting in structural collapse and early osteoarthritis. Although mesenchymal stem cell (MSC) dysfunction has been implicated, the underlying mechanisms remain unclear due to the absence of human disease models. Here, we generated patient-specific induced pluripotent stem cells (iPSCs) from dermal fibroblasts of LCPD patients and differentiated them into mesenchymal stem cells (iMSCs) to establish an in vitro platform for mechanistic interrogation. LCPD-iMSCs exhibited hallmark disease-associated phenotypes, including concurrent suppression of osteogenic, adipogenic and chondrogenic differentiation, accompanied by enhanced phosphorylation of GSK3α/β, reduced β-catenin abundance and attenuated canonical Wnt signalling. Transcriptomic analyses revealed alterations in extracellular matrix organization, adhesion pathways and PI3K-Akt/MAPK signalling, consistent with a cellular environment predisposed to impaired mesenchymal function. Pharmacological inhibition of GSK3 using lithium chloride restored β-catenin levels, improved osteogenic and adipogenic marker expression, and enhanced matrix deposition, demonstrating functional reversibility of the LCPD phenotype. These findings identify GSK3-mediated β-catenin destabilization as a central regulator of MSC lineage impairment in LCPD and establish a patient-derived iPSC-MSC model as a valuable platform for mechanistic and therapeutic exploration in paediatric osteonecrosis.

ObjectiveBlood loss and postoperative anemia are common complications following total hip arthroplasty. Patients with hematologic disorders are at an increased risk of perioperative complications, especially those related to bleeding. This study aimed to investigate the impact of hematologic disorders on blood loss after total hip arthroplasty.MethodsThis single-center, matched retrospective cohort study included 64 patients who had undergone unilateral total hip arthroplasty for osteonecrosis of the femoral head. Patients were allocated in a 1:1 matched design to a control or a hematologic disorders group. Primary outcomes included postoperative red blood cell count, hemoglobin level, reductions in red blood cell count and hemoglobin level, postoperative drainage volume, transfusion rate, and estimated blood loss. Secondary outcomes comprised postoperative white blood cell and platelet counts, maximum perioperative changes, operative duration, length of hospital stay, and the incidence of lower-extremity deep venous thrombosis.ResultsPostoperative red blood cell counts and hemoglobin levels were significantly lower in the hematologic disorders group, and reduction in both parameters was more pronounced in this cohort. The rate of blood transfusion was also significantly higher in the hematologic disorders group. Postoperative white blood cell and platelet counts and perioperative changes in white blood cell counts were less favorable among patients with hematologic disorders. No statistically significant differences were detected in the operative duration, hospital stay, postoperative drainage volume, estimated blood loss, or incidence of lower-extremity deep venous thrombosis.ConclusionsPerioperative blood management following total hip arthroplasty may be more challenging in patients with hematologic disorders. Enhanced and targeted blood management strategies are warranted in this patient population.