Kazuyuki Karasuyama

The role of sclerotic changes in the starting mechanisms of collapse: A histomorphometric and FEM study on the femoral head of osteonecrosis

PURPOSE To assess the distributions of stress, strain, and fractured areas using a finite element model (FEM), and examine the osteoclastic activity histopathologically in osteonecrosis of the femoral head. METHODS Three femoral heads were obtained during hip arthroplasty for femoral head osteonecrosis. One sample with a normal area, two samples with a non-sclerotic boundary without collapse (Type 1), two samples with a non-collapsed sclerotic boundary (Type 2), and two samples with a collapsed sclerotic boundary (Type 3) were collected from each femoral head for the FEM and histopathological analyses. FEM was performed using CT data, and the distributions of von Mises equivalent stress, octahedral shear stress, octahedral shear strain, and simulated fractured area were evaluated. Furthermore, the osteoclast count at the boundary was compared for each type. RESULTS In normal and Type 1 samples, the distributions of von Mises equivalent stress, octahedral shear stress, octahedral shear strain, and the fractured area were equally concentrated along the whole analytical range; however, in the Type 2 and 3 samples, they were concentrated along the thickened bone trabeculae at the boundary, which corresponded to the fractured area. Histopathologically, a significantly increased osteoclast number was observed only at the collapsed sclerotic boundary. CONCLUSION These results demonstrated that both shear stress and shear strain tend to be concentrated on thickened bone trabeculae at the boundary. Fracture analyses revealed that the boundary of sclerotic changes, which results from the repair process, may be the starting point of the fracture. Additionally, the osteoclastic activity increases after collapse.

Impaired differentiation of macrophage lineage cells attenuates bone remodeling and inflammatory angiogenesis in Ndrg1 deficient mice

N-myc downstream regulated gene 1 (NDRG1) is a responsible gene for a hereditary motor and sensory neuropathy-Lom (Charcot–Marie–Tooth disease type 4D). This is the first study aiming to assess the contribution of NDRG1 to differentiation of macrophage lineage cells, which has important implications for bone remodeling and inflammatory angiogenesis. Ndrg1 knockout (KO) mice exhibited abnormal curvature of the spine, high trabecular bone mass, and reduced number of osteoclasts. We observed that serum levels of macrophage colony-stimulating factor (M-CSF) and macrophage-related cytokines were markedly decreased in KO mice. Differentiation of bone marrow (BM) cells into osteoclasts, M1/M2-type macrophages and dendritic cells was all impaired. Furthermore, KO mice also showed reduced tumor growth and angiogenesis by cancer cells, accompanied by decreased infiltration of tumor-associated macrophages. The transfer of BM-derived macrophages from KO mice into BM-eradicated wild type (WT) mice induced much less tumor angiogenesis than observed in WT mice. Angiogenesis in corneas in response to inflammatory stimuli was also suppressed with decreased infiltration of macrophages. Taken together, these results indicate that NDRG1 deficiency attenuates the differentiation of macrophage lineage cells, suppressing bone remodeling and inflammatory angiogenesis. This study strongly suggests the crucial role of NDRG1 in differentiation process for macrophages.

Contralateral osteonecrosis of the femoral head newly developed after increasing the dose of corticosteroids

Nontraumatic osteonecrosis of the femoral head (ONFH) is a debilitating disorder that commonly affects 30to 50-year-old individuals, with corticosteroid use being one of the major causative factors [1]. Although the precise pathogenesis of corticosteroid-induced ONFH remains unclear, both high-dose oral corticosteroid therapy and corticosteroid pulse treatment have been reported to be risk factors, highlighting the importance of the dose of corticosteroids in the development of corticosteroid-induced osteonecrosis [2–7]. Corticosteroid-induced osteonecrosis often affects both femoral heads (50–70 %), and bilateral ONFH is considered to develop concurrently [1, 2]. In contrast, in patients with unilateral ONFH, it is rare that new osteonecrotic lesions subsequently develop in the contralateral femoral head. To our knowledge, there are no reports in the literature regarding the development of new corticosteroidinduced ONFH lesions on the contralateral side. Here we report the case of a patient who developed new ONFH in the contralateral hip after increasing the dose of corticosteroids for a different underlying disease. We clearly indicate that written informed consent for publication was obtained from the patient. Case report

Common site of subchondral insufficiency fractures of the femoral head based on three-dimensional magnetic resonance imaging

ObjectivesThe objective of this study was to investigate the common sites of subchondral insufficiency fractures of the femoral head (SIF) based on three-dimensional (3-D) reconstruction of MR images.Materials and methodsIn 33 hips of 31 consecutive patients diagnosed with SIF, 3-D reconstruction of the bone, fracture, and acetabular edge was performed using MR images. These 3-D images were used to measure the fractured areas and clarify the positional relationship between the fracture and degree of acetabular coverage.ResultsThe fractured area in the anterior portion was significantly larger than in the posterior area. In 11 cases, the fractures contacted the acetabular edge and were distributed on the lateral portion. The indices of acetabular coverage (center-edge angle and acetabular head index) in these cases were less than the normal range. In the remaining 22 cases, the fractures were apart from the acetabular edge and distributed on the mediolateral centerline of the femoral head. The majority of these cases had normal acetabular coverage.ConclusionsThe common site of SIF is the anterior portion. In addition, two types of SIF are proposed: (1) Lateral type: the contact stress between the acetabular edge and lateral portion of the femoral head causes SIF based on the insufficient acetabular coverage, and (2) Central type: the contact stress between the acetabular surface and the mediolateral center of the femoral head causes SIF independent from the insufficiency of acetabular coverage. These findings may be useful for considering the treatment and prevention of SIF.

Bone SPECT/CT of Femoral Head Subchondral Insufficiency Fracture.

Subchondral insufficiency fracture of the femoral head may be confused with osteonecrosis, mainly because of radiological overlap. SPECT/CT with Tc-99 m hydroxymethylene diphosphonate images in 7 patients with subchondral insufficiency fracture were retrospectively reviewed and compared with those from 11 patients with symptomatic early osteonecrosis. In all of the hips with subchondral insufficiency fracture, SPECT/CT showed increased uptake at the subchondral lesions of the femoral head. On the other hand, in all of the hips with osteonecrosis, absence of uptake was confirmed at the subchondral lesions. SPECT/CT may assist in differentiating subchondral insufficiency fracture from osteonecrosis.

Genome-wide Association Study of Idiopathic Osteonecrosis of the Femoral Head

Idiopathic osteonecrosis of the femoral head (IONFH) is an ischemic disorder that causes bone necrosis of the femoral head, resulting in hip joint dysfunction. IONFH is a polygenic disease and steroid and alcohol have already known to increase its risk; however, the mechanism of IONFH remains to be elucidated. We performed a genome-wide association study using ~60,000 subjects and found two novel loci on chromosome 20q12 and 12q24. Big data analyses identified LINC01370 as a candidate susceptibility gene in the 20q12 locus. Stratified analysis by IONFH risk factors suggested that the 12q24 locus was associated with IONFH through drinking capacity. Our findings would shed new light on pathophysiology of IONFH.

Osteonecrosis of the Femoral Head with Collapsed Medial Lesion

A 60-year-old female experienced the gradual onset of left hip pain without any triggering event. Radiographs showed vertical sclerosis in the center of the femoral head and the lesion inside the boundary demonstrated diffuse bony sclerosis. No collapse was observed at the weight-bearing portion on radiograph. However, computed tomography showed a subchondral collapse at the medial lesion. On T2-weighted magnetic resonance imaging, the necrotic lesion showed diffuse high-intensity signals that indicated a prominent repair process. Bone biopsy diagnosed osteonecrosis with associated prominent appositional bone and vascular granulation tissue.

Osteonecrosis of the femoral head extending into the femoral neck

Osteonecrosis of the femoral head (ONFH) is an ischemic disorder that can lead to femoral head collapse and secondary osteoarthritis. Although the condition is usually limited to the femoral head, we report a rare case of biopsy-proven ONFH extending into the femoral neck, which required hip replacement surgery. We emphasize the imaging features of this condition and briefly discuss its potential relevance.

Computed tomography findings of subchondral insufficiency fractures of the femoral head

Objectives The objective of this study was to describe the appearance of Subchondral insufficiency fracture (SIF) by computed tomography (CT). Methods Images of 52 consecutive patients diagnosed with SIF were retrospectively reviewed. CT was available for five patients (7 cases). Results Corresponding to a low-intensity band on MR images, a radiolucent or sclerotic band was observed on CT images. Conclusion The present study is the first to report CT findings of SIF. A radiolucent or sclerotic band was observed on CT images. The results of the present study provide useful information for diagnosis of SIF.

Transient epiphyseal lesion of the femoral head after traumatic hip dislocation: A case report

Highlights • We report a transient epiphyseal lesion of femoral head after hip dislocation.• On MRI performed two days after dislocation, no bony injuries were observed.• Hip pain and a transient epiphyseal lesion appeared four months after dislocation.• Hip pain and a transient lesion disappeared after two-month conservative therapy.• Prolonged rest after the injury may contribute to an insufficiency fracture.