Corticosteroid-induced Osteonecrosis Of Femoral Head Research Articles

Autologous bone plug-sliding with core decompression and bone marrow aspirate concentrate application: a joint-preserving surgical technique for corticosteroid-induced osteonecrosis of femoral head.

This study aimed to describe a surgical procedure for the management of corticosteroid-induced osteonecrosis of the femoral head (ONFH) and report its clinical results. The technique included harvesting a bone plug from the lateral femoral neck, core decompression, and bone marrow aspirate concentrate (BMAC) application; the procedure was completed by press-fit insertion of the autologous bone plug in the debrided area. Autologous bone plug-sliding with core decompression and bone marrow concentrate aspirate application provides good clinical outcomes in the management of ONFH. A retrospective review was performed using records of patients operated on between October 2019 and June 2021. Only patients with Ficat-Arlet stage-2 ONFH, who underwent the procedure described, were included. Twenty- nine hips (18 patients) were included and evaluated clinically and radiologically. Clinical evaluation included the Harris hip score (HHS) and Visual analogue scale (VAS) for pain, while radiological evaluation included direct radiographs. The average age was 39.8 years (± 11.7, range: 24-65 years). The average follow-up was 13.5 months (± 3.4, range: 8-19 months). There were improvements in the VAS pain and Harris hip scores in all patients. Average HHS increased from 61.90 to 87.45 (p < 0.001), while the average VAS pain score decreased from 7.14 to 3.27 (p < 0.001). No complications were encountered in any of the patients during the follow-up. None of the patients had femoral head collapse on the latest radiograph or required total hip replacement. The combination of the novel autologous bone plug-sliding method with conventional regenerative methods is a successful treatment choice for ONFH.

Decreased Proliferation of Mesenchymal Stem Cells in Corticosteroid-induced Osteonecrosis of Femoral Head

The ability of self-repair in patients with corticosteroid-induced osteonecrosis of the femoral head is limited, and it has been suggested the cause is likely relevant to the poor proliferation activity of mesenchymal stem cells in the femoral head region. This study measured the number and proliferation activity of human mesenchymal stem cells in patients both with and without corticosteroid-induced osteonecrosis of the femoral head. Bone marrow was collected from the proximal femur in patients with steroid-induced osteonecrosis of the femoral head (osteonecrosis group, n=18) and patients with new femoral neck fractures without osteonecrosis (control group, n=11). Mesenchymal stem cells were isolated by density gradient centrifugation, and then selected by the adhesive method. The MTT reduction assay method was used to evaluate the level of proliferation. Cells from osteonecrosis patients showed reduced proliferation ability compared with the control patients. The percentage of cells in the S+G2/M phase was decreased significantly (P<.01) in the osteonecrosis group. The decreased proliferation ability of mesenchymal stem cells may play a role in the low repair capacity of steroid-induced osteonecrosis of femoral head. The altered function of mesenchymal stem cells may be responsible for the pathogenesis and progression of osteonecrosis.

Decreased Proliferation of Mesenchymal Stem Cells in Corticosteroid-Induced Osteonecrosis of Femoral Head

The ability of self-repair in patients with corticosteroid-induced osteonecrosis of the femoral head is limited, and it has been suggested the cause is likely relevant to the poor proliferation activity of mesenchymal stem cells in the femoral head region. This study measured the number and proliferation activity of human mesenchymal stem cells in patients both with and without corticosteroid-induced osteonecrosis of the femoral head. Bone marrow was collected from the proximal femur in patients with steroid-induced osteonecrosis of the femoral head (osteonecrosis group, n=18) and patients with new femoral neck fractures without osteonecrosis (control group, n=11). Mesenchymal stem cells were isolated by density gradient centrifugation, and then selected by the adhesive method. The MTT reduction assay method was used to evaluate the level of proliferation. Cells from osteonecrosis patients showed reduced proliferation ability compared with the control patients. The percentage of cells in the S+G 2 /M phase was decreased significantly ( P &lt;.01) in the osteonecrosis group. The decreased proliferation ability of mesenchymal stem cells may play a role in the low repair capacity of steroid-induced osteonecrosis of femoral head. The altered function of mesenchymal stem cells may be responsible for the pathogenesis and progression of osteonecrosis.

Very early development of steroid-associated osteonecrosis of femoral head in systemic lupus erythematosus: prospective study by MRI

The objective of this study was to define prospectively the early development of corticosteroid-induced osteonecrosis of femoral head (ONF) in patients with systemic lupus erythematosus (SLE) and to identify the association of initial steroid treatment with the development of early (silent) ONE Forty-five patients who were newly diagnosed as having SLE and required 40 mg/day or more prednisolone were enrolled. To detect silent ONF, examinations using magnetic resonance imaging (MRI) were done three months after starting steroid therapy, followed by every year's MRI and plain radiography for over five years. Clinical and laboratory data were compared between silent ONF and non-ONF groups. Of 45 patients, 15 (33%) developed silent ONF and five (11%) symptomatic ONE It was of interest that MRI detected silent ONF very early (by three months) in 14 patients (93%). It should be noted that pulse therapy with 1000 mg/day methylprednisolone was found to be done very frequently (13 of 15, 87%) in the silent ONF group compared to non-ONF group (11 of 30, 37%) (P < 0.01) although other clinical features were not significantly different between both groups. High dose corticosteroids caused elevation of serum levels of total cholesterol, albumin, and leukocyte count in most of patients. The degree of elevation of those parameters at one or three months was more prominent in the silent ONF group. In particular, the change ratio of total cholesterol at one month was outstanding in the silent ONF group compared to non-ONF group (0.551 versus 0.374, P < 0.05). In conclusion, pathological ONF develops very early in one-third of SLE patients who received high dose corticosteroids and steroid pulse therapy could be a significant risk factor. An abrupt elevation of serum total cholesterol and/or sensitivity to steroids seem to be associated with the pathogenesis of ONF.