Relationship of α2‐Macroglobulin with Steroid‐Induced Femoral Head Necrosis: A Chinese Population‐Based Association Study in Southeast China

Abstract

Objective The present study aimed to identify the relationship of α‐2‐macroglobulin and microvascular vessel pathology with steroid‐induced femoral head necrosis in the Southeast Chinese population. Methods This study enrolled 40 patients diagnosed with steroid‐induced necrosis of the femoral head. Patients had various stages of femoral head necrosis. The differential expression of serum proteins and mRNA from patients with steroid‐induced necrosis of the femoral head (SINFH) and healthy volunteers was analyzed by western blot and quantitative polymerase chain reaction (QT‐PCR). The pathological change in osteocyte necrosis was indicated by hematoxylin and eosin stain and immunohistochemistry. Results Hematoxylin and eosin stain showed histopathology changes in the necrotic area of patients with steroid‐induced INFH: bone trabeculae were fewer and thinner, became broken, fragmented and structurally disordered; intraosseous adipose cells became enlarged; the arrangement of the osteoblasts became irregular; and vacant bone lacunae increased. QT‐PCR showed significantly lower levels of α‐2‐macroglobulin in the serum of patients with SINFH than in controls (P < 0.05). Immunohistochemical staining and western blotting demonstrated that the expression of α‐2‐macroglobulin was significantly decreased in the necrotic area of SINFH patients (P < 0.05). Conclusion The α‐2‐macroglobulin may be associated with the pathology of SINFH. The multiple pathological reactions occur in SINFH and α‐2‐macroglobulin may serve as a potential biomarker for the diagnosis of SINFH or a promising therapeutic target.

Germline VWF/MPRIP and somatoplasm FGA variants synergically confer susceptibility to non-traumatic osteonecrosis of the femoral head

“…If a necrosis area is ≥ 30% and untreated, non-traumatic ONFH would progress to end-stage arthritis, resulting in severe damage to the hip joint and thus impaired, even disabled functions. Non-traumatic ONFH can be attributed to multiple pathogenic factors, including intravascular coagulation, osteoporosis and lipid metabolism disorders 5 – 7 …”

Germline VWF/MPRIP and somatoplasm FGA variants synergically confer susceptibility to non-traumatic osteonecrosis of the femoral head

“…If necrosis area is ≥ 30% and untreated, non-traumatic ONFH would progress to end-stage arthritis, resulting in severe damage to the hip joint and thus impaired, even disabled functions. Nontraumatic ONFH can be attributed to multiple pathogenic factors, including intravascular coagulation, osteoporosis and lipid metabolism disorders [5][6][7] .…”

Gujiansan Ameliorates Avascular Necrosis of the Femoral Head by Regulating Autophagy via the HIF-1α/BNIP3 Pathway

“…Avascular necrosis of the femoral head (ANFH) is one of the most common osteoarthritic diseases worldwide. Currently, over 30 million people suffer from ANFH globally, including more than 8 million individuals in China [ 1 , 2 ]. In particular, since the development of hormone drugs and their wide application, the incidence of steroid-induced avascular necrosis of the femoral head (SANFH) has gradually increased, and it frequently occurs in patients receiving high-dose steroid treatment, including patients with systemic lupus erythematosus [ 3 ].…”