[Correlation between local microenvironment leptin expression and avascular necrosis of the femoral head].

OBJECTIVE: To discuss the correlation between the letpin level and the pathogenesis of avascular necrosis of the femoral head (ANFH) by measuring the leptin expression of the femoral head in patients with ANFH.

METHODS: Between July 2009 and February 2011, 16 patients with ANFH (including 10 cases of steroid-induced ANFH and 6 cases of alcohol-induced ANFH, ANFH group) and 11 patients with proximal femur fracture (control group) were included in the experiment. There was no significant difference in age, weight, and body mass index between 2 groups (P > 0.05). The peripheral blood and bone marrow were extracted to measure the blood lipid level and the free fat (FF) content, respectively. ELISA was used to detect the levels of the leptin, soluble leptin receptor (sLR), osteoprotegerin (OPG), and soluble receptor activator of nuclear factor kappaB (sRANKL); the leptin biological activity and the activity of osteoclasts were calculated. The femoral head specimens were harvested to count leptin-positive cells by immunohistochemical staining.

RESULTS: No significant difference in the blood lipid level was found between 2 groups (P > 0.05), but the FF content in ANFH group was significantly lower than that in control group (t=14.230, P=0.000). The intramedullary leptin expression was found in both groups; however, the intramedullary leptin level in ANFH group decreased significantly when compared with the level in control group (t=4.425, P=0.002). There were significant differences in the levels of leptin, OPG, and sRANKL between 2 groups (P < 0.05). The leptin biological activity of ANFH group was significantly lower than that of control group (P < 0.05), but the activity of osteoclasts of ANFH group was significantly higher than that of control group (P < 0.05). There was a positive correlation between the leptin level and leptin biological activity (r=0.922 7, P=0.000 0), and a negative correlation between the leptin level and OPG content (r=-0.396 2, P=0.040 8), FF content (r=-0.806 1, P=0.000 0), while it had no correlation between the leptin level and sLR and sRANKL content (P > 0.05).

CONCLUSION: Intramedullary expression and bioactivity of the leptin decrease significantly in ANFH patients, which may play an important role in the pathogenesis of ANFH.