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 gt; 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 κB (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 gt; 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 lt; 0.05). The leptin biological activity of ANFH group was significantly lower than that of control group (P lt; 0.05), but the activity of osteoclasts of ANFH group was significantly higher than that of control group (P lt; 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 gt; 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.
Objective To summary the functional roles and molecular mechanisms of microRNA (miRNA) in osteoblast differentiation so as to supply information for basic and cl inical researches. Methods Recent l iterature concerning miRNA in osteoblast differentiation was reviewed. The information was classified and summarized. Results miRNAs critically regulate bone morphogenetic protein, transforming growth factor β, and Wnt/β-catenin signal ing pathways during osteoblast differentiation. In pathological conditions, especially in some disorders of abnormal osteoblast differentiation, downregulated miRNA expression has been observed. Conclusion miRNA may represent a novel biomarker for diagnosis, and a candidate target therapies for the disorders with abnormal osteoblast differentiation.
ObjectiveTo review the research progress focused on the effects of strontium ranelate (SR) on osteoarthritis. MethodsThe relevant literature about the effects and mechanism of SR intervening osteoarthritis in recent years was extensively reviewed and comprehensively analyzed. ResultsSR not only could improve the microenvironment of bone metabolism in articular cartilage with osteoarthritis, promote activity of osteoblasts, and inhibit activity of osteoclasts, but also could adjust the expression of key proteases which affect cartilage formation, and therefore it has a potential protective effect on subchondral bone during the progression of osteoarthritis cartilage. ConclusionSR is expected to become a drug of osteoarthritis disease remission, but further studies are needed to clarify the mechanism of SR in osteoarthritis, and finally confirm the best application dosage of SR in osteoarthritis treatment.
ObjectivesTo systematically review the influence of antiepileptic drugs on bone mineral density and bone metabolism in adults.MethodsPubMed, EMbase, CNKI, CBM, VIP and WanFang Data databases were electronically searched to collect studies on the influence on antiepileptic drugs on the bone mineral density and bone metabolism in adults from inception to April 1st, 2018. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then, meta-analysis was performed by using RevMan 5.3 software.ResultsA total of 14 studies were included. The results of meta-analysis showed that: VPA could decline the bone mineral density of lumbar spine (SMD=–0.39, 95%CI –0.65 to –0.13, P=0.003); CBZ (SMD=–0.71, 95%CI –1.08 to –0.33, P=0.000 2) and VPA (SMD=–0.3, 95%CI –0.58 to –0.02, P=0.03) could decline the bone mineral density of femoral neck; CBZ could decline the bone mineral density of total hip (SMD=–0.47, 95%CI –0.84 to –0.10, P=0.01). Serum 25-hydroxy vitamin D3 was decreased in OXC group (SMD=–0.67, 95%CI –1.28 to –0.05, P=0.03); serum calcium was decreased in CBZ (SMD=–0.49, 95%CI –0.78 to –0.20, P=0.000 8), LEV (SMD=–0.83, 95%CI –1.15 to –0.51, P<0.000 01) and OXC (SMD=–0.48, 95%CI –0.90 to –0.05, P=0.03) group; serum phosphorus was decreased in LEV group (SMD=–11.36, 95%CI –12.97 to –9.76, P<0.000 01). Serum alkaline phosphatase was increased significantly in LEV (SMD=6.79, 95%CI 5.78 to 7.80, P<0.000 01) and CBZ (SMD=1.90, 95%CI 1.35 to 2.44, P<0.000 01) group.ConclusionsCurrent evidence shows that treatment with antiepileptic drugs may be associated with an decreasing bone mineral density and influence bone metabolism in epileptic adults. Due to limited quality and quantity of the included studies, more high quality studies are required to verify above conclusion.