Icaritin, a novel semisynthesized small molecule with osteoprotective potential, exerts dose-dependent effect on reducing incidence of steroid-associated ON with inhibition of both intravascular thrombosis and extravascular lipid-deposition. Suppression of the up-regulated PPARgamma expression for extravascular adipogenesis of mesenchymal stem cells and protection from activated oxidative stress for intravascular endothelium injury were found to be involved in the underlying mechanisms.

SummaryAgeing is accompanied by chronic inflammatory responses due to elevated circulatory inflammatory cytokine production. Several inflammatory cytokines have been shown to be responsible for a decrease in muscle mass. However, little is known about the possible relationship between inflammation and sarcopaenia. This review aims to summarise the existing evidence about inflammation and sarcopaenia. Sarcopaenia is defined as an age-related decrease of muscle mass and/or muscle strength; it is caused by multiple factors, such as skeletal muscle atrophy, neuromuscular junction degeneration, hormone imbalance, cytokine imbalance, protein synthesis and proteolysis. Several inflammatory cytokines have been considered to promote muscle loss; C-reactive protein levels are significantly upregulated in sarcopaenia and sarcopenic obesity, and high levels of interleukin-6 are associated with reduced muscle mass and muscle strength (the administration of interleukin-6 could lead to a reduction in muscle mass). Up-regulation of tumour necrosis factor-α expression is also related to the development of sarcopaenia. Signalling pathways, such as protein kinase B/mammalian target of rapamycin, Janus kinase/signal transducer and activator of transcription-5 and signal transducer and activator of transcription 3 signalling, involved in muscle metabolism are regulated by insulin-like growth factor-1, tumour necrosis factor-α and interleukin-6 respectively. In conclusion, the inflammatory cytokines produced during chronic inflammation due to ageing, may influence their respective related pathways, thus leading to age-related muscle deterioration.The translational potential of this articleThis review can provide more information for sarcopaenia medicine research in terms of anti-inflammation therapy.

Objective. To examine the features of the intraosseous vasculature, the size of the marrow stem cell pool (MSCP), and expression of vascular endothelial growth factor A (VEGF) during inadequate repair of steroid-associated osteonecrotic lesions in rabbits.Methods. Steroid-associated osteonecrosis was induced in male rabbits. At 0, 1, 2, 4, and 6 weeks postinduction, vascularization and permeability indices were quantified by dynamic magnetic resonance imaging (MRI). In addition, the size of the MSCP in the hematopoietic and mesenchymal compartments was determined, and marrow mononuclear cells expressing specific surface markers for endothelial progenitor cells or periendothelial mural precursor cells were counted. At various time points after the rabbits were killed, the proximal femora were dissected to examine the intraosseous vasculature by angiography, histomorphometry, and ultramorphology. In addition, osteonecrotic lesion repair and marrow VEGF expression were evaluated.Results. Lesion formation without repair was observed at 2 weeks after induction of steroid-associated osteonecrosis. Rabbits displaying destructive repair (DR؉) and those displaying reparative osteogenesis (DR؊) from 4 weeks to 6 weeks postinduction were identified. From week 2 to week 6, the vascularization index was significantly lower in DR؉ rabbits compared with DR؊ rabbits, whereas the permeability index was significantly higher in DR؉ rabbits compared with DR؊ rabbits. The features of the intraosseous vasculature determined by angiography, histomorphometry, and ultramorphology were consistent with those determined by dynamic MRI. The MSCP size and number of marrow mononuclear cells expressing specific surface markers were all significantly lower in DR؉ rabbits than in DR؊ rabbits from week 1 to week 6. The increased VEGF expression at 2 weeks was maintained through week 6 in DR؉ rabbits, whereas VEGF expression decreased in DR؊ rabbits from week 2 to week 6.Conclusion. Continuous occurrence of both insufficient neovascularization and elevated vascular permeability is accompanied by a continuously lowlevel MSCP and uncontrolled VEGF expression during inadequate repair of steroid-associated osteonecrotic lesions.Pulsed steroids are frequently prescribed as lifesaving agents for serious infectious diseases such as severe acute respiratory syndrome and acquired immunodeficiency syndrome, or as disease-modifying agents for chronic autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. However, pulsed administration of steroids often results in osteonecrosis (also known as avascular necrosis). Orthopedic surgeons face the challenge of managing subchondral

In addition to existing evidence that postoperative orthogeriatric collaboration improves mortality and functional outcomes in older patients with hip fractures, this study suggests that allowing preoperative geriatric input in this model of care can produce even more superior results.