No abstract

Only few systematic and comprehensive studies have focused on osteosarcoma in children and adolescents. In the present study, 3,085 patients with osteosarcoma were identified in the Surveillance, Epidemiology and End Results Program database. The patients were <25 years of age and diagnosed between 1973 to 2012. A retrospective study was performed to investigate the factors associated with tumor incidence, metastasis, treatment and survival. The results indicated that the incidence of osteosarcoma was higher in male patients compared with female patients. In addition, the incidence rate of osteosarcoma was higher among male and female patients between the ages of 10 and 19. Osteosarcoma located in the chest and pelvic bones was associated with metastatic disease; however, metastasis in two histological types, parosteal and periosteal, was infrequent. Survival analysis revealed the following were associated with poor outcomes: Sex, patients diagnosed between 1973 and 1982, distant metastasis, treatment without surgery or with radiation, a tumor with a poorly differentiated or undifferentiated grade, tumor size ≥100 mm, and a tumor in the pelvic bones. Patient's whose histologic type was parosteal osteosarcoma and whose tumor was located in one of the limbs, or who underwent local or radical excision, exhibited a good survival outcome. Survival outcomes were ranked according to the type of surgery, from best to worst, as follows: Local excision, radical excision, amputation and no surgery. In summary, the incidence of osteosarcoma is higher in male patients compared with female patients. Furthermore, individuals between the ages of 10 and 19 have a higher risk of osteosarcoma. Osteosarcoma located in the chest and pelvic bones has a high risk of metastasis. Limb-salvage surgery may be the optimal treatment approach for non-metastatic osteosarcoma.

Apoptosis of osteoblasts caused by glucocorticoid (GC) is the biological basis of steroid‐induced avascular necrosis of the femoral head (SANFH). We found that GC can induce osteoblast apoptosis and autophagy through the ROS/JNK/c‐Jun signaling pathway, which contributes to SANFH. Therefore, the autophagy inhibitor 3‐MA might have potential for development into a treatment for SANFH.

HighlightsFirst, it is a population-based study which can provide big sample size.Second, similar articles about chondrosarcoma using big data are lacking.Third, the relationship between treatment type and survival outcomes was analyzed in detail.

Osteoblast apoptosis has been identified as an important event in the development of glucocorticoid (GC)-induced osteoporosis and osteonecrosis of the femoral head. Crocin, a bioactive ingredient of saffron, has been demonstrated to induce antiapoptotic effects on numerous types of cell in vitro ; however, the effects of crocin on the dexamethasone (Dex)-induced apoptosis of osteoblasts remain unclear. In the present study, the protective effects of crocin during Dex-induced apoptosis of MC3T3-E1 osteoblasts, and the underlying mechanisms, were investigated. MTT and Annexin V-FITC/PI flow cytometry assays were performed to evaluate the viability and apoptosis of cells, respectively. The mitochondrial transmembrane potential, reactive oxygen species (ROS), intracellular Ca 2+ levels and apoptosis-associated protein expression were assessed via flow cytometry, fluorescence microscopy and western blotting. It was demonstrated that crocin pretreatment inhibited Dex-induced apoptosis of osteoblasts in a dose-dependent manner. Crocin reversed Dex-induced decreases in the mitochondrial transmembrane potential, and increases in ROS and intracellular Ca 2+ levels. Furthermore, crocin upregulated the expression levels of B-cell lymphoma-2 (Bcl-2) and mitochondrial cytochrome c (Cyt C), and downregulated those of cleaved caspase-9, cleaved caspase-3, Bcl-2-associated X protein and cytoplasmic Cyt C. N-acetylcysteine, a ROS inhibitor, and 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid, a calcium chelator, attenuated Dex-induced osteoblast apoptosis, whereas H 2 O 2 and ionomycin, a calcium ionophore that increases intracellular calcium levels, reversed the antiapoptotic effects of crocin on Dex-treated osteoblasts. These results indicated that crocin may protect osteoblasts from Dex-induced apoptosis by inhibiting the ROS/Ca 2+ -mediated mitochondrial pathway, thus suggesting that crocin has potential value as a treatment for GC-induced bone diseases.