BackgroundTotal hip arthroplasty (THA) is a vital therapy for various hip joint diseases. However, patients have lower hemoglobin level post-operatively, remarkably inconsistent with the measured blood loss. The inconsistence is majorly attributed to hidden blood loss (HBL). In this study, we investigated the HBL and its influential factors among patients after THA.MethodsFrom January 2008 to June 2014, 322 patients (99 males and 223 females) undergoing THA were enrolled in this study. All patients were assessed comprehensively before the operation. The demographic information of the patients was collected. Intra-operative and post-operative blood loss was recorded, and then, the total perioperative blood loss and the HBL were calculated. Influential factors were further analyzed by multiple and stepwise regression.ResultsThe HBL was 429 ± 223 mL, with a percentage of 35.4% ± 11.0% in the total perioperative blood loss (1,155 ± 377 mL). Multiple and stepwise regression analysis revealed that HBL was positively associated with body mass index (BMI), blood transfusion volume, length of incision, change of hematocrit (HCT) between pre-operation and post-operation but negatively associated with age. As compared to male patients, female patients had a risk of increased HBL. Development displasia hip (DDH) patients had a less risk of HBL in all patients.ConclusionHBL is a significant portion of total blood loss in the patients after THA. Gender, age, BMI, blood transfusion, length of incision, change of HCT, and diagnosis are influential factors of HBL.

IntroductionOur previous work has revealed that expression of follistatin-like protein 1 (FSTL1) is elevated in the synovial tissues from osteoarthritis (OA) patients. The aim of this study was to elucidate the underlying molecular mechanisms by which FSTL1 plays a role in the pathogenesis of OA.MethodsCultured fibroblast-like synoviocytes (FLSs) from synovial tissues of OA patients were stimulated with human recombinant FSTL1, and then the expression of inflammatory cytokines in FLS and their concentrations in the cell supernatants were measured by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Nuclear factor kappa B (NF-κB) activation was examined by western blot and chromatin immunoprecipitation (ChIP) assay at the p65 binding site. Finally, the proliferation of FLSs and the expression level of the proliferation-related tumor suppressors (p53 and p21) were determined by MTS assay kit and western blot in the presence or absence of FSTL1, respectively.ResultsFSTL1 remarkably promoted expression levels of several inflammatory cytokines (tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6)) in vitro. Western blot analysis showed that FSTL1 activated the inflammatory-related NF-κB signaling pathway, as validated by ChIP assay detecting p65-binding level on the cytokine promoter region. Moreover, FSTL1 promoted the proliferation of OA FLS by downregulating the expression of p53 and p21. Interestingly, the concentration of synovial fluid IL-6 was remarkably elevated in OA patients, and was correlated with synovial fluid and serum FSTL1 levels.ConclusionsThese findings show that FSTL1 functions as an important proinflammatory factor in the pathogenesis of OA by activating the canonical NF-κB pathway and enhancing synoviocytes proliferation, suggesting that FSTL1 may be a promising target for the treatment of OA.

Chondrocyte apoptosis is closely related to the development and progression of osteoarthritis (OA); however, the underlying mechanisms remain enigmatic. Previous studies have confirmed that cell apoptosis is one of the main pathological alterations during oxidative stress, and chondrocyte apoptosis induced by oxidative stress plays an important role in the development of OA. Rat chondrocytes exposed to hydrogen peroxide (H 2 O 2 ) were used as the experimental oxidative stress model. We assessed cell viability, cell apoptosis, levels of intracellular reactive oxygen species (ROS), nitric oxide (NO) production, gene relative expression level of inducible nitric oxide synthase (iNOS), and expressions of iNOS, PI3K, phospho-Akt, caspase-9, and caspase-3. With the rising of intracellular ROS and increasing iNOS synthesis, producing a large amount of NO in chondrocytes, H 2 O 2 decreased the cell viability and induced cell apoptosis of chondrocytes. Furthermore, the levels of caspase-9 and caspase-3 protein expression were significantly elevated as well as the level of p-Akt protein expression when induced by oxidative stress. These findings suggest that oxidative stress-induced chondrocyte apoptosis occurred via activating both PI3K/Akt and caspase pathways in the early stage in these processes.