Objective To assess the effect of the fusion of rabbit bone marrow stromal cells (rBMSCs) and Nano-hydroxyapatite/poly (l-lactic acid) (Nano-HA/PLLA) in repairing the rabbit knee joint with full-thickness cartilage defect. Method The rBMSCs were isolated and cultured in vitro, and the third generation of rBMSCs was co-cultured with the Nano-HA/PLLA to construct the tissue-engineered cartilage (TEC). Eighteen New Zealand white rabbits were selected and randomly divided into three groups, namely, TEC group, Nano-HA/PLLA group, and control group. A cartilage defect model with the diameter of 4.5 mm and depth of 5 mm was constructed on the articular surface of medial malleolus of rabbit femur. General observation, histological observation, and Wakitani's histological scoring were conducted in the 12th and 24th week postoperatively. Results The results of TEC group indicated that new cartilage tissue was formed on the defect site and subchondral bone achieved physiological integration basically. Histological and immunohistochemical analyses indicated the generation of massive extracellular matrix. In contrast, limited regeneration and reconstruction of cartilage was achieved in the Nano-HA/PLLA group and control group, with a significant difference from the TEC group (p < 0.05). Moreover, the effect of cartilage repair was positively correlated with time. Conclusion The porous Nano-HA/PLLA combined with BMSCs promoted the repair of weight-bearing bone of adult rabbit's knee joint with cartilage defect.

Proximal humeral fractures are common and most challenging, due to the complexity of the glenohumeral joint, especially in the geriatric population with impacted fractures, that the development of implants continues because currently the problems with their fixation are not solved. Pre-, intra-, and postoperative assessments are crucial in management of those patients. Finite element analysis, as one of the valuable tools, has been implemented as an effective and noninvasive method to analyze proximal humeral fractures, providing solid evidence for management of troublesome patients. However, no review article about the applications and effects of finite element analysis in assessing proximal humeral fractures has been reported yet. This review article summarized the applications, contribution, and clinical significance of finite element analysis in assessing proximal humeral fractures. Furthermore, the limitations of finite element analysis, the difficulties of more realistic simulation, and the validation and also the creation of validated FE models were discussed. We concluded that although some advancements in proximal humeral fractures researches have been made by using finite element analysis, utility of this powerful tool for routine clinical management and adequate simulation requires more state-of-the-art studies to provide evidence and bases.

The transforming growth factor β1 (TGFβ1) plays an important role in cartilage development. However, whether TGFβ1 stimulates chondrocyte proliferation and cartilage regeneration in osteoarthritis (OA) remains elusive, especially in the context of different treatment and tissue environments. In the present study, we investigated the role of TGFβ1 in human chondrocyte culture in vitro, focusing on the morphological change of chondrocytes and the expression of angiogenic factors upon TGFβ1 stimulation. We found increased expression of biomarkers indicating chondrocyte hypertrophy and the chondrocytes aggregated to form networks when they were treated with TGFβ1. DNA microarray analysis revealed significantly increased expression of genes related to blood vessel formation in TGFβ1 treatment group compared to control group. Matrigel assay further demonstrated that chondrocytes had the potential to form network-like structure. These results suggested that TGFβ1 induces the hypertrophic change of chondrocytes culture in vitro and induce expression of angiogenic biomarkers. Therefore, application of TGFβ1 for chondrocyte culture in practice should be considered prudentially and targeting TGFβ1 or relevant receptors to block the signaling pathway might be a strategy to prevent or alleviate progression of osteoarthritis.

The present study aimed to investigate idiopathic adhesive capsulitis (frozen shoulder), to gain insights on its pathogenesis, diagnosis and therapeutic targets. Using RNA-sequencing (seq), the present study investigated differentially expressed genes (DEGs) in five samples from five idiopathic adhesive capsulitis patients and two samples from two acromioclavicular dislocation patients, without idiopathic adhesive capsulitis. The DEGs were analyzed using the following tools: Gene Ontology enrichment analysis, Kyoto Encyclopedia of Genes and Genomes pathways analysis and protein-protein interaction analysis. A total of 188 DEGs were identified and it was observed that 150 of these were upregulated and 38 were downregulated. It was hypothesized that various nutrient associated proteins may be associated with idiopathic adhesive capsulitis. The Matrix metalloproteinase family of proteins (MMPs), may exhibit a key role in the formation of abnormal collagen cross-links. Overall, the comprehensive and detailed information collected in the present study, regarding idiopathic adhesive capsulitis, may provide a foundation on which in-depth follow-up experiments may be based, aimed at identifying novel strategies for treatment of this disease.

Frozen shoulder is a common shoulder disorder characterized by a gradual increase of pain and a limited range of motion. However, its pathophysiologic mechanisms remain unclear and there is no consensus as to the most effective treatment. The purpose of the study was to investigate the effect of transforming growth factor-β (TGF-β) on fibrosis and inflammatory response of the shoulder joint of rat models and to explore the therapeutic effect of the peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist. In the study, the effect of PPAR-γ agonist CDDO-IM treatment on cell proliferation, migration, and extracellular matrix proteins synthesis (vimentin, α-smooth muscle actin, collagen I, and collagen III) were tested by cell proliferation test, scratches test, real-time quantitative polymerase chain reaction, and Western blot analysis. The frozen shoulder was also established on the rat model by injecting adenovirus-TGF-β1 into rats' shoulder capsule. Pathological changes of the frozen shoulder tissue of the experimental group and PPAR-γ agonist treatment group were evaluated. The stiffness of joints of the three groups was tested. Inflammatory mediators' expression including cyclooxygenase-1, interleukin-1β, and tumor necrosis factor-α of the shoulder was tested by enzyme-linked immunosorbent assay, and the expression of extracellular matrix proteins was evaluated by hematoxylin and eosin staining and immunohistochemistry. The results showed that pathological changes of the frozen shoulder in the rat model include an abnormal proliferation of fibroblasts, infiltration of inflammatory cells, and disorder of fibrous structure, while rosiglitazone reduced the severity of the frozen shoulder in the treatment group. Clinically, PPAR-γ agonists may be a promising target for the treatment of the frozen shoulder.