Current clinical applications of mesenchymal stem cell therapy for osteoarthritis lack consistency because there are no established criteria for clinical processes. We aimed to systematically organize stem cell treatment methods by reviewing the literature. The treatment methods used in 27 clinical trials were examined and reviewed. The clinical processes were separated into seven categories: cell donor, cell source, cell preparation, delivery methods, lesion preparation, concomitant procedures, and evaluation. Stem cell donors were sub-classified as autologous and allogeneic, and stem cell sources included bone marrow, adipose tissue, peripheral blood, synovium, placenta, and umbilical cord. Mesenchymal stem cells can be prepared by the expansion or isolation process and attached directly to cartilage defects using matrices or injected into joints under arthroscopic observation. The lesion preparation category can be divided into three subcategories: chondroplasty, microfracture, and subchondral drilling. The concomitant procedure category describes adjuvant surgery, such as high tibial osteotomy. Classification codes were assigned for each subcategory to provide a useful and convenient method for organizing documents associated with stem cell treatment. This classification system will help researchers choose more unified treatment methods, which will facilitate the efficient comparison and verification of future clinical outcomes of stem cell therapy for osteoarthritis.

Osteoarthritis (OA) is the most common joint disease, which accompanies pain and inconvenience in daily life owing to degradation of cartilage and adjacent tissues. In this study, we propose a simple point-of-care testing (POCT) kit for the detection of the MTF1 OA biomarker to achieve on-site clinical diagnosis of OA. The kit contains an FTA card for patient sample treatments, a sample tube for loop-mediated isothermal amplification (LAMP), and a phenolphthalein-soaked swab for naked eye detection. The MTF1 gene was isolated from synovial fluids using an FTA card and amplified using the LAMP method at 65 °C for 35 min. A test part of the phenolphthalein-soaked swab was decolorized in the presence of the MTF1 gene due to the pH change after the LAMP, but the color remained pink in the absence of the MTF1 gene. The control part of the swab served as a reference color in relation to the test part. When real-time LAMP (RT-LAMP), gel electrophoresis, and colorimetric detection of the MTF1 gene were performed, the limit of detection (LOD) was confirmed at 10 fg/μL, and the overall processes were completed in 1 h. The detection of an OA biomarker in the form of POCT was reported for the first time in this study. The introduced method is expected to serve as a POCT platform directly applicable by clinicians for easy and rapid identification of OA.

Background: It is known that hepatocyte nuclear factor 4 alpha (HNF4α) is key master nuclear receptor for hepatic fat and bile acid metabolic pathways. But the role of HNF4α in non-alcoholic fatty liver disease (NAFLD) is complex. The current study aimed to investigate role of HNF4α in NAFLD. Methods: Hepatic HNF4α expression evaluated in human NAFLD subjects. Free fatty acid induced lipotoxicity evaluated under HNF4α over- and down regulation. Chenodeoxy cholic acid (CDCA) induced bile acid toxicity evaluated under HNF4α in In Vitro NAFLD model. NAFLD activity score and fibrosis assessed after HNF4α silencing in methionine choline deficiency diet fed mice. Results: Hepatic HNF4α expression was higher in NAFLD than in control group. Overexpression of HNF4α reduced intracellular lipid contents via increasing mitochondria beta-oxidation and hepatic fat excretion. HNF4α overexpression attenuated palmitic acid (PA) induced lipotoxicity. Protective effects of HNF4α on cell death were reversed when CDCA co-treated with PA. CDCA mono-treatment did not affect cell viability, but co-treatment with PA and CDCA decreased cell viability. Bile acid toxicity of HNF4α was exaggerated under PA co-treatment with CDCA. HNF4α knock down using small interfering RNA recovered cell apoptosis and increased cell proliferation from PA and CDCA co-treatment condition. Inhibition of HNF4α using sh-HNF4α adenovirus vector did not reduce hepatic fat accumulation, but decreased intrahepatic inflammation and NAFLD activity score compared to control.Conclusions: HNF4α increased free fatty acid oxidation and attenuated lipotixicity, but increased bile acid toxicity in NAFLD animal model. Inhibition of HNF4α attenuated In vivo NAFLD model.