Objective. Osteoarthritis (OA) is a complex arthritic condition in which the genetic factor plays a major role. One of the candidate genes of is the ADAM12 gene, but no consistency has been reached till now. This study aims to investigate the potential role of four single nucleotide polymorphisms (SNPs) of the ADAM12 gene in susceptibility to knee OA and its progression in Chinese Han population. Methods. The rs1278279, rs3740199, rs1044122, and rs1871054 polymorphisms were genotyped and compared in a population based cohort consisting of 164 OA subjects and 200 age- and gender-matched controls. Results. The SNP rs1871054 was found with increased risk of OA susceptibility in comparing the genotype frequencies between the case and control groups no matter for which model of comparison (allele level, dominant model, recessive model, and extreme genotype model). Additionally, the SNP rs1871054 was found associated with increased OA severity according to the K/L grade. Conclusion. In summary, we have identified that the rs1871054 variant within the ADAM12 gene is a risk factor for increased osteoarthritis susceptibility and severity.

Inflammation of cartilage is a primary symptom for knee-joint osteoarthritis. Matrix metalloproteinases (MMPs) are known to play an important role in the articular cartilage destruction related to osteoarthritis. Naringenin is a plant-derived flavonoid known for its anti-inflammatory properties. We studied the effect of naringenin on the transcriptional expression, secretion and enzymatic activity of MMP-3 in vivo in the murine monosodium iodoacetate (MIA) osteoarthritis model. The assessment of pain behavior was also performed in the MIA rats. The destruction of knee-joint tissues was analyzed microscopically. Moreover, the effect of naringenin was also studied in vitro in IL-1β activated articular chondrocytes. The transcriptional expression of MMP-3, MMP-1, MMP-13, thrombospondin motifs (ADAMTS-4) and ADAMTS-5 was also studied in primary cultured chondrocytes of rats. Naringenin caused significant reduction in pain behavior and showed marked improvement in the tissue morphology of MIA rats. Moreover, a significant inhibition of MMP-3 expression in MIA rats was observed upon treatment with naringenin. In the in vitro tests, naringenin caused a significant reduction in the transcriptional expression, secretion and enzymatic activity of the studied degradative enzymes. The NF-κB pathway was also found to be inhibited upon treatment with naringenin in vitro. Overall, the study suggests that naringenin alleviated pain and regulated the production of matrix-metalloproteinases via regulation of NF-κB pathway. Thus, naringenin could be a potent therapeutic option for the treatment of osteoarthritis.

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BackgroundRheumatoid arthritis (RA) is a chronic auto-inflammatory disorder of joints. The present study aimed to identify the key genes in RA for better understanding the underlying mechanisms of RA.MethodsThe integrated analysis of expression profiling was conducted to identify differentially expressed genes (DEGs) in RA. Moreover, functional annotation, protein–protein interaction (PPI) network and transcription factor (TF) regulatory network construction were applied for exploring the potential biological roles of DEGs in RA. In addition, the expression level of identified candidate DEGs was preliminarily detected in peripheral blood cells of RA patients in the dataset. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to validate the expression levels of identified DEGs in RA.ResultsA total of 378 DEGs, including 202 up- and 176 down-regulated genes, were identified in synovial tissues of RA patients compared with healthy controls. DEGs were significantly enriched in axon guidance, RNA transport and MAPK signaling pathway. RBFOX2, LCK and SERBP1 were the hub proteins in the PPI network. In the TF-target gene network, RBFOX2, POU6F1, WIPF1 and PFKFB3 had the high connectivity with TFs. The expression status of 11 candidate DEGs was detected in , the expression levels of MAT2A and NSA2 were significantly down-regulated and CD47 had the up-regulated tendency in peripheral blood cells of patients with RA compared with healthy individuals. qRT-PCR results of MAT2A, NSA2, CD47 were compatible with our bioinformatics analyses.DiscussionOur study might provide valuable information for exploring the pathogenesis mechanism of RA and identifying the potential biomarkers for RA diagnosis.

The present study aimed to explore genetic association of receptor activator nuclear factor κB (RANK) polymorphisms with individual susceptibility to knee osteoarthritis (OA) in different Kellgren–Lawrence (KL) grades. This case–control study included 138 knee OA patients and 145 healthy individuals. RANK rs1805034 and rs8086340 polymorphisms were genotyped through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The effects of RANK polymorphisms on knee OA risk were analyzed via χ 2 test or Fisher exact test, and the results were expressed using odds ratios (ORs) with corresponding 95% confidence intervals (CIs). The C allele of rs1805034 polymorphism had significantly higher frequency in knee OA patients than in controls ( P = .044), indicating that this allele could increase the risk of knee OA (OR = 1.424, 95% CI = 1.010–2.008). Besides, the CC genotype and C allele of the rs1805034 polymorphism were significantly associated with elevated risk of knee OA in moderate grade (CC vs TT: P = .018, OR = 3.071, 95% CI = 1.187–7.941; C vs T: P = .012, OR = 1.787, 95% CI = 1.131–2.823). However, rs8086340 polymorphism had no significant association with knee OA risk The C allele of RANK rs1805034 polymorphism is closely correlated with increased risk of knee OA, especially for moderate grade.

Introduction Previous clinical studies have reported associations between the acromion index, lateral acromion angle, and critical shoulder angle and the occurrence of rotator cuff tears. The objective of this study was to analyze the correlations of these different anatomic parameters in geriatric Chinese Population. Methods Healthy geriatric Chinese participants (n = 66) and geriatric Chinese patients with rotator cuff tears (n = 70) identified between January 2019 and October 2020 were included in this study. Standardized true anteroposterior radiographs were used to measure the acromion index, lateral acromion angle, and critical shoulder angle in each study participant. Results The mean acromion index was significantly larger, the mean lateral acromion angle was significantly smaller, and the mean critical shoulder angle was significantly larger in geriatric patients with full-thickness rotator cuff tears compared with geriatric healthy participants. Conclusion There were a negative linear relationship between the acromion index and lateral acromion angle and a positive linear relationship between the acromion index and critical shoulder angle in geriatric patients with rotator cuff tear and geriatric healthy participants; we termed this phenomenon “Hypothesis of Acromion Index.” The acromion index, lateral acromion angle, and critical shoulder angle are independent predictors of rotator cuff tears in a geriatric Chinese population.

Background: Pathologic fractures following bone metastasis of rectal cancer are relatively uncommon. Case presentation: A 59-year-old male rectal cancer patient in China with bone metastases in the right femur that caused a right femoral pathological fracture. According to emission computed tomography (ECT) and other examinations, and with the assistance of a multidisciplinary team, bone metastasis was diagnosed. Because the traumatic orthopedic surgeons did not notice his history of colorectal cancer preoperatively, there was no diagnosis of pathological fracture, and open reduction and internal fixation were performed. Additionally, there was no postoperative radiotherapy to the area or systemic treatment. Multiple re-examinations of the patient within 4 months after surgery revealed that the fracture did not heal. The patient was readmitted and treated 9 months after open reduction and internal fixation, and the tumor gradually spread in the proximal right femur.Conclusions: The combination of a medical history, preoperative ECT examination, local DR examination, CT examination and MRI examination are necessary for a preoperative diagnosis. This case report mainly recorded the whole treatment and follow-up process.

Osteoarthritis (OA) is one of the most common forms of arthritis. However, the pathogenesis of OA remains unclear. Previous studies suggested that stromal-cell-derived factor (SDF)-1 was associated with some characteristic changes in cartilage. The aim of this study is, therefore, to explore the mechanism of SDF-1 promotes chondrocyte mineralization in OA. The effect of SDF-1 was analyzed with human C-28/I2 chondrocytes. The chondrocytes were transfected with pEX-4-ANKH or siRNA and treated with related inhibitor. The chondrocytes were subjected to Alizarin red S staining, PiPer phosphate assay kit, Alkaline phosphatase staining , RT-PCR and Western blot analysis. In vitro, SDF-1 markedly promoted the mineralization of chondrocytes and suppressed the expression of ANKH, the endogenous mineralization inhibitor. ANKH overexpressed in the chondrocytes significantly decreased the levels of the mineralization in response to SDF-1 treatment. Moreover, SDF-1 promoted an increase in the expression of p-TAK1 and p-IKKβ、p-IkB、p-NF-kB p65. Furthermore, SDF-1 induced decrease in ANKH expression was blocked by IKKβVI (IkB kinase inhibitor). To conclude, SDF-1 suppresses the expression of ANKH via activating NF-kB pathway to aggravate human chondrocytes calcification, suggesting blockade of SDF-1 might be a novel therapy for treatment of OA patients.