The Study Of Early Diagnosis Of Traumatic Osteoarthritis By Articular Chondrocytes And Their Metabolism

Objective: Traumatic osteoarthritis(Post-traumatic osteoarthritis,PTOA)is one of the common types of(Osteoarthritis,OA)in osteoarthritis.This study explored the molecular mechanism of early PTOA from the point of view of articular chondrocytes and its related metabolic factors.To observe the interaction and inconsistency of related metabolic factors in chondrocytes and synovial fluid before and after joint injury,and then to find meaningful biomarkers to elucidate the molecular mechanism of early pathogenesis of PTOA.It is found that the clinical biomarkers are beneficial to the early diagnosis of PTOA.Methods: The cartilage and synovial fluid of knee joint in patients with potential PTOA(joint injury)and normal subjects were used as experimental materials to study the interaction between structural damage and triggered biological cascade reaction after joint injury.The distribution,density,migration and infiltration of chondrocytes were observed from the point of view of tissue in situ.To study the expression of nuclear transcription factors in the early stage of chondrocytes,the initiation and expression of proinflammatory factors,the relationship between intercellular signaling,programmed cell death and the changes of antiangiogenic factors.From March 1,2015 to December 1,2017,a total of 30 patients(16 males and 14 females,aged 20 ~ 51 years,mean(36.1012.34)years)diagnosed by the Department of Trauma Orthopaedics of Tianjin Hospital were collected.According to the inclusion criteria of the experimental group and the control group,15 cases were divided into experimental group: the cartilage in MRI images of knee joint showed normal cartilage tissue,but the pathological findings were that the surface of cartilage was damaged and repaired,and the degeneration of cartilage matrix showed mucinous degeneration.The necrosis of chondrocytes proved to be in the early stages of PTOA.Control group(n = 15): the cartilage tissue and synovial fluid of the knee joint were not significantly changed on MRI images and pathological findings in the patients with femoral destruction and uninvolved knee joint.Pathological staining was used to observe the changes of chondrocytes and matrix from a microscopic point of view.At the same time,immunohistochemical staining of FGF-1 and CMP(Cartilage Matrix Protein)markers was performed to further observe the degeneration of cartilage.The degradation of collagen and proteoglycan in cartilage and synovial fluid and the related proteases and important cytokines including ADAMTS4,ADAMTS5,FGF10,COMP,CTX Ⅱ,TGF β,HA were systematically studied by multi-factor detection platform and enzyme-linked immunosorbent assay(Elisa),TIMP2,COL2,TNF α,TIMP1,MMP13,BMP2,IL-1,BMP7,The relationship between PTOA and cartilage degeneration was considered from many aspects of pathophysiology,and the sensitive methods of predicting PTOA and clinical biomarkers were explored.Results: The common indexes including FGF10,CTX Ⅱ,ADAM-TS5,BMP2,tgfs,COMP,IL,cols and other factors were detected,and pathological examination was performed at the same time.According to the preliminary analysis of the relevant experimental data,it was found that the concentrations of FGF10(t ≤ 2.58,p ≤ 0.014)and ADAM-TS5(t ≤ 2.23,p ≤ 0.033)in the synovial fluid of the experimental group were lower than those of the control group(normal cartilage).The concentrations of CTX Ⅱ(t ≤ 2.34,p ≤ 0.026)and BMP-2(t ≤ 2.519,p ≤ 0.017)in articular cartilage lysate in the experimental group were significantly different from those in the control group.Conclusion: In the early stage of joint trauma,the levels of FGF-10 and ADAM-TS5 factors in synovial fluid decreased,the levels of CTX Ⅱ in cartilage tissue decreased and the level of BMP2 increased,indicating that before the imaging changes of joints in PTOA patients,That is to say,the factor levels of FGF10,CTX Ⅱ,ADAM-TS5 and BMP-2 in synovial fluid and cartilage can be detected to achieve the purpose of early diagnosis of PTOA.