Project description:Background: Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease marked by the progressive degeneration of cartilage and underlying bone, resulting in pain and functional impairment. Despite current conservative treatments such as physical therapy and NSAIDs, the etiology and pathophysiology of TMJOA are unclear, making effective management difficult. Finding reliable biomarkers for early identification and new therapeutic targets is crucial to improve treatment outcomes.
Project description:Synovial fibroblasts contribute to the inflammatory temporomandibular joint under pathogenic stimuli. Synovial fibroblasts and T cells participate in the perpetuation of joint inflammation in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. IL-17 is an inflammatory cytokine produced primarily by Th17 cells that plays critical roles in the pathogenesis of numerous autoimmune and inflammatory diseases. Here, we investigated the roles of IL-17A in temporomandibular joint disorders (TMD) by using genome-wide analysis of synovial fibroblasts isolated from patients with TMD. We analyzed the gene expression profiles of synovial fibroblasts that were treated with or without IL-17A. IL-17 induced gene expression in synovial fibroblasts from human temporomandibular joint was measured at 4 hours after treated with IL-17A (10 ng/ml) and untreated control samples. This experiment used one donor sample.
Project description:To investigate the functions of ncRNAs in temporomandibular joint osteoarthritis, we established temporomandibular joint osteoarthritis model induced by unilateral anterior crossbite. We then performed gene expression profiling analysis using data obtained from RNA-seq of condylar cartilage at 8 weeks of modeling.
Project description:To investigate the functions of ncRNAs in temporomandibular joint osteoarthritis, we established temporomandibular joint osteoarthritis model induced by unilateral anterior crossbite. We then performed gene expression profiling analysis using data obtained from RNA-seq of condylar cartilage at 8 weeks of modeling.
Project description:We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells from post-traumatic temporomandibular joint osteoarthritis model to investigate the signaling pathways critical for cellular functions during temporomandibular joint osteoarthritis pathology.
Project description:To investigate differentially expressed miRNAs in synovium of human temporomandibular joint osteoarthritis (TMJOA), we performed miRNA high-throughput sequencing in synovium of human TMJOA.
Project description:To investigate differentially expressed lncRNAs,circRNAs,miRNAs and mRNAs in synovium of human temporomandibular joint osteoarthritis (TMJOA), we performed RNA high-throughput sequencing in synovium of human TMJOA. We then performed gene expression profiling analysis using data obtained from RNA-seq .
Project description:Synovial fibroblasts contribute to the inflammatory temporomandibular joint under pathogenic stimuli. Synovial fibroblasts and T cells participate in the perpetuation of joint inflammation in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. IL-17 is an inflammatory cytokine produced primarily by Th17 cells that plays critical roles in the pathogenesis of numerous autoimmune and inflammatory diseases. Here, we investigated the roles of IL-17A in temporomandibular joint disorders (TMD) by using genome-wide analysis of synovial fibroblasts isolated from patients with TMD. We analyzed the gene expression profiles of synovial fibroblasts that were treated with or without IL-17A.
Project description:Temporomandibular joint osteoarthritis (TMJ-OA), a subtype of temporomandibular joint dysfunction (TMD), is characterized by progressive cartilage degradation, subchondral bone erosion, and chronic pain. Although there has been extensive research on TMJ-OA, its etiology remains unknown. Age, hormonal factors, and excessive mechanical stress on the TMJ are proposed risk factors for TMJ-OA. Using microarrays, we discovered two disease susceptibility genes that have been suggested to be involved in the pathogenic mechanism of TMJ-OA.