Project description:We performed gene expression profiling analysis using data obtained from RNA-seq of condylar cartilage 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 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:Internal derangement (ID) in the temporomandibular joint (TMJ) compromises a group of clinical problems, and holds a relative high prevalence in populations. However, the temporal change in gene expression of condylar cartilage during continous ID remains unclear. The aim of current study is investigating the differential expressed gene pattern in condylar cartilage of rabbits with ID from 1 to 8 weeks. Immunohistochemical results indicated that abnormal collagen fiber arrangements, fragmentation of fibrils, inflammatory cells infiltration were detected from 1 week to 4 week in joint disc specimens, while newly formed vessels, mucoid degeneration, meniscal tears, osteoclasts and osteoblasts were observed later. The microarray analysis showed 6478 genes have more than two-fold changes among all the tested transcripts. The inflammation gene group including ACE and IL1βincreased rapidly in the early stage while decrease later. On the contrary, the bone construction related genes showed a low level at first and increased at later period in the ID progression. Besides, the current study found some genes such as HLA2G, which had never been reported, might be relevant with ID. Our findings might provide useful insights into the pathological mechanism of ID in TMJ.
Project description:Temporomandibular joint osteoarthritis (TMJOA) is a common group of clinical diseases and is an important subtype of temporomandibular joint disorder (TMD). Increased intrajoint pressure or weakened penetration can exacerbate the hypoxic state of the condylar cartilage microenvironment. In this study, TMT labeling quantitative proteomic technology was used to comprehensively explore the impacts of and pathways affected by LIPUS on the biological functions of chondrocytes under hypoxic conditions. Bioinformatic analysis revealed differentially expressed proteins (DEPs) in the N group versus the L group and the L group versus the LP group. Considering the results of gene ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, and protein-protein interaction (PPI) network analyses, we hypothesized that LIPUS can activate the FAK signaling pathway. This study identified a new molecular marker to determine the efficacy of LIPUS in TMJOA, providing a theoretical basis for the clinical application of LIPUS in the treatment of TMJOA.
Project description:Background Extracellular matrix (ECM) protein malfunction or defect may lead to temporomandibular joint osteoarthritis (TMJ OA). Dentin sialophophoprotein (DSPP) is a mandibular condylar cartilage ECM protein, and its deletion impacted cell proliferation and other extracellular matrix alterations of postnatal condylar cartilage. However, it remains unclear if long-term loss of function of DSPP leads to TMJ OA. The study aimed to test the hypothesis that long-term haploinsufficiency of DSPP causes TMJ OA. Materials and Methods To determine whether Dspp+/- mice exhibit TMJ OA but no severe tooth defects, mandibles of wild-type (WT), Dspp+/-, and Dspp homozygous (Dspp-/-) mice were analyzed by Micro-computed tomography (micro-CT). To characterize the progression and possible mechanisms of osteoarthritic degeneration over time in Dspp+/- mice over time, condyles of Dspp+/- and WT mice were analyzed radiologically, histologically, and immunohistochemically. Results Micro-CT and histomorphometric analyses revealed that Dspp+/- and Dspp-/- mice had significantly lower subchondral bone mass, bone volume fraction, bone mineral density, and trabecular thickness compared to WT mice at 12 months. Interestingly, in contrast to Dspp-/- mice which exhibited tooth loss, Dspp+/- mice had minor tooth defects. RNA sequencing data showed that haplodeficency of DSPP affects the biological process of ossification and osteoclast differentiation. Additionally, histological analysis showed that Dspp+/- mice had condylar cartilage fissures, reduced cartilage thickness, decreased articular cell numbers and severe subchondral bone cavities, and with signs that were exaggerated with age. Radiographic data showed an increase in subchondral osteoporosis up to 18 months and osteophyte formation at 21 months. Moreover, Dspp+/- mice showed increased distribution of osteoclast in the subchondal bone and increased expression of MMP2, IL-6, FN-1, and TLR4 in the mandibular condylar cartilage. Conclusions Dspp+/- mice exhibit TMJ OA in a time-dependent manner, with lesions in the mandibular condyle attributed to hypomineralization of subchondral bone and breakdown of the mandibular condylar cartilage, accompanied by upregulation of inflammatory markers.