Osteoarthritis (OA) is the most prevalent articular disease, especially in aged population. Caused by multi-factors (e.g., trauma, inflammation, and overloading), OA leads to pain and disability in affected joints, which decreases patients’ quality of life and increases social burden. In pathophysiology, OA is mainly characterized by cartilage hypertrophy or defect, subchondral bone sclerosis, and synovitis. The homeostasis of cell–cell communication is disturbed as well in such pro-inflammatory microenvironment, which provides clues for the diagnosis and treatment of OA. MicoRNAs (miRNAs) are endogenous non-coding RNAs that regulate various processes via post-transcriptional mechanisms. The miR-17-92 cluster is an miRNA polycistron encoded by the host gene called MIR17HG. Mature miRNAs generated from MIR17HG participate in biological activities such as oncogenesis, neurogenesis, and modulation of the immune system. Accumulating evidence also indicates that the expression level of miRNAs in the miR-17-92 cluster is tightly related to the pathological processes of OA, such as chondrocyte apoptosis, extracellular matrix degradation, bone remodeling, and synovitis. In this review, we aim to summarize the roles of the miR-17-92 cluster in the underlying molecular mechanism during the development and progression of OA and shed light on the new avenue of the diagnosis and treatment of OA.
In bone tissue engineering, tailored biomaterials mimicking mesenchymal stem cells (MSCs) niche could regulate cell behavior and fate decision. The mechanisms, however, remain obscure. Recently, increasing evidence has shown that non-coding RNAs (ncRNAs) are critical modulators of the mechano-induced MSCs’ responses. Mechanosensitive ncRNAs could convert various physical forces into biochemical signals, and orchestrate signaling networks that regulate the osteogenic differentiation of MSCs in their unique microenvironment. In this review, we focus on the mechanosensitive ncRNAs which could interpret mechanical stimuli during the osteogenesis of MSCs, summarize the signaling pathway networks by which these ncRNAs drive MSCs fate, and point out the limitations and the areas waiting for further exploration.
The number of people suffering from temporomandibular joint osteoarthritis (TMJOA) has been increasing. TMJOA cause joint noise, pain on TMJ and/or masticatory muscles, and restricted mandibular movement, which disturb eating, laughing and conversation, and impose serious lifestyle impediments. Chondrocyte apoptosis, extracellular matrix degradation, synovitis, and subchondral bone remodeling are the main pathological features of TMJOA. Various drug delivery systems are developed to controlled release at specific activation sites with high bioactivity and inhibit rapid dilution to enable long-term therapeutic response, which present great potential for the treatment of TMJOA. This review focuses on recently developed drug delivery systems by different administration in the TMJOA treatment, and summarizes their effects, duration, safety, and limitations, which would pave the way for development of TMJOA therapy.
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