Abstract
Exosomes are nanosized vesicles (30–140 nm) of endocytic origin that play important roles in regenerative medicine. They are derived from cell membranes during endocytic internalization and stabilize in biological fluids such as blood and synovia. Temporomandibular joint osteoarthritis (TMJ OA) is a degenerative disease, which, in addition to chronic pain, is characterized by progressive cartilage breakdown, condylar bone remodeling, and synovitis. However, traditional clinical treatments have limited symptom- and structure-modifying effects to restore damaged cartilage and other TMJ tissues. This is due to the limited self-healing capacity of condylar cartilage. Recently, stem-cell-derived exosomes have been studied as an alternative therapeutic approach to tissue repair and regeneration. It is known that trophic regulation of mesenchymal stem cells (MSCs) has anti-inflammatory and immunomodulatory effects under pathological conditions, and research on MSC-derived exosomes is rapidly accumulating. MSC-derived exosomes mimic the major therapeutic effects of MSCs. They affect the activity of immune effector cells and possess multilineage differentiation potential, including chondrogenic and osteogenic differentiation. Furthermore, exosomes are capable of regenerating cartilage or osseous compartments and restoring injured tissues and can treat dysfunction and pain caused by TMJ OA. In this review, we looked at the uniqueness of TMJ, the pathogenesis of TMJ OA, and the potential role of MSC-derived exosomes for TMJ cartilage and bone regeneration.
Highlights
The temporomandibular joint (TMJ) is a unique joint that connects the mandibular condyle with the articular surface of the temporal bone, accompanied by hinge and gliding activity
Potential prognostic indicators or diagnostic markers for Temporomandibular joint osteoarthritis (TMJ OA) have not been identified to date, and further investigation is needed to determine whether the markers for cartilage degradation in TMJ synovial fluid increase
Another possible mechanism by which TMJ OA may arise is from alterations in the ECM; this might be due to genetic disturbances that directly alter the composition of the ECM in the TMJ, or indirectly due to changes in composition and/or turnover of the ECM caused by other genetic factors
Summary
The temporomandibular joint (TMJ) is a unique joint that connects the mandibular condyle with the articular surface of the temporal bone, accompanied by hinge and gliding activity. Traditional clinical treatments mainly include nonsurgical options, such as psychotherapy, physical therapy, occlusal stabilization splints, medication, and arthrocentesis, while surgical intervention has been applied to patients with severe symptoms [11,12] These abovementioned treatments can prevent disease progression to a certain degree, they are unable to completely restore degraded cartilage or subchondral bone lesions, as well as disc deteriorations. In the developmental stages of the TMJ, MSCs split within themselves to divide into even smaller cells, eventually attaining full size These MSCs migrate into the interior condyle and into is the high density of fibers that can withstand static load and forces of movement, which are less likely to break down over time and less affected by aging than are other joints [24]. These MSCs migrate into the interior condyle and into the cartilage, where cell differentiation occurs, and the differentiated cells become immature tchheoncadrrtoilcaygtees, w[2h1e].reTcheellgdroiffwetrhenitniatthioenToMccJucras,rtailnadgethoecncuthrse mdiaffienrleyntthiartoeudgcheltlhsebdecifofmereenitmiamtioanturoef cmheosnednrcohcyymteasl [ti2s1s]u. e,Trhaethgerrotwhathn uinndtheer tThMe iJncflauretinlacgeeofomcciutorssismoafincalyrtitlhargoeupgrhogtheneitdoirffceerlelns.tiTahtieoTnMofJ mis ensoent cfhuyllmy aclhtaisrsaucete,rriaztehderbtuhtanshuonwdserhtihsetoilnoflguiceanlc, eaonfamtoimtoisciasl,ofancadrtdileavgeelporpomgeennittaolrdcieflflesr. eTnhceesTMfroJmis notohtefrulbloydcyhajoraincttse,riwzehdicbhuatrsehloikweslyhitsotoalfofegcictatlh,eancaautosme,ipcarle,dainspdodseitvioelno,pomr epnrotaglrdesiffsieornenocfeTs MfroJmdiosethaseer banoddyrejoqiunitrse, fwurhtihcehr asrteudliyk.ely to affect the cause, predisposition, or progression of TMJ disease and require further study
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