LAUSR

Craniofacial secondary cartilages of the mandibular condyle and temporomandibular joint (TMJ) eminence grow in response to the local mechanical environment. The intervening TMJ disc distributes normal loads over the cartilage surfaces and provides lubrication. A better understanding of the mechanical environment and its effects on growth, development, and degeneration of the TMJ may improve treatments aimed at modifying jaw growth and preventing or reversing degenerative joint disease (DJD). This review highlights data recorded in human subjects and from computer modeling that elucidate the role of mechanics in TMJ ontogeny. Presented data provide an approximation of the age-related changes in jaw-loading behaviors and TMJ contact mechanics. The cells of the mandibular condyle, eminence, and disc respond to the mechanical environment associated with behaviors and ultimately determine the TMJ components’ mature morphologies and susceptibility to precocious development of DJD compared to postcranial joints. The TMJ disc may be especially prone to degenerative change due to its avascularity and steep oxygen and glucose gradients consequent to high cell density and rate of nutrient consumption, as well as low solute diffusivities. The combined effects of strain-related hypoxia and limited glucose concentrations dramatically affect synthesis of the extracellular matrix (ECM), which limit repair capabilities. Magnitude and frequency of jaw loading influence this localized in situ environment, including stem and fibrocartilage cell chemistry, as well as the rate of ECM mechanical fatigue. Key in vivo measurements to characterize the mechanical environment include the concentration of work input to articulating tissues, known as energy density, and the percentage of time that muscles are used to load the jaws out of a total recording time, known as duty factor. Combining these measurements into a mechanobehavioral score and linking these to results of computer models of strain-regulated biochemical events may elucidate the mechanisms responsible for growth, maintenance, and deterioration of TMJ tissues.