Using "Mighty Mouse" to understand masticatory plasticity: myostatin-deficient mice and musculoskeletal function

Knockout mice lacking myostatin (Mstn), a negative regulatorof the growth of skeletal muscle, develop significant increasesin the relative mass of masticatory muscles as well as the abilityto generate higher maximal muscle forces. Wild-type and Mstn-deficientmice were compared to investigate the postnatal influence ofelevated masticatory loads due to increased jaw-adductor andbite forces on the biomineralization of mandibular articularand cortical bone, the internal structure of the jaw joints,and the composition of temporomandibular joint (TMJ) articularcartilage. To provide an interspecific perspective on the long-termresponses of mammalian jaw joints to altered loading conditions,the findings on mice were compared to similar data for growingrabbits subjected to long-term dietary manipulation. Statisticallysignificant differences in joint proportions and bone mineraldensity between normal and Mstn-deficient mice, which are similarto those observed between rabbit loading cohorts, underscorethe need for a comprehensive analysis of masticatory tissueplasticity vis-à-vis altered mechanical loads, one inwhich variation in external and internal structure are considered.Differences in the expression of proteoglycans and type-II collagenin TMJ articular cartilage between the mouse and rabbit comparisonssuggest that the duration and magnitude of the loading stimuluswill significantly affect patterns of adaptive and degradativeresponses. These data on mammals subjected to long-term loadingconditions offer novel insights regarding variation in ontogeny,life history, and the ecomorphology of the feeding apparatus.