The effects of hypermuscularity on shoulder morphology in myostatin-deficient mice.
ABSTRACT Mechanical loads, particularly those generated by skeletal muscle, play a significant role in determining long-bone shape and strength, but it is less clear how these loads influence the morphology of flat bones like the scapula. While scapular morphology has been shown to vary with locomotor mode in mammals, this study seeks to better understand whether genetically modified muscle size can influence scapular shape in the absence of significant locomotor differences. The soft- and hard-tissue morphological characteristics were examined in 11 hypermuscular, mutant (myostatin-deficient), 20 heterozygote, and 15 wild-type mouse shoulders. Body mass did not significantly differ among the genotype groups, but homozygous mutant and heterozygote mice had significantly larger shoulder muscles than wild-type mice. Mutant mice also differed significantly from the wild-type controls in several aspects of scapular size and shape, including glenohumeral joint orientation, total scapular length, superior border length, and supraspinous and infraspinous fossa length. Conversely, several traits describing superoinferior scapular breadth measures (e.g. total breadth and dorsal scapular fossa breadth) did not significantly differ between mutant and wild-type mice. Since the intrinsic musculature of the scapula is oriented in a mediolateral fashion, it follows that mediolaterally configured hard-tissue features like scapular length were most distinct among genotype groups. As had been noted previously with long bones, this study demonstrates that genetically enhanced muscle size has marked effects on the morphological characteristics of the shoulder.
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ABSTRACT: Bone is a dynamic tissue that is constantly renewed. The cell populations that participate in this process--the osteoblasts and osteoclasts--are derived from different progenitor pools that are under distinct molecular control mechanisms. Together, these cells form temporary anatomical structures, called basic multicellular units, that execute bone remodeling. A number of stimuli affect bone turnover, including hormones, cytokines, and mechanical stimuli. All of these factors affect the amount and quality of the tissue produced. Mechanical loading is a particularly potent stimulus for bone cells, which improves bone strength and inhibits bone loss with age. Like other materials, bone accumulates damage from loading, but, unlike engineering materials, bone is capable of self-repair. The molecular mechanisms by which bone adapts to loading and repairs damage are starting to become clear. Many of these processes have implications for bone health, disease, and the feasibility of living in weightless environments (e.g., spaceflight).Annual Review of Biomedical Engineering 02/2006; 8:455-98. · 12.21 Impact Factor