title: Morphological changes of skeletal muscle, tendon and periosteum in the senescence-accelerated mouse (SAMP6): a murine model for senile osteoporosis.
abstract: SAMP6, a substrain of senescence-accelerated mouse, was developed as an animal model for senile osteoporosis. Previously we observed age-related changes of the bone in SAMP6. In the present study, we investigated the morphology of the skeletal muscle, tendon and periosteum in SAMP6 and age-matched normal mouse SAMR1. We did not find any significant differences between SAMR1 and SAMP6 at 1 and 2 months of age. As compared with SAMR1, the cross-sectional area of type I and type II muscle fibers of the soleus muscle were significantly low in SAMP6 at 8 months of age. The projections in the interface of the muscle-tendon junctions were significantly decreased in SAMP6 at 8 months of age. The number of fibroblasts and the diameter of the tendon collagen fibers in Achilles fiber were significantly reduced in SAMP6 at 8 months of age. The diameter of Sharpey's fiber reduced in SAMP6 at 5 and 8 months of age. Some chondrocytes in the insertions of Achilles tendon and some osteogenic cells in the periosteum showed degenerative changes in SAMP6 at 5 and 8 months of age. The pronounced degenerative changes were detected in the skeletal muscle, muscle-tendon junction, tendon, tendon-bone interface and periosteum in SAMP6 with age. These findings indicated the atrophy of skeletal muscle, degeneration of tendon and periosteum in SAMP6, which may be involved in the bone loss for senile osteoporosis.
authors.affiliation: Department of Anatomy, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan. huayue@cc.gifu-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Chen
authors.forename: X F
authors.initials: XF
authors.lastname: Yao
authors.forename: S
authors.initials: S
authors.lastname: Emura
authors.forename: S
authors.initials: S
authors.lastname: Shoumura
mesh_terms: D000125:Achilles Tendon / Q000473:pathology / Q000503:physiopathology; D019588:Aging, Premature / Q000235:genetics / Q000473:pathology*; D000818:Animals; D019902:Chondrocytes / Q000473:pathology; D003094:Collagen / Q000648:ultrastructure; D004195:Disease Models, Animal; D004721:Endoplasmic Reticulum / Q000473:pathology; D005260:Female; D005347:Fibroblasts / Q000473:pathology; D051379:Mice; D008817:Mice, Mutant Strains; D008855:Microscopy, Electron, Scanning; D046529:Microscopy, Electron, Transmission; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D018482:Muscle, Skeletal / Q000473:pathology* / Q000503:physiopathology; D009133:Muscular Atrophy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D010024:Osteoporosis / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D010521:Periosteum / Q000473:pathology* / Q000503:physiopathology; D013710:Tendons / Q000473:pathology* / Q000503:physiopathology
chemical_list: D003094:Collagen