Abstract:The experimental increase in mechanical usage or overloading of the left hindlimb was produced by immobilization of the contralateral hindlimb. The right hindlimb was placed in a flexed position against the body and was immobilized using an elastic bandage. Some control animals were sacrificed initially at time zero and increased mechanical usage and age-matched control animals were sacrificed after 2, 10, 18, and 26 weeks of treatment. All animals received double bone fluorochrome labeling prior to sacrifice.… Show more
“…For example the coefficient of variation for cortical bone area in rodent long bones is in the range of 10-15% (42, 64). As area weighted moments of inertia, these small differences in bone geometry will lead to different structural stiffnesses among bones such that stresses applied to the ulnae (and resulting local strains) will differ among animals for the same applied load magnitude.…”
Recent experiments point to two predominant forms of fatigue microdamage in bone: linear microcracks (tens to a few hundreds microns in length) and “diffuse damage” (patches of diffuse stain uptake in fatigued bone comprised of clusters of sublamellar-sized cracks). The physiological relevance of diffuse damage in activating bone remodeling is not known. In this study microdamage amount and type were varied to assess whether linear or diffuse microdamage have similar effects on the activation of intracortical resorption. Activation of resorption was correlated to the number of linear microcracks (Cr.Dn) in the bone (R2=0.60, p<0.01). In contrast, there was no activation of resorption in response to diffuse microdamage alone. Furthermore, there was no significant change in osteocyte viability in response to diffuse microdamage, suggesting that osteocyte apoptosis, which is know to activate remodeling at typical linear microcracks in bone, does not result from sublamellar damage. These findings indicate that inability of diffuse microdamage to activate resorption may be due to lack of a focal injury response. Finally, we found that duration of loading does not affect the remodeling response. In conclusion, our data indicate that osteocytes activate resorption in response to linear microcracks but not diffuse microdamage, perhaps due to lack of a focal injury-induced apoptotic response.
“…For example the coefficient of variation for cortical bone area in rodent long bones is in the range of 10-15% (42, 64). As area weighted moments of inertia, these small differences in bone geometry will lead to different structural stiffnesses among bones such that stresses applied to the ulnae (and resulting local strains) will differ among animals for the same applied load magnitude.…”
Recent experiments point to two predominant forms of fatigue microdamage in bone: linear microcracks (tens to a few hundreds microns in length) and “diffuse damage” (patches of diffuse stain uptake in fatigued bone comprised of clusters of sublamellar-sized cracks). The physiological relevance of diffuse damage in activating bone remodeling is not known. In this study microdamage amount and type were varied to assess whether linear or diffuse microdamage have similar effects on the activation of intracortical resorption. Activation of resorption was correlated to the number of linear microcracks (Cr.Dn) in the bone (R2=0.60, p<0.01). In contrast, there was no activation of resorption in response to diffuse microdamage alone. Furthermore, there was no significant change in osteocyte viability in response to diffuse microdamage, suggesting that osteocyte apoptosis, which is know to activate remodeling at typical linear microcracks in bone, does not result from sublamellar damage. These findings indicate that inability of diffuse microdamage to activate resorption may be due to lack of a focal injury response. Finally, we found that duration of loading does not affect the remodeling response. In conclusion, our data indicate that osteocytes activate resorption in response to linear microcracks but not diffuse microdamage, perhaps due to lack of a focal injury-induced apoptotic response.
“…In addition, the effect of mechanical strain on bone-resorbing activity and mRNA expression of osteoclast marker enzymes (tartrate-resistant acid phosphatase, TRAP; cathepsin K) was examined using isolated osteoclasts (Kurata et al, 2001). In an isolated osteoclast culture, the bone-resorbing activity was up-regulated (Kurata et al, 2001), although it is known that bone mass increases by mechanical strain (Jee et al, 1991;Turner et al, 1991;Mosley et al, 1997;Srinivasan et al, 2003). Therefore, a suitable in vitro model system will be necessary to analyze osteoclastic function under unloading or loading conditions.…”
“…Force exerted by a muscle is proportional to the product of the physiological cross-sectional area and fiber length and thus to muscle volume (Van Eijden et al, 1997). The present findings may be explained by previous animal experiments demonstrating that bone mass increases as an effect of mechanical load on long bones (Jee and Li, 1990;Jee et al, 1991) and that the increase in bone mass has a linear relationship with the magnitude of strain (Rubin and Lanyon, 1985). Although inheritance clearly has a strong influence on facial features (Proffit, 1993), skeletal morphology is modified by the mechanical stresses placed on it.…”
Although several investigators have reported associations between masticatory muscles and skeletal craniofacial form, there is no agreement on the association. We tested the hypothesis that masticatory muscle volume correlates with the size and form of the adjacent local skeletal sites. For this purpose, we investigated the morphological association of the cross-sectional area and volume of temporal and masseter muscles with zygomatico-mandibular skeletal structures using computerized tomography (CT) in 25 male adults with mandibular prognathism. Muscle variables significantly correlated with widths of the bizygomatic arch and temporal fossa but not with the cranium width. Masseter volume significantly correlated with cross-sectional areas of the zygomatic arch and mandibular ramus. Masseter orientation was almost perpendicular to the zygomatic arch and mandibular antegonial region. The zygomatic arch angle significantly correlated with the antegonial angle. The results of the study suggest that the masticatory muscles exert influence on the adjacent local skeletal sites.
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