Morse, A. et al. Mechanical load increases in bone formation via a sclerostin-independent pathway.
Two weeks of mechanical loading increased BV/TV, trabecular thickness and trabecular BMD in the loaded tibia by 12%23%% when compared to non-loaded tibia in all four groups of mice but there was no significant difference in the bone response between the groups in response to loading.
In this study, we observed that changes in mechanical loading increased mTORC1 activity in subchondral bone preosteoblasts in mice and in vitro.
Two weeks of mechanical loading increased total bone volume (TV) by 7%–10%, BMD by 7%–8% and cortical thickness by 10%13%% in the loaded tibia when compared to non-loaded tibia of control sham, H IGF-I KO sham and control pOVX mice.
The osteocyte activity, resulting from excess mechanical loading, increases the respective activities of osteoblasts and osteoclasts, as evident from increase in the expression of matrix proteins (COL1A, SPARC, and IBSP) and osteoclast-specific enzymes (CTSK and ACP5) (Table 3 & 4; Figure 5).
The loading-condition dependence addresses recent debates about whether mechanical load increases or decreases the MMP cleavage rate of a monomer.
Because mechanical loading increases during development and facilitates cardiac maturation, we hypothesized that afterload would promote maturation of EHTs.
An example of reduced or inhibited apoptosis leading to scarring is in a model of hypertrophic scarring, where mechanical loading increases survival of myofibroblasts and was found to lead to greater scar formation.
Due to the yielding, the elastic region of the material is not permanently destroyed when the same mechanical load is increased.
Combined with our previous work and the work of others showing increases in Cx43 in synovial cells the OA joint, the present data support a model in which OA-associated changes in the joint (e.g., inflammation, altered mechanical load) can increase Cx43 expression.
