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Bone adapts its shape in response to prevailing loads by bone modeling and remodeling at the outer and inner envelopes of the cortical shaft.
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It consists of primary spongiosa, which is directly connected with the growth plate and is mainly shaped by bone modeling during longitudinal growth, and secondary spongiosa, which is derived from the primary spongiosa by a bone remodeling process.
The delayed ossification persists into adulthood and is accompanied by impaired bone modeling and remodeling, resulting in short stature, increased bone mass, and gross morphologic abnormalities of the bones and joints, but normal bone strength.
Mechanical stress also modifies the contour and shape of subchondral bone by means of bone modeling and remodeling [ 16].
These findings could indicate that AMBN plays a role in early bone formation and modeling, but they have been contradicted by a study showing no implication in bone modeling and repair [ 38].
In bone modeling and remodeling, osteoclasts resorb mineral by acidifying the bone matrix (Blair 1998).
In addition, the expansion of bone marrow and buccal bone by the bone-derived mesenchymal matrix is thought to contribute to bone modeling and remodeling.
These signals are sensed by the bone cells and converted to biochemical events which regulate bone modeling and remodeling.
Bone metabolism in children is characterized by predominant bone modeling with simultaneous activity of both osteoblasts and osteoclasts on different parts of the bone.
However, the decrease in bone resorption despite heightened inflammation could have been caused by age-dependent bone modeling processes [ 42, 62] between 4 and 8 days as bone has a rapid rate of turnover.
No detrimental effects of high Ca were observed on bone modeling (assessed by histomorphometry and bone markers), at least in this short-term intervention.
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