Biomedical Engineering Reference
In-Depth Information
sections through remodeling. In particular, mechanical loading has a
significant influence on bone remodeling. Disused or reduced loading due to
long-term bed rest, casting immobilization, or microgravity conditions (such
as experienced by astronauts in a space station or shuttle) induces obvious
bone loss and mineral changes [7,8], probably because of a lack of convective
fluid flow in the canalicular network. Overuse or increased loading, such
as experienced with weightlifting exercises, causes damage to bone tissues,
which in turn stimulates bone remodeling and eventually achieves bone gain.
The two important roles of bone remodeling are continuously to replace
and repair (1) damaged bone tissues and (2) mineral homeostasis by provid-
ing access to stores of calcium and phosphate. Osteoclasts start resorbing
bone in response to signals that are as yet unknown but may include direct
damage to osteocytes via microcracks in the bone matrix.
The adaptive response of bone to mechanical loading is highly site spe-
cific. This is clearly evident at the whole-bone level, with only the bone that
is actually loaded undergoing adaptation [9]. This concept is supported by
much human research investigating skeletal health indices in athletes, espe-
cially in players of racquet sports such as tennis, whose bones of the racquet
arm or dominant arm display significantly greater bone mineral density and
cortical bone content than in the nonplaying arm [10,11]. The site-specific
depositing of new bone is functionally important. The site-specific deposit-
ing process puts newly formed bone where it is most required and increases
bone strength in the resistible direction of loading, while not necessarily
increasing the bone mass or density [12].
Experimental observations [13] show that, in comparison with other organ
systems, skeleton tissue is hypocellular and composed primarily of extracel-
lular matrix. Atrabecular bone is a porous latticework of struts or plates of
long bones, whereas cortical bone is a dense tissue of low porosity found in
the diaphyses of long bones. The microstructure of a cortical bone is orga-
nized as a hierarchical arrangement of porosities, including a network of
cellular spaces (lacunae), interconnections (canaliculi), and larger vascular
(osteonal) canals. This spectrum of microarchitecture features implies the
transformation of whole-skeleton loading via localized changes in remodel-
ing cycles.
Current understanding of bone remodeling is primarily based on experi-
mental results in vivo and in vitro. A great deal of research has been carried
out on the interactions of autocrine, paracrine, and endocrine activities of
receptors and ligands in bone remodeling and mechanotransduction path-
ways; the role of bone cells involved in this process at cellular and even genic
levels; and the influence of mechanical loading on bone formation in bone
remodeling. Based on these observations, many hypotheses have been pro-
posed as to the role played by different signaling pathways and the commu-
nication between bone cells in bone remodeling. Similarly, many hypotheses
have also been reported in the literature regarding bone-cell dynamics of
both trabecular and cortical bones under mechanical stimulus. However,
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