Biomedical Engineering Reference
In-Depth Information
microstrains (με). Above this threshold, remodeling was inhibited and bone
formation was initiated at the periosteal surface, which is consistent with the
Mechanostat theory. Detailed experiments by Jee, Li, and Ke [41] indicated
that a contralateral overloaded limb showed increased cancellous bone mass
due to inhibited remodeling and increased bone formation rate. An increase
of cortical bone mass on the periosteum was also observed. How, then, do
bone tissues sense strain-related signals, and how are the thresholds distin-
guished? The foregoing theories do not explain these functions.
It is well known that two kinds of bone cells are involved in the bone
remodeling (modeling) process: osteoblasts and osteoclasts. The for-
mer are responsible for bone formation and the latter for bone resorption.
Evidence has shown that age-related bone osteoporosis differs between
males and females. Accelerated bone loss in women during menopause is
associated with reduced levels of estrogen. Estrogen receptors are abun-
dantly expressed in osteocytes [42], but their expression is less in other cells
of the osteoblast lineage, which suggests that osteocytes are likely involved
in the regulation of estrogen-mediated bone remodeling (modeling).
Osteocytes can then be considered as mechanosensitive bone cells [43,44]
that are thought to activate other bone cells to initiate remodeling (modeling)
activity in response to environmental stimuli, thus playing a key role in the
regulation of bone remodeling (modeling) [45].
How the osteocytes participate in the remodeling (modeling) is still
unknown. Investigations [27,28,46] showed that PDGF, IGF, BMP, and TGF-β
exist in considerable quantities in bone matrix and play an important role in
bone formation and remodeling (modeling). Normally, they are retained in
osteocytes. Once the osteocytes are resorbed, the growth factors are released
into the bone fluid and stimulate osteoblasts to refill the resorption cavities.
Experiments have shown that a pulsed extremely low-frequency electromag-
netic field can stimulate the multiplication of growth factors [29-31]. Thus, it
can be seen that an electromagnetic field can influence the bone remodeling
(modeling) process indirectly.
5.2.4 Adaptive Bone Modeling and Remodeling
As we can see from the Mechanostat model described earlier, it is a relatively
mature hypothesis for a bone modeling and remodeling mechanism. But it
is far from perfect. It does not describe how local mechanical signals are
detected and how they are translated to bone formation and resorption. Nor
does it indicate what the signals and nonmechanical agents are during the
modeling and remodeling processes. Furthermore, although it distinguishes
the strain thresholds of each mode, the reason for the existence of these
thresholds is beyond its explanation capacity. To bypass these issues, elec-
trical signals are defined as stimuli and growth factors as nonmechanical
agents in this subsection. Then the modeling and remodeling processes of
bone under electromagnetic loads are shown.
