Biomedical Engineering Reference
In-Depth Information
poroelasticity theories for fractured geological structures are democratic; their fluid
transport channels of a particular size may exchange fluid with transport channels
of any pore size. The primary objective of this work is to provide a model of a
poroelastic pore structure that is appropriate for bone tissue; it is a model that is
easily extended to other tissues such as the tendon and the meniscus. Concerning
bone, the principal focus is on the modeling of the mechanical and blood pressure
load-driven movements of the interstitial bone fluid flow.
The absence of the assumption of incompressible constituents is a significant
difference between the version of poroelasticity theory employed in [91] and the
poroelasticity theory used for previous published solutions involving soft tissues.
The assumption of incompressible constituents, while appropriate for soft tissues,
is inaccurate for hard tissues. The solution for the unconfined compression of
an annular, transversely isotropic, poroelastic hollow cylinder with compressible
constituents was recently presented [57]. On the basis of this solution, a protocol has
been devised for an experimental test procedure to determine tissue permeabilities
for the smallest nested bone porosity, the osteonal lumen wall, and the osteonal
cement line. This protocol will extend to bone tissue an experimental technique
that has been very effective in determining soft tissue poroelastic properties [56].
As noted above, current theoretical and experimental evidence suggests that the
bone cells in the lacunae (pores) of the PLC are the principal mechanosensory cells
ofthebone,andthattheyareactivatedbytheinduceddragfromfluidflowing
through the PLC [1, 2]. The movement of bone fluid from the region of the bone
vasculature through the canaliculi and the lacunae of the surrounding mineralized
tissue accomplishes three important tasks. First, it transports nutrients to the cells
in the lacunae buried in the mineralized matrix. Second, it carries away the cell
waste.Third,thebonefluidexertsaforceonthecellprocess- aforcethatislarge
enough for the cell to sense. This is thought to be the basic mechanotransduction
mechanism in the bone - the way in which the bone senses the mechanical load to
which it is subjected. Understanding bone mechanotransduction is fundamental
to the understanding of how to treat osteoporosis, how to cope with microgravity in
long-term manned space flight, and how to design prostheses that are implanted
in bone tissues to function for longer periods.
These considerations suggest that the PV and PLC function almost indepen-
dently, the prime mechanical influences for the two porosities being very different
as are the timescales of their response. The mechanical loading of the whole bone
moves the bone fluid in the PLC. When the bone is compressed, the bone fluid is
driven from the PLC into the low-pressure PV, and when the bone is in tension,
or the compression is reduced, the bone fluid is sucked from the PV into the PLC.
These drainage and imbibing processes occur on a pressure timescale that is much
larger than the short pressure adjustment relaxation time for the PV and therefore
have minimum influence on the pressure in the PV. The change in interstitial pore
fluid pressure in the PV due to inflow or outflow of bone fluid from the PLC is
insignificant because of the time period of pressure adjustment, which is much
shorter (estimates of these time periods are in Zhang
et al
. [53]) than the pressure
adjustment time period for the PLC. While the bone fluid in the PLC is significantly
