Biomedical Engineering Reference
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attached to the exterior surface of the bone. It has been reported that the periosteum
acts as a barrier to bone fluid flow [61]. The endosteum is simply a monolayer
of cells. Multiple layers of cells at various stages of differentiation lie under the
periosteum.
There are two interfaces between the three levels of bone porosity within the cor-
tical bone and within the trabeculae of the cancellous bone: the PV/PLC interface
and the lacunar- canalicular/collagen- hydroxyapatite porosity interface. Topologi-
cally, the entire lacunar-canalicular/collagen- hydroxyapatite porosity interface is
completely contained within the PV/PLC interface.
The first important point concerning these interfaces, and the porosities de-
scribed above, is that they change rapidly after birth, being quite porous at birth
and subsequently reducing their porosity as the bone tissue becomes fully min-
eralized [61, 62]. Experimental permeability studies clearly show time-dependent
changes in the interstitial pathways as the bone matures. At the earliest times,
the unmineralized collagen-proteoglycan bone matrix is porous to large solutes.
A study [63] with ferritin (10 nm in diameter) in a two-day-old chick embryo
shows a continuous halo around primary osteons 5 min after the injection of
this tracer. The halo passes right through the lacunar- canalicular system sug-
gesting that, before complete mineralization, pores of a larger size can exist
throughout the bone matrix. It was later demonstrated [64, 65] that such halos
were very likely an artifact of histological processing and could be eliminated by
shortened fixation methods [4]. These studies found that ferritin was confined
exclusively to the vascular canals and blood vessels and did not enter the PLC.
The porosity in puppies is 3.5 times higher than that in dogs [61]. In this work,
only the adult or fully mineralized situation is described. The PV/PLC interface,
which separates the mineralized tissue from the vascular channels, is considered
first.
The region interior to the PV/PLC is called the '' milieu interieur ,'' and the
existence of a ''bone membrane'' that would coincide with what we call the
vascular/lacunar-canalicular porosity interface was suggested [66]. This interface is
a continuous layer of bone lining cells [67]; all the surfaces of the Haversian canals
and the Volkmann canals are a part of this interface as is the endosteum. There
is a report on tight junctions occurring in the bone lining cells on the interface
[62]. In [15], it was noted that the bone fluid of the PV (serum) and the bone fluid
of the PLC (extracellular fluid) were nearly equivalent in composition (pH, Ca ++ ,
Na + , etc.), but it was argued that there must be some diffusion barrier, some ion
gradient or ion pump, between the two fluid compartments, a view revised later
[17]. It has been analytically demonstrated that there are high transient pressure
gradients across the interface that serve to move the bone water across the interface
[53]. The bone lining cells with tight junctions do not form a significant barrier
to the transport of bone water across this interface. During each cycle of bone
loading, the bone fluid of the PV (serum) briefly mix with the bone fluid of the PLC
(extracellular fluid). As a first approximation it appears reasonable to assume that
the permeability of this interface is equal to the permeability of the PLC.
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