Biomedical Engineering Reference
In-Depth Information
Notwithstanding the genetic or environmental effects on trabecular bone
structure prior to adulthood [
45
], future susceptibility to osteoporotic fractures will
be minimised, for an individual, if consideration is given to maximizing bone
health during these formative years. It has been shown that the skeleton is capable
of very high calcium absorption during growth [
45
], which allows for rapid
modeling and optimization of the trabecular architecture, particularly at sites
where the majority of osteoporotic fractures occur.
6 Trabecular Bone Structure in the Adult
Peak bone mass and thus, maximal bone strength is attained late in the 3rd decade
of life [
45
]. Complete cessation of endochondral bone formation means that further
change in trabecular bone structure is primarily through remodeling of existing
trabeculae. Regulation of the bone basic multicellular unit (BMU) through the
coordinated action of osteoclasts and osteoblasts has been well characterised at
morphological, physiological and molecular levels, which has provided insights
into how trabecular bone is maintained, repaired and remodeled in response to
physiological or mechanical stimuli. Histomorphometric studies have shown that
the sequence of cellular events that occur when bone is removed and subsequently
replaced by unmineralized matrix (osteoid) can be quantified in time and space and
in vivo fluorochrome labeling has enabled the rate of mineralization of the osteoid
to be measured. Together these measured parameters provide a detailed snapshot of
an individual's bone metabolism at the site of sampling. It has been suggested that
remodeling can be targeted or untargeted [
82
,
83
], where targeted remodelling is
most usually a reparative process in response to damage accumulation [
13
,
82
,
83
],
which is initiated by disturbance to the cannilicular network as microcracks pro-
gress within the bone matrix. The amount of bone turnover has been shown to be in
excess of the that required to maintain mechanical competence therefore it is has
been suggested that, while initially targeted, there is some remodeling that con-
tinues even when the initiating stimulus is no longer present [
82
,
83
].
From the 4th to 6th decades studies have shown that trabecular bone volume
fraction can decline by up to 40-50% for males and females [
1
,
45
,
68
,
73
]
although the rate of decline is sex-dependent, site-dependent and study cohort
dependent. An exception to this general pattern is in lactation, where up to 10% of
bone mass is lost in response to the nutritional imperative of milk production,
where the bone loss is mediated by mammary gland-derived parathyroid hormone
related-protein (PTHrP) in combination with low estrogen levels [
16
]. Fortunately,
this insult to the skeleton is transient with rapid restoration of bone mass after
weaning and it is not thought to infer greater susceptibility to fracture later in life.
In clinically relevant skeletal sites, there are significant differences in the
bone volume fraction of trabecular bone between males and females [
4
], which
are associated with differences in the trabecular microstructure [
1
]. There is
also considerable variability in trabecular microstructure within skeletal sites
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