Characterisation of Trabecular Bone Structure - Skeletal Aging and Osteoporosis: Biomechanics and Mechanobiology - page 33

osteoporosis [ 69 , 70 , 89 , 91 ], but ethical issues and the availability of clinical non-
invasive imaging have greatly reduced this source of material. Societal sensitivi-
ties and government regulation have also restricted the availability of cadaveric
material, which has tended to constrain these studies to an older age range thus
limiting the clinical relevance of studies [ 34 , 36 ].
Metaphyseal bone structure is determined early in development as secondary
trabeculae emerge from the primary spongiosa in the epiphyseal plates during
endochondral bone growth [ 14 , 42 ]. Modelling of individual bones in childhood
and adolescence occurs through periosteal apposition and endosteal resorption to
change the size and shape of the cortical shell of the bone and the trabeculae in the
trabecular bone compartment; these appeat to adapt in a coordinated manner to
maintain the ability to withstand the extant loads [ 45 , 82 , 83 , 109 ].
After closure of the epiphyseal growth plates at skeletal maturity, bone
remodelling becomes the predominant means by which bone is added or removed
from the trabecular compartment [ 45 ]. It is now well established that the archi-
tecture of trabecular bone is dependent on the forces acting upon it and the high
surface area of the bone mineral in the bone tissue marrow facilitates the cellular
events, which remove or deposit bone in a highly dynamic environment [ 45 ].
Coordination of the cellular events may be at the tissue level for events such as
removal of damaged bone [ 82 , 83 ], at the organ level for modelling due to changed
usage pattern, or the whole body level for involutional events such as the meno-
pause in females [ 90 ]. The consequences of these scenarios at all size scales can be
to decrease the load needed to cause a fracture, where in-built safety margins in
load carrying capacity are reduced [ 8 ].
From the time of attainment of peak bone mass, studies show that there is a
decrease in trabecular bone volume with aging in both sexes [ 68 ], although not at all
sites and not uniformly for males and females [ 9 ]. The specific cause of these age-
related changes in individuals is unclear as most studies were cross-sectional in
nature making it difficult to track the many factors that influence bone mass, such
as the loading history of the individuals. While it is known that trabecular bone
architecture changes according to the loading history of the individual, there are
other factors, such as nutrition, co-morbidities, social activities and work activities
that affect bone metabolism, independent of direct mechanical stimuli [ 54 ].
In females, changes in trabecular bone are most evident at and after the men-
opause, which is associated with decreased estrogen [ 22 ]. The greatly increased
activation of osteoclasts associated with decreased oestrogen in menopausal
females results in an imbalance between resorption and formation with a conse-
quent net bone loss [ 90 ]. In males, the reduction in sex-hormone (androgen)
production is typically more gradual but is associated with significant net bone loss
over time as a consequence of increased resorption relative to formation [ 55 , 103 ].
The consequence of menopausal or age-related bone loss for females and males,
respectively, is a marked increase in fracture incidence, although the changes to
the trabecular bone architecture are different between sexes [ 43 , 109 ]. In general,
menopausal females lose trabecular bone through perforation of trabeculae, which
are then either completely removed or transformed from plate-like to rod-like