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which compose 10% of bone
’
s organic matrix, also may affect bone
mechanical properties. Osteocalcin stimulates mineral maturation,
inhibits bone formation, recruits osteoclast precursors to bone
resorption sites, and helps with their differentiation into mature
osteoclasts [107]. Osteopontin plays a role in mineralization and assists
the bone resorption process by anchoring osteoclasts to the mineral
matrix of the bone surface [88]. More importantly, these proteins have
been recently considered to act as the glue that holds mineralized
collagen fibers together. When a force is applied, these components
stretch, help dissipate energy by breaking sacrificial bonds between
adjacent collagen fibrils, and prevent harmful crack formation and
propagation [108]. Thus, alterations to the matrix composition of both
collagenous
and
non-collagenous proteins may alter bone biomech-
anical properties. Increased serum osteocalcin and osteopontin has
been reported in postmenopausal womenwith osteoporosis compared
to healthy controls [109,110].
In summary, there is increasing evidence of the role of bone
’
s
organic matrix on age- and disease-related changes in bone
’
s
mechanical properties. Enzymatic crosslinking of collagen is generally
considered to have a positive effect on bone
’
s mechanical properties,
while non-enzymatic crosslinking can lead to deteriorated bone
mechanical properties with aging and disease. Non-collagenous
proteins play a role in the prevention of harmful microdamage
formation. Though osteoporosis is generally defined as a loss of bone
mass, there are considerable matrix changes, particularly in collagen
crosslinks, which cause a loss of bone quality.
Conclusions
The bone
’
s inorganic and organic composition, its trabecular and
cortical nano-, micro-, and macroscopic architecture, and the hetero-
geneity of these structural features all have impact on age- and disease-
related changes in bone
’
s mechanical properties. Though osteoporosis
is generally defined as a loss of bone mass, there are considerable
changes of the structure and matrix itself, which can cause a loss of
bone quality.
It is known, that cortical bone plays a major role in determining the
mechanical competence of bone and the risk of fracture; the age-
related alterations of its geometrical features and its local porosity,
though, have long been poorly understood and underestimated. The
number of trabeculae in trabecular bone, trabecular thickness and the
degree of connectivity all influence the mechanical strength of a bone.
In osteoporosis a decrease of all these characteristics is seen. Especially
in bones with increased risk for osteoporotic fractures, however, the
remaining trabecular tissue is largely heterogeneous, with regions of
different mineralization, stiffness and strength.
Both, the trabecular and the cortical component undergo different
changes at different times. Bone remodelling occurs on osseous
surfaces and, thus, osteoporotic bone loss is a function of surface
available for bone remodelling. The bone loss in early osteoporosis is
mainly trabecular and with increasing age the bone loss becomes
primarily endo- and intracortical.
The knowledge about this evolution in matrix and structure in
osteoporotic bone and about the differences between trabecular and
cortical bone could help with predicting, avoiding and treating
osteoporotic fractures. Future clinical imaging techniques will have to
consider structural measures of cortical and trabecular bone rather
than focusing on bone mineral density alone. In prophylactic treatment
regimens, the aimed for therapeutic region (i.e. trabecular versus
cortical) and mechanisms of action within the cascade of bone
remodelling might have to be chosen according to the patient
’
s age
and the individual advancement of bone changes. Eventually, when a
fracture has occurred, the non-operative or surgical treatment has to
be guided by both: the personality of a patient and the personality of
their bone.
Conflict of interest
The authors report no conflict of interest related to the content of
the manuscript.
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