Biomedical Engineering Reference
In-Depth Information
includes effects of porosity as well, which increases with bone loss and is well
related to skeletal failures [
13
,
14
,
55
]. BMD is distinct from degree of mineral-
ization (DOM), which is quantitated microscopically and measured at tissue level
(refer to
Sect. 2.1
) and is often represented as a ratio against collagen matrix.
Earlier studies observed higher degree of mineralization in trabecular bone of
osteoporotic individuals (low BMD) suggesting that despite bone loss, individuals
can still have higher DOM [
7
]. Bone mineralization was also found to correlate
highly with strength [
62
] implying bone quality measures may complement BMD
in predicting fracture risk.
Degree of mineralization was observed to be greater in individuals with hip
fractures [
142
,
157
]. Wu et al. suggested that low turnover may possibly be
responsible for the increase in DOM, yet, a lower bone turnover assumption does
not align well with the reduction in bone mass in osteoporotic individuals or the
positive association between bone turnover and fracture risk. An alternative
explanation of increasing average mineralization in the face of increasing
resorption and less bone is based on a relative increase in more mineralized
interstitial bone with greater turnover of selective osteons [
55
]. In other words,
bone of younger tissue age is preferentially resorbed and the bone that remains
tends to have older tissue age and thus be more mineralized. In contrast to above
mentioned studies, reduced mineralization is reported in osteoporotic humans [
96
]
and overectomized monkeys [
70
], a good model for post-menopausal osteoporotic
women [
87
]. Loveridge reported less mineralization in the femoral neck regions of
patients with hip fractures when compared to controls and they could not establish
any relationship between mineralization and remodeling dynamics. In their
opinion vitamin D deficiency might be the potential cause for decreased miner-
alization in fractured individuals because involvement of vitamin D deficiency was
earlier implied in hip fractures [
60
], which is believed to increase bone turnover
and decline mineralization rate, resulting in fast removal and slow maturation of
bone mineral. Other reasons like genetic defects in collagen and osteocyte apop-
tosis were also considered in interpreting their results. However, the samples had
no known genetic defects and were neither measured for vitamin D nor analyzed
for osteocytes.
Boskey et al. has pointed out that osteoporosis can occur by high turnover
(greater than normal resorption rate) or low turnover (lower than normal formation
rate) [
23
]. High turnover regime tends to shift the balance to lower mineralization
and lower crystallinity, whereas the low turnover regime may result in a relatively
greater mineralization and mineral maturity. Therefore, while both regimes result
in lower bone mass there may be differing outcomes of osteoporosis in terms of
matrix mineralization. It is clear that remodeling dynamics shapes the degree of
mineralization, besides the rate of crystal growth, and such associations remain to
be investigated. Biochemical markers can be used to distinguish high and low
turnover osteoporosis as a systemic indicator of remodeling [
44
,
53
,
107
]. Yet,
occurrence of fractures in specific anatomical locations indicates the need for site
specific means to determine resorption and formation dynamics. As of yet, such
analyses cannot be conducted non-invasively and mostly depend on assessment of
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