Biomedical Engineering Reference
In-Depth Information
Various studies assessed treatment strategies of osteoporosis to counter bone loss,
particularly the bisphosphonates and anabolic agents. In most cases, bishphospho-
nates succeeded in increasing bone density [
59
,
111
] and degree of mineralization
[
20
,
135
] by prolonging secondary mineralization. Hormone replacement therapy
(HRT) was used for the treatment and prevention of osteoporosis, which improved
mineral content and the statistical distribution of the population of crystal sizes in
postmenopausal women [
118
]. A decrease in the average crystal size was observed
in early postmenopausal women treated with HRT [
118
]. Fluoride therapy was one
of the treatments that directly affected mineral properties, especially crystal size,
along with mineral density [
12
]. Though crystal length was increased, crystal width
was decreased, which would reduce the ability of bone tissue to bear high loads [
40
].
That may be one reason why fluoride treatment failed to reduce the incidence of hip
fractures [
130
]. In addition, the mineral crystal's interaction with organic matter
may have been disturbed by the altered crystal size in fluoride therapy [
109
].
Intermittent parathyroid hormone treatment (PTH) increased formation of new
bone matrix and mineral crystals [
119
]. This conclusion was based on the
observation of shifts in mineral/matrix ratio and crystallinity towards lower values
in both animals [
138
] and humans [
110
]. Other bone quality properties like
compositional changes in bone minerals caused by anabolic agents were also
investigated. Overiectomized rats [
19
] and monkeys [
70
] treated with bisphos-
phonates and monitored using infrared spectroscopy demonstrated no change in
carbonate and acid phosphate content. However cancellous bone in dogs treated
with calcitonin, which inhibits osteoclasts, exhibited increased levels of carbonate
which possibly may have happened due to delayed mineralization.
5 Conclusion
Remodeling holds the key in terms of determining the mean tissue age.
A mechanically competent tissue structure depends on temporally and spatially
orchestrated remodeling process. A delicate balance between activation, resorption
and formation processes is essential to turn over older tissue fragments and repair
in vivo damage accumulation. The relative rates of these three processes can
potentially alter in many different combinations during aging and osteoporosis.
It may be why there is a lack of consensus in the literature on compositional,
architectural and microstructural changes during aging and osteoporosis. The
number of cells involved in the basic multicellular unit and their metabolic
capacity may change with age and osteoporosis as well. Another variable at play is
the rate of mineralization of the osteoid. Finally, aging of unresorbed moieties via
prolonged crystal growth and non-enzymatic crosslinks further complicates the
picture. A complete reliance on biopsies in terms of investigating these factors
reliably curbs the progress of research. Novel technologies reporting on matrix
quality and remodeling dynamics in situ and non-invasively (or minimally inva-
sively) would be a quantum-leap in the field.
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