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Abstract
An overview of biochemical markers of bone metabolism is presented along with indications
for their clinical utilization.
The structure, cyclical metabolism, and hormone regulation of bone is reflected by
markers of resorption, formation and/or turnover. Markers of resorption representing
degradation of type 1 collagen, include N-telopeptides, C-telopeptides, hydroxyproline,
and the collagen crosslinks pyridinoline and deoxypyridinoline; acid phosphatase,
a marker of osteoclast activity, and urinary calcium are also indicators of bone resorption.
Bone formation markers indicate osteoblast activity; bone-specific alkaline phosphatase
and the N-terminal and C-terminal extension peptides of procollagen reflect formation
of organic matrix in bone. Osteocalcin, produced by osteoblasts but also released
during osteoclastic degradation, may indicate either formation when resorption and
formation are coupled or turnover when they are uncoupled.
Bone markers respond to intervention more rapidly than techniques such bone mineral
density. Resorption markers respond approximately 1 to 3 months after intervention;
markers of formation respond later, after 6 to 9 months. Bone markers may add useful
information for assessing fracture risk and for monitoring osteoporosis, Paget's disease
of bone, cancer metastasis, and metabolic disease. Various therapeutic interventions
may affect release of some bone markers.
Bone disease has high prevalence in adults so bone markers will become even more important
for assessing fracture risk and monitoring therapy as populations age. Characteristics
of bone markers are dependent on biology and the assay used. Substantial work remains
in characterizing existing assays, identifying better markers and performing the clinical
studies to define which bone markers should be measured and when.