Biochemical markers of bone turnover in osteonecrosis of the jaw in patients with osteoporosis and advanced cancer involving the bone.
Osteonecrosis of the jaw (ONJ) has been hypothesized to result in part from a relative "oversuppression" of normal physiologic bone remodeling at the jaw brought about by bisphosphonate therapy. Biochemical markers of bone turnover give readily measurable information on integrated systemic bone remodeling activity, as measured by blood and urine assays. The intra- and interassay variability of most currently available assays is less than 10%, although many biological factors can influence levels of bone turnover markers. Bone turnover markers may show a dynamic response to changes in clinical status for a given disease state. Elevated bone turnover on and off treatment appears to predict adverse clinical consequences in both osteoporosis and cancer. Bisphosphonates effectively decrease the level of the bone turnover markers with a pattern depending on the marker, the bisphosphonate, the dose regimen, and the disease. However, long-term (10-year) treatment with bisphosphonates for osteoporosis does not appear to result in a progressive decline in bone turnover, as measured by markers and bone histology. The effects of long-term (greater than 2 years) treatment with monthly intravenous bisphosphonates on bone turnover markers in cancer are unknown. Discontinuation of bisphosphonate therapy appears to allow a recovery of bone turnover, which is related to the bisphosphonate, the duration of therapy, and the disease being treated. At this time, data are limited with regard to the utility of bone turnover markers in assessing risk for ONJ and whether bone marker-directed bisphosphonate holidays would be useful in prevention or treatment of ONJ.
Cremers
Serge
S
Department of Medicine, Endocrinology, College of Physicians and Surgeons, Columbia University, New York, New York, USA. sc2752@columbia.edu
Farooki
Azeez
A
D015415:Biomarkers / Q000032:analysis*; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D024042:Collagen Type I / Q000032:analysis; D004164:Diphosphonates / Q000009:adverse effects* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D007571:Jaw Diseases / Q000139:chemically induced* / Q000378:metabolism; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism; D010020:Osteonecrosis / Q000139:chemically induced* / Q000378:metabolism; D010024:Osteoporosis / Q000188:drug therapy / Q000378:metabolism; D010455:Peptides / Q000032:analysis
D015415:Biomarkers; D024042:Collagen Type I; D004164:Diphosphonates; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide