The Use of Bone Remodeling Markers
ABSTRACT & COMMENTARY
Synopsis: The amount of bone and the rate of loss of bone both determine the risk of fracture.
Source: Bjarnason NH, et al. Climacteric 1998; 1:72-79.
Bjarnason, hassager, and christiansen from Denmark reviewed the current knowledge regarding postmenopausal bone remodeling. Bone remodeling is initiated by the activation of osteoclasts, which then produce bone resorption. This is followed by bone formation stimulated by osteoblasts. The postmenopausal time of life is characterized by increased osteoclastic activity that causes higher bone turnover. Recent studies indicate that low bone mass at the time of menopause predicts the risk of fracture due to osteoporosis. Equally predictive is a high rate of bone loss after menopause, the so-called "fast loser." Importantly, the combination of a low bone mass and fast losing is additive, and, thus, these individuals are at the highest risk for fracture. Inhibition of bone resorption by estrogen treatment is a rapid process, yielding full suppression after 3-6 months. The use of biochemical markers for bone resorption will reflect a rapid change, with a difference being seen within 3-6 weeks and a change that can be used clinically within 2-3 months. Studies with these markers indicate that those individuals demonstrating the highest bone turnover (fast losers) have the largest response in bone mass to estrogen therapy. The new agents, raloxifene and tibolone, are associated with changes in bone markers that are comparable to treatment with estrogen. However, bone density studies indicate differences among these agents, and it remains to be seen whether there will be a difference in fracture rates with each of these treatments.
COMMENT BY LEON SPEROFF, MD
There are three practical observations based upon the recent literature dealing with postmenopausal bone remodeling and are as follows: 1) Because the rate of bone loss after the menopause contributes equally to the risk of fracture as the total bone mass present at the time of the menopause, a normal bone density measurement at the time of the menopause does not mean that the patient will not be at risk of fracture later in life; 2) because those patients who have the highest bone turnover, according to biochemical marker assessment, have a higher risk of fracture, it is gratifying to note that those women who need the treatment most demonstrate the best response; and 3) biochemical markers of bone resorption respond quickly and offer the potential of assessing patients for response and proper dosage.
Important questions remain. Will patients who demonstrate a lack of bone response to estrogen treatment (approximately 10-15% of treated women) respond to other agents, such as alendronate, raloxifene, or tibolone? Is it appropriate to increase estrogen doses according to bone marker response, and, specifically, can this be done without adverse effects on the risk, for example, of thrombosis? There are clinicians in the bone world who strongly believe that patients receiving bone treatment, regardless of which agent, should be monitored for response with the new biochemical markers. Others are not certain that the clinical use of this approach has been demonstrated, especially in view of individual variability with these tests. This is an area receiving intensive study, and I suspect data will soon emerge to help us answer these clinical questions. In the meantime, is the increased expense of biochemical marker testing justified? Only you, your patient, and your managed care program can provide the answer.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content