ABSTRACT
The usual effect of an antiresorptive agent is to produce a temporary increase in measured bone mineral density (BMD) in the first 1-2 years, after which a plateau or resumed loss occurs (Figures 6.1, 6.4). One explanation for this is that initially the bone antiresorptive agent dissociates the activities of the osteoclast and osteoblast in such a way that resorption ceases and the remaining cavities are filled in with bone produced by osteoblasts2. Subsequently, new bone formation falls as the osteoblasts detect (probably by biochemical messages) the reduced activity of the osteoclasts, no further resorption cavities remain to be refilled, and
bone turnover rate falls. The reason for this apparent waning of the effect of an antiresorptive agent is not fully understood. The effect of an antiresorptive agent will also depend on the initial rate of bone turnover (being more effective where bone turnover is increased), the number of resorbing sites and the agent used (Figure 6.1). The magnitude and duration of the initial increase in bone density seem too great to be explained entirely by the refilling of the increased numbers of resorption cavities present when the bone turnover rate is high. Long-term studies of antiresorptive agents are not always available and most deal with bone density but not fracture rate. Some antiresorptive agents may also have anabolic as well as antiresorptive effects.
