SAN FRANCISCO — A plateau in bone mineral density improvement while on antiresorptive therapy for osteoporosis does not mean the treatment has stopped working, Dr. Steven T. Harris said at a diabetes update sponsored by the University of California, San Francisco.
Explain this to patients at the start of therapy to avoid disappointment or worse when their T scores stop rising, suggested Dr. Harris, of the university.
The most important clinical objective is to prevent fractures, not to produce changes in surrogate markers like bone mineral density or biochemical markers of bone turnover, he emphasized.
The risk of fracture declines significantly despite a slight improvement in T score or even no change in T score in the first year on antiresorptive medication because of improvements in bone quality. The fracture protection continues while the patient is on therapy, despite no further changes in bone mineral density.
Antiresorptive agents such as bisphosphonates, selective estrogen receptor modifiers, calcitonin, and estrogen decrease bone resorption and bone formation. This typically produces an increase in bone mineral density in the first year of therapy and a smaller increase the second year, followed by a plateau. Despite the plateau, fracture protection continues.
“It is the rule, not the exception, that bone density goes up a little, then stabilizes. That is not nonresponse. That does not mean you have to change the therapy. That does not mean your patients are not taking their medications. This is physiology in action,” Dr. Harris commented.
Explain this concept early to patients, because many of them logically assume that if a T score of −3.2 won them a diagnosis of osteoporosis, for example, then the goal of therapy is to get the T score back to zero. “As much as we'd all like to have the bone density of the average 19-year-old … it ain't happening, and it doesn't have to happen,” he said.
Studies of the bisphosphonates risedronate and alendronate, for example, show that therapy increases spinal bone density 5%–8% and hip bone density by 3%–5% after 3 years in osteoporotic women.
“Not terribly impressive” numbers until you look at the fracture protection, he noted.
The drugs reduced the incidence of vertebral fractures by 40%–65% and the incidence of hip fractures by 40%–60%. “If you had asked me 4 years ago what I thought a 4% increase in bone density could accomplish,” these benefits wouldn't have been guessed, Dr. Harris said.