Ladies, Don’t Fall Into the Bone Mineral Density (BMD) Testing and Osteoporosis Medication Trap

Remember that commercial where the graceful but aging woman is talking about

how she got shorter? And that if you had the same problem you should ‘talk to your doctor’.

Well I don’t recommend talking to your doctor for any reason unless you are really sick.

But what about my bone mineral density (BMD) test, you protest? What if I have hidden

osteoporosis and my leg snaps off while I am pirouhetting across the skating rink?

The most disabling of fractures occur in the elderly, in the hipbone, specifically

the femoral neck, which is associated with considerable loss of mobility.

More commonly, fractures occur in the vertebral body (bones in your spine), which usually

are not associated with pain; they may cause a bowing of the back, and shortness.

Bone density, or how thick your bones are, is currently tested using a bone mineral density test (BMD).

Normal values for these tests are based on how far off the patient’s results are from those of

the average healthy young woman, using something called t scores. However bone density normally declines with age, and therefore there is no reason to think that this is necessarily a cause for concern.

For example, if you are a woman who gets BMD testing and follows the WHO criteria, there is a 50% chance you will be diagnosed with osteoporosis at the age of 72 (t score less than -2.5), and a good chance your doctor will recommend medication treatment. Your risk of having osteopenia (t score less than -1.0), for which your doctor may recommend medication to “prevent” osteoporosis, is 50% by age 52. In other words, according to the guidelines, at least half of postmenopausal women should be taking medication for osteoporosis. And even more women have “osteopenia” (i.e. loss of bone mineraldensity that is not severe enough to qualify for osteoporosis) and are taking medications to “prevent” osteoporosis. However, recommendations for

so many women to take bone medications don’t make any sense.

Osteoporosis is commonly treated with bisphosphonates like Fosamax (alendronate), Actonel (risedronate), Boniva (ibandronate), Didronel (etidronate), Skelid (tiludronate), Aredia (pamidronate), and Zomeda (zoledronate).Bone turnover is regulated by cells called osteoblasts and osteoclasts. While the osteoblasts are building up bone in area, the osteoclasts are breaking down bone in another. This leads to a balance in normal bone. What the bisphosphonates drugs do is turn off the osteoclasts, so that bone isn’t broken down, thereby slowing the loss of bone

density with aging. But they also turn off the osteoblasts, so that if there is a fracture, it won’t heal. All of the studies have shown that bisphosphonates increase BMD and reduce the risk of

vertebral fracture in women with osteoporosis (t score of less than -2.5). But what is the significance of a vertebral fracture? Vertebral fracture is merely defined as a reduction of the height of the vertebra by 20% on radiological tests like MRI. To have a vertebral fracture defined in this way, you don’t have to have pain, change in posture, or anything at all

that would make you aware of any problem. In fact, most of the time the only person who knows you have a vertebral fracture is your radiologist.

What about fractures that matter? Most of the studies, including the Alendronate Phase III Osteoporosis Treatment Study, the Fracture Intervention Trial (FIT), the FOSamax International Trial (FOSIT), and the Vertebral Efficacy with Risedronate Therapy (VERT) studycollectively performed in thousands of women with osteoporosis based on BMD, did not show a reduction in hip fractures, the kind of fracture most clearly associated with lasting disability. In terms of fractures in other parts of the body, referred to collectively as nonvertebral fractures (in places like the clavicle or the wrist) the findings are more mixed, with differing findings depending on whether there is a prior history of fractures and other factors.

The Hip Intervention Program (HIP) Study assessed the effects of three years of risedronate or placebo in 9331 women over age 70 with dramatic losses of bone mineral density (t score less than -4), with -2.5 being regular osteoporosis) or t score less than -3 with a risk factor for hip fracture, like propensity to fall. Overall 2.8% of women on risedronate suffered hip fracture versus 3.9% on placebo, a difference of 1.1% that although statistically significant was not very impressive. In the only study of men to date, bisphosphonates did not prevent painful vertebral fractures or nonvertebral fractures, including fractures of the hip.

And what about treatment beyond three years? The implication of the educational campaigns about osteoporosis is that this is a disease for which you need to be treated for the rest of your life. But is there evidence of added benefit of long-term treatment, or perhaps harm? The studies I reviewed above showed that after five years there is no benefit.

In other words after five years they seem to stop working. How could this be?

Again, bisphosphonates act by inhibiting osteoclasts, the cells that act to break down bone. So although they increase BMD for a few years, in the long run they decrease bone turnover. Animals treated with bisphosphonates have a decrease in bone turnover. Women on alendronate were found to take up to two years to heal after a fracture, and had markedly suppressed bone formation on biopsy. In the long run bisphosphonates may decrease the ability of bones to resist fracture, making bones more brittle. They also are not metabolized, meaning that they bisphosphonates you are taking now will be in your bones for life, resulting in a long term reduction in bone turnover.

This decrease in bone turnover underlies the scariest potential side effect of bisphosphonates: osteonecrosis. Osteonecrosis is a degeneration of the bone in the jaw that may require surgery. Osteonecrosis was seen in “Fossy Jaw” or “Phossy Jaw”, which developed in workers in 19th Century match making factories exposed to phosphorus. The phosphorus would get into the bone of the jaw, much like the bisphosphonates do, and stop bone turnover, leading to death of the bone tissue. The outcome was so painful and disfiguring that it sometimes led people to kill themselves.

Although most of the cases of osteonecrosis of the jaw have been reported in patients with bone metastases or myeloma treated with intravenous bisphosphonates, there are now emerging cases in patients who took the medication only for the “prevention of osteoporosis.” This shows there are those out there for whom there is little potential benefit and unfortunately much to lose in taking bisphosphonates.

A total of 15 cases of osteonecrosis have been reported with oral alendronate, one with oral risedronate and one with ibandronate, taken for the treatment of osteoporosis or Paget’s Disease (a disease of that makes bones weak and fragile).

Bottom line? If you don’t have a history of fracture these medications don’t help much. Better to exercise and stop smoking– those interventions work better at preventing fractures.