Boniva®, Fosomax®, Actonel®, Forteo®… Evista®? If you’ve been diagnosed with osteoporosis or osteopenia, and changes in diet and lifestyle haven’t resulted in raising those T-scores, you may be poised on the brink of a new and very confusing world: drug treatment.
Right now, I’m trying the supplements and exercise route to increase my bone density. But if that doesn’t work—and I’ll find out next month—I’ll probably have to make some decisions about drugs. So I decided I’d best find out as much about them as I can. And since I’m pretty good at explaining things in language we all can understand, I thought I’d share with you what I’m discovering.
Let’s start with the main classes of osteoporosis drugs: bisphosphonates; parathyroid hormone/anabolic drugs; estrogen; calcitonin; and selective estrogen receptor modulators (SERMs).
Do you really need to remember these words? No; they won’t be on the next quiz. But be aware that you may hear them as your doctor rattles off information about the drug you’re about to start taking. Let’s look at what they are, and how they work, one by one. This will be a general overview; later on, I’ll go into more depth about each drug.
Bisphosphonates (bis-foss-fo-nates, if you want to know how to pronounce it): This is the most common class of osteoporosis drugs, and includes Boniva, Fosomax, Reclast®, and Actonel. Also called anti-resorptives, these drugs work by slowing the rate at which your bones “shed,” or lose their substance.
Your bones are always “remodeling;” they break down, and they build back up. Over the course of your life, the pendulum swings from more bone growth/less breakdown (when you’re young), to more breakdown/less growth (when you’re older). But the pendulum swings farther for some of us than for others; if your bones break down way quicker than they build up, then you have osteoporosis.
And what do bisphosphonates do? They slow the pace of bone breakdown, putting it more in balance with bone buildup. Thus your bone density increases. How do they do this? By hindering the cells (osteoclasts) that break down your bones; and perhaps by stimulating the cells (osteoblasts) that build up your bones.
Parathyroid hormones: Currently, there’s only one FDA-approved drug in this class, thus only one used for osteoporosis treatment in the U.S.: Forteo.
Your body manufactures parathyroid hormones, which stimulate your osteoblasts to build bone. Forteo is the synthesized (manufactured) version of this hormone. In effect, it increases bone density by just the opposite method of a bisphosphonate: it stimulates bone buildup (osteoblasts), rather than slowing down bone breakdown (osteoclasts). Forteo also helps your body absorb calcium, which is key to bone buildup.
Estrogen: There are various forms of estrogen available on the market. The broader class of these drugs, known as hormone replacement therapy drugs (HRT), have been taken by millions of women to deal with the side effects of menopause, one of which is osteoporosis. The most common examples of HRT include Prempro® and Premarin®.
How does estrogen strengthen your bones? Basically, estrogen hinders osteoclasts, and helps osteoblasts. Estrogen slows the amount of bone osteoclasts can absorb; and it increases the amount of calcium osteoblasts (the “good guys”) can absorb. So bone breakdown is slowed, and the pace of bone buildup is increased.
Sounds good, right? Well, yes and no. Estrogen definitely helps slow/reverse osteoporosis. It’s also been identified as a significant breast cancer risk factor. So the use of HRT for osteoporosis has declined.
Calcitonin: This is a manufactured version of a naturally occurring hormone, and it comes in two brands: Fortical®, and Miacalcin®.
And how does it work? Exactly like bisphosphonates: by slowing the work of those bone-destroying osteoclasts, and (perhaps) encouraging osteoblasts to increase the pace of bone buildup.
Selective estrogen receptor modulators (SERMs): This type of drug has a split personality: in some parts of the body it acts like estrogen, while in others, it doesn’t. Evista (raloxifene) is the SERM most commonly prescribed for osteoporosis.
So what’s with the seemingly opposite effect SERMS have in different parts of your body? Why is that important? As mentioned above, estrogen is great for building bones. Unfortunately, for women with breast cancer (or those at identified high risk of getting it), estrogen is a no-no; it encourages breast cancer growth. Evista acts like estrogen on the bones, yet at the same time isn’t recognized as estrogen by breast tissue. Thus it helps bones, but doesn’t encourage breast cancer; a win-win for women.
Tamoxifen, a drug taken for over 30 years by breast cancer patients, is another common SERM. Its ability to build bone isn’t as great as that of raloxifene (Evista). Another promising option, bazedoxifene (Viviant), appears comparable to Evista, but it hasn’t yet been given FDA approval.
Whew, are you still with me? Congratulations! I hope you now know a bit more than you did about osteoporosis drugs, and how they work. In future posts, I’ll break this all down to more specific levels.
Published On: October 16, 2008