#80 Where Are We in the Treatment of Osteoporosis

We often think of bones as being dead, like the leg of a table or wood timbers for a house. The fact is that bones are very much alive, including the marrow. The bone cortex, or outside of the bone, includes osteoblasts, cells which make bone, and osteoclasts, cells which remove the old bone. Estradiol is responsible for stimulating osteoblasts. With the decrease in estradiol after menopause, osteoblasts lose some of their stimulation for producing new bone cells. With osteoporosis, you begin to lose bone mass and your bones grow thin.

With fewer bone-producing cells, your bones become thin and prone to breaking. Women have smaller bones than men, which puts women at a disadvantage compared to men.

The person most at risk for osteoporosis is the thin, Caucasian female smoker who is menopausal and inactive. Smoking reduces the benefit of estradiol. However, exercise does increases bone size, so the more active a person is, the bigger the person’s bones will be to begin with.

Most of the pharmacologic agents used to prevent bone loss increase bone size by decreasing the body’s osteoclast activity. There is a large group of bisphosphonates which decrease osteoclast activity. However, necrosis of the mandible (jaw bone) in one of the side-effects of these drugs.

Men have less osteoporosis and fewer bone fractures than women. Because men have bigger skeletons than women, men start out with more bone in their bodies. In addition, men run out of testosterone at a later time in life than women run out of estradiol from menopause.

There is a condition called osteopenia, which is a precursor to osteoporosis. While men have fewer fractures than women, they have more osteopenia. There is a pharmacologic agent, calcitonin, which is helpful in promoting the healing of fractures. However, calcitonin can make bones brittle, so should only be used a month or two to avoid brittle bones.

Whenever women move into menopause, they are faced with the question of whether or not to start  hormone therapy.

There’s a well-known Women’s Health Initiative (WHI) study from 40 years ago involving Premarin. The purpose of the study was to show Premarin would be good for hormone replacement in women. The study involved three groups of women, one group taking only Premarin (manufactured from horse urine), a second group taking Premarin and Provera (a synthetic form of progesterone), and a third group taking Premarin and natural progesterone. This study showed that women taking hormone replacement therapy including Premarin had more cardiovascular disease than did women who took no Premarin and the study was suspended.

If you make a decision to take hormone replacement therapy, start as soon as menopause begins. However, many physicians in this country have been scared off by the WHI study, they do not consider estradiol separately from Premarin, and hence they often do not recommend estradiol as part of post-menopausal health maintenance. In the WHI study, one group took Premarin and natural progesterone and had better results than the other two groups. However, estradiol, the natural estrogen, was not used in the WHI study.

A Danish study has demonstrated the benefits of taking progesterone if the therapy is begun as soon as menopause begins. In this study, if a woman waited five years before beginning hormone replacement therapy, there appeared to be no benefit.

This Danish study also used natural progesterone instead of a synthetic form of progesterone such as Provera. If you choose to begin hormone replacement therapy, be sure to take estradiol or natural progesterone, or both.

I am still waiting for the definitive study of estradiol.