In attending the recent International Osteoporosis Foundation’s World Congress on Osteoporosis, Osteoarthritis and Musculoskeletal Disease in Seville this month, I was intrigued by the very subtle reminder from this prestigious forum that bone mineral density (BMD) is just one factor in bone strength and remains a limited one at that.

I say the reminder was subtle because it was certainly not the main message of the conference, and the primary attendees and presenters were approaching the condition from a medical and pharmacological viewpoint (which relies heavily on BMD measurement) examining medications as well as the epidemiology and etiology (populations affected, risk factors and causes of the disease.) But as one of the only attendees who was not a scientist, researcher, physician, nurse, lab technician, pharmaceuticals representative, device manufacturer, or osteoporosis association official, this acknowledgment was a significant take-away for me to hear from such a conference of osteoporosis leaders.

I’ve long been discouraged by the reliance on bone mineral density in our diagnosis and discussions of osteoporosis, despite the standing acknowledgment that it is just one of many clinical risk factors. We know that the strength and quality of our bones stem from various other characteristics including their microarchitecture, shape, composition and ability to self-repair. In fact, the World Health Organization defines osteoporosis as a skeletal disease of low bone mass as well as architectural deterioration which makes the bones susceptible to fracture.

[1] And yet the diagnosis of osteoporosis is made on the scoring of BMD, a measurement of bone mass within a given area.

Furthermore, we’ve seen evidence of fractures occurring more in people in the classification of osteopenia than osteoporosis.[2] Clearly there is more to the picture than just bone density measurement, which is usually provided by a DEXA scan — a low radiation measurement tool that’s considered the gold-standard for measurement although other methods also exist.  For this reason, other clinical risk factors, including age, smoking history, steroid medications and fracture history, are being taken into account in most treatment scenarios.

But beyond measurement of bone mineral density, the technology to fully examine bone quality, such as that of a high resolution CT scan, is not clinically feasible and involves additional radiation exposure. So the density measurement of bone is the best method we’ve had, even though research over the last decade has growingly pointed to the importance of bone quality.

I’ve just seen new technology at the conference that I’m very excited about which enables feasible assessment of bone microarchitecture, one component of bone quality, without additional radiation. I’m very excited about this technology and curious to experience it.

You see, when I was diagnosed with osteoporosis ten years ago, my BMD measurement categorized me in the range of osteoporosis.  And indeed my low vitamin D levels indicated that my bones were in fact undermineralized. I also had another clinical risk factor indicating that I may not have accrued my peak bone mass as a teenager when our bodies are typically building the bone reserves for our adult lives.

But I also wondered if there wasn’t more to the picture, since all my other biomarkers were normal, suggesting that no unusual or dangerous metabolic activity was occurring. I questioned, as suggested even by my endocrinologist, whether my mere size wasn’t predisposing me to low bone mass. I’m very petite and as you’d expect, my bones are in fact just downright small!  Bone size is a risk factor for osteoporosis, but should low mass, in the absence of major clinical risk factors including those such as glucocorticoids, necessarily mean that my skeleton can’t sustain certain loading forces without risk for fracture, especially if I’ve trained it to do so?

This brings me to my question I’m posing about exercise and its effects on bone tissue. We’ve seen the ability of exercise to improve bone mass, strength and quality. Why are we not including more mechanical stimulus – i.e., movement – in our osteoporosis treatment and prevention strategies within our health care systems?

This month, I learned first-hand some answers to that question.

First, PROOF. We need more scientific evidence.  The medical world and the world of patient advocacy understandably rely on proof. Yet the amount of proof needed to show the benefits of exercise to the osteoporosis population, and to those at especially high risk of fracture, is far greater than many people realize. And we’re only just beginning to mix the world of biochemistry with physics in the osteoporosis research realm. I was surprised at the conference by the limited discussion of mechanical factors impacting bone tissue, but pleased to see that the interest exists, and I believe that we are on the brink of change.

Second, FEAR. The skepticism that underlies the question of whether exercise can improve bone density and quality for those with osteoporosis stems not only from the need for more evidence, but from the valid concern over a patient’s fragility. Thus we need to provide evidence and programming of safe exercise and movement regimens. As many of us recognize, not all exercise is beneficial and in fact we certainly do need to be cautious of overloading forces stemming from movements that can indeed lead to an osteoporotic fracture. To give a very personal example, I myself don’t perform loaded spinal flexion exercises (lying on the back with hips in the air, placing all body weight on a curved back) due to the high forces that I can’t guarantee my spine would sustain — and I have no need to test that out!

Third, DISBELIEF. We believe what we know. And we know what we experience. Sure, part of the disbelief stems from lack of proof, going back to the first point. But part of it also relates to an individual physician’s personal understanding of exercise and movement. If a doctor knows the benefits firsthand, he or she may well be more likely to recommend and prescribe it, even in the absence of extensive published evidence. After all, why would someone recommend something that he or she does not believe in or know to be true? So another goal here is to involve and integrate the medical community into the exercise community to cultivate interest and discussion, which then leads to conducting more research to obtain more proof.

Fourth, DEFINITION.  What is exercise, after all? I attended a televised PBS presentation a few years ago on healthy aging and how lifestyle changes could slow this course of physical decline as we know it.  When the lecturing physician spoke about exercise he referred to cardiovascular and aerobic activity separate from resistance training (which in fact often coexist these days in the exercise physiology and personal training realms) and never mentioned anything in the realm of Tai Chi, yoga, Pilates or other movement forms. I think we need to redefine the traditional definition of exercise as the medical world traditionally considers it. Someone recovering from an ankle fracture may be told not to exercise so as to promote healing, but should that stop this person from doing arm stretches or using a resistance band with her upper body while seated? Not only will the individual benefit from maintaining strength and mobility in unaffected areas of her body; she will feel grateful to remain active in some way and will be relieved to overcome the powerlessness we all feel when sidelined from an injury or physical setback.

Moving forward, I propose that we as health advocates of ALL types consider how we can work together to promote the inclusion of exercise as prevention and management of osteoporosis. In the exercise realm, many are aware of the countless benefits, but the general public and some in the greater health care community need more convincing. The task is daunting, but if we each spread the word, share information and encourage dialogue, the mountain to climb grows less steep, and our bones grow all the stronger.

 


[1] World Health Organization. 1994. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. WHO Technical Report Series, No. 843. WHO Geneva.

[2] Stone, KL et al. BMD at multiple sites and risk of fracture of multiple types: Long-term results from the study of osteoporotic fractures. Journal of Bone and Mineral Research. 2003;18(11):1947-1954; Pasco JA, Seeman E, Henry MJ et al. The population burden of fractures originates in women with osteopenia, not osteoporosis. Osteoporosis International 2006;17:1404-1409.