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Bone Loss on Steroids – It Must Be Stopped!

  • 7/24/2013 9:16:00 AM
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Bone Loss on Steroids – It Must Be Stopped!

Ramon Boudreaux, M.S.

A common misconception is that the skeleton is a relatively fixed structure that undergoes few changes during adulthood. In actuality, bones are an extremely active tissue that continuously rebuild themselves throughout an individual’s lifetime (referred to as turnover). Bone cells are in constant communication with each other to remove areas of damaged bone (resorption) and replace them with newer, healthier bone (formation). In fact, the entire skeleton is completely rebuilt every 10 years.


Healthy cell communication is key to the overall health and strength of bone. However, many factors can disrupt bone cell communication and thereby shift bone turnover in favor of resorption, resulting in bone loss. Glucocorticoid (GC) therapy is one such contributing factor. Within the first six months of GC therapy, bone density declines by as much as 27%, according to researchers in Italy [1]. Although GC therapy is very effective in treating a variety of conditions, such as asthma, COPD, rheumatoid arthritis, and Crohn’s disease, it may lead to bone loss in over 97%, and fractures in over 50%, of the patients receiving the therapy [2,3,4]. Even with these staggering statistics, less than 14% of patients receiving GCs are treated for bone loss [5]. To broaden public awareness of this major clinical issue, physicians must communicate with their patients the risks of GC therapy and offer suggestions for treatment options to help maintain their bone health.


The current gold standard treatment for GC-induced bone loss are bisphosphonate (BP) medications. BPs are a family of drugs (e.g., Fosamax, Actonel, Boniva – remember the Sally Field commercials?) that work by binding to the surfaces of bone. Months later they will be ingested by bone-resorbing cells (osteoclasts) and eventually slow down osteoclasts’ ability to remove bone. While BP treatments have shown relative success, their intent is only to slow down the process of bone loss since they cannot actually grow new bone. But what if there was something people could do, prior to GC therapy, to build up their bone mass and strength in order to protect themselves from GC-induced bone loss? Researchers at Texas A&M University think this is entirely possible. It is well documented that bone responds to resistance exercise, such as weight lifting, much like skeletal muscle does.


While this phenomenon may be more visually apparent in skeletal muscle, bone also increases in size and strength with resistance exercise. For example, the dominant playing arm of professional tennis players can have up to 20% more bone than the non-playing arm [6]. Thus, by incorporating this idea of growing bone mass through resistance exercise, and then suppressing resorption of bone with BPs, patients may be able to better protect themselves from the rapid bone loss associated with GC therapy. Be on the lookout for data coming from TAMU scientists testing this theory through a novel exercise protocol developed in their laboratory.



For further reading on this topic, please refer to:



  1. LoCascio, V., et al., Bone loss in response to long-term glucocorticoid therapy. Bone Miner, 1990. 8(1): p. 39-51.

  2. Cohen, S., et al., Risedronate therapy prevents corticosteroid-induced bone loss: a twelve-month, multicenter, randomized, double-blind, placebo-controlled, parallel-group study. Arthritis Rheum, 1999. 42(11): p. 2309-18.;2-K/pdf

  3. Wallach, S., et al., Effects of risedronate treatment on bone density and vertebral fracture in patients on corticosteroid therapy. Calcif Tissue Int, 2000. 67(4): p. 277-85.

  4. Muchmore, J.S., et al., Prevention of loss of vertebral bone density in heart transplant patients. J Heart Lung Transplant, 1992. 11(5): p. 959-63; discussion 963-4.

  5. Peat, I.D., et al., Steroid induced osteoporosis: an opportunity for prevention? Ann Rheum Dis, 1995. 54(1): p. 66-8.

  6. Calbet, J.A., et al., Bone mineral content and density in professional tennis players. Calcif Tissue Int, 1998. 62(6): p. 491-6.



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