Do stress fractures indicate underlying bone disease?

This is a question that comes up often in a metabolic bone disease clinic, particularly when the patient has sustained more than one such fracture.

I don’t think there is a simple answer to this somewhat rhetorical question because stress fractures tend to occur in persons healthy enough to overload their skeletons. My thinking is that damage to trabecular bone micro-architecture occurs constantly during activities of daily living but the bone remodeling process is usually able to overcome this. As micro-cracks occur osteoblasts are recruited to heal them before they can propagate into true clinically apparent stress fractures. It is only if one keeps overloading the skeleton to a point where the accumulation of micro-cracks exceeds the ability to repair the damage that stress fractures happen.

All too often I see younger women who take on a vigorous exercise program (I have had a number of patients who somehow find time to put in two or more hours of exercise every day) and sustain a stress fracture within a few weeks or months of starting their program. Undaunted they allow themselves a week or so to “recover” before starting up again. However, this time they tend to protect the injured limb and simply overload the good one, increasing their risk of another such event. In that circumstance, a metabolic bone disease work-up is probably not indicated but a complete history particularly looking for any change in menstrual function is appropriate — ie, looking for the “female athlete triad.” I face an angry response almost every time I suggest that the patient tones down his or her load-bearing exercise program.

Sustained use of corticosteroids is clearly detrimental to skeletal health since they stimulate bone resorption and inhibit bone formation, limiting the body’s ability to repair micro-damage in a timely manner. Steroids also tend to impair muscle function such that the extent to which the patient can engage in vigorous exercise is reduced. However, the disruption of the normal bone remodeling cycle is likely to lead to fractures even when skeletal loading is reduced.

Osteoporosis therapies that inhibit bone resorption, particularly bisphosphonates with a long half-life in the skeleton, are also likely to diminish the ability of the skeleton to self-repair. The skeletal response is different to that of steroid exposure in that both resorption and formation are suppressed. There is usually a delay of three months or slightly longer between inhibition of resorption and inhibition of formation, and for some time, this leads to positive skeletal balance. There is mounting evidence that over time, in some patients, there is no longer any positive skeletal balance. To me, this should be a warning sign that it is time to give the skeleton a rest from therapy as I have discussed before. As long as bone mineral density is continuing to increase between successive DXA studies performed two years apart, the bisphosphonates should be continued.

Once you have demonstrated with successive DXA studies that there is no ongoing increase in bone mass, give serious consideration to temporarily discontinuing the therapy and give the remodeling cycle a chance to recover. Remember this is “off label” use of bisphosphonates so make certain you understand the rationale for interrupting therapy and have carefully explained that to the patient. Take the time to note that discussion carefully in the patient’s record. At the time when positive skeletal balance is no longer evident, your patient may still have a worryingly low bone density and be at increased risk for fracture. This is the time to remind the patient about safety and fall prevention as well as maintaining an adequate calcium, vitamin D and protein intake. If you and/or the patient are still concerned about fracture risk, consider initiating therapy with teriparatide. The insurance company may balk at first but not responding to bisphosphonates (which you have demonstrated with serial DXA) is an indication to use teriparatide in patients with increased risk of fracture.