Describe the relationship between menopause and hip fracture risk.Describe the relationship between body mass and hip fracture risk.
We know with certainty that hip fracture incidence is higher after menopause. The precise mechanism –or rather, the relative contribution of known mechanisms—is debated. (The interested student is pointed to Bernstein, J., Grisso, J.A. and Kaplan, F.S. Body Mass and Fracture Risk. Clinical Orthopedics and Related Research. 364:227-230 1999).
Menopause, with its decreased estrogen production, leads to increased osteoclast activity. Thus, at menopause, women begin to experience a 2% loss in bone mass per year as bone resorption outpaces bone formation.
A low BMI is a risk factor for hip fracture. A BMI of 20 is estimated to have a 2.0 relative risk of hip fracture compared to an individual with a BMI of 25. (Note that a really low BMI is best thought of as cachexia –and that’s a sign of general decline, bones included.)
There are two schools of thought why low BMI leads to fracture, both centered on the role of fat.
- Fat is a substrate for the synthesis of estrogen and thus is an indirect osteoclast inhibitor. More fat = more estrogen = more bone.
(don’t memorize this until you start cramming for step I) - Fat provides soft tissue padding. The energy absorbed by the bone in a fall is equal to the energy generated by the fall, minus the energy absorbed by other tissues. Hence, More fat = more energy absorbed by soft tissues = less energy absorbed by bone = lower risk of fracture.
What is the practical distinction between the two? Basically, it’s the question of whether low energy fractures are an intrinsic bone problem or an extrinsic, medical problem and in turn, whether the best plan to decrease fractures is to optimize the bone or minimize the energy to which the bone is exposed at the time of falling.