Patients who have had fractures of the distal forearm do not lose bone as expectedBMJ 1996; 313 doi: https://doi.org/10.1136/bmj.313.7060.821 (Published 28 September 1996) Cite this as: BMJ 1996;313:821
- R W Keen, Clinical research fellow,
- G O Griffiths, Statistician,
- T D Spector, Consultant rheumatologist
EDITOR,—Women's lifetime risk of experiencing a fracture of the distal forearm is 15%.1 Such fractures are associated with considerable pain and morbidity. They are also associated with an increased risk of vertebral fracture,2 although these anatomical sites have different bone compositions, with the forearm being composed predominantly of cortical bone whereas the spine is composed predominantly of trabecular bone.
In response to the work by N F A Peel and colleagues3 we have prospectively examined rates of bone loss at the lumbar spine over five years in 1003 women (age range 45-64) who had been recruited from a general population cohort.4 Data on prevalent fractures of the distal forearm during the 10 years before the baseline were collected from subjects, and incident fractures were recorded during the study. Bone mineral density at the lumbar spine (L1-4) was measured with dual energy x ray absorptiometry (Hologic QDR-1000) at the baseline and at 12, 24, 36, 48, and 60 months. Short term reproducibility (the coefficient of variation) calculated with repeat measures in normal volunteers was 0.8%. Annual percentage rates of change in bone mineral density at the lumbar spine in individual subjects were calculated by linear regression analysis.
Data were available on 32 women who had sustained a fracture of the distal forearm and on 664 controls who had not. Table 1 shows characteristics of the cases and controls. Bone mineral density at the lumbar spine was reduced in the women with a fracture, and this relation was unaltered by adjustment for age. The rate of change in bone mineral density at the lumbar spine was significantly different from zero in the controls (P<0.001) but not in the patients with a fracture (P = 0.15) and was significantly greater in the controls than in the patients with a fracture. The results were not affected by adjustment for age, weight, height, menopausal status, and use of hormone replacement therapy.
Our data confirm Peel and colleagues' findings that patients with a fracture of the distal forearm did not lose bone as expected. The data support the hypothesis that the low spinal bone mineral density of these women may be a consequence of either reduced peak bone mineral density or a period of accelerated bone loss before the menopause. This rapid loss could also affect the microarchitecture of bone and may explain the increase in forearm fractures seen at the time of the menopause. Large prospective studies in younger premenopausal and perimenopausal women will be required to clarify these findings.