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Age-related fractures are considered to be primarily the consequence of bone loss and increased bone fragility. In line with this dominant view on fracture etiology, prevention studies have primarily focused on pharmacologic interventions to increase bone density of the femoral neck. However, osteoporotic fracture occurrence is not entirely accounted for by bone strength but also related to the incidence and impact of falls. Recent data have provided evidence that an intensive multifactorial intervention strategy can be used to decrease the incidence of falls, but it remains to be determined whether fall prevention can be used successfully to prevent fall-related injuries or hip fracture. In fact, while more than 90% of hip fractures involve falls, hip fracture occurs in only about 1% of falls, suggesting that falls that cause hip fracture may differ qualitatively from other falls. These differences relate to the biomechanical aspects of falls, i.e., the energy that is ultimately transmitted to the proximal femur. Fall severity, rather than fall initiation, may therefore have to be the primary subject of future research.

Objective: To estimate the numbers of hip fractures among Dutch women caused by senescence in contrast to decreasing postmenopausal bone loss., Design: A Markov chain model in a multi-state life table., Setting: Department of Public Health, Erasmus University of Rotterdam, the Netherlands., Method: Cross-sectional data of prevalences of femoral neck bone mineral density, measured in an epidemiological survey (1993), were related to numbers of hospital admissions for hip fractures among women aged 55 and older, using a (published) relative risk for hip fracture of 2.6 (95% confidence limits: 1.9-3.6) per decrease by I SD of bone mineral density. We varied the prevalences of bone mineral density in the multi state life table and looked at changes in the expected number of fractures., Results: If bone loss were to cease after the age of 55, this would decrease the number of fractures by 39.4% (30.4%-45.2% in sensitivity analysis). If bone loss were delayed by 7.5 years, the number of hip fractures would decrease by 14.8% (10.0%-19.9% after 5 to 10 years' delay). If compliance decreases by age (3% per year), then the number of hip fractures would decrease by 5.6% (3.4%-11.0% after 1%-5% decrease of compliance per year)., Conclusion: Bone loss is only one of the many age related causes of hip fractures. Population based interventions targeting only bone mineral density, while ignoring comorbidity, have only a limited potential for preventing hip fractures.

Vitamin D deficiency is common in the elderly, especially in patients with hip fracture. Elderly people infrequently stay outside in the sunshine, and nutrition is deficient in vitamin D. In addition, the hydroxylation of vitamin D into active metabolites decreases with age. Vitamin D deficiency ultimately leads to osteomalacia, but in an earlier stage it causes secondary hyperparathyroidism, which is accompanied by increased bone turnover and cortical bone loss. Along these pathways vitamin D deficiency may contribute to the pathogenesis of hip fractures. In a survey in Amsterdam vitamin D deficiency was observed in more than 60% of the patients with hip fracture. Transilial bone biopsy showed signs of high turnover and cortical bone loss in more than 20% of patients. The elderly which are institutionalized carry an increased risk. Prevention or vitamin D deficiency is possible by adequate exposure to ultraviolet light. Primarily, the elderly should be encouraged to go out into the sunshine regularly. Advice on nutrition may be given additionally. When sunshine exposure is negligible, as in many disabled and institutionalized elderly, a daily supplement of vitamin D3 400 IU should be given. Preventive measures have to be evaluated prospectively. Vitamin D deficiency is not the most important risk factors for hip fractures, but the easiest to correct.