By Eric S. Orwoll, Robert Marcus (auth.), Eric S. Orwoll MD (eds.)
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Extra resources for Atlas of Osteoporosis
67. } C/in Endocrinol 2002,87:2883-2891. GENETICS OF OSTEOPOROSIS Robert F. Klein O steoporosis is onc of thc most (ommon bone and mineral disorders in all aging communitics. Ir is characterizcd by low hone mass, and rhus low bone strcngth, which rcsuhs in fractuTes from rclatively minor trauma. Although ostcoporotic fracturcs are most commonly obscrvcd among thc cldcrly, rhe pathogcncsis of ostcoporosis starts early in life and involves the interaction of multiple factors [1,2]. Genet;c epidemiologie studies providc dcscriptive data that convincingly demonstrate population and crhnie differences.
Genetic linkage refers to the fact that genes are physically attached to one another along the length of the chromosome. Consequently, two genes that are dose together on a chromosome are usually transmitted together, unless a recombination event separates them. Recombination, which occurs during meiosis, is useful for mapping genes, because it provides alandmark that delineates borders for the location of a gene. The odds of a crossover, or recombination event, are proportionate to the distance that separates them.
30 ATLAS OF OSTEOPOROSIS FIGURE 3-6. A commonly used explanation for such a relationship is that there is an underlying susceptibility distribution for osteoporosis and fractures in the general population. When bone mineral density (BMD) is used as an example, the individuals who are on the high end of the BMD distribution have little chance of developing osteoporosis (ie, they have few alleles or environmental factors that contribute to skeletal fragility). Those who are closer to the low end of the BMD distribution (T I), however, have more of the disease-causing genes and environmental factors and are therefore more likely to experience an osteoporotic fracture.