A type of mutant mouse which is fine at birth, but which has a slowed growth rate and develops osteoporosis-like symptoms should help our understanding of the genetic basis of the condition, according to a report in Nature Genetics .
Osteoporosis can lead to fracturing as the bone density decreases with age.
The most severe osteoporotic fracture is a hip fracture, which may affect as many as 15 per cent of women as they become elderly. Bone contains a number of substances but gains its strength and resilience from an internal network of mineralized 'extracellular matrix' proteins. Tianshun Xu from the National Institutes of Health in Bethesda, Maryland, and colleagues, have now found that a lack of one of these non-collagenous bone matrix proteins, biglycan, is important in the development of osteoporosis. By breeding mice with a deficient form of the Bgn gene, which encodes biglycan, the researchers hoped to find out its role in connective tissue metabolism and bone strength. The research showed that the biglycan-deficient mice seemed normal at birth, and grew normally until three months of age, at which point their growth rate decreased.