Potential preventative therapy for rickets discovered
A new therapy could reduce the risk of rickets in children that have a predisposed risk of developing the condition.
Hypophospatasia (HPP) is a congenital form of rickets, also known as osteomalacia. A team of researchers from the Burnham Institute for Medical Research, in California, US, found that enzyme replacement therapy can be used to prevent the development of the condition in mice, when administered from birth.
Unlike most cases of rickets, which are caused by a lack of vitamin D or calcium, HPP comes about through the mutation of a gene called TNAP, which is crucial to the depositing of minerals in developing bones and teeth.
Professor Jose Luis Millan, lead researcher, explained that a bone-targeted form of the TNAP gene was able to completely preserve the skeletal and dental structures of mice with HPP 15 days after treatment, with bone lesions still not seen after 52 days.
"While the biochemical mechanism that leads to skeletal and dental defects of HPP is now generally understood, there is currently no established medical treatment," he said, explaining that the team is now looking to find a way of reversing bone defects in mice where the disease is advanced.
According to a study published in the journal Paediatrics, vitamin D insufficiency can increase the risk of rickets and osteoporosis in children, and may also contribute to low bone mass or aggravate metabolic bone diseases.
The Arthritis Research Campaign, which produces a booklet on osteomalacia, is also funding research into reducing thinning bones in children with arthritis who are on long-term steroids.
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