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New link found between osteoporosis and celiac disease
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Patients with celiac disease may develop osteoporosis because their immune system attacks their bone tissue, according to a study conducted in Scotland.
It is the first time an autoimmune response has been shown to cause direct damage to bones, Stuart H. Ralston, MD, of the Institute of Genetics and Molecular Medicine at the University of Edinburgh, said in a press release.
Researchers at the university studied a protein called osteoprotegerin in people with celiac disease, a digestive condition that affects one in 100 people.
In healthy people, osteoprotegerin plays a crucial role in maintaining bone health by controlling the rate at which bone tissue is removed.
The latest research, which appears in the Oct. 8 issue of The New England Journal of Medicine, indicates that 20% of celiac patients produce antibodies that attack the osteoprotegerin protein and stop it working properly. This results in rapid bone destruction and severe osteoporosis, according to the press release.
Ralston said most researchers believed that osteoporosis — a known complication of celiac disease — develops in celiac patients because they cannot properly absorb calcium and vitamin D from their diet. Both nutrients are essential for healthy bone development.
The team found that although this new form of osteoporosis did not respond to calcium and vitamin D supplements, it can be easily treated with drugs that prevent bone loss.
Ralston, who led the team, said in the press release, “This is a very exciting step forward. Not only have we discovered a new reason to explain why osteoporosis occurs in celiac disease, but we have also found that it responds very well to drugs that prevent bone tissue removal.
“Testing for these antibodies could make a real and important difference to the lives of people with celiac disease by alerting us to the risk of osteoporosis and helping us find the correct treatment,” he said.
Riches PL. N Eng J Med. 2009;361:1459-1465.
The association of gluten enteropathy and low bone mass is well known but the cause has not always been obvious. For those patients with the disorder who are vitamin D-deficient the bone disease is poor mineralization (osteomalacia), not osteoporosis. This report provides an explanation of how gluten enteropathy may lead to osteoporosis. An antibody against osteoprotogerin, the decoy molecule that inactivates RANK ligand (the factor that recruits osteoclasts) has been identified. The unregulated production of RANK-L then can lead to increased bone resorbtion, low bone mass and increased fragility. This discovery should open the way to uncovering other specific causes of osteoporosis and specific solutions. The new RANK-L antibody awaiting further evaluation by the FDA might provide a specific remedy to this specific cause of osteporosis although the bisohosphonates currently provide the appropriate treatment.
– Donald A. Bergman, MD
Endocrine Today Editorial Board member
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