Osteoporosis researchers were dumbfounded by the report. “I am very excited,” said Dr J Christopher Gallagher, an osteoporosis specialist and professor of medicine at Creighton University. “It is a groundbreaking paper. One is completely surprised.”

Dr Ronald N Margolis, senior adviser for molecular endocrinology at the National Institute of Diabetes and Digestive and Kidney Diseases, said: “I was astonished. My jaw was dropping.”

Dr Clifford J Rosen, a senior scientist at the Maine Medical Center Research Institute, was no less impressed. “This is amazing science,” Dr. Rosen said. “Amazing. The science is spectacular.”

Dr Ethel S Siris, who directs the Toni Stabile Osteoporosis Center at Columbia, cautioned that the work was not with humans but instead involved mice that were engineered to have human genes. “This stuff is really exciting basic — underscore basic — research,” Dr Siris said. The story of the serotonin-bone connection began with reports of a rare inherited condition causing fragile bones and blindness. Children with the condition had bones so weak that they needed wheelchairs or devices to assist them in walking.

The problem turned out to be a mutation that inactivated a gene called LRP5. A few years later, another mutation was found in LRP5 that produced the opposite effect: extremely dense bones and resistance to osteoporosis. In this case, LRP5 was overactive. People with this gene mutation, Karsenty said, had jawbones so dense that it was difficult to extract their teeth.

Researchers jumped on those findings, realising that LRP5 could hold clues to the disease. But most assumed that LRP5’s role was in bone itself. With Karsenty’s work, said Dr Bjorn R Olsen, a bone growth researcher at Harvard Medical School, “that has now been proven completely wrong.”

... contd.