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All Languages. More filters. Sort order. Start your review of Flesh and Bones of Surgery. Torki Hami rated it liked it Oct 23, Mrs Bert rated it it was amazing Dec 26, But they failed to find a mutation unique to people with FOP. The group arranged for some of those families to attend its gatherings, along with foreign doctors who wanted to learn how to recognize the disorder.

When these doctors went home, they added more patients to the network. Eventually, this broadening community led Kaplan to patients who had children who also suffered from the disorder.

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Studying families is one of the best ways to pinpoint a mutated gene. By comparing the DNA of parents and children, geneticists can identify certain segments that consistently accompany a disorder. But then the online patient network began surfacing exceptions: a family in Bavaria, one in South Korea, one in the Amazon.

All told, seven families emerged; Kaplan traveled to meet a few of them and draw their blood.

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Back in Philadelphia, Shore and her colleagues examined the DNA from these samples and narrowed down the possible places where the FOP gene could be hiding. By , they had tracked the gene to somewhere within a small chunk of Chromosome 2. By a fortunate coincidence, scientists at the University of Rochester had just studied one of those several hundred genes. They had discovered that the gene, called ACVR1, made a receptor. The receptor grabbed BMP proteins and relayed their signal to cells. Shore and her staff inspected the gene as it occurred in people with FOP.

Once they had double- and triple-checked their results, once they had written a paper describing the mutation, Kaplan and Shore planned a press conference. In the spring of , Kaplan called Peeper to tell her something she had doubted she would live long enough to hear. A rare disease is a natural experiment in human biology. A tiny alteration to a single gene can produce a radically different outcome—which, in turn, can shed light on how the body works in normal conditions.

The new bones contain marrow. If fractured, they heal nicely. They are much like the bones of other mammals, of reptiles, of fish. In all those animals, bones develop under the control of the same network of genes—a network that, having shaped the bodies of our pre-vertebrate ancestors, is older even than bone itself. What is not normal is when these bones form. Normally, new bones develop only in embryos. As children grow, those bones extend; when those bones break, new cells repair them.

But almost no one develops entirely new bones outside the womb. They set about studying baby teeth from young patients, as well as mice they genetically altered, to observe the mutation in action.

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Seven years later, they had pieced together an understanding of the far-reaching effects. But in people with FOP, the receptors become hyperactive.

The signal they send is too strong, and it lasts too long. In embryonic skeletons, the effects are subtle—for example, deformed big toes.

Fractures (Broken Bones) - OrthoInfo - AAOS

Only later, after birth, does the mutation start to really make its presence known. Say you bruise your elbow, killing off a few of your muscle cells. Your immune cells would swarm to the site to clear away the debris, followed by stem cells to regenerate the tissue. As they got to work, the two kinds of cells would converse via molecular signals.

Shore and Kaplan suspect that BMP4 is an essential part of that exchange. But in someone with FOP, the conversation is more of a screaming match. The stem cells kick into overdrive, causing the immune cells not just to clear the damage but to start killing healthy muscle cells. The immune cells, in turn, create a bizarre environment for the stem cells. And instead of becoming muscle cells, they become bone. In the context of FOP, new bone is a catastrophe.

But in other situations, it could be a blessing. Some people are born missing a bone, for example, while others fail to regenerate new bone after a fracture. FOP may be an exquisitely rare bone condition, but low bone density is not: 61 percent of women and 38 percent of men older than 50 suffer from it. The more bone matter people lose, the more likely they are to end up with osteoporosis, which currently afflicts nearly one in 10 older adults in the United States alone.

For decades, doctors have searched for a way to bring back some of that bone. Some methods have helped a little, and others, such as estrogen-replacement therapy, have turned out to have disastrous side effects in many women. Giving someone a second skeleton is not a cure for osteoporosis. But if Kaplan and his colleagues can finish untangling the network of genes that ACVR1 is a part of, they could figure out how to use a highly controlled variation on FOP to regrow bones in certain scenarios.

This would not be the first time the study of a rare disease unearthed new treatment options for more-common afflictions. In , Don Frederickson of the National Heart Institute discovered a strange disorder, now called Tangier disease, which caused tonsils to turn orange. The color resulted from a buildup of cholesterol, he found.

Forty years later, scientists identified the mutated gene that causes Tangier disease and figured out how it helps shuttle cholesterol out of cells. Researchers are now trying out drugs that boost the performance of this gene as a way to lower the risk of heart disease. Framed photographs of his patients covered most of the surfaces and blocked part of his narrow window. Kaplan pointed to a picture of Tiffany Linker, the patient who, as a baby, had persuaded him to stake his career on FOP.


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He told me that last July, at 23, Linker had passed away. When I talked with young people with the disease, though, I was struck by their optimism.

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In the s, Peeper had to type out letters to reach a dozen other people with her condition.