Philadelphia Woman's Skeleton With Rare Bone Disease

Fibrodysplasia Ossificans progressiva is an extremely rare genetic disorder causing the body to replace muscle tissue with bone, slowly over time. There is no known cure

This is Harry Eastlack. His choice to donate his body to science was a significant contribution to the understanding of this disease. His remains are usually housed at the Mütter Museum, however they do travel briefly to attend conferences on FOP.

Harry Raymond Eastlack, Jr. (17 November 1933 – 11 November 1973) was the subject of the most recognized case of FOP (fibrodysplasia ossificans progressiva) from the 1900s.

His case is also particularly acknowledged, by scientists and researchers, for his contribution to medical advancement. After suffering from a rare, disabling, and currently incurable genetic disease, Eastlack decided to have his skeleton and medical history donated to the Mütter Museum of the College of Physicians of Philadelphia in support of FOP research.

His skeleton is one of the few FOP-presenting, fully articulated ones in existence, and it has proved valuable to the study of the disease. As is characteristic of FOP patients, Eastlack did not demonstrate any possible sign of a disease at birth except for a malformation of the big toes. At the time it was not recognized as the first clinical sign of FOP. It was not until 1937 when the first Heterotopic ossification symptom surfaced. By the time of his death, Eastlack's skeleton bore sheets of bone along the vertebrae, which fused to and locked his skull, and branches of bone along his limbs, which immobilized his shoulders, elbows, hips, and knees. He died in Philadelphia of bronchial pneumonia six days before his 40th birthday.

What is Fibrodysplasia Ossificans Progressiva?

People who have fibrodysplasia ossificans progressiva (FOP), an ultra-rare and disabling genetic disease, form two skeletons — a primary one like everyone else and a second one created from their skeletal muscles and other connective tissues. FOP affects approximately one in two million people. About 900 people in the world have been diagnosed with FOP.

FOP is caused by a gene mutation that transmits incorrect signals in cells and transforms soft connective tissue (such as muscle, ligaments, and tendons) into bone. This formation of bone where it is not supposed to be is called heterotopic ossification (HO). FOP is difficult to diagnose at birth because there are no visual signs except for malformed big toes. Diagnosis usually occurs after the body begins creating extraskeletal bone, often following an injury or a viral infection.

No racial, ethnic, sex, or geographic preferences are seen in people with FOP. Because of its rarity and early tumorlike symptoms, FOP is often misdiagnosed, usually as cancer. FOP is deadly; the median estimated life expectancy is 56 years. Most FOP deaths are caused by cardiorespiratory failure due to fusion of the rib cage. In 2006, a research team at Penn identified the genetic mutation that causes FOP in all affected people. No cure or effective treatment exists, however, as of 2019, three drugs are in clinical trials.

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