Onderzoekers onthullen details over rol veroudering op de botten
Researchers have unraveled crucial details of how aging causes broken bones to heal slowly, or not at all, according to study results published today in the Journal of Bone and Mineral Research. The research team also successfully conducted preclinical tests on a potential new class of treatments designed to "rescue" healing capability lost to aging.In the worst cases, an age-related delay in healing keeps the two sides of a fractured bone from ever rejoining (non-union), leaving many confined to wheelchairs, unable to walk or to live independently. Of the estimated 5.6 million fractures in the United States each year, between five and ten percent (up to 560,000) will heal slowly or incompletely. Researchers have known for 30 years that aging interferes with fracture healing, and have been filling in the details since on the complex web of biochemicals, stem cells and genes that bring about healing. The field is now reaching the point where precision designed drugs are in different stages of animal and human trials.The current study is focused on cyclooxygenase 2 (COX-2), an enzyme known from past studies to drive stem cells to differentiate into cartilage, which then matures into bone. Researchers at the University of Rochester Medical Center 20 years ago discovered the gene in humans that is responsible for producing the COX-2 enzyme and revealed the enzyme's role in causing inflammation, the reason drugs like the painkiller Vioxx were developed to shut down its action. Then about seven years ago another research team here determined that COX-2 also plays an essential role in bone formation during skeletal repair.
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