Some Painkillers May Slow Bone Healing Process
Studies on rats suggest that non-steroidal anti-inflammatory drugs (NSAIDs) can delay or even prevent the mending of fractures, according to a report in the magazine **** New Scientist ****.
NSAIDs, which include aspirin and drugs made from ibuprofen such as nurofen, are taken by millions of people every day around the world. One of the ways they are commonly used is to ease the pain of broken bones.
But researchers are now worried that some of the newer NSAIDs might seriously hamper bone healing. A team led by Patrick o'Connor at the University of New Jersey in the U.S. gave two of the drugs, rofecoxib and celecoxib, to rats with bone fractures.
None of the bones in rats treated with rofecoxib healed. In those treated with the celecoxib, none healed completely but about half had some form of bone growth.
For over 20 years there have been occasional reports of impaired bone healing in patients taking NSAIDs, said **** New Scientist ****. The magazine said: The issue may have escaped attention because the older generation of NSAIDs, such as ibuprofen and indomethacin, only appear to delay healing by a few weeks instead of blocking it. Aspirin is one of the few NSAIDs that appears to kill pain without this side effect, the report said.
O'Connor said ibuprofen and indomethacin delayed bone healing by about one to two weeks in rats, which was equivalent to slowing it down by 25 per cent to 50 per cent in humans.
Merck, the pharmaceutical company that makes rofecoxib, sold as Vioxx, said a study on spinal fusion operations found no bone-healing problems in people given the drug. But Thomas Einhorn, a U.S. orthopaedic surgeon at Boston University Medical Center in Massachusetts and a paid consultant to Merck, told **** New Scientist ****: "It would seem that a prudent approach is to temporarily avoid the use of these drugs during bone healing."
Traditional NSAIDs inhibit the enzymes Cox-1 and Cox-2. The latter catalyzes the production of hormone-like chemicals known as prostaglandins, involved in inflammation, while Cox-1 has a variety of roles.
New generation NSAIDs such as rofecoxib are designed as far as possible to block only Cox-2 to minimize side effects. But research now indicates that Cox-2 may be crucial in helping bone-forming stem cells and growth-triggering chemicals to do their work, said **** New Scientist ****. Jeremy Saklatvala, of the Kennedy Institute of Rheumatology in London, was quoted as saying the area needed to be investigated urgently. He added: "In the meantime, people with healing fractures should steer clear of these drugs."