New study findings indicate that popular painkillers such as non-steroidal anti-inflammatory drugs (NSAIDs) like rofecoxib (Vioxx) and celecoxib (Celebrex) may delay or even prevent the healing of broken bones.
“It’s time to tell the public,” says Thomas Einhorn, an orthopaedic surgeon at Boston University Medical Center and also a paid consultant to Merck, which makes one of the drugs under scrutiny. “It would seem that a prudent approach is to temporarily avoid the use of these drugs during bone healing.”
When researcher Patrick O’Connor and his team at the University of New Jersey administered NSAID painkillers to rats their broken bones didn’t fully heal. Both drugs, rofecoxib and celecoxib, are often used to ease the pain of arthritis and broken bones.
Merck, the maker of rofecoxib, rejects the claim that healing could be impaired in people too. It pointed out a study on spinal fusion operations that found no bone healing problems in people given rofecoxib. Celecoxib’s maker Pharmacia did not respond to queries before the study published in the journal New Scientist went to press.
For over twenty years there have been occasional reports of impaired bone healing in patients taking NSAIDs. 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.
“Ibuprofen and indomethacin delay bone healing by about one to two weeks in rats, which is the equivalent to slowing it down by 25 to 50 per cent in humans,” says O’Connor. None of the rats treated with rofecoxib managed to heal their bones. In those treated with celecoxib, none managed to completely heal their bones but about half had some form of bone regrowth.
Traditional NSAIDs inhibit the enzymes cox-1 and cox-2. Cox-2 catalyses the production of hormone-like chemicals known as prostaglandins involved in inflammation, while cox-1 has a variety of roles not specific to the inflammatory response. Since the new generation of NSAIDs such as rofecoxib block cox-2 almost exclusively, it was hoped they would have fewer side effects.
But it now seems that cox-2 may be crucial in helping bone-forming stem cells and growth factors do their work. This area now needs to be investigated urgently, says Jeremy Saklatvala of the Kennedy Institute of Rheumatology in London. “In the meantime, people with healing fractures should steer clear of these drugs.”