The paper, published in Science Translational Medicine, suggests that inflammation, a normal part of injury recovery, helps resolve acute pain and prevents it from becoming chronic. Blocking that inflammation may interfere with this process, leading to harder-to-treat pain.
In a surprising discovery that flies in the face of conventional medicine, McGill University researchers report that treating pain with anti-inflammatory medication, like ibuprofen or aspirin, may promote pain in the long term.
Senior study author Jeffrey Mogil, Ph.D., a professor in the department of psychology at McGill said “What we’ve been doing for decades not only appears to be wrong but appears to be 180 degrees wrong, we should not be blocking inflammation. we should be letting inflammation happen. That’s what stops chronic pain.”
As it appears to be risky to meddle with inflammation, which happens for a reason. one of the study’s authors claims. To understand why some people’s pain goes away quickly while it lasts a long time for others, researchers examined the processes of pain in both mice and humans. They discovered active gene alterations over time in those whose lower back pain subsided when they examined the DNA of lower back pain sufferers. They discovered that the neutrophil, a particular kind of white blood cell, appears to be crucial in this regard. Researchers suppressed neutrophils in mice to explore this connection and discovered that the pain persisted 2 to 10 times longer than usual.
Even though they offered temporary alleviation, anti-inflammatory medications also prolonged pain; however, giving the mice neutrophil injections appeared to prevent this from happening. Separate research involving 500,000 people in the UK indicated that those who took anti-inflammatory medications to alleviate their pain were more likely to still experience pain two to ten years later.
When an injury first occurs, neutrophils arrive early in the inflammatory process, right when many of us turn to painkillers. According to this research, it could be preferable to let the neutrophils “do their thing” rather than suppressing inflammation. It may be preferable to use an analgesic like acetaminophen, which reduces pain without inhibiting neutrophils, as opposed to an anti-inflammatory medicine or steroid.
Nevertheless, the researchers emphasised that even while the results are strong, clinical trials are still required to directly compare anti-inflammatory medications to other painkillers.
This study could pave the way for the creation of novel drugs to treat people with chronic pain.
“Our data strongly suggests that neutrophils act like analgesics themselves, which is potentially useful in terms of analgesic development,” Mogil says. “And of course, we need new analgesics.”
Parvathy Sukumaran 
