Taking anti-inflammatory drugs after surgery is fairly standard protocol. But a new study from researchers at Michigan State University suggests this approach may be backfiring and that blocking inflammation during this critical time may, in fact, delay recovery and prolong pain rather than relieve it.
In the new study, published recently in the Journal of Pain Research, the researchers report that letting inflammation run its course led to a quicker cessation of pain and an overall quicker recovery after a surgery or injury.
“The idea was that blocking inflammation would reduce pain overall,” said Geoffroy Laumet, the study’s senior author and associate professor in the Department of Physiology and the Neuroscience Program at MSU. “Instead, blocking inflammation increased pain in the long run. It was an unexpected result.”
The team used a mouse model to study postoperative pain with versus without activity from a key immune signaling molecule called TNF-α, or tumor necrosis factor alpha. To compare, they inhibited TNF-α, which is involved in promoting inflammation, and mimicked surgery with a small incision. They expected that blocking TNF-α would reduce pain, but the opposite happened: The mice stayed in pain for much longer. “It prevented the body from turning off the pain normally,” Laumet explained.
A surprising discovery
Laumet initially thought the result was a glitch. But after the experiment was repeated by multiple lab members and using three different methods for inhibiting TNF-α — including Etanercept, an FDA-approved drug used in humans — the findings were clear.
If you look across all types of surgeries — anything from an extracted tooth to a hip replacement — the pain resolves normally for 90% of patients. But the other 10% develop chronic pain, Laumet said. That persistent pain is very hard to treat; it’s very resistant to medication and it can last for years.
More than 40 million Americans undergo surgery each year — meaning an estimated 4 million Americans develop chronic postsurgical pain annually. Laumet’s work suggests the body’s ability to promote TNF-α in response to the injury from the surgical incision could be a critical factor in whether a person’s pain resolves or not.
The problem with pain
Should you throw out your ibuprofen? Not exactly. There are many different molecules in the body involved in inflammation, pain and healing.
“We don’t have a good understanding of what is doing what, so the key will be to identify which molecules are contributing to pain and which are contributing to the resolution of pain,” Laumet said. “The goal is to target the bad and keep the good ones.”
Although this study suggests that blocking TNF-α after surgery is likely unwise, there are other scenarios where it may still make sense, such as improving mobility by reducing arthritic inflammation in the joints for autoimmune diseases like rheumatoid arthritis.
In defense of inflammation
“Inflammation is not necessarily a bad thing,” Laumet said. “Yes, it hurts, but it’s also working on the inside to promote the resolution of that pain. The idea in the medical field that when you have an injury, you should absolutely block the inflammation right away might not always be the best strategy.”
Does Laumet think that one day we’ll be able to block the pain but allow the healing inflammation? “Yeah, I do think so,” he says. “If not, I would do a different job.”
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This article was sourced from MSU Today.
Opportunities for Partnership
The MSU Innovation Center is seeking companies and organizations interested in pain management, inflammation research, and post-surgical recovery solutions.
Whether you’re exploring sponsored research, licensing opportunities, or co-developing targeted pain therapeutics, inflammation modulation strategies, or chronic pain prevention innovations, we’re ready to collaborate.
Interested in partnering with MSU faculty on pain physiology research and next-generation recovery therapies?
Visit innovationcenter.msu.edu or contact us to start the conversation.
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