Are We Treating Chronic Pain All Wrong?

In a recently published study, researchers at McGill University in Canada reported that treating acute pain with NSAIDS like ibuprofen and aspirin may promote chronic pain in the long term. The study, published by Science Translational Medicine, suggests that inflammation is a normal part of injury recovery and overall helps to resolve acute pain and prevents it from transitioning into chronic pain.

“You should let inflammation happen” states the senior author of the study, Jeffrey Mogil. He went on to say that what we have been doing for decades has been entirely wrong, noting that inflammation is what stops chronic pain overall, “Inflammation occurs for a reason and it is dangerous to interfere with it”.

Inflammation and Neutrophils

“In analyzing the genes of people suffering from low back pain, they observed active changes in the genes as the pain went away”, said Luda Diatchenko, PhD, a professor and chair of human genetics at McGill. Changes in the blood cells especially in the neutrophils seemed to be the most important factor.

To validate this factor, the researchers blocked neutrophil activity in mice and found pain lasted 2-10 times longer than normal. Anti-inflammatory medications like NSAIDS and Aspirin, had a similar prolonged effects that was reversed after re-injecting neutrophils.

An analysis of 500,000 patients in the UK supported McGill’s results. The UK study showed those who took anti-inflammatory medicines were more likely to have pain in 2-10 years.

Neutrophils appear on the site of injury at it’s onset, and are involved in the inflammatory response. This research suggests that it may be more important to let the inflammatory response occur rather than blocking it.

Mogil stated, “ our data, strongly suggests that neutrophils act like analgesics themselves which is potentially useful in terms of analgesic development”

Neutrophils are recruited from the blood stream into inflamed and infected tissues where they release proinflammatory cytokines to attract other inflammatory cells to clear bacterial and fungal infections. Neutrophil recruitment is critical for immunity. This recruitment must be tightly regulated as excessive inflammatory disorders can cause tissue destruction.

Platelets

Platelets are recognized as the essential regulators of the recruitment of many types of leukocytes, including neutrophils under a wide range of inflammatory conditions. These pro-inflammatory roles of platelets are distinct from their role in blood clotting.

It has been shown that platelets are required for neutrophil recruitment in many inflammatory situations. Inflammatory stimuli induce the activation and upregulation of adhesion molecules on the surface of the platelets that enables the cells to stick to neutrophils and other bio-active substances.

A highly significant adhesion molecule for platelet-neutrophil interactions is P-selectin and is found on the platelet surface. The P-selectin is stored in the membrane of the alpha granules under basal conditions. The degranulation of the platelet’s alpha granules in response to stimuli is required for platelet neutrophil interactions.

It should be stressed that neutrophil recruitment is only one of the many pro-inflammatory functions of the platelets.

Authors note, although the study from McGill is very interesting, the exclusion of platelets from the discussion should be noted here. Overall, it is still very interesting and can change the overall treatment of pain as we know it.

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