A new study from King’s College London offers clues as to why chronic pain can persist, even when the injury that caused it has gone.
Although still in its infancy, this research could explain how small and seemingly innocuous injuries leave molecular ‘footprints’ which add up to more lasting damage, and ultimately chronic pain.
All of us are likely to know someone who suffers from persistent pain — it is a very common condition, which can be caused by sports injuries, various diseases and the process of ageing.
Treatment options are limited and doctors are often unable to offer anything more than partial relief with painkillers, leaving their patients resigned to suffering.
While chronic pain can have many different causes, the outcome is often the same:
an overly sensitive nervous system which responds much more than it normally would.
However, a question still remains as to why the nervous system should remain in this sensitive state over long periods of time, especially in instances where the underlying injury or disease has gone.
In the study, published today in Cell Reports, they found that nerve damage changes epigenetic marks on some of the genes in these immune cells.
Epigenetics is the process that determines which gene is expressed and where.
Wikipedia: Epigenetics is the study, in the field of genetics, ofcellular and physiologicalphenotypic traitvariations that are caused by external orenvironmental factors that switch genes on and off and affect how cells read genes.
Some epigenetic signals have direct functional consequences, while others are just primers: flags that indicate a potential to act or be modified.
The cells examined in this King’s study still behaved as normal, but the existence of these novel epigenetic marks may mean that they carry a ‘memory’ of the initial injury.
We are ultimately trying to reveal why pain can turn into a chronic condition.
We already knew that chronic pain patients have nerves that are more active, and we think this is probably due to various proteins and channels in those nerves having different properties.
We want to know why these proteins and channels should maintain their altered function over such a long period of time.
Cells have housekeeping systems by which the majority of their content are replaced and renewed every few weeks and months — so why do crucial proteins keep being replaced by malfunctioning versions of themselves?
Our study is the very first step towards trying to answer this question by exploring the possibility that changes in chronic pain may persist because of epigenetics.
Franziska Denk, Megan Crow, Athanasios Didangelos, Douglas M. Lopes, Stephen B. McMahon. Persistent Alterations in Microglial Enhancers in a Model of Chronic Pain. Cell Reports, 2016; DOI: 10.1016/j.celrep.2016.04.063
The National Pain Report has an article about this as well:
Cells Can Remember Injury, Which May Reveal Why Chronic Pain Persists