Completed Bones, Joints & Muscles Brain & Nervous System

Arthritis Research UK Pain Centre

Funder VsArthritis Charity-funded
Recipient organisation University of Nottingham
Funding £2.0M
Period Mar 2015 — Mar 2020

In plain English

AI plain-English summary

Osteoarthritis pain does not come from a single source—it arises from a mix of joint damage, nerve changes, brain rewiring, and psychological distress, and researchers are now mapping exactly how these factors combine. This matters because current treatments for osteoarthritis pain often fail. They target one mechanism at a time, but the pain itself is driven by multiple, interacting systems. Without understanding which mechanism dominates in which patient, clinicians cannot match treatments to individuals. The Pain Centre has spent five years identifying discrete pain pathways—such as the role of nerve growth factor (NGF), spinal sensitisation, and altered brain structure—and linking them to specific patient pain profiles. If the next five years succeed, clinicians could test treatments that target the right mechanism for the right patient, rather than prescribing by trial and error. This would reduce the burden of chronic pain for millions of people living with arthritis. The research is translational: it moves directly from lab-based mechanism discovery into clinical trials, with input from industry and patient partners. There is no immediate cure, but a shift from one-size-fits-all pain management to precision-targeted therapy is the realistic goal.

View original technical description
The integration of preclinical and clinical expertise within the Arthritis Research UK Pain Centre, coupled with external collaborations, has led to fundamental advances in our understanding of OA pain mechanisms. Key achievements during our first 5 years include identifying discrete pain mechanisms that map to OA pain phenotype both in patients and in animal models, and the integration of preclinical and clinical studies to demonstrate the mechanisms by which NGF, osteoclasts, TRPV1, and CGRP in the joint, spinal sensitization, psychological distress and augmented central pain processing each contribute to OA pain. This new knowledge has informed a multimodal model of knee OA pain, which integrates joint pathology, alterations in peripheral and central pain processing, changing brain morphology and function and psychological factors. During the next 5 years, we will capitalise on these achievements to test mechanistically targeted and novel treatment strategies which reduce the burden of pain in people living with arthritis identify mechanisms of pain progression which can be targeted to substantially reduce the future burden of arthritis. An integrated, multidisciplinary approach combining preclinical and clinical research, in collaboration with academic, industrial, health care and public/patient partners, will underpin our future success.

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Researchers

David Walsh (EPMC Awardee)

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Original classification

Centre of Excellence Full

Plain English summaries and category classifications on this site are generated by AI and may not perfectly reflect the original research.