Cartilage innervation is the driving force behind the development of osteoarthritis and back pain, or does degeneration of the osteoarthritis joints affect the nerves and cause pain?
This was the issue that underpinned a fascinating debate at the OARSI 2021 World Congress, with two giants from the OA research community: Anne-Marie Malfait, MD, Ph.D., professor of medicine in the rheumatology division at Rush Medical College, Chicago, i Stefan Lohmander, MD, Ph.D., Professor Emeritus of Orthopedics at Lund University (Sweden) in Sweden.
The discussion is at stake in better understanding the physiological processes that underpin both the development of AO in the joints and the experience of pain in patients with OA.
Lohmander began by pointing out that while pain is the main symptom of OA, it does not always overlap with the physiological processes of the disease, as measured by techniques such as MRI, X-ray, biomarkers, and gait analysis.
“This lack of complete overlap is often a problem when we do our clinical trials,” Lohmander said at the conference, sponsored by the International Osteoarthritis Research Society. “When we talk about osteoarthritis, we also have to remember from time to time that we talk about symptoms or disease and maybe not always about both.”
Although a healthy joint has pain receptors everywhere except cartilage, studies have found that the osteoarthritic joint carries blood vessels, sensory nerves, and cells that express nerve growth factor from the bone. subchondral even in uncalcified articular cartilage.
These nociceptor neurons are mechanosensitive, so mechanical damage to the joint triggers inflammation and the inflammatory proteins themselves act on the nociceptors to generate signals of pain in the brain, “so clearly, it is the joint that signals to the brain.” , said Lohmander.
However, Malfait noted that there is evidence from animal studies showing that the absence of sensory nerves in the joints, either due to disease or elimination, is associated with the onset or worsening of OA.
“Healthy nerves are really important to ensure healthy joints,” Malfait said. He said age-related sensory nerve loss always preceded age-related OA and was also associated with loss of proprioception and age-related vibratory perception.
Interestingly, animal studies suggest that removal of intraarticular nociceptors may have a protective effect on the osteoarthritic joint, Malfait said. Studies in humans who have experienced neurological lesions also suggest an improvement in conditions such as rheumatoid arthritis.
He raised the idea of neurogenic inflammation: that peripheral neurons release vasoactive mediators that contribute to tissue inflammation. “These nerves and nerve products talk to all the different cells in the joints,” he said.
Defending his argument that joint pathology is the cause of pain, not the pain caused by joint pathology, Lohmander gave the example of studies that analyzed radiographic abnormalities between two knees in the same patient that also had measures of discordant pain for each knee. This research “showed a strong association between radiographic osteoarthritis and knee pain, supporting the argument that structural abnormalities cause knee pain,” he said.
Martin van der Esch, PhD, Amsterdam University of Applied Sciences, said the debate was one of the highlights of the conference because it addressed such an important and long-standing issue at OA.
“Osteoarthritis causes widespread pain, so it affects the nervous system, but the source, the causality, is in the joint?” he said in an interview. “Or is it the other way around, so it means that there is first a problem within the nervous system (including the vascular system as well) and that it presents to the joint?”
It is more than an academic discussion because the findings of this fact could mean different treatment approaches for different groups of patients and it raises different ways of thinking about OA, he said.
None of the sources in this story claimed to have relevant conflicts of interest.
This article originally appeared on MDedge.com, which is part of the Medscape professional network.
