Image by Vilius Kukanauskas from Pixabay
September 27, 2026 - By - Osteoarthritis is a chronic disease of the entire joint and is often assumed to be an inevitable part of aging. But researchers are working to better understand the condition in a much more nuanced way.
Chuan-Ju Liu, PhD, Charles W. Ohse Professor of Orthopaedics & Rehabilitation and vice chair of research with the Department of Orthopaedics & Rehabilitation at Yale School of Medicine is one of the world’s leading experts in osteoarthritis research.
Although osteoarthritis was traditionally viewed largely as wear-and-tear cartilage loss, research now shows that it is a complex disease of the entire joint. Beyond cartilage, it involves underlying bone, ligaments, menisci, fat pads, and nerves. Rather than just mechanical breakdown, drivers include inflammation, abnormal cell signaling, metabolic changes, and nervous-system interactions.
Although factors like age, obesity, joint alignment, and previous injuries are well-documented risk factors, Liu's work focuses on the deeper cellular drivers. Research increasingly shows that cellular aging, immune activity, and communication between different organs dictate how osteoarthritis begins and progresses, providing vital targets for novel medical treatments.
In this Q&A, Liu shares more about osteoarthritis, the groundbreaking research taking place at Yale, and what future treatments may look like.
Can osteoarthritis be reversed?
Chuan-Ju Liu, PhD: Established osteoarthritis is a chronic condition that does not simply disappear. While standard care focuses on symptom management, such as physical therapy, weight management, and medications, new research aims to move beyond symptom relief to develop therapies that actively slow or stop the progression outright.
And at present, clinical treatments cannot reliably reverse advanced osteoarthritis. Once substantial tissue is lost, natural regeneration is limited.
Laboratory and preclinical studies increasingly suggest that some biological pathways responsible for cartilage degeneration can be interrupted and that, under the right conditions, cartilage repair may be stimulated.
Our recent work at Yale has shown in preclinical models that targeting a specific protein called the Nav1.7 sodium channel and delivering a medication called lacosamide locally through a collagen-II-based hydrogel can do more than reduce pain. These therapies may also protect cartilage and promote cartilage repair. While investigational, these studies offer optimism that future treatments will stimulate meaningful tissue repair.
Can osteoarthritis be prevented?
Liu: Genetics influence susceptibility, but osteoarthritis is not inherited through a single gene. A family history can increase risk, but genes interact with age, weight, joint anatomy, and prior injuries, meaning a family history does not guarantee development, nor does its absence prevent it.
While non-modifiable factors like genetics and prior injuries play a role, individuals can manage modifiable risk factors. Maintaining a healthy body weight, avoiding excessive joint loading, and staying physically active help support joint mobility and muscle strength without accelerating preventable wear and tear.
Is osteoarthritis an autoimmune disease?
Liu: Osteoarthritis is not a classic autoimmune disease like rheumatoid arthritis. In autoimmune diseases, the immune system mistakenly attacks the body’s own healthy tissues. Osteoarthritis is neither simply a result of wear and tear nor a classic autoimmune disease. It is better understood as a complex degenerative disease involving mechanical stress, inflammation, aging, metabolism, and abnormal cellular responses within the joint.
What does the future look like for osteoarthritis research?
Liu: The future of osteoarthritis research is shifting away from the traditional view that the condition is simply the result of aging and mechanical wear. The next generation of treatments should ideally do two things at the same time: relieve pain and change the biological course of the disease.
A major breakthrough centers on our findings with the Nav1.7 sodium channel. Traditionally studied for transmitting pain signals in nerve cells, this channel has also been discovered in cartilage cells known as chondrocytes. Preclinical models reveal that inhibiting Nav1.7 not only reduces pain but also protects cartilage, indicating that joint pain and degeneration are deeply connected. To maximize these benefits, researchers are developing advanced delivery systems, combining the Nav1.7-targeting drug lacosamide with an injectable collagen-II hydrogel. This approach releases the medication gradually inside the joint, providing prolonged relief and protection while minimizing whole-body drug exposure, though it remains preclinical and is not yet an approved treatment.
Beyond nerve signaling, ongoing work explores how inflammation and cellular aging actively drive cartilage breakdown. By identifying the molecular switches behind these processes, scientists hope to intervene before permanent joint damage occurs.
Ultimately, the future of osteoarthritis care is moving toward a personalized, mechanism-based model. Because the condition is driven by a mix of factors including inflammation, metabolic dysfunction, previous trauma, and nerve-joint signaling, future therapies will likely identify specific biological subtypes to match patients with targeted treatments. The overarching goal is to redefine an osteoarthritis diagnosis entirely by detecting the condition early, preserving the natural joint, stopping its progression, and ultimately repairing damaged tissues.
What is the best treatment for osteoarthritis?
Liu: Current treatments have a major limitation: There is still no medication approved by the U.S. Food and Drug Administration that can reliably regenerate damaged cartilage while controlling pain. Developing treatments that address both symptoms and underlying disease remains the primary goal at the Liu Lab for Translational Orthopaedic Research.
Source: Yale School of Medicine
