Osteoarthritis, the most common form of arthritis, is a condition where the cartilage cushioning the joints gradually breaks down. Over time, this leads to bone-on-bone friction, joint stiffness, and pain with movement.
Affecting over 32 million people in the United States alone, it can severely impact daily life, with no current treatment capable of halting its progression.
The risk of developing osteoarthritis depends on several factors, including injury, aging, obesity, and genetics. Recent research highlights that nearly half of this risk is genetic, sparking interest in understanding the genetic components of the disease.
A new study led by researchers at the UNC Thurston Arthritis Research Center has made significant progress in this area. By identifying 13 genes directly involved in joint tissue loss, the team hopes to pave the way for new therapies that can slow or stop the progression of osteoarthritis.
Dr. Richard Loeser, Dr. Doug Phanstiel, and Dr. Brian Diekman brought their diverse expertise together for this groundbreaking study. Published in Cell Genomics, their research builds on prior studies that pinpointed over 100 regions in DNA linked to osteoarthritis risk.
However, these earlier studies struggled to identify the specific genes responsible. By focusing on “causal” genes—those directly influencing the disease—the team has filled a critical gap in understanding.
The researchers began by collecting joint tissue samples from more than 100 human donors. In the lab, they created a model of osteoarthritis by exposing these cells to molecules that mimicked the disease’s effects.
Using advanced tools in genomics and bioinformatics, Dr. Phanstiel’s team analyzed gene expression data to identify genes strongly linked to the disease. Meanwhile, Dr. Diekman’s expertise in gene editing helped confirm the role these genes play in osteoarthritis.
Of the 13 identified genes, six were previously unknown in connection to osteoarthritis. This discovery is particularly exciting because it opens new doors to understanding the biological processes involved in joint damage.
Some of these genes are linked to known osteoarthritis mechanisms, while others point to entirely new pathways that researchers are just beginning to explore.
Currently, osteoarthritis treatments focus on symptom management. Doctors often recommend nonsteroidal anti-inflammatory drugs, physical activity, and weight loss to ease pain and improve mobility.
However, there is no treatment that can prevent or reverse the damage caused by the disease. The hope is that targeting these newly identified genes will lead to therapies that address osteoarthritis at its root, stopping joint deterioration before it becomes severe.
The UNC research team is now expanding their work to include more samples and cell types, aiming to uncover additional genes involved in the disease.
They are also investigating how the identified genes influence biological processes that contribute to joint damage. In parallel, they are conducting drug screening studies to find compounds that could block these harmful processes.
Dr. Loeser, a leading expert in rheumatology, expressed optimism about the potential of this research.
“The hope is that we will be able to find new therapeutics that will stop the progression of joint damage at its earliest stages,” he said. “This could prevent the pain and disability that so many patients with osteoarthritis experience.”
This study marks an important step forward in the fight against osteoarthritis. By identifying specific genetic targets, researchers are laying the groundwork for therapies that could transform how the disease is treated, offering hope to millions living with its challenges.
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The research findings can be found in Cell Genomics.
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