Possible Personalized Treatment for Osteoarthritis


The whole-joint gene expression profile for osteoarthritis discovered by researchers.

In a recent study, researchers analyzed the whole-joint gene expression through RNA sequencing at 1 day, 1 week, 6 weeks, and 12 weeks after anterior cruciate ligament (ACL) rupture from a single high-impact injury in a mouse model.

Joint injury can cause post-traumatic osteoarthritis (PTOA), as approximately half of people who rupture their ACL developing PTOA within 10 to 20 years, according to the study published in the Journal of Orthopaedic Research.

Osteoarthritis is caused by the cartilage between joints breaking down and is usually asymptomatic until there has been significant joint damage that can be treated by surgery or pain management.

Researchers believe that characterizing OA biomarkers can help detect and track progression of the disease. This, and new therapies that minimize cartilage damage, could personalize osteoarthritis treatments and could possibly prevent the development of PTOA.

"The goal of the study was to see if there are biomarkers associated with cartilage degradation, which could then be further explored as therapeutic targets in future experiments," said lead author Jiun Chang.

The researchers were able to identify 1446 genes expressed in injured joints, including 18 long noncoding RNAs, according to the study.

"This study provides the first account of gene expression changes associated with PTOA development and progression in this tibial compression model," said study co-author Aimy Sebastian.

Researchers in the study were the first to analyze the whole genome expression profiles to gain new insights into the progression of osteoarthritis, the authors wrote.

"By comparing our data to gene-expression data generated using the surgical destabilization of the medial meniscus PTOA model, we identified several common genes and shared mechanisms,” concluded researcher Gabriela Loots, PhD. “Our study highlights several differences between these two models and suggests that the tibial compression model may be a more rapidly progressing model of PTOA.”

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