Injuries to the joints can cause post-traumatic osteoarthritis (PTOA). Furthermore, almost half of the people who managed to rupture the anterior cruciate ligament in their knee at a given moment of their lives will develop PTOA at a given moment during the course of the next 10-20 years.
Unfortunately, the entire process that causes cartilage degeneration or PTOA as a result of trauma hasn’t been fully comprehended yet.
A recent study done by scientists from Lawrence Livermore National Laboratory (LLNL), University of California, Davis, University of California, Merced and Regeneron Pharmaceuticals analyzed how PTOA develops by RNA sequencing at different stages after a person has suffered the injury. In order to get a most accurate data the team of researchers used a non-invasive tibial compression mouse model of PTOA, which can replicate an anterior crucial ligament rupture which can be caused by just one high-impact injury. The study was published in the Journal of Orthopedic Research.
The most common form of arthritis is osteoarthritis (OA), also known as “wear and tear” arthritis. This type of arthritis develops over time due to the constant damage done to the cartilage between the joints which starts breaking down, causing symptoms such as pain, stiffness and swelling.
Most of the time, people who develop osteoarthritis don’t know they have arthritis until a long period of time has passed, leaving them with less treatment options. By identifying the disease early and tracking its progression while treating its symptoms with the new medical options available could personalize medical treatment before the disease gets to a more advanced stage. The most important part is that there can be developed treatments to prevent the apparition of PTOA years after the injury.
According to Jiun Chang, a UC Merced graduate student, the study wanted to see if there are any biomarkers associated with cartilage degradation in order to discover if they can be used as therapeutic targets.
The study managed to identify 1 446 genes in injured joints, including some OA regulators which were already known and a large number of new genes. Aimy Sebastian, another UC Merced graduate student stated that the study offers the first account of gene expression changes related to the development and progression of PTOA in the tibial compression model.
Loots, the LLNL biologist who leads the research team said that when they compared their new data to the gene-expression data generated by the surgical destabilization of the medial meniscus PTOA model they noticed that the tibial compression model could be a faster progressing model of PTOA.
This new study is the first account of the entire genome expression profiles to gather new information of the temporal progression of the disease.