Doctors discover arthritis starts much earlier than they thought

By Stephen Beech

Arthritis begins long before the painful symptoms start to show, reveals new research.

The seven-year study identified new "early warning signs" that could help doctors spot at-risk patients most likely to develop the debilitating condition.

The discovery will enable more targeted monitoring and earlier intervention, say scientists.

Rheumatoid arthritis is a common autoimmune disease that causes painful joint inflammation and damage.

It affects around one in 100 people worldwide, and is significantly more common in women than men.

Rheumatoid arthritis typically develops in adults between the ages of 30 and 60.

The new study reveals that people at risk experience "dramatic" immune system changes long before they feel any symptoms.

During that early phase, the research team explained that their bodies fight an autoimmune battle invisibly. 

The study, published in the journal Science Translational Medicine, was led by researchers at the Seattle-based Allen Institute.

They say it is the most detailed look available into how rheumatoid arthritis develops, mapping immune changes in at-risk people long before symptoms appear - paving the way for earlier treatment and prevention. 

Study co-senior author Dr. Mark Gillespie, of the Allen Institute, said: “Overall, we hope this study raises awareness that rheumatoid arthritis begins much earlier than previously thought and that it enables researchers to make data-driven decisions on strategies to disrupt disease development.”

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During the seven-year study period, the research team tracked people carrying ACPA antibodies, which are known biomarkers for individuals at risk for developing RA.

They identified previously unknown factors associated with disease development, including widespread inflammation, immune cell dysfunction, and cellular reprogramming. 

The research team found that systemic inflammation was already present throughout the body in at-risk individuals.

Several types of immune cells also showed "significant" abnormalities.

B cells, which normally produce protective antibodies, had shifted toward a pro-inflammatory state, while T helper cells were "dramatically expanded" beyond normal levels.

The research team explained that those cells play "crucial" roles in directing immune responses, and their overactivity helps explain why the immune system begins attacking healthy tissue. 

The study also found that even "naive" T cells - immune cells that haven't encountered threats before -showed epigenetic changes.

The researchers said the cells' DNA wasn't mutated, but the way genes were turned on and off had been altered - essentially "reprogramming" the cells before they even encountered their first threat. 

The team also identified monocytes - a type of white blood cell - in the bloodstream that were producing high levels of inflammatory molecules.

The blood cells closely resembled the macrophages found in the inflamed joint tissue of arthritis patients, suggesting the disease process was already preparing to target joints. 

The researchers believe that, if caught early, arthritis could be stopped before it starts – saving patients years of pain and disability.

They say the study may enable a "major shift" away from reactive treatments that rely on the appearance of joint damage and towards proactive prevention. 

Co-author Dr. Kevin Deane, of the University of Colorado Anschutz, added: “We expect that going forward the findings from this study will support additional studies to identify ways to better predict who will get rheumatoid arthritis, identify potential biologic targets for preventing  rheumatoid arthritis as well as identify ways to improve treatments for those with existing rheumatoid arthritis."