How Do RA Drugs Prevent Further Joint Damage?

Medically Reviewed by Brunilda Nazario, MD on February 10, 2022
Written by Susan Bernstein
4 min read

Rheumatoid arthritis (RA) inflammation attacks the tissue lining your joints and causes swelling and pain. Inflamed joint tissue breaks down and wears away. Without medications to treat and control RA, your joints can become permanently damaged, unstable, and twisted out of shape.

Joint damage in RA can be permanent if you don’t treat your disease with medications to control RA disease activity, and slow or stop joint damage as soon as possible.

The inflammation that comes with  RA can wear away bone and cause progressive damage. Normally, bone tissue grows back to replace areas where there is damage. When you have active inflammation in RA, bone breaks down faster than new bone cells can replace those that are lost. When you take medications to stop inflammation in your joints, new bone cells called osteoblasts can catch up to form new bone.

Some RA medications can help prevent joint damage, delay or stop it from getting worse, or may even repair or heal some harm. You and your rheumatologist can choose the right medications to lower RA disease activity and safeguard your joints.

Nonsteroidal anti-inflammatory drugs (NSAIDs) treat arthritis joint pain and swelling because they block an enzyme called cyclooxygenase (COX). Your body makes it when your joints are injured or inflamed.

NSAIDs can treat occasional symptoms of inflammation from RA like joint swelling, heat, redness, and pain.

While NSAIDs can treat RA symptoms, these drugs do not prevent joint damage from RA. They do not slow down the progress of your disease, so if you already have joint damage, NSAIDs won’t keep it from getting worse.

Disease modifying antirheumatic drugs (DMARDs) are used to treat RA disease activity. They ease pain and swelling, but can also slow down or stop joint damage from getting worse.

RA is an autoimmune disease that causes your immune system to become overactive. It releases inflammatory proteins that attack your joints and healthy tissues by mistake. DMARDs target your immune system to slow down that process and reduce the inflammation that damages your joints.

DMARDs ease inflammation in your joint tissues, which can prevent joint structure breakdown. This also helps preserve joint function, and can relieve pain and swelling.

DMARDs need to be taken for weeks or months before they start to work or you notice decreased inflammation. You need to keep taking your DMARDs regularly, even when you no longer notice any RA symptoms.

DMARDs may not relieve symptoms like pain or swelling right away, but don’t stop taking your drug because you don’t think it’s working. Over time, DMARDs can delay or prevent joint damage from RA.

Biologics and biosimilars are a newer type of DMARD made from living cells. Each biologic drug targets a specific molecule on the surfaces of cells released by your immune system, or cells in your joints or joint fluid that cause RA inflammation and joint damage. Biologics can block those molecules to lower inflammation and prevent further joint damage.

Some biologics seem to help repair or partially heal damaged bone in your joints caused by RA. These drugs could help damaged joints start to function and move better, and restore normal spacing between the structures of your joint.

Biologics each attack specific targets in your immune system that cause inflammation to slow down or halt joint damage:

  • TNF inhibitors block tumor necrosis factor, an immune system protein that causes inflammation. These drugs reduce inflammation and keep RA damage from getting worse. TNF inhibitors can also partially repair bone tissue to make joint erosions, small holes in bone, less deep. 
  • T-cell costimulatory blockers stop the action of T lymphocytes, immune cells that can cause inflammation. With long-term use, these drugs can stop joint destruction.
  • B-cell depleting drugs stop the action of B lymphocytes. These are immune cells that are involved in RA inflammation in different ways. B cells can produce autoantibodies called rheumatoid factor and anti-citrullinated protein antibody (ACPA) that cause joint inflammation. B cells can also activate T cells and produce cytokines that inflame and destroy the soft tissue lining your joints. B-cell depleting therapy can slow down RA joint damage even when other biologics or DMARDs haven’t worked.
  • Other biologics target and block inflammatory cytokines like interleukin-1 (IL-1), interleukin-1-Ra, and interleukin-6 (IL-6) to slow down joint damage in RA. IL-1 and IL-6 inhibitors can both promote new bone growth for limited repair of joint erosions.

Janus kinase or JAK inhibitors are another type of biologic that can treat RA. They’re also called targeted synthetic DMARDs. These drugs block signals between cells and cytokines that cause joint inflammation and damage.

JAK inhibitors interrupt communication between cells that cause inflammation of the synovium, the tissue that lines and protects your joints, and causes joint destruction in RA. JAK inhibitors can stop bone erosion, reduce joint inflammation, and prevent joint damage from getting worse for people with RA.