What is RA?

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RA is short for rheumatoid arthritis, a chronic disease characterized by joint inflammation, pain, stiffness, and swelling.1 RA is one of over one hundred different types of arthritis. Some of the most common types of arthritis include osteoarthritis, infectious arthritis, and gout. What they each have in common is joint pain. In fact, the word arthritis is made up of the Greek words arthros, for joint, and itis, for inflammation.

 

How does RA affect me?

What sets one form of arthritis apart from another is the cause of joint involvement and pain. In RA, inflammation and joint damage is caused by an autoimmune process. In RA, like other autoimmune diseases, such as psoriasis, lupus, type I diabetes, and Crohn’s disease, the body’s immune system mistakenly attacks its own healthy tissue. In fact, the word autoimmune combines the words auto, which means self, and immune to communicate the idea of the immune system attacking the body itself.

Normally, inflammation is a sign that our immune system is fighting invasion by substances or organisms that are foreign and potentially harmful to our bodies. However, in RA, joint inflammation and damage results when our immune system malfunctions and attacks healthy tissue.

Are there effective treatments for RA?

Over the last couple decades, great strides have been made in understanding RA and developing effective treatments for the disease. Although RA is associated with symptoms that negatively affect the way joints function, now more than ever, it is possible to get treatment that will improve these symptoms and allow you to lead an active and full life. Some of the most exciting developments in RA treatment have been made with disease-modifying anti-rheumatic drugs (DMARDs) and new biologic treatments. These drugs can help to slow or prevent joint damage and provide relief from many of the symptoms of RA.

 

RA and the autoimmune process

A group of immune cells made up mainly of white blood cells (also called leukocytes) and a wide range of immune system chemicals called inflammatory mediators carry out the work of our immune system. This work includes patrolling the body to watch for invasion by potentially harmful foreign substances or organisms and responding to an invasion by mounting an inflammatory response designed to destroy the invader.

In RA, the immune system malfunctions and an inflammatory response is launched against the body’s healthy joint tissue. RA specifically affects the type of joints called synovial joints (also called diarthrodial joints) that connect bones that are highly mobile. Synovial joints typically affected by RA include the hip, the elbow, the hands and feet, the knees, and the shoulders.2

 

RA and its effects on joints and other structures

As a disease, RA directly affects the joints. However, it also impacts other structures including bones, organs, and soft tissues, such as muscles, tendons, ligaments, and bursae.

In RA, immune cells, principally white blood cells (leukocytes), travel to joint cavities, the spaces where two or more bones meet. An inflammatory response is launched, making the joint painful and swollen. As leukocytes, including B and T lymphocytes (B- and T-cells, for short), neutrophils, monocytes, dendritic cells, and macrophages, continue to multiply in the joint cavity, they release a wide range of inflammatory mediators, including cytokines, enzymes, and signaling molecules called leukotrienes and prostaglandins. Some of these substances promote the growth of blood vessels, which supply nutrients to the growing mass of leukocytes, resulting in the formation of pannus (this Latin word literally means a piece of cloth), a flap of fibrous tissue that forms over the synovial cartilage.2

RA affects many different parts of the joint, including the synovial fluid that fills the joint cavity and functions as a kind of shock absorber and lubricant to reduce friction between bone and joint cartilage during movement. Normally clear with a consistency like egg yolk, inflammation associated with RA causes the synovial fluid to become cloudy and increase in volume. The synovial lining on the inside of the joint becomes inflamed and swollen. With continued exposure to inflammation, thickening of the synovial lining, and pannus formation, over time the joint space decreases. The bony structure of the joint itself may become deformed and, in extreme cases, the joint may cease to function.2

 

How does RA affect soft tissue?

While joints themselves are stationary, soft tissues, including muscles, tendons, ligaments, and bursae (bursae is plural of bursa) are responsible for actually making movement happen. RA can have direct and indirect effects on these soft tissues.

Tendons, which attach muscle to bone, and ligaments, which attach bone to bone, provide both mobility and stability to joints. Movement is driven by muscular contraction (a shortening of the muscle) and pulling of a tendon, which moves over a joint. Bursae are small pouches lined with synovial membrane and filled with synovial fluid (the same fluid that fills the joint capsule). These structures serve as cushions between bones and muscles and/or tendons which are under extreme stress. Inflammation that affects tendons or bursae is called tendonitis and bursitis, respectively.

The function of a joint depends to a large degree on the muscle mass that surrounds the joint. Muscles are designed to absorb some of the stress that ordinary movement places on joints. Joint pain can result in disuse and inactivity and lead to muscular deterioration (sometimes called atrophy). This deterioration can, in turn, have a negative effect on joint function by interfering with proper joint alignment and increasing stress on joints. Loss of alignment with muscular disuse can eventually lead to joint deformity. RA can result in tendonitis and ultimately lead to tendon damage. For instance, the rupture of tendons in the hand is common as RA progresses.

 

How does RA affect bone?

The human body contains approximately 300 individual bones that are connected by over 140 joints. Bones are made up of a mineral called hydroxyapatite, which provides rigidity, and collagen (a type of protein), which provides elasticity. Bones in the body are in a constant process of repair (called remodeling) driven by two types of bone cells. Osteoclasts are responsible for the removal (resorption) of old existing bone and osteoblasts are responsible for forming new bone. Normally, osteoclasts and osteoblasts work together to maintain a balance between bone formation and resorption of bone, so that the overall mass of bone is kept constant. The inflammatory process that occurs with RA and other diseases can upset the balance between bone loss and formation. In RA, bone loss is common and is associated with the severity of inflammation and the duration of the disease.3

view references
  1. Posalski J, Weisman MH. Articular and periarticular manifestations of established rheumatoid arthritis. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatoid Arthritis. Philadelphia, Penn: Mosby Elsevier; 2009:49-61.
  2. McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med 2011;365:2205-19.
  3. Schett G, Redlich K. Osteoclasts and osteoblasts. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatoid Arthritis. Philadelphia, Penn: Mosby Elsevier; 2009:163-167.
further reading
Paget SA, Lockshin MD, Loebl S. Rheumatoid Arthritis Handbook. New York, NY: John Wiley and Sons, Inc; 2002. Fox B, Taylor N, Yazdany J. Arthritis for Dummies. Hoboken, NJ: Wiley Publishing, Inc; 2004. Emery P. Pocket Reference to Early Rheumatoid Arthritis. London: Springer Healthcare Ltd; 2011.
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