cartilage (cart’ ill idge): tough elastic tissue found in various parts of the body, including the joints. It is largely converted into bone.
cytokines (site’ o kynes): Any of several proteins that are released by cells in the immune system to signal for an immune response. Examples include tumor necrosis factor-α, interleukin-1, and interleukin-8.
synovial joint (sin o’ vee uhl): the synovial tissue lines the joints and produces synovial fluid, which is a clear fluid that nourishes and lubricates the cartilage and bone in the joint.
tumor necrosis factor-α (TNF-α): a protein that triggers inflammation as part of the body’s normal immune system response. Overproduction of TNF-α can lead to excessive inflammation such as that found in patients with RA.
white blood cell: also called leukocyte (luke’ o site) or white cell; any of various blood cells that separate into a thin white layer when whole blood is separated. White blood cells are responsible for protecting the body from infection and disease.
HOW IT OPERATES
The joint pain and inflammation of rheumatoid arthritis (RA) begins when white blood cells,
which are a part of the immune system responsible for fighting infection,
accumulate in the synovial (sin o' vee uhl) tissue. The synovium is a
layer of cells that lines the joints and produces synovial fluid, which
is a clear fluid that nourishes and lubricates the cartilage and bone
in the joint. The white blood cells produce cytokines (site' o kynes),
which experts have described as "the messenger molecules of the
immune system." Cytokines can cause inflammation, which can result
in pain and swelling, which is a normal healthy process when your
body has an infection but is inappropriate when no infection exists.
They also attract other immune cells and cause the production of
excess synovial fluid.
In severe cases, RA can often reduce the movement of limbs.
Researchers at the National Institute of Arthritis and Musculoskeletal
and Skin Diseases (NIAMS) have suggested that an imbalance between
cytokines that promote inflammation and those that perform healthy
functions within the immune system play a key role in the development
of many autoimmune diseases. In RA, several cytokines,
including tumor necrosis factor-α, interleukin-1, and interleukin-8, appear to
contribute to the ongoing destruction of cartilage, bone, and other
joint-related tissues.
ENTERING A NEW ERA OF DISCOVERY AND TREATMENT
Scientists have advanced their understanding of the process of rheumatoid arthritis (RA),
and this knowledge has led to the successful development of medicines that slow or help inhibit joint damage. According to leading scientists J.
Bruce Smith, MD, and Mark Haynes, PhD, "the newer treatments represent
the 'tip of the iceberg,' and as our basic knowledge increases, so too,
will the armamentarium [the
Animation showing a joint broken down by RA. In joints with RA, white blood cells enter the
synovial space and produce cytokines, which contribute to the destruction
of cartilage, bone, and other tissues.
complete range of weapons] with which we can fight rheumatoid arthritis and other similar autoimmune diseases."
Richard Shirley is but one example of how this continuing research is
helping patients with RA. After receiving a biologic DMARD,
(disease-modifying antirheumatic drug), he reports "I am doing better
now than I have in many years." He also finds that he has dramatically
less pain, is able to walk long distances, and can do light housework
and minor repairs around the house. As he said so simply, "I enjoy my life."
There is no single test that doctors can use to determine if someone has rheumatoid arthritis (RA). Experts recommend that doctors perform several tests to accurately diagnose RA. In fact, the American College of Rheumatology (ACR) has developed guidelines for diagnosing RA. The ACR guidelines have been reviewed by rheumatologists (specialists), primary care providers who practice rheumatology, and other health care professionals. According to these experts, a doctor may do all or some of the following to diagnose RA:
Ask the patient about the amount of joint pain they have, which joints are affected, how long any fatigue or morning stiffness lasts, and if they have problems completing everyday activities like housework or exercise
Perform a physical examination to count how many joints are tender or swollen and to evaluate mechanical joint problems, such as loss of motion and/or deformity
Perform blood tests for signs of RA
Take X-rays of selected joints that appear to be affected by RA
The ACR guidelines also suggest that additional tests be performed to assess liver function and evaluate overall health before beginning treatment for RA and to monitor disease progression as treatment continues over time.
The health information contained herein is intended
for use by United States residents only and is provided for informational
purposes only and is not intended to replace a discussion with a healthcare
provider. All decisions regarding patient care must be made with a
healthcare provider and consider the unique characteristics of each patient.
The joint pain and inflammation of rheumatoid arthritis (RA) begins when white blood cells,
which are a part of the immune system responsible for fighting infection,
accumulate in the synovial (sin o' vee uhl) tissue. The synovium is a
layer of cells that lines the joints and produces synovial fluid, which
is a clear fluid that nourishes and lubricates the cartilage and bone
in the joint. The white blood cells produce cytokines (site' o kynes),
which experts have described as "the messenger molecules of the
immune system." Cytokines can cause inflammation, which can result
in pain and swelling, which is a normal healthy process when your
body has an infection but is inappropriate when no infection exists.
They also attract other immune cells and cause the production of
excess synovial fluid.
In severe cases, RA can often reduce the movement of limbs.
