Pathophysiology of arthritis pain

by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

Click here: Second Opinion Arthritis Treatment Kit

There are more than 100 different types of arthritis. The pathophysiology varies according to diagnosis. Let’s look at a couple of the more common types of arthritis.

Osteoarthritis is a disease most often seen in older individuals but it also may occur in younger people, following injury.

According to studies, more than 80% of people older than 75 have clinical OA, and more than 80% over the age of 50 have x-ray evidence of OA.

The joint consists of bone, cartilage, synovial lining, and ligaments. Subchondral bone is covered by hyaline or articular cartilage that consists of type II collagen, chondrocytes and proteoglycans which are high molecular weight glycoproteins that retain water and increase resiliency of cartilage. Collagen fibrils are arranged in a a fashion which provide tensile strength, and the proteoglycans provide distensibility by retaining water. The synovial cell layer that lines the joint produces a viscous synovial fluid that provides lubrication for joint motion.

Located on the outer side of the synovial membrane is a flexible joint capsule with ligaments and tendons. Outside the joint, bursae provide cushioning for muscle, tendon, and ligaments to pass over roughened bone surfaces. These joint components allow for both motion and load bearing across nearly frictionless surfaces.

OA is primarily a disease of cartilage. The disease typically affects weight-bearing joints asymmetrically. Local inflammation is also present.

The osteoarthritis process can result from excessive or repetitive loading of the normal joint, including work-related repetitive activities that damage cartilage or subchondral bone, trauma, or increased load to the joint from obesity.

As cartilage is damaged, it becomes thinner, develops fissures or large clefts, and proteoglycan synthesis decreases. That process leads to decreased load-bearing capacity. The chondrocyte- the cartilage cell- can respond initially by attempting to repair its surrounding extracellular matrix, but as it is overwhelmed there is increased release of metalloproteinases and lysosomal proteases leading to further matrix loss.

By contrast, let’s now look at another type of arthritis.

Rheumatoid arthritis (RA) has a different pathophysiology. RA begins in the synovium and systemic features include fever, weight loss, skin thinning, scleritis, corneal ulcers, and the formation of subcutaneous or subperiosteal nodules. Multiple organs may be involved leading to premature death. The etiology of RA is unknown. Possibilities include various viral or bacterial infections or infection with mycobacteria. Recent evidence suggests bacteria located in the mucosa may play a significant role. In any event, an environmental trigger stimulates an immune response in the appropriate genetic host leading to a host immune response that may cross react with similar antigens in the host joint tissue.

When dendritic cells, monocytes, and macrophages are activated by the autoimmune process, they interact with and present antigen to the appropriate T cells. A series of events occurs that leads to the further activation of more monocytes and macrophages, T cells, B cells, and increased endothelial cell activity. Endothelial cells are the cells that line blood vessels. What occurs is a proliferation of blood vessel.

These events increase the synthesis of adhesion molecules. Inflammatory white blood cells are attracted to the inflamed joint fluid by the elaboration of multiple cytokines, some of which act as chemoattractants that increase the delivery of inflammatory cells to the synovium and synovial fluid.

Cytokines such as IL-1 alpha or beta, IL-8, tumor necrosis factor (TNF)-alpha, platelet-derived growth factor, heparin binding growth factor, GM-CSF, IFN-gamma, TGF-beta, IL-2, and IL-6 and others lead to increased activation of fibroblast-like cells in the synovium and chondrocytes, as well as macrophages. The activation releases increased amounts of prostaglandins, neutral proteinases such as collagenases, and stromelysin. Also, bone breakdown cells are produced and attracted to the area. All of these factors lead to the destruction of bone and cartilage by the invading proliferative synovium.

Therefore, RA is a progressive destructive inflammatory disease of the synovium. Release of cytokines and other pro-inflammatory mediators and proteinases lead to the destruction of the joint.

Other forms of arthritis have other types of pathophysiology. For example, gout is an inflammatory arthritis that is induced by crystals of monosodium urate. Tese crystals induce an acute and chronic inflammatory destructive response.

A similar inflammatory pattern is established for calcium pyrophosphate crystal induced arthritis although the production of crystals occurs through a different mechanism.

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