Osteoarthritis (OA) is the most common joint disorder. It affects 30% of people ages 45 to 64, and 68% of those over age 65.1 While management of symptoms is central focus of care for OA patients, other measures, geared toward prevention of the disease or removing its underlying causes, have also been promoted. As these approaches (many of them considered complementary therapies) gain popularity and receive more attention in the literature, it is vital that healthcare providers be familiar with them.2  

OA is more than simply “wear and tear” on a joint. It is a heterogeneous disease with four
key etiological factors: 1) disorders in chondrocyte cell biology, 2) genetic predisposition, 3) the influence of biomechanical forces, 4) inflammation. OA may be classed as noninflammatory or inflammatory. In noninflammatory OA, patients tend to only have disability-related complaints and pain, whereas
in inflammatory OA, they also have articular swelling, nighttime pain, and morning stiffness, as well as synovitis and calor.

Joint health is dependent on the function of chondrocytes. Chondrocytes synthesize joints’ extracellular matrix, which is made of three main components: water, collagen, and proteoglycans (made of protein, chondroitin sulfate, and keratin sulfate). Proteoglycans, which have a half-life of just weeks, provide elasticity through their highly negatively charged sulfated glycosaminoglycans. Collagen, which has a half-life of many years, lends tensile strength by holding proteoglycan molecules in a structural framework.

Early in OA chondrocytes begin making more proteoglycans, but eventually, as chondrocytes begin to fail, proteoglycan synthesis decreases as well. Ultimately loss of elasticity and increased water permeability lead to further chondrocyte dysfunction, which leads to further joint damage. Eventually chondrocytes begin
to produce degradative enzymes (primarily metalloproteinases) and various mediators of inflammation, which lead to additional joint destruction and steady worsening of symptoms.³

Any force that leads to biomechanical changes in cartilage can lead to OA. This can include injury, overloading of the joint, ligament damage, muscle atrophy, and metabolic diseases that lead to joint deposits. Ultimately osteoblasts below the cartilage increase bone formation as cartilage is compromised. Microfractures occur leading to callus formation and additional vulnerability to more microfractures. Osteophytes form, subchondral cysts grow as the body tries to equalize joint pressure, and muscles and ligaments lose their ability to provide the joint with structural support.

OA tends to strike the following joints:

• Cervical spine
• Lumbar spine
• Hips
• Knees
• First carpometacarpal and metatarsophalangeal joints
• Distal interphalangeal joints (DIPs)