Osteoarthritis (OA), also known as degenerative arthritis, is the most common of the arthritides and is a progressive joint disease. Described commonly as a "wear and tear" process, OA is caused by mild inflammation in the joint secondary to abnormal degradation of the articular cartilage that covers the bones forming the joint. As the articular cartilage wears away, the bone it covers is exposed and becomes a participant in joint movement, increasing friction. This process also involves decreasing the synovial fluid in the joint that normally lubricates its moving parts. This decrease can occur through consumption of the fluid over time and/or through slowly diminishing its production in the joint space by the synovial membrane. The combination of these two progressive events leads to pain in the joint. In response to the pain, the joint gets used less and atrophy of the muscles and ligaments associated with the joint occurs. These secondary effects cause further dysfunction in addition to the pain and stiffness that comes with cartilage erosion.
The joints most commonly affected are ones that are most frequently in use, i.e. knees, hips and metacarpals. The spine and feet are also frequently involved and in theory a patient can have OA changes in any joint.
Anatomy and Mechanism
Articular cartilage exists on the bones opposed inside most mobile joints and provides cushion and protection against friction when the joint is in motion. Note that this is a different entity altogether than the cartilage that redistributes weight through the joint (e.g. the menisci of the knee). This can be a point of confusion when the term "cartilage" is used.
Articular cartilage is a type of hyaline cartilage that is hard yet smooth. It is composed of Type II collagen and proteoglycans. It is different from fibrocartilage in its collagen type (II vs. I) and its relative composition of collagen and proteoglycans (articular cartilage has more proteoglycan and less collagen vs. fibrocartilage). Proteoglycans help trap water in the hyaline matrix and therefore an increase in their concentration provides articular cartilage with its ability to significantly reduce friction.
Due to a poor blood supply and a network of materials that restrict chondrocyte movement, response to damage in articular cartilage typically either leads to fibrocartilage deposition or calcification. In either case, articular cartilage repair is rare as chondrocytes are trapped by the hyaline cartilage matrix in the lacunae they reside. Poor vascularization also contributes to the poor healing quality of articular cartilage. Thus, the wear and tear that articular cartilage experiences over time cannot be repaired as efficiently as in other tissue systems.
While articular cartilage may not be as active in turnover as, say, bone or skin, it is not a dead tissue. A balance is struck by the chondrocyte between anabolic and catabolic processes within the matrix. Recent studies suggest upregulation of metalloproteinases (MMPs) by chondrocytes in response to stress is much more prominent in OA joints vs. normal joints of the same biological age. The role of MMPs as catabolic entities in the OA process continues to be actively investigated.
OA can either be primary or secondary. Primary OA is correlated with (not caused by) increasing age. Up to 80% of people over the age of 55 are affected by OA but it should not be accepted as a normal process of aging. It is caused by chronic joint use combined with age-related changes in the composition and health of articular cartilage. This includes reduced proteoglycan deposition that alters its friction-reducing properties, as well as, the accumulation of poorly repaired micro-trauma over years of chronic use.
Primary OA is diagnosed when no specific disease or event is identified as the cause; if one was found, the diagnosis would be secondary OA. While the pathology is the same as with primary OA, secondary OA is caused directly by another disease process or by an event or series of events. Common causes of secondary OA include joint trauma, ligamentous instability, obesity, inflammatory diseases (Perthes' disease, Lyme disease), other chronic joint diseases (gout, pseudogout, RA), congenital disorders (hip dysplasia), hemochromatosis, et al.
Genetic predisposition to OA is a subject of intense research at present. Twin studies have shown that the influence of genetic factors may approach 70% in OA in certain joints. Extracellular matrix component genes are suspected and polymorphisms or mutations in these ECM proteins could dictate early changes in articular cartilage health. MMPs, and more specifically their expressions by chondrocytes, are cited as potential explanations for genetic variability. Please check references for more information.
As the cartilage in the joint breaks down, free-sulfated proteoglycans are released into the synovium. These byproducts combined with continued use provoke inflammatory synovitis. Thus, cartilage break down occurs first, then inflammation follows. Articular cartilage lacks nerves. The pain caused by OA is related to the synovial inflammation and its effects on the area, i.e. ligament stretch, muscle spasm, and increased venous pressure in the bone. It is then that the patient begins to feel pain, most notably while the joint is in use. Pain is the most common symptom reported in OA; it is also usually the first symptom reported. The pain becomes chronic and is usually symmetrical and can be accompanied by reduced range of motion or stiffness. It can be described as a sharp, grinding or burning ache and is typically exacerbated by use. This information is crucial in differentiating OA from rheumatoid arthritis, where symptoms improve as the joint is used throughout the day.
Other signs of OA include bony enlargements of the DIP and PIP joints called Heberden and Bouchard's nodes, respectively. Both are caused by the aforementioned calcification of articular cartilage that occurs following either chronic or acute injury. They may or may not cause pain but frequently distort the form and function of the joint of origin.
OA is a clinical diagnosis made based on careful history and physical exam findings. Some x-ray findings correlate with an OA diagnosis but do not exclusively correlate with the given history. These findings include subchondral sclerosis, subchondral cysts, joint-space narrowing and bone spur (osteophyte) formation. Because OA is usually stress-induced, changes within the joint are mostly asymmetric. As the joint receives stress unevenly distributed across its components, this is visible in radiographic studies. Compare this to RA or gout changes, where, for instance, joint space narrowing will be symmetric across the joint over time.
OA is not a curable disease. While it is a progressive process that is not reversible, treatment options are available that can help. These options can best be broken down into non-surgical and surgical options.
Lifestyle Modification: depending on the suspected cause of the OA, the patient may be asked to alter their daily living. Losing weight can help decrease stress of weight-bearing joints. Restricting high-impact activities in favor of low-impact activities can also help reduce joint stress. While some activities should be avoided make sure that physical activity in general is maintained for the overall health of the patient, if possible.
Pain Management: NSAIDs are the foundation of pain control in OA. Corticosteroid injections can also be used for symptomatic pain control when needed.
Diet: Some studies have suggested glucosamine and chondroitin sulfate are supplements that when taken orally can have positive effects on joint health.
Physical Therapy: As a patient compensates for pain associated with OA, the corresponding changes in the joint can make symptoms worse. Muscle atrophy from lack of use and joint laxity can exacerbate OA. PT can help combat these secondary effects while attempting to reduce pain and inflammation without sacrificing activity level.
Osteotomy: Realignment of bones articulating in a joint to alter the pressure distribution in that joint.
Arthroscopy: Minimally-invasive procedure where instruments are inserted through small incisions into the joint to remove or address the byproducts of the OA process.
Arthrodesis: Joint fusion that sacrifices flexibility and function of the joint for symptomatic pain relief.
Arthroplasty: Joint replacement involving replacing diseased joint with plastic or metal parts to function artificially.
Currently, OA is the number one cause cited for joint replacement today in the United States. Short-term complications include deep vein thrombosis, blood loss, scarring and infection. Long-term complications include late infection, wearing down or loosening of the components. As materials and techniques improve, arthroplasty will continue to improve as a viable option for OA and other joint diseases.
Tuetken, Rebecca S. Osteoarthritis. In Turek's Orthopaedics, 6th ed. Eds. Stuart L Weinstein, Joseph A Buckwalter. 154-162. (Lippincott Williams & Wilkins, 2005)