Osteoarthritis (OA) is a chronic disease process which affects the synovial joints, particularly large weight-bearing joints. OA is particularly common in older patients but can occur in younger patients either through a genetic mechanism or, more commonly, because of previous joint trauma. Another name for OA is degenerative joint disease which is considered to be the most common form of arthritis (2004). It is characterized by degenerative loss of articular cartilage, subchondral bony sclerosis, and cartilage and bone proliferation at the joint margins with subsequent osteophyte formation. Secondary synovial inflammation is common.
OA is classified as secondary when the cause is another disease or condition, an infection, deformity, injury, or overuse of a joint. It may be secondary to chronic trauma or underlying joint disease. Much of the risk for osteoarthritis of the knee comes from occupations that involve bending of the joint.
Normal Structure and Function
Synovial joints make up most joints of the body. They are found in fluid-containing cavities which permits much movement as possible. Its stability depends on articular surfaces, ligaments, and muscle tone (2000).
Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are comprised of a synovial membrane, articular or hyaline cartilage, subchondral bone, synovial fluid, and a joint capsule. Although traditional teaching prescribes that OA affects primarily the articular cartilage of synovial joints, pathophysiologic changes also occur in the synovial fluid, as well as in the underlying (subchondral) bone and overlying joint capsule.
Joints normally have such a low friction level that they are protected from wearing out, even after years of use. The ends of two bones which meet to form the joint are covered with articular cartilage, a surface material much like a tread of a tire. It is composed of tough, fibrous tissue – collagen – which gives it its strength (1994).
In the mature adult, articular cartilage has no blood vessels, no nerves, and no lymphatic channels. Its living cells are nourished by joint fluid, called synovial fluid which is also extremely good lubrication. The specialized tissue lining called the synovium produces synovial fluid, the prime lubricant for the joint and the nutritional source for joint surface cartilage and meniscus cartilage.
The synovial fluid is a thick, stringy fluid found in the cavities of synovial joints. It has an egg-like consistency which reduces friction between the articular cartilage and other tissues in joints to lubricate and cushion them during movement. The inner membrane of synovial joints is called the synovial membrane, which secretes synovial fluid into the joint cavity. This fluid forms a thin layer (approximately 50 micrometers) at the surface of cartilage, but also seeps into the articular cartilage filling any empty space.
The fluid within articular cartilage effectively serves as a synovial fluid reserve. During normal movements, the synovial fluid held within the cartilage is squeezed out mechanically to maintain a layer of fluid on the cartilage surface.
The cause of OA is unknown, but genetic, metabolic, endocrine, biochemical, and hydrolytic enzyme factors have been suggested. Abnormal biochemical stresses may lead to chondrocyte damage and proteolytic enzyme release resulting in articular cartilage degeneration. OA develops when cartilage repair does not keep pace with degeneration.
In children, the articular cartilage does have some blood supply and can repair itself. In adults, the cartilage repairs with scar tissue which is mechanically inferior. The tearing down of these surfaces (articular cartilage) is osteoarthritis or degenerative arthritis, also called wear and tear arthritis.
Osteoarthritis is a non-inflammatory disease of joints characterized by deterioration and erosion of articular cartilage and by the formation of new bone at the articular margins sometimes producing so-called spurs ( 1998). Osteoarthritis may occur as a monoarticular or polyarticular involvement. The large joints of the body and the spine are principally affected. The principal anatomic alterations are degeneration of the cartilage rather than inflammation of the synovia.
OA probably begins most often with an abnormality of the cells that synthesize the components of cartilage, such as collagen and proteoglycans. The cartilage may swell because of water retention, become soft, and then develop cracks on the surface. Tiny cavities are then formed in the bone beneath the cartilage, causing the bone to become weak. This destroys the articular cartilage found in edges of the bones.
The affected cartilage initially develops small tears known as fibrillations, followed by larger tears, and eventually it fragments off into joints. The cartilage-forming cells, the chondrocytes, replicate in an attempt to keep up with the cartilage loss; however, they eventually are unable to do so, and the underlying bone becomes exposed because of gross areas of bone denuded of cartilage.
With the destruction of the articular cartilage, the underlying bone is exposed. The subarticular bone becomes thickened because of either compression or new bone formation. The marrow spaces in this region are often filled with fibrous tissue and small islands of cartilage that are either driven in by traumatic injury or are formed from the endosteum or connective tissue in the marrow spaces. At the same time, small islands of cartilage, which later become ossified, project above the surface of the articular cartilage, usually about its margins, to produce the characteristic bony spurs of osteoarthritis.
Bone can overgrow at the edges of the joint, producing bumps (osteophytes) that can be seen and felt. Ultimately, the smooth, slippery surface of the cartilage becomes rough and pitted, so that the joint can no longer move smoothly and absorb impact. When large spurs project from opposing bones, they may come into contact with each other to cause pain and limitation of motion (1998). All the components of the joint—bone, joint capsule, synovial tissue, tendons, ligaments, and cartilage—fail in various ways, thus altering the joint.
Onset is usually gradual and localized to one or a few joints. Pain, usually the earliest symptom, is greatest after exercise. Stiffness or fibrositis commonly follows inactivity but is usually of short duration. Joint motion is limited in severe cases. Tenderness and crepitus or grating are present. Joint enlargement is present due to proliferative chondrocyte reactions in cartilage and bone. Synovial effusion may occur. Deformity and subluxation are late findings. Constitutional symptoms and extra-articular manifestations are absent.
The manifestation of OA usually varies depending on the joint involved. Enlargement of the terminal interphalangeal joints (Heberden’s nodes) is common; painful gelatinous cysts may also be present. Women are affected by this form of the disease more often than men. Similar deformities may develop at the proximal interphalangeal joints (Bouchard’s nodes). Disease of the first carpometacarpal joint causes pain and limitation of the use of the thumb. Knee involvement produces pain, swelling, and instability. Osteoarthritis of the hip causes local pain and a limp; pain may be present at the knee due to referral along the obturator nerve. Spinal osteoarthritis is common; severe degenerative changes may occur without symptoms. Osteoarthritic changes are most common in the midcervical and lower lumbar areas of maximal spinal motion. Compression of contiguous neurologic structures by large osteophytes or a degenerated disc may cause severe radicular pain. Vascular insufficiency syndromes may follow compromise of cervical vascular structures.
The synovial fluid acts to provide nutrients to the avascular articular cartilage and to provide viscosity for shock absorption with slow movements and elasticity for shock absorption with rapid movements. The joint affected by OA is characterized by decreased concentration of hyaluronic acid because of reduced production and increased water content as a result of inflammation, particularly during later stages of the disease.
Grossly, the cartilage becomes yellow-white and soft in OA. Fibrillation, pitting, and ulcers are found in superficial cartilage layers. Marginal osteophytes form. Histologically, fissuring and fibrillation are prominent. Degenerating chondrocyrtes and reactive clonal chondrocyte proliferation are present. Subchondral bone is thickened; cyst formation occurs. Synovitis is mild to moderate.