Osteoarthritis (OA) is an ancient disease which dates back to the Neolithic period and is also the most common form of arthritis. Perhaps also indicates the reason for the use of this particular name which actually means inflammation of the joints, whereas OA is a non-inflammatory, degenerative disease of the movable joints. This means that the disease worsens with the passage of time, and age is an important risk factor for this particular disease. Degenerative joint disease or Osteoarthrosis would fit to the disease pathologically. To summarise OA may be defined as a slowly progressive disease of monoarticular joint with no known cause.
It is a relatively common disease in the elderly population as the most important predisposing factor is age. According to C.M.Stein and G.Taylor (2004), 80% of people at the age of 65 years will have radiological proof of OA but maybe 10% of these will actually present with some sort of symptoms like pain and loss of range of motion. Before the actual clinical presentation of symptoms, the disease is reversible if the factors initiating the disease are corrected. At an age of less than 50 years more males are affected than females but beyond 50 years more females are affected indicating a hormonal relationship with the condition. Genetic mechanical and hormonal factors are being demonstrated by Ghosh P, Cheras PA (2001). There are recent studies by Sheng-Yu Jin et.al (2004) which predicts the association of ER*- α* gene haplotype with primary knee OA in the Korean population, and that genetic variations in the ER- * α* gene might play a role in susceptibility to OA.
!http://www.indmedica.com/cyberlecturespics/22605_osteoknee.png"(comparison of Healthy knee and Osteoarthritic knee)!
Figure 1 compares normal knee joint with osteoarthritic knee joint.
When two bones meet at a point called the joint, some form of cushion is required to protect the end of the bones from trauma against each other. So the joint line is covered by this flexible and smooth form of connective tissue called Cartilage to absorb the shock which arises when two bones come closer as in heel strike during the stance phase of the gait, climbing down stairs ect. The cartilage is four layered with a thickness of about one-eighth of an inch, lacks blood supply and nerve supply but one of the layers mostly contains a complex molecule known as the proteoglycans which has the property of holding the fluid around the joint to keep it lubricated by the synovial fluid. (R.H.Phillips 2001)
When the catabolism by Collagenolytic enzymes exceeds the anabolism the result is osteoarthritis. Usually the first changes are seen in the cartilage in the form of fibrillation due to the advance in age, which may be seen microscopically but the visible abnormality is a local swelling in the matrix of the cartilage. At the cellular level, the chondrocytes surrounding the matrix increase in number than the normal but the general layout is same as the normal. There also occurs a deposition of fine fat molecules in between the matrix which may increase in size at the chondrocyte capsule. This particular condition, though degenerative, also involves new bone formation at the joint surfaces which is the Remodeling in response to the disease process, resulting in changes in the shape of the joint with age, the varus deformity of the knee. In relation to the joint line there are two places where new bone formation occurs i.e. at the margins, called the marginal osteophytes, and at the part adjacent bone marrow. It is these marginal osteophytes which travel to the joint space and limit the range of motion in one pattern of growth. In the second pattern the osteophytes develop in the soft tissue attachments to the joint causing an inflammatory response, ultimately giving rise to pain. The degeneration of the joint cartilage also gives rise to Eburnation, a phenomena in which the bone becomes smooth and shiny due to loss of cartilage and constant rubbing against each other giving rise to crepitus. This describes the major signs and symptoms of this condition which are pain, limitation or range of motion, crepitus and deformity.
A history of trauma around the knee joint, or injury to the anterior cruciate ligament showed an increase in incidence of degenerative changes. This may explain that altered biomechanics can initiate damage to the joint cartilage though the cartilage has the ability to structurally adapt to the loading of the joint.