Osteoarthritis And Rheumatoid Arthritis Biology Essay

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Osteoarthritis is a degenerative joint disease caused by bio-mechanical process and an age -related wear and tear disorder of the synovial joints; it is the most common type of arthritis (Yuan, 2003). In addition, it is the main leading cause of disability in elderly and affects at least 10% of the population ( Ge, 2006). The cause of osteoarthritis is still unknown to researchers (Sakkas, 2007) but Berenbaum (2010) stated that osteoarthritis is a complex polygenetic disease. McCance (2006) added that osteoarthritis is characterized by areas of local damage and loss of the articular cartilage, osteophytosis, subchondral bone changes, mild synovitis and thickening of the joint capsule. The synovial is considered to be the key area of osteoarthritis due to the clinical symptoms shown in synovial inflammation. Synovial inflammation is seen in the signs and symptoms osteoarthritis such as joint swelling, effusion and redness (Pelletier, 2001). The risk factors for osteoarthritis are genetic predisposition, obesity, aging, female gender, bone density, joint laxity and excessive mechanical loading (GE, 2006).

The main consequence in osteoarthritis is the loss of articular cartilage during the early phases of the disease; in fact, it loses its appearance and become brownish gray (McCance, 2006). As the disease progresses, the top of the articular cartilage flakes off and fibrillation occurs as well as presenting as a degenerated cartilage (McCance, 2006). The cartilage becomes more degenerated due to constant trauma as related to aging. As the articular cartilage degenerates, the osteophytes (bone spurs) may alter the bone contours. The osteophytes fragments have a chance to irritate the synovial membrane, synovitis (where most symptoms occur) and joint effusion occurs. This causes limitation in movement as the joint capsule becomes thickened (McCance, 2006). As aging occurs, McCance (2006) stated that the proteoglycans content is decreased and the water content inside the cartilage can increase up to 8%. The articular cartilage is made out of chondrocytes (cartilage cells) and the extracellular matrix (Yuan, 2003). The extracellular matrix is made out of collagen and proteoglycans and other proteins that are needed (Yuan, 2003). In Osteoarthritis, there will be an enzymatic destruction of the articular cartilage on the collagen and proteoglycans. When there is loss of proteoglycans from the articular cartilage, osteoarthritis is confirmed. During the early stages of osteoarthritis, the immune response may be responsible for the initial destruction of the articular cartilage (Sakkas, 2007). Normally the cartilage is avascular and therefore it is excluded from the immune surveillance but with constant stress, trauma and aging factors, it results in the release of cartilage antigenic determinants (Yuan, 2003). This will in turn cause an influx of inflammation process. In the inflammatory response, it shows features of a T cell immune response (Sakkas, 2007). The activated T cells have a chance of contributing to the destruction of joint by inducing production of collagenase in synovial membrane (Sakkas, 2007). Cytokines and growth factors are involved in osteoarthritis which is release from the chondrocytes. These cytokines increase the rate of osteoarthritis by increasing the production of proteinases. The most important cytokines which are involved in the Osteoarthritis are the Interleukin- 1(IL-1) and tumor necrosis factor (TNF) which are released by the chondrocytes involved in the cartilage destruction (GE, 2006). GE also stated that TNF α initiates acute inflammation while IL-1 is said to have a pivotal role in sustaining the inflammation and erosion as the disease progresses. The two pathways, p38 mitogen-activated protein (MAP) kinase and nuclear factor kB (NF-kB) are seen to be the major ones involved in mediation of synthesis of the inflammatory cytokines (Pelletier, 2001). There are many other pro-inflammatory cytokines such as IL-8, LIF, IL-6, IL-11 and IL-17 which are over expressed in the osteoarthritis tissues (Pelletier, 2001). In the synovial membrane, leukocytes and endothelial adhesion are also expressed ( Sakkas, 2007). These leukocytes release enzymes that degrade the collagen. The excess production of Nitrogen Oxide (NO) causes apoptosis in chondrocytes along with the activation of the caspase cascade (Pelletier, 2001). With the enzymes degrading the collagen on a constant level, the fibrils get destroy and sunder the chondrocytes to stress and attack. Bone resorption occurs as well. (Intema, 2010)

Rheumatoid arthritis (RA) is known as a chronic, heterogeneous autoimmune disorder with an unknown etiology (Guidelines for Management, 2002). It is inflammatory auto immune diseases that cause pain and disability in the long term (Huyser, 1998). Rheumatoid Arthritis affects 1- 2% of the adult population (Guidelines for Management,1996). In Rheumatoid Arthritis, the first joint tissue that is affected is the synovial membrane which lines the joint cavity (McCance, 2006). This disorder develops most often in women with a female/male ratio of 3: 1respectively. In rheumatoid arthritis, the inflammation affects the articular cartilage, the fibrous joint capsule, ligaments and tendons. Rheumatoid arthritis also causes fever, malaise, rash, lymph node, spleen enlargement and Raynaud phenomenon (McCance, 2006). Long term Rheumatoid Arthritis leads to joint deformity, joint malalignment, functional disability, work disability and premature death (Biovitrum, 2008). McCance stated that the initiating event that releases the immune response leading to inflammation of the joint lining is the synovial membrane. The antibodies that are released and transformed are known as the rheumatoid factors which are 2 classes of immunoglobin antibodies; IgM and IgG.

The immune response to the antigenic expression is by the synovial cells and chronic release of this, triggers the body to release the rheumatoid factors. With that complement activation and polymorphonuclear leukocytes infiltration cause an inflammatory response to the joint (Vu Ngugen, 2004). Chronic inflammatory synovitis is defined with the increase number of cells on the surface of the synovium with the infiltration of lymphocytes and plasma cells in the subintimal synovium (Odeh, 1997). When an antigen of unknown etiology attacks, it activates the CD helper T cells and the B lymphocytes. This leads to the induction of the cytokines which recruits inflammatory cells in to the joint sub lining area. The T cells stimulate the synovial membrane and fibroblast. The cytokines, TNF and interleukin-1 stimulate the synovial cells to proliferate and cause mediators of inflammation which leads to the destruction of cartilage. The T cells which are active along with the synovial fibroblast activate osteoclasts promoting bone destruction (McCance, 2006). IL-1 is the key mediator of inflammation and known as the most effective cytokine to induce cartilage destruction (Odeh, 1997). The inflamed synovial tissues also produce other cytokines and chemokines which moderate the synovial cell functions. Proper functions of the many cytokines that are involved in pathogenesis are still unclear (Tak, 2000). TNF α also plays a major role in pathogenesis of rheumatoid arthritis and also directly promotes connective tissue degraduation and is involved in the chronic inflammatory state of the disease (Odeh, 1997). In rheumatoid arthritis , the pannus which is made out of proliferating fibroblast and inflammatory cells are formed by the granulation while inflammation occurs. The pannus produces collagenases and other proteolytic enzymes that destroy the cartilage leading to destruction of the ligaments and causes bony erosions (Vu Nguyen, 2004). The pannus formation leads to the formation of scarring which in turn immobilizes the joint (McCance, 2006). While the pannus proliferates, chondrocyte-derived cells appear and when stimulated by TNF α and IL- 1β produces enzymes which causes cartilage matrix degradation (Tak, 2000). Tak also stated that mast cells are seen at the site of cartilage erosion. An interest fact was about synovial angiogenesis. Synovial tissues are very rich in blood vessels. Angiogenesis is a feature in synovial inflammation and pannus formation where the endothelial cells proliferate and migrate from existing synovial blood vessels (Tak, 2000) The inflammatory cells generate angiogenic factors that increase angiogenesis and this permits continuing growth of the proliferating synovial pannus (Tak , 2000).

As stated the most common symptom of osteoarthritis is pain in the affected joints as aging progression therefore treatment has been attempting to relieve the pain, improve the range of motion and regeneration of the articular cartilage (Ge, 2006). In patients with osteoarthritis, the symptoms differ from person to person. In severe cases, there will be complete loss of cartilage cushion. The symptoms of osteoarthritis are asymptomatic with aging. An x-ray of the affected joints may suggest osteoarthritis has occurred in which the findings include the lost of joint cartilage, the narrowing of the joint and bone spur formations. When in the induction stage of treatments, a treatment that was advised was to stop the inflammation process by the usage of nonsteroidal anti-inflammatory drugs (Yuan, 2003). For rheumatoid arthritis, the evaluation is done by physical examination, roentgenography of the joint as well as serologic test for rheumatoid factors (McCance, 2006). In managing, rheumatoid arthritis, the goals are to control the inflammatory symptoms, to decrease pain, to prevent and control the joint damage as well as reduce the loss of functionality. The treatments options for rheumatoid arthritis is by conservative (rest of the inflamed joints and body rest hours a day with the usage of diet meals and drugs and immunosuppressors by oral or injection) or surgical methods (arthrodesis ,arthroplasty or joint replacement) (McCance, 2006).

This review has provided me with a better understanding of the clinical presentation of both disease and their differences in their signs and symptoms which has contributed to the updates on the treatments that available. Rheumatoid arthritis is a disease that progresses over times and is three times more common in women than men while osteoarthritis is another form of arthritis experienced by the elder through aging. In rheumatoid arthritis, the duration of the joint symptoms such as the stiffness worsens after rest lasting at least 30 minutes or longer but osteoarthritis seems to be brief. Osteoarthritis is the cause of destruction of the cartilage in the joints and begins with a joint while rheumatoid arthritis affects the synovium (lining of the joint) and there are systemic effects and affects multiple joints.