Essay On Pathogenesis Of Arthritis

Rheumatoid Arthritis(RA) is the most common type of autoimmune arthritis. RA is a progressive and debilitating musculoskeletal disorder that affects the joints symmetrically, causing a range of systemic effects. What it causes is still not well known; nevertheless, findings of new research points towards a believe that it is triggered by a defective immune system, which causes the release of inflammatory chemicals. These chemicals cause damage to cartilage and bone, usually affecting the wrists, the joints of the hand, including the knuckles, the middle joints of the fingers and feet. While this condition can affect any joints, besides, important body organs such as the eyes and the lungs can also be affected by the inflammation that occurs as a result of this chronic condition. Only in America 1.3 million of people are affected by this ailment, and 75 % of them are mainly women. Its onset usually occurs between fourth and sixth decades; however, RA can occur at any age("Diseases And

These types of disorders are sometimes treated by using TNF inhibitor. This inhibition is usually done with a monoclonal antibody such as Infliximab, an anti-TNF drug. Infliximab is used to treat rheumatoid arthritis by administering infliximab intravenously, in 6-8 week intervals (The British Pharmacology Society, 2011). Infliximab works by preventing TNF - alpha from binding to its receptors in the cell, as a result inhibiting TNF - alpha from carrying out functions in the immune response. Rheumatoid arthritis, is a disease associated with chronic joint inflammation, severe pain, stiffness, and swelling. Rheumatoid arthritis occurs when the body mistakenly attacks itself, in most cases inflammation is supposed to occur when the body is fighting off an invasion however with this disease, it occurs when the immune system malfunctions and starts to attack itself (Health Union,

Rheumatoid Arthritis or (RA) is an autoimmune disease that attacks the joints and connective tissue. The result is inflammation that produces permanent damage in the joints. Rheumatoid arthritis is a chronic syndrome that tends to be progressive and destructive as compared to Osteoarthritis or (OA), which is more of an age related disease caused by “wear and tear” of the joints. In contrast to (OA), rheumatoid arthritis is characterized by inflammation mostly of the joints, but is a general body disease.

Rheumatoid arthritis is an autoimmune etiology that affects the patient in ways like, progressive disability, systemic complications, socioeconomic costs, and premature death. No cause, to date, has been found, and the prognosis is guarded, (McInnes & Schett, 2011). Unfortunately, rheumatoid arthritis is a debilitating disease that affects the body in the following ways: swelling and damage of the joints (synovitis); bone destruction; formation of autoantibodies, like rheumatoid factor (RF) and anti-citrullinated peptide (ACPA); persistent functional decline; vasculitis; fatigue; increased disability; dysphasia; stiffness and pain, mostly in the hands and wrist; functional limitations and physical disabilities; systemic manifestations that may include renal, eye , and vascular issues; cardiovascular disease and myocardial infarctions; ultimately leading to an increased

Rheumatoid Arthritis is an autoimmune disease and chronic inflammatory illness that causes the body’s immune system to attack its joints rather than the usual foreign substances such as viruses and bacteria (Arthritis Foundation, 2015; Mayo Foundation, 1998-2015). Unlike wear-and-tear osteoarthritis, Rheumatoid Arthritis attacks the lining of the joints and often other body tissues such as the heart, skin, eyes and lungs (Arthritis Foundation, 2015; May Foundation, 1998-2015). Due to the body’s normal immune response, redness, inflammation, pain, and swelling, arise and can ultimately result in the destruction of bone and joint, causing for deformity (Mayo Foundation, 1998-2015). In the United States, about 1.5 million people have Rheumatoid Arthritis (Arthritis Foundation, 2015). Within this population, women are three times more likely to experience this than men. It has been noted to commonly occur between the ages of 30-60 for women and later in life for men (Arthritis Foundation, 2015). Men may be protected by hormonal factors and require a stronger genetic component to develop disease. Rheumatoid Arthritis is thought to stem from a combination of genetic susceptibility and exposure to an appropriate environmental trigger. (Ollier, W. E., Harrison, B., & Symmons, D. 2001). Within the aspect of genetics it is most likely hereditary. Although infectious triggers of RA have long been suspected, no definitive evidence has been obtained. Previous blood transfusion,

Rheumatic arthritis (RA) is a chronic, progressive disorder that commonly presents a group of mechanically related disorders concerning the degenerative nature of joints that is specifically affecting the articular cartilage and subchondral bone (1). Thus, causing a dip in the quality of life in RA patients. The aetiology for RA is unclear, however, a combination of hereditary susceptibility causes a reaction that causes severe inflammation in the synovial membrane (1). However, other factors such as the immunological, hormonal and environmental factors plays a role in development of RA (2). The pathology of RA is characterised by an insidious order of biological events that will eventually lead to articular cartilage destruction and secondary changes in surrounding tissues (1). The pathological changes to joints consequently lead to structural deformity and functional disability. The clinical presentation of RA patients are often intermittent joint pain, worse on movement; stiffness; and, limited range of motion (ROM) and joint instability, either due to loss of articular cartilage, or effusions into the joint cavity (1-3).

In rheumatoid arthritis, patients have persisting inflammation of their joints, together with pain and fatigue. "This is most likely due to the formation of immune complexes by ACPAs with citrulline containing antigens and subsequent binding of RF, which can lead to abundant complement activation" (Smolen, Aletaha, & McInnes, 2016, p. 2024).

Rheumatoid arthritis is characterized by excessive inflammation, particularly in the joints leading to irreversible damage (Contreras-Yáñez, Ponce De León, Cabiedes, Rull-Gabayet, and Pascual-Ramos, 2010). Pain and joint damage leads to limited mobility, decreased function and a reduced quality of life (Elliot, 2008). TNF blockers provide significant improvement in patient outcomes “by reducing pain,

RA is associated with inflammation of the synovium, autoantibody production, progressive cartilage and bone destruction, early morbidity, and other systemic consequences in which many include cardiovascular events. Although structural changes can be visualized by conventional imaging techniques, joint damage is rarely apparent in early stages of disease, but rather accumulates over time (4). Various immune modulators and signalling pathways are involved in the pathophysiology of RA. The influx of mononuclear cells, including T and B cells results in synovitis, which is inflammation of the synovial joint. The synovial lining becomes hyperplastic and the membrane expands and destroys bone, due to osteoclast-rich regions. Cartilage is also degraded by enzymes secreted from synoviocytes and chondrocytes (4).

A critique of an article published by The New York Times suggests a Breakthrough in treatment for joint pain of patients suffering from Rheumatoid arthritis. The article suggests that a drug known as a Biologic taken with Methotrexate may effectively treat pain and swelling symptoms caused by Rheumatoid Arthritis. Before critiquing the article, it is necessary to discuss the anatomy and physiology of Rheumatoid Arthritis so you may have a better understanding of the disease and the possible treatments. Rheumatoid Arthritis is classified as an autoimmune disease; it is a chronic inflammatory disorder in which the immune system attacks the tissues of the synovial joints of the individual who is suffering from the disease (Marieb and Hoehn 2013). The attacks cause inflammation to the synovial joints; the onset of inflammation brings both pain and swelling to the joint (Marieb and Hoehn 2013). Inflammatory cells appear in the joint cavity of the synovial joint and release inflammatory chemicals that destroy the body tissue at the joint (Marieb and Hoehn 2013). The disease is bilateral, meaning that if it affects a joint on one side of the body, for example the left wrist; chances are that it will affect the same joint on the opposite side of the body (Marieb and Hoehn 2013).

People have long feared rheumatoid arthritis (commonly called RA) as one of the most disabling types of arthritis. The good news is that the outlook has greatly improved for many people with newly diagnosed and detected RA. Of course, RA remains a serious disease, and one that can vary widely in symptoms and outcomes. Even so, treatment advances have made it possible to stop or at least slow the worsening of joint damage. Rheumatologists now have many new treatments that target the inflammation that RA causes. They also understand better when and how to use treatments to get the best effects.

The human body’s immune system provides protection from foreign invaders. Inflammation is one of our body’s line of defense to get rid of infection and prevent disease. In rheumatoid arthritis, a deluded immune system may unintentionally attack the joints through uncontrolled inflammation, which can lead to bone, cartilage and joint erosion. “Rheumatoid arthritis occurs when the inflammatory response of the joint synovial membrane and periarticular tissues is conveyed by influx and activation of immune cells and release of inflammatory mediators such as chemokines and cytokines, resulting in tissue destruction and dysfunction” (Costa VV, Amaral FA and et al. 2015). Although the exact etiology of R.A is unknown, biological and environmental factors can contribute to the disease. Treatment goals are to reduce pain, improve function, and prevent further

Synovial macrophages and fibroblast-like synoviocytes increase in number and infiltrate the surrounding cartilage and bone; these cells are the primary source of inflammatory mediators, involving proinflammatory cytokines, chemokines, and adhesion molecules. The cytokine tumor necrosis factor alpha (TNF alpha) is present in the RA synovium, and so anti-TNF alpha therapy has proved to be effective in controlling disease progression in many RA patients (76).

Rheumatoid arthritis (RA) is a chronic, complex and systemic inflammatory disorder that affects up to 1% of the population (1-2). It’s an autoimmune disease of unknown etiology. RA is associated with progressive joint destruction, systemic complications and early morbidity. The disease is characteristic of inflammation of the synovium, autoantibody production, cartilage and bone destruction and other systemic consequences, many of which include cardiovascular events. Although structural changes can be visualized by conventional imaging techniques, joint damage is rarely apparent in early stages of disease, but rather accumulates over time (3). Various immune modulators and signalling pathways are involved in the pathophysiology of RA. The influx

Rheumatoid arthritis (RA) is an auto-immune disease, meaning that the body’s own antibodies react negatively in the body by attacking its own healthy cells. RA is a disorder that causes extreme and painful swelling in the joints, prolongs healing times, and also puts affected individuals at a higher risk of many other conditions, such as cardiovascular disease (Carmona, Cross, Williams, Lassere, & March, 2010). It affects 0.5% of the adult population worldwide, though the majority of this percentage is women over the age of 40 (Carmona, Cross, Williams, Lassere, & March, 2010). RA is like most other diseases in that the earlier the disease is diagnosed and treatment is begun, the higher the success rate of slowing the disease progression or putting it into remission.