Connective Tissue Disorders in Rheumatoid Arthritis and Osteoarthritis - Case Study Example

ar Connective tissue disorders in Rheumatoid Arthritis and Osteoarthritis 5/17 Introduction Connective Tissue The human body is madeup of various types of tissue which work in an organized manner to complete the normal functions of the body. Connective tissue is a tissue which supports and protects different tissues which are found in the body. Connective tissue is formed of both cellular and extracellular matrix and both of these help the tissue to fulfill its functions. Most of the connective tissue in the body is formed from embryonic mesoderm. Ligaments are type of connective tissue which contain elastin whereas connective tissue sheaths found in vessels and muscles are the ones consisting collagen. (Chaurasia 2006; Snell 2004) Connective Tissue Disorders Connective Tissue Disorders can be either acquired or innate. These disorders specifically target the connective tissue and the fibers present in the connective tissue. Examples of hereditary connective tissue disorders are Marfan Syndrome, Ehlers Danlos Syndrome, Stickler Syndrome etc. All thee hereditary connective tissue disorders have different effects on the body of an individual. However most of these disorders affect the collagen fibers present in the connective tissue. Inflammation of the connective tissues is seen to be common in the individuals suffering from these disorders. Above all many of these connective tissue disorders are seen to be on an increase in developed nations. In some cases these disorders can also be caused because of the deficiency of the immune system to recognize the body’s own organs or tissues. In other words these are called auto-immune disorders which are usually caused by genetical disorders. One such example of an auto immune connective tissue disorders is known as the Mixed Connective Tissue Disease. This disease is characterized by different symptoms of different diseases such as arithritis, leucopenia, anemia, fever and swelling of hands. (90). Connective Tissue Disorders at times can be so lethal that they may cause death in an individual. It is seen that most of the connective tissue disorders usually occur largely in women rather than in males. The reason for this is possibly the high rate of osteoporosis in women. The main emphasis of this essay would be on Rheumatoid Arthritis and Osteoarthritis which is a connective tissue disorder. It would provide the pathogenesis of both the diseases and provide with its diagnosis (Moore & Dalley 1999; Pal 2005). Connective Tissue Fibroma (BABA & CĂTOI, 2007). Fibroma Molle, Fine Fiber reticular and fibrocits (BABA & CĂTOI, 2007). Top of Form Bottom of Form Bottom of Form Bottom of Form Osteoarthritis General Information on Osteoarthritis One of the most common disorders of connective tissue is osteoarthritis which has become a great concern for the developed nations. Osteoarthritis is characterized by degeneration of the articular cartilages which are attached to the bones. These cartilages help in the free movement of bones and also help to distribute weight on to the joints uniformly. (Aigner & Mckenna 2002). Top of Form Bottom of Form Pathogenesis of Osteoarthritis It is also found that genetic factors also affect the vulnerability of osteoarthritis in an individual. The specific genes which play a role in this increasing risk factor have yet not been recognized but it is assumed that chromosome 2 and 11 play an important role in it. Bone density also has an effect on osteoarthritis as if bone density increases, chances of osteoarthritis also increase. Hormones are also suggested to play an important as it has been found that increased levels of estrogen can cause osteoarthritis to occur in an individual (Robbins et al 2005). The cartilage which is affected in osteoarthritis clearly shows changes in its structure and properties. The proteoglycans in the cartilage are decreased as the disease progresses and a significant amount of water is found in it. The collagen network is then disrupted as it is seen that the collagen type II fibers are destroyed and the new ones are not produced in proportion to the destroyed ones. It is believed that some of the molecular messengers cause these abrupt changes in the composition of a cartilage. The molecular messengers which are believed to cause these changes are Interleukin I, Tumor Necrosis Factor, and Nitric Oxide. Lastly apoptosis is also increased in these cartilages because of which the number of chondrocytes decreases. All these changes together cause the cartilage to be less resilient and elastic because of which the arthritis spreads. In the beginning the immune system of the body prevents the changes in the cartilage but after some time the negative influences increase and the degeneration increases in the cartilage (Robbins et al 2005). Diagnosis of Osteoarthritis The typical symptoms of osteoarthritis include pain of the joints which usually gets worse with its usage, morning stiffness, crepitus and loss of motor movements of the muscles. The joints most affected by osteoarthritis are knee joint, hip joint, lumbar vertebrae, cervical vertebrae, and tarsal joints of the fingers. Diagnosis of osteoarthritis can be difficult as different kinds of arthritis involve the degeneration of the cartilages. The symptoms are first checked to determine the level of arthritis in a patient. Then several tests are carried out to find as to if arthritis exists in the patient or not. X rays are carried out to find the disease. These x-rays will show osteophytes on the margins of the joints along with narrowing of the joint space (Robbins et al 2005; Hunter 2009). Subchonrdal sclerosis is also witnessed in these x-rays. Another type of test which is done to find out about arthritis is Magnetic Resonance Imaging. MRI can look deep into the tendons, bone and cartilages. The laboratory test to check synovial fluid is also important to determine the level of osteoarthritis in a patient However till date X-rays are the most important forms of tests to determine arthritis. (Robbins et al 2005; Payne 2009). Top of Form Bottom of Form Bottom of Form Treatment Options for Osteoarthritis Osteoarthritis should be treated as soon as possible as it can affect a variety of tissues all over the body. If it is not treated it may adversely affect the tissue causing it to degenerate on a whole. It is believed that the first cause of arthritis is related to weight and thus it is recommended that the weight should be lost as soon as possible. The level of arthritis also determines the treatment strategies of different patients. It is believed that exercise can be really helpful in reducing the pain of arthritis as it would help the joints to move freely and become stronger. Hence these joints would then be able to move freely without any feeling of pain. It is also recommended that besides weight control, chondritin sulfate and glucosamine are being taken by the patient as these two together help to form the ground substance of a cartilage (Hua et al 2002; Pothacharoen et al 2006). Medications are usually recommended for patients for whom the general practices of weight loss and exercise have proved to be a failure (Hunter 2009; Robbins et al 2005). These medications vary from simple creams to anti inflammatory drugs. The creams contain salicyclates or capsaicin which helps in decreasing the pain of arthritis. Analgesics such as acetaminophen are also recommended so that pain can be relieved. And finally anti inflammatory drugs such as ibuprofen or naproxen are also used so that the inflammation of cartilages is reduced. In individuals in which these medications also fail it is recommended that a surgery be done. (Katzung et al 2008; Robbins et al 2005; Rang & Dale 2007). Top of Form Bottom of Form Choice of Test for the Diagnosis of Osteoarthritis The tests carried out to diagnose osteoarthritis are related to the specifics of the degeneration. X-rays are usually recommended for the diagnosis as they are the best possible options. In an x-ray a doctor is clearly able to distinguish the subchondral sclerosis and narrowing of the joint space. MRI in comparison is a better technique to even show the soft structures but it is quite expensive in relation to an X-Ray. Synovial Fluid Test is an after test if arthritis is detected hence the best option of diagnosis for osteoarthritis is that of an x-ray (Hunter 2009). Rheumatoid Arthritis General Information about Rheumatoid Arthritis Rheumatoid Arithritis is a inflammatory disorder that is capable of affecting many joints and tissues together. Joints are most vulnerable to rheumatoid arthritis such that these joints get inflamed and in result the articular cartilage gets destroyed. It is believed that genetic factors yet again play an important role in the onset of this type of arthritis. It is affecting more women than men in this world and is usually seen in adults of 40 to 70 years old (Robbins et al 2005). Pathogenesis of Rheumatoid Arthritis Rheumatoid Arthritis is caused after an individual is exposed to an unknown antigen which is supposed be causing the arthritis. It is believed to be caused by the immune system itself as CD4+Helper cells and other lymphocytes cause this destruction of the joint (Firestein 2003; Lee & Weinblatt 2001 ) 1307. The autoimmune response which is believed to cause the onset of the disease is related to the actions of CD4+ T cells as these are the ones which stimulate still other cells to cause the destruction of the cartilage. Cytokines are believed to the most important in causing this destruction of cartilage. TNF and IL-1 are secreted by macrophages which stimulate the synovial cells to produce inflammatory products and metalloproteinases. These two then act together to cause harm to the cartilage itself. T Cells are also believed to play a role in the pathogenesis of the disease as they along with fibroblasts produce RANKL which further activates the bone destructing cells known as osteoclasts. The synovium then expands over the articular surface to form a pannus. This pannus then starts to reabsorb the adjacent cartilage which causes its destruction and simultaneously the destruction of the subchondral bone (Gravallese & Goldring 2000). It is believed that Class II HLA locus is an important mediator of the disease (Gregersen 2003). It has not yet been established as to which antigens cause the immune system to react in such a way (Hyrich & Inman 2001). Top of Form Bottom of Form Bottom of Form Diagnosis of Rheumatoid Arthritis Rheumatoid Arthritis is a slowly progressing disease which generally is asymptomatic. Patients with the disease initially complain about muscle fatigue and musculoskeletal pain. It is after this pain that the joints generally get involved in the whole process. The small joints are the most affected after the onset of the disease and then the large ones are affected such as the hip, wrist, ankle, elbow and knees. The joints which get affected by the disease usually get swollen and warm after which the pain arises. Radiography is usually suggested for individuals suffering from the disease. But x-rays are of no help in the beginning of the disease as no prominent signs are seen in the beginning. Later onwards the x-rays show juxta-articular osteopenia and erosion of bones along with the joint space narrowing. MRI and ultrasonography are also done in order to establish the level of arthritis. Color Dopler and Power Doppler ultrasound help to find the defect in synovium of the joints (Robbins et al 2005; Majithiav & Geraci 2007; Hochberg 2009). Laboratory Tests are not usually recommended to find out about Rheumatoid Arthritis however serum tests show rheumatoid factor along with IgM antibody complex with that of IgG. (Feldmann 2002).Top of FormBottom of Form Treatment Options for Rheumatoid Arthritis Treatment of Rheumatoid Arthritis is important as it can affect a variety of tissues in the body. It is recommended that patients whose Rheumatoid Arthritis is in its first stage be advised to lose weight in accordance to the pressure inflicted on the joints. Exercise can also help to establish regular movement of the joints which are less functional because of the pain. Physical therapies can help to reduce the level of inflammation in the joint. It is recommended for these people to consume a lot of calcium also so that they do not suffer from any bone loss. The patients who are suffering vigorously from this disease are recommended with medications and physical exercise both. The medications which are recommended in rheumatoid arthritis are of two types i.e. Non-Steroidal Anti inflammatory drugs and disease modifying antirheumatic drugs. The NSAIDS are believed to reduce the pain suffered by the patient and decrease the inflammation of the disease but on a large scale it does not decrease the progression of the disease to its latter stages. On the other hand DMARDS can be of a great help to patients suffering from rheumatoid arthritis. These drugs can help to prevent the progression of the disease by reducing the damage to the joints and protect the functions of these joints at the same time. Some examples of these drugs are hydroxychloroquine, methotrexate and cyclosporine etc (Katzung et al 2008; Robbins et al 2005; Rang & Dale 2007). Choice of Tests for Rheumatoid Arthritis In Rheumatoid Arthritis it is recommended that a test for a defect in synovium is carried out first. Color Dopler and Power Doppler ultrasound is the best way to find out any defect in the synovium. It is this synovium which is the most affected part of a joint after the onset of the disease. X-rays are again also very helpful in the diagnosis of the disease but these x-rays can only tell about the disease after its progression (Hochberg 2009). References AIGNER T, & MCKENNA L. (2002). Molecular pathology and pathobiology of osteoarthritic cartilage. Cellular and Molecular Life Sciences : CMLS. 59, 5-18. BABA, A. I., & CĂTOI, C. (2007). Comparative oncology. Bucharest, The Publishing House of the Romanian Academy. CHAURASIA, B.D. (2006). Chaurasias Handbook of General Anatomy. Gardners Books. FELDMANN M. (2002). Development of anti-TNF therapy for rheumatoid arthritis. Nature Reviews. Immunology. 2, 364-71. FIRESTEIN GS. (2003). Evolving concepts of rheumatoid arthritis. Nature. 423, 356-61. GRAVALLESE, E. M., & GOLDRING, S. R. (2000). Review: Cellular Mechanisms and the Role of Cytokines in Bone Erosions in Rheumatoid Arthritis. ARTHRITIS AND RHEUMATISM -ATLANTA-. 43, 2143-2151. GREGERSEN, P. K. (2003). Teasing apart the complex genetics of human autoimmunity: lessons from rheumatoid arthritis. Clinical Immunology : the Official Journal of the Clinical Immunology Society. 107, 1. HOCHBERG, M. C. (2009). Rheumatoid arthritis. Philadelphia, Mosby/Elsevier. HUNTER, D. (2009). Osteoarthritis. Philadelphia, Pa, Saunders. HYRICH KL, & INMAN RD. (2001). Infectious agents in chronic rheumatic diseases. Current Opinion in Rheumatology. 13, 300-4. KUMAR, V., ABBAS, A. K., FAUSTO, N., ROBBINS, S. L., & COTRAN, R. S. (2005). Robbins and Cotran pathologic basis of disease. Philadelphia, Elsevier Saunders. LEE, D. M., & WEINBLATT, M. E. (2001). Rheumatoid arthritis. The Lancet. 903-911. MAJITHIA V, & GERACI SA. (2007). Rheumatoid arthritis: diagnosis and management. The American Journal of Medicine. 120, 936-9. MOORE, K. L., & DALLEY, A. F. (1999). Clinically oriented anatomy. Philadelphia, Lippincott Williams & Wilkins. PAYNE JW. (2009). Osteoarthritis. U.S. News & World Report. 146. PAL, G. (2005). General anatomy: basic concepts in human gross anatomy. New Delhi, Peepee publishers and distributors. SNELL, R. S., & SNELL, R. S. (2004). Clinical anatomy. Philadelphia, Lippincott Williams & Wilkins TREVOR, A. J., KATZUNG, B. G., MASTERS, S. B., & KATZUNG, B. G. (2008). Katzung & Trevors review of pharmacology. New York, McGraw-Hill Medical.Top of Form Bottom of Form Top of Form Bottom of Form Bottom of Form Top of Form Pothacharoen P, S Teekachunhatean, W Louthrenoo, W Yingsung, S Ong-Chai, T Hardingham, and P Kongtawelert. "Raised Chondroitin Sulfate Epitopes and Hyaluronan in Serum from Rheumatoid Arthritis and Osteoarthritis Patients." Osteoarthritis and Cartilage / OARS, Osteoarthritis Research Society. 14. 3 (2006): 299-301. Top of Form Hua J, K Sakamoto, and I Nagaoka. "Inhibitory Actions of Glucosamine, a Therapeutic Agent for Osteoarthritis, on the Functions of Neutrophils." Journal of Leukocyte Biology. 71. 4 (2002): 632-40. Top of Form RANG, H. P., & DALE, M. M. (2007). Rang & Dales pharmacology. [Edinburgh], Churchill Livingstone. Bottom of Form Bottom of Form Bottom of Form Top of Form Top of Form Bottom of Form Top of Form Top of Form Top of Form Top of Form Bottom of Form Top of Form Top of Form Top of Form Bottom of Form Bottom of Form . Top of Form Read More