An Overview Of Gingivitis Biology Essay

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Gingivitis is an acute inflammation of the gums surrounding the teeth, including the gums, soft tissues, and bone. Gingivitis is a periodontal disease that affect the health of the periodontium.1 Accumulation of Plaque, a sticky material made of bacteria, mucus and trapped food between the teeth2, is the most common cause of Gingivitis. The plaque contains the bacteria and debris that are responsible for this inflammatory disease. Sometimes hormonal changes in the body during pregnancy, puberty, and steroid therapy leave the gums vulnerable to bacterial infection.1

Pathogenesis:

It is usually necessary for the person to have an underlying illness or take a particular medication that renders their immune system susceptible to gingivitis.1 As the plaque accumulate in between the teeth and gum, the gum becomes inflamed and susceptible of bleeding. If the plaque is not removed, it will then calcify and become calculus. Bacterial Exotoxins such as Hyaluronidase will destroy the intercellular connections between epithelial cells lining the gingival sulcus. Collagenase, another exotoxin secreted by the bacteria, enable them to enter the barrier of the gingival sulcus by destroying the base membrane. There are three stages in the pathological development: the early stage (first 4-7, up to 14 days), the established stage (after 14 days), and the advanced stage (toxin is secreted). In the early stage, approximately prior to day 12, numbers of neutrophils will increase in the periodontal pocket. B-cell, a type of lymphoid cells, will become dominant at the end of the early stage. Numbers of neutrophil will increase in the established stage. At the same time, the B-cells will be converted into plasma cell, and monocytes into macrophage. In the advanced stage (periodontitis), the toxic secreted by the bacteria has already damaged the bone, gum and the teeth, making the teeth loose easy to fall out. 3,4

Diagnosis:

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The diagnosis is made by the dentist after examining the patient’s mouth. Signs include soft, swollen, red-purple gums, bleeding. At the base of teeth, the dentist will look for deposits of plaque and tartar. The gums are usually painless or mildly tender.

No further testing is usually necessary, although dental x-rays and dental bone measurements may be done to determine whether the inflammation has spread to the supporting structures of the teeth.5

Patient history should be taken properly for diagnosing underlying causes.

Clinical Manifestations

Clinical Manifestations of gingivitis include swelling, redness, pain and bleeding of the gums, foul breath. The gums appear red and inflamed color, and becomes loose and weak.1

Treatment

The main aim in treating gingivitis is to remove the plaque. By brushing teeth regularly with a toothbrush and fluoride toothpaste approved by dentists, plaque build-up can be kept to a minimum.1 Root planning, also known as conventional periodontal therapy, can remove factors that cause inflammation (plaque and calculus). On more severe cases, antibiotics are used to help the body fight against the bacteria.

Prognosis

Gingivitis is a reversible inflammatory disease, with no breakdown of the attachment fibers connecting them to the teeth and underlying bone.

Case Study IIâ€" Rheumatoid Arthritis

Etiology:

Rheumatoid arthritis (RA) is an autoimmune disorder that causes chronic inflammation in the joints. The disease affects synovial tissue. RA can occur at any age. Women are affected more often than men. The cause of RA is still unclear. It is considered a autoimmune disease in which the body’s defensive mechanism attacks itself, causing the chronic inflammation. RA usually affects joints on both sides of the body equally. Wrists, fingers, knees, feet, and ankles are the most commonly affected. The course and the severity of the illness can vary considerably. Infection, genes, and hormones may contribute to the disease. 6

Pathogenesis:

The first stage of the pathogenesis is marked by the activation of the T cells by antigens in the immunogenetically susceptible host. After the T-cells are activated, multiple effects, including the inflammatory response is triggered. Synovial lining and endothelial cells will be activated and proliferated; additional proinflammatory cells from the bone marrow and circulation will be signaled to recruit and activate; cytokine and proteases will be secreated by macrophages and fibroblast-like synovial cells. Autoantibody production is also triggered. 7

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The synovium in RA organizes itself into an invasive tissue that, if unchecked, can degrade cartilage and bone. The rheumatoid synovium has many characteristics of a locally-invasive malignancy, but it never becomes completely unresponsive to antiinflammatory and antiproliferative factors.7

Diagnosis:

A specific blood test, called anti-CCP antibody test will be done for distinguishing between the common normal arthritis and Rheumatoid arthritis. Many other tests are available, including complete blood count, c-reactive protein, Erythrocyte sedimentation rate, Joint ultrasound or MRI, Joint x-rays, Rheumatoid factor test (positive in about 75% of people with symptoms) and Synovial fluid analysis.7 When diagnosing RA, the physician will make the diagnosis based on the above examinations and factors that associate with this disease. The factors include: morning stiffness in and around the joints for at least one hour, swelling or fluid around three or more joints simultaneously, at least one swollen area in the wrist, hand, or finger joints, symmetric arthritis and Rheumatoid nodules.8

Clinical Manifestations

RA often begins with symptoms that are not distinctive, such as fatigue, loss of appetite, low fever, swollen glands and weakness. As it progresses, joint pain appears. The type of joint pain is typical and mentioned above in the pathogenesis. Joints are often boggy and swollen and warm to touch. Joints will lose their range of motion as it progresses.7

Treatment:

RA treatments are usually lifelong, working with medications, physical therapy, exercise and possibly surgery. Medications used on patients include disease modifying antirheumatic drugs (DMARDs), anti-inflammatory medications, antimalarial medication, corticosteroids and biologic drug.7

Prognosis:

People with rheumatoid factorrheumatoid factor, the anti-CCP antibody, or subcutaneous nodulessubcutaneous nodules seem to have a more severe form of the disease. People who develop RA at younger ages also seem to get worse more quickly.7 However, treatment for rheumatoid arthritis has improved. Many people with RA work full-time. About 10% of those with RA are severely disabled, and unable to do simple daily chores such as walking, washing and dressing.7