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Transcript
Unit 3 Unit 3 Immunity Unit 3 Objectives: Students will be able to: 1. Describe the role of the immune system/response in controlling and causing disease. Include the common cells of the immune system and their functions. 2. Describe the clinical features of desquamative gingivitis and give examples of diseases in which it may occur. 3. Apply descriptive and histologic terminology to describe and differentiate the clinical and histologic manifestations of each of the following autoimmune diseases: a. b. c. 4. Lupus erythematosus Pemphigus vulgaris Cicatricial pemphigoid For each of the following infectious diseases a) name the organism causing it, b) summarize the route or routes of transmission of the organism and the oral manifestations of the disease, and c) explain how the diagnosis is made: a. b. c. d. e. f. Tuberculosis Actinomycosis Syphilis (primary, secondary, tertiary) Verruca vulgaris Condyloma acuminatum Primary herpetic gingivostomatitis 5. Compare the clinical features of intraoral herpes and minor aphthous ulcers. 6. Differentiate between the humoral immune response and the cell-mediated immune response. 7. Differentiate between active and passive immunity. 8. Describe, compare, and contrast the clinical features of each of the three types of aphthous ulcers. 9. Describe using correct descriptive terminology the clinical and histologic features of lichen planus. Point out differences in the different types of lichen planus. 1 Unit 3 10. Describe the oral manifestations of each of the following autoimmune diseases: a. b. c. d. e. Sjogren’s syndrome Lupus erythematosus Pemphigus vulgaris Cicatricial pemphigoid Behcet’s syndrome 11. List, describe and differentiate between the four forms of oral candidiasis listed in your text. 12. Describe the clinical features of herpes labialis. Distinguish between herpes labialis and other forms of herpes. 13. Compose a well thought out differential diagnosis for lesions and conditions that resemble aphthous ulcers, lichen planus, desquamative diagnosis and herpes infections. Be able to give reasons for your decisions by comparing clinical and histological features. 14. Recognize from a slide those lesions reviewed in chapter 3. The Immune Reaction The immune reaction is designed to help the healthy body resist and defend against certain injurious agents. The immune reaction plays a helping role in the cellular stage of acute inflammation and a sustaining role in both nonspecific and granulomatous chronic inflammation. These are very important functions. The immune system also functions to prevent injurious agents such as certain microbes, toxins, parasites, and even altered cells (cancer, transplantation) from becoming established, proliferating, and causing harm. Basically, four types of diseases can result from immune system dysfunction. 1. 2. 3. 4. Immune deficiency disorders Hypersensitivity disorders Autoimmune disorders Immune cellular proliferative disorders (leukemia, lymphoma). The normal immune system functions to destroy and isolate antigen-bearing injurious agents. Remember that most body tissues are antigenic. However, the immune system learns to recognize “self” during development and therefore usually does not attack the body’s own cells. The immune system is composed of two distinct classes of lymphocytes: T Lymphocytes, and B Lymphocytes. It is also composed of antigen-processing and antigen-presenting cells (APC’s), which are most frequently macrophages. The lymphocytes are memory cells. When a lymphocyte precursor is stimulated and becomes sensitized to a specific nonself antigen--usually a protein on a microbe or cell--the sensitized lymphocyte will react to that antigen. All progeny of the sensitized lymphocyte will also develop 2 Unit 3 a memory for the specific antigen and will react (ATTACK) when the antigen (INJURIOUS AGENT) reappears. Example: If you were cheated in a business relationship, Mr. Jones stole all of your money from the partnership you were in and left town. You now go home and tell your kids all about Mr. Jones--He wore a silk tie, drove a big car, wore a Rolex watch and had a big silver cross around his neck. This is the antigenic code, which your children pass on to their children and grandchildren. Generations later a similar-appearing cheater wearing the silk tie, Rolex and silver cross appears. He is instantly recognized by your great-grandchildren, who might tar and feather him, and tie him up (the antibodies at work), tear his suit and tie it into shreds (cytolytic cells), or call the police (the lymphokines). The antigen would be inhibited and the damage prevented or restricted. The lymphocytes are the primary WBC involved in immune response...20 to 25% of WBC’s. B-Lymphocytes: Developed from the stem cell in the bone marrow (B = Bone marrow). The B lymphocyte precursor cells reside is in the lymphoid tissue, usually found in the lymph nodes. The lymphocytes travel to the site of injury after stimulated by an antigen. There are two types of B lymphocytes: l. Plasma cells: produce antibodies specifically directed against the antigen. The antibody binds itself to the antigen material. Once the binding occurs, Ag is inactivated: the Ag-Ab complex may be opsonized, agglutinated, or precipitated for inflammatory phagocytosis. Antibodies, also called immunoglobulins, are carried in blood serum. There are five different types, all with the same basic structure; however, in each type of antibody, this structure is arranged differently: IgM, IgA, IgD, IgG, IgE = MADGE. 2. B memory cell: retains the memory of the previously encountered antigens. T-Lymphocytes: The T lymphocytes develop from the bone marrow stem cell, travel to the thymus, and mature, (are processed), (T = Thymus), and subsequently reside in the lymphoid nodules that they share with B-lymphocyte precursors. They produce lymphokines. These T cells develop a memory for a single specific foreign antigen associated with an injurious agent. The antigenic memory is passed down through generations to numerous T-cell progeny. When sensitized T cells encounter the “silk tie antigen,” they react by sending messages to other cells, including T cells, B cells, and macrophages. These chemical messages are termed lymphokines or cytokines, and they instruct the other cells to shred, club, punch, and generally disable the antigenic agent. Some sensitized T cells (cytolytic) can directly destroy the agent, whereas some simply call other cells to help. (Fig 4-2 p.41 Miller) The net result is that the silk tie bandit is destroyed or at least inhibited. AG-Processing Cells: The third series of cells to participate in the immune reaction is the AG-processing cells. In many cases the T lymphocytes are quite farsighted and do not 3 Unit 3 immediately recognize the antigenic substances. Antigen-processing cells such as macrophages initially change or process the Ag until it is recognizable to the lymphocytes. Then the lymphocytes can react and function. Coordination of Cells: The three cell systems usually function as a team, and therefore, communications are important. The T-helper lymphocyte In many situations the t-helper functions as a team leader to call and coordinate signals. They are also called the T4 lymphocytes. The T-helper cells are involved in the activation of effector cells. Once the T4 lymphocyte has been presented with the Ag by the APC, it sends chemical lymphokines, termed interleukins, to other T4 and T8 lymphocytes and B lymphocytes, instructing them to proliferate and function. Other lymphokines have effects on macrophages, such as initiation of macrophage chemotaxis, activation of phagocytosis, and aggregation at the area of injury (antigen). (See table 3-1 in text, page 110) T8 lymphocytes = T-suppressor cells function to (1) directly destroy the antigenic agent and (2) send messages back to T4 - helper cells (again via interleukins). Some of these messages inhibit further immune response so that there is not an overreaction. Because T8 cells function to limit the immune response, they are often referred to as suppressor cells. Activated macrophages and B cells also communicate by interleukins. Other types of lymphocytes (NK cells = Natural Killer) and macrophages participate in the immune reaction with extensive communication and feedback by interleukins. The system therefore is very complex, precise, and is easily distorted (Miller p.40). Lymph Nodes and Lymphatics Blood and lymphatic systems parallel each other throughout the body. Lymphocytes make up 70 - 80 % of nucleated cells in blood and more than 99% of nucleated cells in lymph. Principal functions of lymphoid system: Concentrate antigens into distinct structures Circulate lymphocytes through tissues Carry products of immune responses to bloodstream and tissues 4 Unit 3 Major Divisions of the Immune Response Humoral Response: Antibodies secreted by B lymphocytes. Associated with the fluid phase of blood (plasma or serum--humoral means liquid). The humoral response is effective against extracellular stages of bacterial and viral infections. Cell-mediated Response: lymphocytes working alone (usually T lymphocytes) or assisted by macrophages. Associated with lymphoid system. Primarily effective against intracellular viruses, fungi, parasites, neoplastic cells, and foreign tissue. Types of Immunity Active Immunity: Occurs naturally when a disease is caused by a microorganism. This type of immunity is also acquired by artificial means. Vaccine: a person is injected with or ingests either altered pathogenic microorganisms or products of those microorganisms = Vaccination. The immune system produces a stronger, faster response next time the pathogen is encountered. This production of acquired immunity is called immunization. Antibacterial: 1. Low skin surface pH and its general dryness inhibit bacterial growth. 2. Epithelial desquamation, mucus barrier, ciliary activity, pH of the lumen, and fluid flow of mucous membranes limit bacterial colonization. 3. Bactericidal agents include lysozyme, lactoferrin, leukin and plakin. 4. Phagocytosis is the most important element in host resistance to infectious disease. Antiviral: 1. Interferons inhibit viral infection of healthy cell Antifungal Passive Immunity: using antibodies produced by another person to protect against infectious disease. Natural: mother to fetus Acquired: short-lived but active immediately (HBiG: hepatitis B immunoglobulin) 5 Unit 3 Immunopathology Hypersensitivity (allergic reaction) is an immune response to a harmless substance (Langlais, p88). Type I (IgE mediated immediate hypersensitivity) Histamine mediated. Can be life threatening because tissues swell and bronchioles constrict. Occurs immediately after exposure to a previously encountered antigen (e.g., penicillin). 1. 2. Local allergic reactions: (hay fever--allergic rhinitis, asthma, and allergic dermatitis) Systemic (termed anaphylaxis) involves several organs, may be triggered by insect venom, drugs, or certain foods. Type II Hypersensitivity (Cytotoxic): (Hemolytic anemia of the newborn, aka erythroblastosis fetalis), also includes transfusion reactions, and Rh incompatibility). Type III Hypersensitivity (complex-mediated) Autoimmune type, e.g. lupus. Type IV (Delayed) Cell-mediated --initiated by T cell lymphocytes-- of no benefit (ex. tissue rejection, tuberculin test, and poison ivy allergy). Drug Hypersensitivity (Types I, II, III, and IV) Route of administration: Topical causes more reactions Parenteral reaction is severe and widespread--increased risk if : infection present multiple allergies autoimmune diseases present adults more than children Immediate localized hypersensitivity is managed with antihistamines, whereas delayed hypersensitivity is best treated with corticosteroids. Autoimmune Diseases: In autoimmune diseases (connective tissue diseases) certain body cells are no longer tolerated, and the immune system treats them as antigens. Autoimmune disease may involve a single cell type, single organ, or multiple organs. Genetic factors may play a role as may viral infection. Immunodeficiency: A condition involving a deficiency in number, function, or interrelationships of the involved white blood cells and their products. Can be congenital (present at birth) or acquired (developing after birth). 6 Unit 3 Oral Diseases with Immunologic Pathogenesis 1. Aphthous Ulcers (aka canker sores, recurrent aphthous stomatitis-RAS) (Langlais, p. 94). Painful recurrent ulcers usually on vestibular and buccal mucosa, tongue, soft palate, fauces, and floor of the mouth (movable mucosa). Prevalence tends to be higher in professional persons and those in upper socioeconomic groups. Affects about 20% of the population. Unknown etiology, but possibly defect in the immune system--see higher levels of Ab’s to oral mucous membranes--. Other causes that may have a triggering role include trauma (most common), food allergy (nuts, chocolate, gluten), stress, hormonal alterations, and nutritional factors (deficiencies of vitamin B12, folic acid, iron). Familial patterns have been demonstrated. Non-smokers are more frequently affected than smokers. Not caused by the herpesvirus. Peridex has been used to treat with some success. Patients with severe aphthous may be given steroids (due to relation to immunologic defect). Three forms of aphthous ulcers have been classified according to size; all are believed to be part of the same disease spectrum. Differences are essentially clinical and correspond to degree of severity. a. b. Minor aphthae: most commonly occurring type. On movable mucosa-mucosa not covering bone--and occasionally on gingiva. Yellow membrane surrounded by erythematous halo, less than 1 cm in size. Often a 1 to 2 day prodromal period. Generally lasts 7 to 10 days. Invariably recurrent. Minor ulcers usually heal spontaneously without scar formation within 14 days. Occurs as single ulcer usually, occasionally in crops but not more than 5. They are more common in the anterior of the mouth. Major aphthous (aka Sutton’s disease, periadenitis mucosa necrotica recurrens--PMNR, major scarring aphthous stomatitis, scarifying stomatitis) (Langlais, p. 96). Regarded as the most severe expression of aphthous stomatitis. Lesions are larger, deeper, more painful and persist longer (up to 6 weeks with immediate recurrence) than minor aphthae. Lesions heal with scarring. Pain may result in difficulty in eating and psychological stress and systemic health may be compromised. Young female adults with anxious personality traits are most commonly affected. (Aphthous ulcers usually occur as single lesions located on oral mucous membranes that contain minor salivary glands. These locations include all oral mucosa except gingiva, anterior and lateral surfaces of the hard palate. 7 Unit 3 c. Herpetiform are tiny (1-2mm) recurrent crops of small ulcers. Mostly on movable mucosa but also see on gingiva, palate and tip of tongue. Smaller than aphthae. Very painful. May be clinically confused with primary herpes. Recurrent history of aphthous and lack of gingival involvement (usually) in aphthous help make the distinction between this and primary herpes. 2. Urticaria: (hives) (Langlais, p. 88) Immediate allergic responses are histaminemediated and occur within minutes of exposure to Ags (ex. anaphylaxis)..Individual wheals (aka urticaria, hives) arise following ingestion of certain foods such as shellfish, citrus fruits, chocolate, or systemically administered drugs. Managed with antihistamines. 3. Angioedema: (Langlais, p. 88) Swelling is the most prominent feature. It appears rapidly and lasts for 24 to 36 hours. Sensations of warmth and tenseness. Commonly perioral and periorbital tissues. May occur with urticaria. Managed with antihistamines. 4. Contact Mucositis (aka allergic mucositis): (Langlais p88) Delayed (Type IV) reaction. (ex. flavoring ingredients, topical anesthetics, mouthwashes, cast alloy restorations) 5. Contact Dermatitis: ex. Latex glove allergy, reaction to lipstick or sunscreen. Treat delayed hypersensitivity with corticosteroids. 6. Fixed Drug Eruptions: These are lesions that appear in the same site each time a drug is introduced. A complex-mediated allergic reaction (type III). 7. Erythema Multiforme (EM, aka ectodermosis erosiva pluriorificialis) (Langlais, p. 90). Unknown etiology but in about half the cases precipitating factors (infections--esp. herpes simplex, stress, and drugs) can be identified. Malaise, headache and low-grade fever typically precede lesions by 3 to 7 days. Characteristic skin lesion is called a target, iris, or bull’s eye. It consists of concentric erythematous rings separated by rings of near-normal color. Lesions rapidly appear on arms and legs. Oral lesions can occur with or without skin lesions and are usually painful ulcers. Oral lesions frequently form on the lateral borders of the tongue. Dark, redbrown, hemorrhagic crusts are characteristically present on the lips. 8. Stevens-Johnson syndrome: the most severe form of EM. “If eye, mouth and genital lesions are involved it is usually Steven Johnson syndrome” (Dr. Wooley). More widespread involvement, and more systemic signs (fever, malaise, headache, cough, chest pain, diarrhea, vomiting, arthralgia). Hemorrhagic lip lesions are intensely painful. Topical corticosteroids for mild EM, systemic corticosteroid treatment usually needed. 8 Unit 3 9. Lichen Planus: (Langlais) Benign, chronic disease affecting the skin and oral mucosa. Frequently misdiagnosed. Disease of middle age; often severity parallels stress level. The most common oral pattern of presentation is termed reticular lichen planus. It is so named because of the presence of a lace-like pattern of intersecting, somewhat angular to curved white striations--Wickham’s striae. These are present to some extent in all forms of lichen planus. Oral lesions occur most commonly on buccal mucosa, often bilateral and symmetrical. A single patient may have more than one form: a. b. c. d. e. Reticular form = striated form: Most common type with numerous interlacing keratotic lines (striae of Wickham) producing a lacy pattern. Most commonly on buccal mucosa but may be on almost any mucosal tissue. Plaque-like lichen planus looks like leukoplakia and is usually on buccal mucosa and dorsum of tongue. Asymptomatic. Least common type. Atrophic form comes with burning or pain complaints. Attached gingiva is frequently involved; keratotic striae radiate from atrophic dark areas. When the attached gingiva is affected the term “desquamative gingivitis” has been used. Erosive form shows granular and brightly erythematous surface. A pseudomembrane covers areas of significant erosion. Intermittently painful. Erosive lichen planus shows striations, as well as irregular painful ulcers (Miller p. 270). Bullous variant is the most unusual form. Bullae rupture and leave ulcerated, painful surface. Commonly on posterior buccal mucosa and lateral margin of tongue. Corticosteroids are used to treat symptomatic lesions. Stress reduction can bring about abrupt and dramatic resolution of the lesions. Lichen planus is a chronic condition. Erosive and atrophic forms may rarely transform to malignancy if associated with tobacco use, so patients should be observed periodically (especially with history of tobacco or alcohol abuse). The etiology of lichen planus is not understood. However, considerable attention has been directed toward the identification of predisposing factors. While it should be emphasized that metallic restorations only rarely induce lichen planus, two mechanisms are known. It is recognized that certain amalgam alloys in rare cases will induce development of lichen planus in the adjacent buccal or lingual mucosa. Even less common is lichen planus arising under the influence of galvanic currents flowing between metallic restorations composed of dissimilar metals (Miller, p. 271) Different drugs are a common and important predisposing factor in lichen planus. Beta blockers used to treat hypertension are in this group. Because it is the oral expression of an important dermatologic condition, it would be reasonable to anticipate that oral lichen planus would usually occur with concurrent skin disease. In like manner, lichen planus of the skin would be expected to typically include 9 Unit 3 oral disease. Interestingly, neither pattern is frequently observed. Paradoxically, oral lichen planus usually occurs in patients without cutaneous disease, and the majority of patients with lichen planus of the skin are free of oral disease. However, concurrent oral and cutaneous lichen planus do occur with some frequency. The finding of typical cutaneous lichen planus in a patient with suspected oral lichen planus provides additional support for the oral diagnosis. 10. Reiter’s Syndrome: Unknown etiology but possibly genetic influence. Major components (triad) are arthritis, urethritis, and conjunctivitis. Oral lesions are relatively painless aphthous type ulcers occurring almost anywhere in the mouth. If on tongue, looks like geographic tongue. Abnormal immune response to microbial antigen(s) is now regarded as a likely mechanism for the multiple manifestations of this syndrome. Predominantly in white males in their third decade. Self-limiting: It lasts weeks to months; recurrence is common. 11. Histiocytosis X (aka idiopathic histiocytosis, Langerhans-cell granulomatosis, Langerhans cell disease) Associated primarily with an abnormal histiocyte. A condition of children and young adults. Oral changes may be the initial presentation in all forms of this disorder. Classic presentation in the jaws often results in loosening or premature exfoliation of teeth. Tenderness, pain and swelling are frequent patient complaints. Loosening of teeth in the area of the affected alveolar bone is a common occurrence. The gingival tissues are frequently inflamed, hyperplastic, and ulcerated. Three disorders grouped because of similar microscopic appearance but clinical manifestations are diverse. There are debates on the appropriateness of this classification scheme. In all 3 diseases, the proliferating cell is the macrophage. Also present are eosinophils. a. b. Letterer-Siwe Disease (aka acute disseminated histiocytosis) shows rapidly progressive, usually fatal clinical course. Widespread, proliferative organ, bone, and skin involvement in infants. Most likely represents a malignant neoplastic process. Significant oral involvement is rare due to rapid and usually fatal course. Hand-Schuller-Christian Disease (aka multifocal eosinophilic granuloma, chronic disseminated histiocytosis) Presents with a clinical triad of single to multiple, well-defined or “punched-out” radiolucent areas in the skull 10 Unit 3 c. (may occur in jawbones); unilateral or bilateral exophthalamos (abnormal protrusion of the eyeball), and diabetes insipidus. (Triad seen in about 25% of cases). Usually in children younger than 5. Oral manifestations include: 1) sore mouth with or without ulcerative lesions, 2) loose and sore teeth, 3) early exfoliation of teeth, 4) nonhealing extraction sites, and 5) loss of alveolar bone mimicking periodontal disease is characteristic. Eosinophilic Granuloma refers to patients with solitary or multiple bone lesions only. More localized form of the disease. Patient may complain of redundant gingival tissue, pain, swelling of focal areas of the gingiva, or a loosening of isolated teeth. Be especially suspicious of the presence of a single loose tooth without apparent cause. Radiographically: “teeth floating in air.” Treated with conservative surgical excision or radiation therapy... recurrence is rare. 11