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Tags : Oral, Manifestations, Allergic, diseases, Hypersensitivity, reactions, immune, mechanisms, immunopathology, allergen, reaction, anaphylactic, allergy, skin, urticaria, eczema, eyes, conjunctivitis, nasopharynx, rhinorrhea, rhinitis, bronchopulmonary, tissues, asthma, gastrointestinal, tract, gastroenteritis, Aphthous, Burning, Candida, Carcinoma, Caries, Dental, Drug reaction, Gingiva, Herpes, Hu

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Khushbu Shrivastava Gupta Editor @MedicPresents Master of Technology (M.Tech.), Biotechnology Oral Manifestations of Allergic diseases
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Hypersensitivity reactions The immune system is an integral part of human protection against disease, but the normally protective immune mechanisms can sometimes cause detrimental reactions in the host. Such reactions are known as hypersensitivity reactions, and the study of these is termed immunopathology.
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An allergen is a substance that triggers an allergic reaction in people who are sensitive to that substance.
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Types of hypersensitivity reactions: Hypersensitivity reactions can be divided into four types ( by R. Coombs and P. Gell) : type I, type II, type III and type IV, based on the mechanisms involved and time taken for the reaction. Type V (Autoimmune disease, receptor mediated)- This is an additional type that is sometimes (often in Britain) used as a distinction from Type 2. Instead of binding to cell surface components, the antibodies recognize and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling. Some clinical examples: Graves' disease Myasthenia gravis The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically segregated into its own subcategory of Type 2.
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TYPE I HYPERSENSITIVITY Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 - 12 hours).
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Immediate hypersensitivity is mediated by IgE. The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils. A biopsy of the reaction site demonstrates mainly mast cells and eosinophils. The mechanism of reaction involves preferential production of IgE, in response to certain antigens (often called allergens). The precise mechanism as to why some individuals are more prone to type-I hypersensitivity is not clear. However, it has been shown that such individuals preferentially produce more of TH2 cells that secrete IL-4, IL-5 and IL-13 which in turn favor IgE class switch. IgE has very high affinity for its receptor (Fcε; CD23) on mast cells and basophils. A subsequent exposure to the same allergen cross links the cell-bound IgE and triggers the release of various pharmacologically active substances . Cross-linking of IgE Fc-receptor is important in mast cell triggering. Mast cell degranulation is preceded by increased Ca++ influx, which is a crucial process; ionophores which increase cytoplasmic Ca++also promote degranulation, whereas, agents which deplete cytoplasmic Ca++ suppress degranulation. The agents released from mast cells and their effects are listed in Table 1. Mast cells may be triggered by other stimuli such as exercise, emotional stress, chemicals (e.g., photographic developing medium, calcium ionophores, codeine, etc.),anaphylotoxins (e.g., C4a, C3a, C5a, etc.). These reactions, mediated by agents without IgE-allergen interaction, are not hypersensitivity reactions, although they produce the same symptoms.
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TYPE I HYPERSENSITIVITY The reaction is amplified by PAF (platelet activation factor) which causes platelet aggregation and release of histamine, heparin and vasoactive amines. Eosinophil chemotactic factor of anaphylaxis (ECF-A) and neutrophil chemotactic factors attract eosinophils and neutrophils, respectively, which release various hydrolytic enzymes that cause necrosis. Eosinophils may also control the local reaction by releasing arylsulphatase, histaminase, phospholipase-D and prostaglandin-E, although this role of eosinophils is now in question. Cyclic nucleotides appear to play a significant role in the modulation of immediate hypersensitivity reaction, although their exact function is ill understood. Substances which alter cAMP and cGMP levels significantly alter the allergic symptoms. Thus, substances that increase intracellular cAMP seem to relieve allergic symptoms, particularly broncho-pulmonary ones, and are used therapeutically (Table 2). Conversely, agents which decrease cAMP or stimulate cGMP aggravate these allergic conditions.
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TYPE I HYPERSENSITIVITY Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests, measurement of total IgE and specific IgE antibodies against the suspected allergens. Total IgE and specific IgE antibodies are measured by a modification of enzyme immunoassay (ELISA). Increased IgE levels are indicative of an atopic condition, although IgE may be elevated in some non-atopic diseases (e.g., myelomas, helminthic infection, etc.). There appears to be a genetic predisposition for atopic diseases and there is evidence for HLA (A2) association.
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TYPE II HYPERSENSITIVITY Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples. The reaction time is minutes to hours. Type II hypersensitivity is primarily mediated by antibodies of the IgM or IgG classes and complement. Phagocytes and K cells may also play a role.
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TYPE II HYPERSENSITIVITY The lesion contains antibody, complement and neutrophils. Diagnostic tests include detection of circulating antibody against the tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence. The staining pattern is normally smooth and linear, such as that seen in Goodpasture's nephritis (renal and lung basement membrane) and pemphigus (skin intercellular protein, desmosome) .
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TYPE III HYPERSENSITIVITY Type III hypersensitivity is also known as immune complex hypersensitivity. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs (e.g., aspergillosis), blood vessels (e.g., polyarteritis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms.
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TYPE III HYPERSENSITIVITY The reaction may take 3 - 10 hours after exposure to the antigen (as in Arthus reaction). It is mediated by soluble immune complexes. They are mostly of the IgG class, although IgM may also be involved. The antigen may be exogenous (chronic bacterial, viral or parasitic infections), or endogenous (non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE). The antigen is soluble and not attached to the organ involved. Primary components are soluble immune complexes and complement (C3a, 4a and 5a). The damage is caused by platelets and neutrophils. The lesion contains primarily neutrophils and deposits of immune complexes and complement. Macrophages infiltrating in later stages may be involved in the healing process.
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TYPE III HYPERSENSITIVITY
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TYPE III HYPERSENSITIVITY The affinity of antibody and size of immune complexes are important in production of disease and determining the tissue involved. Diagnosis involves examination of tissue biopsies for deposits of immunoglobulin and complement by immunofluorescence microscopy. The immunofluorescent staining in type III hypersensitivity is granular (as opposed to linear in type II such as seen in Goodpasture's syndrome). The presence of immune complexes in serum and depletion in the level of complement are also diagnostic. Polyethylene glycol-mediated turbidity (nephelometry) binding of C1q and Raji cell test are utilized to detect immune complexes.
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TYPE IV HYPERSENSITIVITY Type IV hypersensitivity is also known as cell mediated or delayed type hypersensitivity. The classical example of this hypersensitivity is tuberculin (Montoux) reaction which peaks 48 hours after the injection of antigen (PPD or old tuberculin). The lesion is characterized by induration and erythema.
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TYPE IV HYPERSENSITIVITY Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, histoplasmosis, toxoplasmosis, leishmaniasis, etc.) and granulomas due to infections and foreign antigens. Another form of delayed hypersensitivity is contact dermatitis (poison ivy, chemicals, heavy metals, etc.) in which the lesions are more papular. Type IV hypersensitivity can be classified into three categories depending on the time of onset and clinical and histological presentation
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TYPE IV HYPERSENSITIVITY Mechanisms of damage in delayed hypersensitivity include T lymphocytes and monocytes and/or macrophages. Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes and macrophages, which cause the bulk of the damage. The delayed hypersensitivity lesions mainly contain monocytes and a few T cells. Major lymphokines involved in delayed hypersensitivity reaction include monocyte chemotactic factor, interleukin-2, interferon-gamma, TNF alpha/beta, etc. Diagnostic tests in vivo include delayed cutaneous reaction (e.g. Montoux test ) and patch test (for contact dermatitis). In vitro tests for delayed hypersensitivity include mitogenic response, lympho-cytotoxicity and IL-2 production.
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Anaphylactic shock Anaphylaxis is a severe, whole-body allergic reaction to a chemical that has become an allergen. After being exposed to a substance such as bee sting venom, the person's immune system becomes sensitized to it. On a later exposure to that allergen, an allergic reaction may occur. This reaction happens quickly after the exposure, is severe, and involves the whole body. Tissues in different parts of the body release histamine and other substances. This causes the airways to tighten and leads to other symptoms. Some drugs (morphine, x-ray dye, and others) may cause an anaphylactic-like reaction (anaphylactoid reaction) when people are first exposed to them. Aspirin may also cause a reaction. These reactions are not the same as the immune system response that occurs with "true" anaphylaxis. However, the symptoms, risk for complications, and treatment are the same for both types of reactions. Anaphylaxis can occur in response to any allergen. Common causes include: Drug allergies Food allergies Insect bites/stings Pollens and other inhaled allergens rarely cause anaphylaxis. Some people have an anaphylactic reaction with no known cause. Anaphylaxis is life-threatening and can occur at any time. Risks include a history of any type of allergic reaction.
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Symptoms Symptoms develop rapidly, often within seconds or minutes. They may include the following: Abdominal pain or cramping Abnormal (high-pitched) breathing sounds Anxiety Confusion Cough Diarrhea Difficulty breathing Difficulty swallowing Fainting, light-headedness, dizziness Hives, itchiness Nasal congestion Nausea, vomiting Palpitations Skin redness Slurred speech Wheezing
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Presentation There is often (but not always) a history of previous sensitivity to an allergen, or recent history of exposure to a new drug (e.g. vaccination). Initially, patients usually develop skin symptoms, including generalised itching, urticaria and erythema, rhinitis, conjunctivitis and angio-oedema. Signs that the airway is becoming involved include itching of the palate or external auditory meatus, dyspnoea, laryngeal oedema (stridor) and wheezing (bronchospasm). General symptoms include palpitations and tachycardia (as opposed to bradycardia in simple vasovagal episode at immunisation time), nausea, vomiting and abdominal pain, feeling faint - with a sense of impending doom; and, ultimately, collapse and loss of consciousness. Airway swelling, stridor, breathing difficulty, wheeze, cyanosis, hypotension, tachycardia and reduced capillary filling suggest impending severe reaction.
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Quick reference anaphylaxis algorithm Rapid assessment: Airway: look for and relieve airway obstruction; call for help early if there are signs of obstruction. Remove any traces of allergen remaining (e.g. nut fragments caught in teeth, with a mouthwash; bee stings without compressing any attached venom sacs). Breathing: look for and treat bronchospasm and signs of respiratory distress. Circulation: colour, pulse and BP. Disability: assess whether responding or unconscious. Exposure: assess skin with adequate exposure, but avoid excess heat loss. Consider anaphylaxis when there is compatible history of rapid-onset severe allergic-type reaction with respiratory difficulty and/or hypotension, especially if there are skin changes present. Give high-flow oxygen - using a mask with an oxygen reservoir (greater than 10 litres min-1 to prevent reservoir collapse). Lie the patient flat: Raise the legs (care, as this may worsen any breathing problems). In pregnant patients, use a left lateral tilt of at least 15° (to avoid caval compression).
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Emergency Adrenaline (epinephrine) intramuscularly (IM) in the anterolateral aspect of the middle third of the thigh (safe, easy, effective): Adult IM dose 0.5 mg IM (= 500 micrograms = 0.5 mL of 1:1000) adrenaline (epinephrine). Child IM dose (the equivalent volume of 1:1000 adrenaline (epinephrine) is shown in brackets): >12 years: 500 micrograms IM (0.5 mL), i.e. the same as the adult dose. 300 micrograms (0.3 mL) if the child is small or prepubertal. >6-12 years: 300 micrograms IM (0.3 mL). <6 years: 150 micrograms IM (0.15 mL). Note: half doses of adrenaline (epinephrine) may be safer for patients on amitriptyline, imipramine, monoamine oxidase inhibitor (MAOI) or beta-blocker.
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When skills and equipment are available: Establish airway (in anaphylaxis, airway obstruction from tissue swelling is difficult to overcome and early expert intubation is often needed). IV fluid challenge: Insert one or more large-bore IV cannulae (enable the highest flow). Use intraosseous access (if trained to do so) in children when IV access is difficult. Give a rapid fluid challenge: Adults - 500 mL of warmed crystalloid solution (e.g., Hartmann's or 0.9% saline) in 5-10 minutes if the patient is normotensive or one litre if the patient is hypotensive. Use smaller volumes (e.g. 250 mL) for adult patients with known cardiac failure and use closer monitoring (listen to the chest for crepitations after each bolus). The use of invasive monitoring, e.g., central venous pressure (CVP), can help to assess fluid resuscitation. For children - give 20 mL/kg of warmed crystalloid.
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When skills and equipment are available: Chlorphenamine (after initial resuscitation). Dose depends on age: >12 years and adults: 10 mg IM or IV slowly. >6-12 years: 5 mg IM or IV slowly. >6 months-6 years: 2.5 mg IM or IV slowly. <6 months: 250 micrograms/kg IM or IV slowly. Hydrocortisone (after initial resuscitation). Dose depends on age: >12 years and adults: 200 mg IM or IV slowly. >6-12 years: 100 mg IM or IV slowly. >6 months-6 years: 50 mg IM or IV slowly. <6 months: 25 mg IM or IV slowly. Monitor: Pulse oximetry ECG BP
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Antihistamines (after initial resuscitation) Antihistamines are a second line treatment for an anaphylactic reaction. The evidence to support their use is weak, but there are logical reasons for them. 55 Antihistamines (H1-antihistamine) may help counter histamine-mediated vasodilation and bronchoconstriction. They may not help in reactions depending in part on other mediators but they have the virtue of safety. Used alone, they are unlikely to be lifesaving in a true anaphylactic reaction. Inject chlorphenamine slowly intravenously or intramuscularly. The dose of chlorphenamine depends on age: >12 years and adults: 10 mg IM or IV slowly >6 – 12 years: 5 mg IM or IV slowly >6 months – 6 years: 2.5 mg IM or IV slowly <6 months: 250 micrograms/kg IM or IV slowly There is little evidence to support the routine use of an H2-antihistamine (e.g., ranitidine, cimetidine) for the initial treatment of an anaphylactic reaction.
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Steroids (give after initial resuscitation) Corticosteroids may help prevent or shorten protracted reactions. In asthma, early corticosteroid treatment is beneficial in adults and children. 57 58 There is little evidence on which to base the optimum dose of hydrocortisone in anaphylaxis. In hospital patients with asthma, higher doses of hydrocortisone do not seem to be better than smaller doses. 59 Inject hydrocortisone slowly intravenously or intramuscularly, taking care to avoid inducing further hypotension. The dose of hydrocortisone for adults and children depends on age: >12 years and adults: 200 mg IM or IV slowly >6 – 12 years: 100 mg IM or IV slowly >6 months – 6 years: 50 mg IM or IV slowly <6 months: 25 mg IM or IV slowly
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Quincke's edema Angioedema or Quincke's edema is the rapid swelling (edema) of the dermis, subcutaneous tissue,mucosa and submucosal tissues.
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Symptoms The skin of the face, normally around the mouth, and the mucosa of the mouth and/or throat, as well as the tongue, swell up over the period of minutes to several hours. The swelling can also occur elsewhere, typically in the hands. The swelling can be itchy or painful. There may also be slightly decreased sensation in the affected areas due to compression of the nerves. Urticaria(hives) may develop simultaneously. In severe cases, stridor of the airway occurs, with gasping or wheezy inspiratory breath sounds and decreasing oxygen levels.
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Causative factors Food related products for Quincke's edema associated with urticaria. Drugs like penicillin, aspirin, phenytoin and others, Infection- bacterial and viral Venoms, medication and food can induce anaphylaxis in sensitized individuals. Hereditary angio-oedema is an autosomal-dominant disorder associated with recurrent episodes of edema of the subcutaneous tissue without. Onset is usually in early childhoodbut may be delayed even into late adult life.
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Treatment Angioneurotic odema is a medical emergency, it always better to seek the medical help immediately To give airway support in case of medical support Antihistamines Corticosteroids Adrenaline in acute condition C1 esterase inhibitors in case of hereditary angioneurotic edema
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Erythema multiforme Erythema multiforme (EM) is an acute, self-limited, and sometimes recurring skin condition that is considered to be a type IV hypersensitivity reaction associated with certain infections, medications, and other various triggers.
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Symptoms Fever General ill feeling Itching of the skin Joint aches Multiple skin lesions: Start quickly and may return May spread May appear as a nodule, papule, or macule and may look like hives Central sore surrounded by pale red rings, also called a "target", "iris", or "bulls-eye" May have vesicles and blisters of various sizes (bullae) Located on the upper body, legs, arms, palms, hands, or feet May involve the face or lips Usually even on both sides (symmetrical)
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Other symptoms that may occur with this disease: Bloodshot eyes Dry eyes Eye burning, itching, and discharge Eye pain Mouth sores Vision problems
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Erythema multiforme
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History: In EM, there may be no prodrome or a mild upper respiratory tract infection. The rash starts abruptly, usually within 3 days. It starts on the extremities, being symmetrical and spreading centrally. Half of children with the rash have recent herpes labialis. It usually precedes the erythema multiforme by 3 to 14 days but it can sometimes be present at the onset.
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Examination: The iris or target lesion is the classical feature of the disease. Initially there is a dull red flat spot or wheal that enlarges slightly up to 2 cm over 24 to 48 hours. In the middle, a small bump, vesicle, or bulla develops, flattens, and then may clear. The intermediate ring forms and becomes raised, pale, and swollen. The periphery slowly becomes purple and forms a concentric lesion, resembling a target. Some lesions are atypical targets with only 2 concentric rings. The Koebner phenomenon may occur. This is where a lesion occurs along the line of trauma and it is typical of psoriasis and lichen planus. Lesions appear first on the extensor surfaces of the periphery and extend centrally. The palms, neck and face are often involved but the soles and flexures of the extremities less often. There may be mucosal involvement in 70% of patients but it tends to be mild and limited to just one mucosal surface (for example mouth or vulva). Oral lesions are most common with lips, palate and gingiva affected. There may be red conjunctivae and tearing, but eye involvement tends to be mild. Genital involvement can produce painful hemorrhagic bullae and erosions.
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Erythema multiforme Investigations: No specific investigations are indicated. Nikolsky's sign is positive A punch biopsy may be required to confirm diagnosis. Management: In recurrent disease due to HSV, antiviral therapy is helpful. Symptomatic treatment may include analgesics, mouth wash and local skin care. Steroid creams may be used. If the mouth is very sore, attention may have to be given to hydration and nutrition. Lubricating drops for eyes may be required.
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Stevens–Johnson syndrome Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are two forms of a life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis The syndrome is thought to be a hypersensitivity complex that affects the skin and the mucous membranes. Although the majority of cases are idiopathic (without a known cause), the main class of known causes is medication, followed by infections and, rarely, cancers.
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Symptoms SJS usually begins with fever, sore throat, and fatigue, which is misdiagnosed and usually treated with antibiotics. Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children who develop SJS. A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.
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Stevens-Johnson syndrome
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Treatment: SJS constitutes a dermatological emergency. All medications should be discontinued, particularly those known to cause SJS reactions. Patients with documented mycoplasma infections can be treated with oral macrolide or oral doxycycline. Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g. intravenous fluids and nasogastric or parenteral feeding) and symptomatic (e.g.,analgesic mouth rinse for mouth ulcer). Dermatologists and surgeons tend to disagree about whether the skin should be debrided. Beyond this kind of supportive care, there is no accepted treatment for SJS. Treatment with corticosteroids is controversial. Early retrospective studies suggested that corticosteroids increased hospital stays and complication rates. There are no randomized trials of corticosteroids for SJS, and it can be managed successfully without them. Intravenous immunoglobulin (IVIG) treatment has shown some promise in reducing the length of the reaction and improving symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a warm environment, and intravenous analgesics. An ophthalmologist should be consulted immediately, as SJS frequently causes the formation of scar tissue inside the eyelids, leading to corneal vascularization, impaired vision and a host of other ocular problems.
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Skin Tests Scratch test (also known as a puncture or prick test). This test is done by placing a drop of a solution containing a possible allergen on the skin, and a series of scratches or needle pricks allows the solution to enter the skin. If the skin develops a red, raised itchy area (called a wheal), it usually means that the person is allergic to that allergen. This is called a positive reaction.
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Intradermal test. Intradermal test. After examining and cleaning the skin, a small amount of the allergen is injected just under the skin, similar to a tuberculosis test. During this test, a small amount of the allergen solution is injected into the skin. An intradermal allergy test may be done when a substance does not cause a reaction in the skin prick test but is still suspected as an allergen for that person. The intradermal test is more sensitive than the skin prick test but is more often positive in people who do not have symptoms to that allergen (false-positive test results).
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Patch test. Patch test. For a skin patch test, the allergen solution is placed on a pad that is taped to the skin for 24 to 72 hours. This test is used to detect a skin allergy called contact dermatitis.
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Allergy blood tests Allergy blood tests look for substances in the blood called antibodies. Blood tests are not as sensitive as skin tests but are often used for people who are not able to have skin tests. The most common type of blood test used is the enzyme-linked immunosorbent assay (ELISA, EIA). It measures the blood level of a type of antibody (called immunoglobulin E, or IgE) that the body may make in response to certain allergens. IgE levels are often higher in people who have allergies or asthma. Other lab testing methods, such as radioallergosorbent testing (RAST) or an immunoassay capture test (ImmunoCAP, UniCAP, or Pharmacia CAP), may be used to provide more information.