Download pdf - Alergen & Hypersensitive Dlm KG 2011

8/4/2019 Alergen & Hypersensitive Dlm KG 2011

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Alergen &

Hypersensitivitydlm Kedokteran

Gigi


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Alergen

Bahan /material/antigen yang bisamenyebabkan terjadinya alergi

Alergi: respon immune patologik ,terjadi secara berlebihan sehinggamerusak jaringan, diperantarai olehIg E . Sensitivitas thd Ag >>>>

Terkait dengan reaksihypersensitivitas type I


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Ag, Alergen

Hidrat arang (polisakarida)umumnya imunogenik

Lipid

non imunogenik + carrierimunogenik, ex Sfingolipid Asam Nukleat

Non imunogenik +carrier

imunogenik Protein

imunogenik yang multideterminanunivalen


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Berdasar epitope

Unideterminan,univalen; hapten

Unideterminan, multivalen;

polisakarida Multideterminan, univalen;

protein

Multideterminan, multivalen;

kimia kompleks


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Terminology

Ag

immunogen

allergen


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Exogenous materials (Ag,allergen) and the Skin/mucosa

response

1. Allergic contact

Dermatitis/Stomatitis/Mucositis

2. Irritan contact

Dermatitis/Stomatitis/Mucositis

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Allergic contact dermatitis(ACD)

The term contact dermatitissometimes is used incorrectly as asynonym for allergic contactdermatitis (ACD).

Contact dermatitis is inflammationof the skin induced by chemicalsthat directly damage the skin as

ussualy Irritant Contact Dermatitis

by specific sensitivity in the case ofACD.


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ACD

ACD is inflammation of the skinmanifested by varying degrees oferythema, edema, andvesiculation.

It is a delayed type of inducedsensitivity (allergy) resulting from

cutaneous contact with a specificallergen to which the patient hasdeveloped a specific sensitivity.

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Pathophysiology: ACD

The pathology is a subepidermal blister withcollections of neutrophils present within the tipsof the dermal papillae associated with edema

(papillary microabscesses). Direct immunofluorescence (DIF) reveals a

granular deposits of IgA at the dermal papillae of

lesional and perilesional skin. It is not found inpatients with celiac disease who do not have theskin disease.


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Most chemicals able to provoke ACD have smallmolecules (


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Diagnosis :ACD

History: A detailed history, both before and afterpatch testing, is crucial in evaluating individualswith ACD.

Potential causes of ACD and the materials towhich individuals are exposed should be patchtested.

Patients with ACD require a much more detailedhistory compared to those with most other

dermatologic disorders.


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Clinical : ACD

Physical: Acute ACD is characterized bypruritic papules and vesicles on anerythematous base.

Lichenified pruritic plaques may manifestchronic ACD.

Occasionally, ACD may affect the entire

integument (ie, erythroderma, exfoliativedermatitis).

The initial site of dermatitis often provides thebest clue regarding the potential cause of

ACD.


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Frequency: the prevalence of contact dermatitis to be 13.6 cases per

1000 population using physical examinations bydermatologists of a selected sample of patients.. TheNational Ambulatory Medical Care Survey conducted in

1995 estimated 8.4 million outpatient visits to Americanphysicians for contact dermatitis. This was the secondmost frequent dermatologic diagnosis.

Of office visits to dermatologists, 9% are for dermatitis.At a student health center dermatology clinic, 3.1% of

patients presented for ACD, and 2.3% presented forirritant contact dermatitis.

Internationally: A Swedish study found that prevalenceof ACD of the hands was 2.7 cases per 1000 population.

A Dutch study found that prevalence of ACD of thehands was 12 cases per 1000 population.

Epidemiology: ACD


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Epidemiology: ACD

Sex: ACD is more common in women than inmen.

This predominately is a result of allergy to

nickel, which is much more common inwomen than in men in most countries.

Age: ACD may occur in neonates. In elderly

individuals, the development of ACD may bedelayed somewhat, but the dermatitis may bemore persistent once developed


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Mortality/Morbidity: ACD

Death from ACD is rare in the US. ACD to theweed wild fever few caused deaths


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ACD

Picture 1. Onycholysis developingfrom allergic contact dermatitis toformaldehyde used to harden nails

Picture 2. Nickel contact allergy
http://www.emedicine.com/cgi-bin/foxweb.exe/makezoom@/em/makezoom?picture=/websites/emedicine/derm/images/Large/829hogan5ACD.jpg&template=izoom2


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Allergic Contactstomatitis/Mucositis


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Allergic Contactstomatitis/Mucositis

A contact allergy in the mouth or contactstomatitis is a hypersensitivity mechanism

of the cellular or delayed type and is, likecontact dermatitis on the skin, the resultof a sensitization to a substance withwhich one has previously come in

contact, the "contact allergen".


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a contact stomatitis produces primarilysubjective symptoms: loss of the sense of

taste, numbness, burning sensations, and pain(rarely itching), and sometimes evencomplaints of generalized itching, dizziness,headache, gastro-intestinal problems, and

malaise.

Allergicstomatitis/Mucositis


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Allergic

stomatitis/Mucositis Immediate hypersensitivity to

drugs or contact allergy may often

lead to inflammatory oral mucosalred lesions.

Antibiotics, sulfonamides,barbiturates and iodine are

capable of causing hypersensitivereactions.


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symptoms can be unpleasant and include pain,numbness, a burning sensation and loss of taste

Unlike contact allergic dermatitis, which can spread

to other parts of the body, the effects of allergiccontact stomatitis remain confined to the mouth,strictly where direct physical contact has occurred.

Fortunately the condition is rare, as in most people

saliva dilutes and washes the allergens away.

Burning of the mucosa or itchiness are consistentfeatures in both hypersensitive and contact allergy

patients.

Allergicstomatitis/Mucositis


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Clinical Feature Allergicstomatitis/Mucositis

1. Diffuse mucosal redness is the hall mark ofallergic mucositis.

Pseudomembrane and desquamation of

epithelium may occur in some cases Contact allergic respone on the other hand is

generally discrete.

The redness occurs in the area that is in direct

contact with the allergen


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Some known allergens include; dental materials, topical medications, cosmetics,. toothpaste, including any dyes they contain mouthwash medication applied within the mouth, such as lozenges for sore

throats and ulcers fillings, crowns, dentures etc. lipstick nail varnish, if you bite your nails

nickel, from sucking jewellery foods

Allergen in the chewing gum can sometimes evoke a generalizederythematous respone of the oral mucosa and the gingiva. Thiscondition is called plasmacytosis gingivae

Allergen of Allergic stomatitis/Mucositis


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Treatment of Contact Allergic

Stomatitis History and elimination of the known allergen are

of the most importance in the diagnosis and

management of these conditions. Try to identify the cause of your contact allergic

stomatitis and then avoid it.

Antihistaminics help to control systemic reaction

and Triamcinalone acetonide in orabase isuseful for contact allergy


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Irritant stomatitis

Caused by irritant agents ; Self CuringAcrylic Resin, H2O2`,stain removalagent (Ocho), Acids

Direct injury from irritan (burning)

High concentration chemicals

burning mouth syndrome

trauma or physical injuries.


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Irritant stomatitis

Clinical signs are frequently lesspronounced than subjective symptoms,and patients commonly experience

severe functional problems despite onlymild mucosal alterations.


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The clinical manifestations of contactstomatitis are extremely variable and include

erythema, erosions, ulcerations, leukoplakia-like lesions, and lichenoid reactions.

Clinical Feature; Irritant

stomatitis


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Treatment of Irritant Stomatitis

A careful history and an accurate examination of the oralcavity, teeth, and dental restorations are essential for acorrect diagnosis

Patch testing is indicated in all lesions that are not clearlyrelated to trauma or physical injuries.

Successful treatment requires the identification andelimination of the causative factor, and

Used carefully and optimal concentration of chemicals

Topikal medication of lession


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Reaksi Hipersenstivitas

(Gell & Combs) Membagi berdasar kecepatan dan

mekanisme immun

Ada 4 tipe; tipe 1, tipe 2, tipe 3,tipe 4

Reaksi dpt terjadi sendiri-sendiri,atau bersamaan


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Type I Hypersensitivity

Allergy

Immediate type

Local anaphylaxis

Systemic anaphylaxis

IgE mediated hypersensitivity

Mast cells are involved

the antigen is typically called an allergen


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Anaphylaxis: Example ofType I Hypersensitivity

1. Types of Anaphylaxis

Generalized anaphylaxis

Cutaneous anaphylaxis - localized 2. Cutaneous anaphylaxis- local reaction

of antigen with homocytotropic antibody.

Contributor to spontaneous disease:hypersensitivity reactions to insect bites, post-

vaccinal wheal and flare reactions


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Generalized anaphylaxis

a. Pathogenesis and Mediator Release

Sensitization to antigen with IgEresponse

IgE binds to mast cells and basophils

Re-exposure causes degranulation ofmast cells

Mediators of immediate hypersensitivity

disease


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Mast cell product and


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Mast cell product andfunction

1) Histamine and serotonin:Increase venular permeability, induce smooth musclecontraction in pulmonary airways, cause arteriolar dilation

2) Leukotrienes:LTC4, LTD4, LTE4

Causes sustained smooth muscle contraction; may beimportant in prolonged airway constriction in immediatehypersensitivity reaction. LTB4: chemotactic for neutrophilsand eosinophils

3) Eotaxin: chemotactic for eosinophils; released from mast

cells4) PAF: released by basophils, neutrophils, macrophagesStimulate:Platelet aggregation, increased vascularpermeability, smooth muscle contraction,

5) Prostaglandins: PGE2 stimulates vasodilation


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Phase of Reaction Type IHypersensitivity

Sensitization Phase

Production Ig E Bind to FCe-R of Mast cell/basophil

Activation Phase

Re-exposure released granule of mast cell; MetilationPhospholipid membraneCa influx>> phospholipase

GlikolisisEnergigranule movement

cAMP degranulation

Effector Phase

Complex response from mediator of granule;histamin,bradikinin


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Alergen Sel B Sel Th2

Sel Plasma

Ig E

Sel Mast+IgE Alergen

Sel Mast

Degranulasi Sel Mast

Sel MasAmin Vasoaktif, sitokin


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Sel mast+IgE+Alergen

Degranulasisel mast Sekresimediator inflamasi Sekresi sitokin

Amin vasoaktif,

proteasePG

Leukotrin

TNF alfa

Delatasi vas,

Kerusakan jarDelatasi vas,

Kontraksi otot polos

Reaksi inflamasi


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Clinical manifestation

Erythem ( red) vena delatation

Edema release serum into tissue

bronchoconstriction Peak 10-15 min after re-

exposure


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Type II Hypersensitivity

Cytotoxic antibody -- IgG or IgM reacts withantigen on cells and then complement activationdestroys cells. (Also may have NK cell viaADCC cells involved)

Hemolytic disease of the newborn(erythroblastosis fetalis)

Transfusion reactions

Anti-streptococcal M-protein crossreacts withheart muscle in rheumatic fever malaria infectedRBCs coated with malaria antigens


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Type II Hypersensitivity - Cytotoxic Reactions

1. Examples

Autoimmune hemolytic anemia

Isoimmune hemolytic anemia andtransfusion reactions

Drug-induced hemolytic anemia(e.g.-penicillin)

Autoimmune thrombocytopenia


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Penyakit Hipersensitivitas Tipe 2

Anemia hemolitik autoimun; fagositosiseritrosithemolisis,anemia

Trombositopenia purpuraautoimun;fagositosisTrombositperdarahan

Vaskulitis;degranulasi netrofil & inflamasi Goodpasture;inflamasi oleh komplemen &R-Fc

nefritis

Demam reumaaktifasimakrofage,inflamasimiokarditis

Miastenia gravis: ikatan asetilkolin dihambatparalisis

Diabetes insulin resisten; Ab mencegah ikataninsulinhiperglikemia

Anemia pernisiosa; netralisasi faktor intrinsikenemia


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Goodpastures syndrome-Type II

smooth deposition


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2. Mechanisms:


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Komplek imune ( antigen+antibodi)

Aktifasi komplemen

Mediator inflamasi

Aktifasi makrofage Stimulasi sel mast

Release C3a dan C5a

Kerusakan jaringan

Mekanisme Kerusakan jaringan pada Hypersensitivitas Type III

T III H iti it I (T i )


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Type III Hypersensitivity - Immune (Toxic)

Complex Disease

1. Examples of Immune ComplexDisease

Serum Sickness

Immune ComplexGlomerulonephritis

Arthus reaction

Extrinsic Allergic Alveolitis

SLE


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Antigen-Antibody complexes formin antigen excess and aredeposited in vessel walls, joints

and glomeruli. Fixation of complement and

neutrophil infiltration induces tissuedamage and vasculitis, arthritis

and glomerulonephritis. Antigen, Antibody and complement

can be demonstrated in lesions

Serum Sickness as a model of immune

complex injury


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Serum Sickness as a model of immunecomplex injury


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Immune complex glomerulonephritis

1. Examples of immune complexglomerulonephritis

Viral Diseases Lymphocytic choriomeningitis

Equine infectious anemia Chronic hog cholera Aleutian mink disease Feline leukemia virus infection

Parasitic Diseases: Dirofilariasis Autoimmune diseases: Systemic lupus

erythematosus Idiopathic (largest group of cases)

M h i f f i f i i


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Mechanisms of formation of toxic immunecomplexes in glomeruli

Morphologic changes:


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Morphologic changes:glomerulonephritis

SLE Butterfly Rash


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SLE Butterfly Rash


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SLE

antibodies against DNA

Women, primarily affected

collection of syndromes, fever, joint

paint, CNS damage, kidneytype III hypersensitivity-leading to

glomerulonephritis

Type IV Hypersensitivity - Cell Mediated (T-cell


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yp yp y (

Hypersensitivity )

Mechanisms :1. Helper T-cell Mediated Hypersensitivity CD4


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2. Cytotoxic T-cell Mediated Hypersensitivity

CD 8
http://www.vetmed.ufl.edu/path/pbteach/wlc/vem5161/il85.gif


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Type IV

Type I DM

Arthritis reumathoid

Neuritis perifer Dermatitis kontak karena kimia

Sklerosis multiple


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Tugas

Kel Putra & Kel Putri;

Manifestasi Oral alergi

Presentasi besuk pagi oleh wakildari masing2x kelompok