Man Ali

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Transcript of Man Ali

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IMMUNOLOGICALDISEASES OF THE

ORAL CAVITYBY MISS MANALI NAGAONKAR

3RD

BDS

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RECURRENT APTHOUS STOMATITIS

• RECURRENT APTHOUS MAJOR

• RECURRENT APTHOUS MINOR

RECURRENT APTHOUS HERPITIFORM

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ETIOLOGY

• BACTERIAL INFECTION

• IMMUNOLOGICAL ABNORMALITIES

• IRON VIT B 12 DEFICIENCY ….FOLIC ACID

DEFICIENCY• ENDOCRINE

• TRAUMA

•PRECIPITATING FACTORS

• PSYCHIC FACTORS

• ALLERGIC FACTORS

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RECURRENT APTHOUS MINOR

(CANKER SORES)• MORE IN WOMEN

• BTWEEN 10 TO 30 YRS OF AGE SINGLE OR MULTIPLESOLITARY ,COVERED BY GREY MEMBRANE,NECROTICCENTRE ,ERYTHEMATOUS HALO

VERY PAINFUL,DIFFICULTY IN SPEECH AND EATING• 2 TO 3 MM IN DIAMETER MANIFESTATIONS …..BURNING

SENSATION ,PARASTHESIA ,MALAISE,EDEMA ,VESICLE LIKELESIONS CONTAINING MUCUS

• SITES …..BUCCAL AND LABIAL MUCOSA ,BUCCAL AND

LINGUAL SULCI ,SOFT PALATE ,PHARYNX• PERSISTS FOR 7 TO 14 DAYS

• NO EVIDENCE OF SCARRING

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RECURRENT APTHOUS MAJOR

• LARGE,PAINFUL,1 TO 10 N NO ,MORE SEEN IN HIV

• SITE- LIPS ,CHEEK ,TONGUE,SOFT PALATE

• DYSPHAGIA AND PAIN

• 1 CM IN DIAMETER ,PERSISTS FOR UPTO 6 WEEKS

,LEAVE A SCRA UPON HEALING

• FEMALES MORE AFFECTED

• SEVERE FORM…..PENIS,VAGINA,RECTUM,LARYNX

,RHEUMATOID ARTHRITIS ,CONJUCTIVITIS

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RECURRENT APTHOUS HERPITIFORM

• CROPS OF MULTIPLE,SMALL ,SHALLOW ULCERS ,UPTO 100IN NO

• SITE ….IN THE ORAL CAVITY

• LESIONS ON THE INTRA ORAL MUCOSAL SURFACE

• AS SMALL PIN HEAD EROSIONS THAT ENLARGE• MORE PAINFUL

• PRESENT CONTINOUSLY FOR ONE TO THREE YRS

• TEMPORARY RELIEF WITH 2% TETRACYCLINE MOUTHWASH

NON KERATINISED MOVABLE AREAS ARE MOSTLY• AFFECTED

• SIMILAR TO HSV INFECTION

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HISTOLOGIC FEATURES

• MINOR APTHOUS SHOWS FIBRINOPURULENT

MEMBRANE

• INTENSE INFLAMMATION,LYMPHOCYTES ON

….PMNS ,LYMPHOCYTES ,EPITHELIAL

PROLIFERATION ,GRANULATION TISSUE

• TISSUE INVOLVEMENT GENERALLY

SUPERFICIAL

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NON-SPECIFIC MICRSCOPIC PICTURE

• Early – central zone of ulceration covered byfibrinoprulent memberane

• Connective tissue – increased vascularity andmixed inflammatory cellular infiltrate

• Marginal epthelium – spongiosis and

numerous mononuclear cells• Presence of band of lymphocytes intermixed

with histocyte in superficial connective tissue.

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DIFFERENTIAL DIAGNOSIS

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• No defINitive lab. Diagnosis, depends on theclinical presentation

• Lesions can be mistaken for recurrent

aphthous stomatitis include herpecticstomatitis, herpangina, erythema multiforme,

erosive lichen planus, pemphigus and

pemphigoid.

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TREATMENT AND PROGNOSIS

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Immune enhancement

• Levimisole

• Vaccine

Immunosupression, inflammatory suppression

• Prednisone• Triamcicinolo acetonide

• Betamithasone-17-benzoate

• Antihistamine

Antibiotics• Suspension ,topical

• Chloramphenicol.

• Broad-spectrum antibiotics.

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Diet supplementation.

• Vitamin B12,folic acid .

• Iron.

• Zinc sulfate.

Symptomatic treatment .

• Xylocaine/lidocaine.

• Silver nitrate .

• Benadryl ,topical.

• Camphor – phenol .

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BEHCTES SYNDROME

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• Disease of uncertain etiology .

• May resemble infectious diseases.

• National institute of health in 1977- humoral

antibodies and cell mediated immune responsesmay act either jointly or independently upon oralepithelium .

• Recurrent aphthous ulcer and Behcet ‘s syndromecan not be distinguished by antibodies and cellmediated immune responses .

• HLA MARKERS DIFFERENTIATE

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CLINICAL FEATURES

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• More common in young adults (25 to 40 yrs).

• 5 to 10 times more common in males .

• Characterized by oral , genital ulcerations and ocular , skin lesions .

• First manifestation – appearance of oral and genital lesions witherythematous border .

• Genital ulcers are small located on scrotum, root of the penis ,orlabia majora .

• Ocular lesions – photophobia ,irritation , simple conjunctivitisuveitis

• Skin lesionssmall puspules or macules , erythema nodosum and

erythema multiform.• DISTINGUISHING FACTORS – CLASSIC TRIAD OF THE DISEASE

PRESENT

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A common case of HLA B 27 UVEITIS

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Histologic features :

• Nonspecific remarkably similar to recurrentaphthous ulcer .

• Endothelial proliferation .

• Vasculitis .Laboratory findings .

• Hypergyamaglobulinemia .

Mucocytrosis• Eosinophilia .

• Elevated ESR .

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TREATMENT AND PROGNOSIS

SYMPTOMATIC OR SUPPORTIVE MEASURES

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REITERS SYNDROME

• TYPICAL TETRAD ….NON ONOCCAL URETHRITIS,ARTHRITISCONJUNCTIVITIS,MUCOCUTANEOUSLESIONS

MALE TO FEMALE RATIO ….9 : 1• URETHRITIS IS THE FIRST SIGN

• ARTHRITIS …BILATERAL POLYARTICULAR 

• SKIN LESIONS – RED OR YELLOW KERATOTICMACULES OR PAPULES WHICH DESQUAMATE

• HLA B 27 IS THE FACTOR PRESENT ,SEEN IN HIV

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SITES …. 

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ORAL MANIFESTATIONS

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• Painless ,red,slightly elevated areas

,sometimes granular or even vesicular with

white circinate border on buccal mucosa ,lips

and gingiva .(pindborg etal)

• Palatal lesions – small bright red purpuric spot

which darken and coalesce .

• Geographic tongue appearance

• Circinate balanitis

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GEOGRAPHIC TONGUE

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Histologic features.

• No diagnostic findings .

• Parakeratosis ,acanthosis and

polymorphonuclear leukocyte infiltration of 

epithelium .

• Microabscess formation .

• Connective tissue – lymphocyte and plasma

cell infiltrate .

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Sarcoidosis (boeck’s sarcoid ,besnier-

boeck-schaumann disease)• Multi system granulomatious disease of unknown origin

characterized by the formation of uniform discrete compactnoncaseating epitheloid granulomas ,black>white .

• Etiology – infective and non infective .

Most favored infective (mycobacterium and propionibacterium).

• Associated with tuberculosis .(Gupta D et al)

• Most common in lungs ,skin , lymph nodes ,salivaryglands,spleen and bones.

DEPRESSION OF DELAYED TYPE HYPERSENSITIVITY,IMPAIREDCELL MEDIATED IMMUNITY ,INCREASE OR ABNORMALSERUM IMMUNOGLOBULINS ,LYMPHOPROLIFERATION

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Clinical features .

SITES …LUNGS,SKIN,LYMPH NODES,SALIVARY

GLANDS ,SPLEEN AND BONE

• Commonly seen in young and middle age.

• Mild malasise and cough – chief features .• Cutaneous lesions – 25 to 35 %.

• Multiple red patches that occur in group growslowly and do not tend to ulcerate .

• Hepatomegaly and splenomegaly .

• ERYTHEMA NODOSUM

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MULTIPLE RED PATCHES

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Oral manifestation .

• Sarcoid granulomas – labial glands – 58%.

• Lesions on lip – small papular nodules or

plaques resemble fever blisters .

• Palate and buccul mucosa- bleblike ,

containing clear yellowish fluid OR SOLID

NODULES

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Histologic features .

• No acid fast organisms can be demonstrated .

• Nest of epithelioid cells with multinucleated

giant

• cells-chief feature .

• Also contains T and B cells, various

immunoglobulins .

• Caseation and necrosisn do not occour .

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Uveoparotid fever .

• Form of sarcoidosis .• Firm painless usually bilateral .Enlargement of parotid gland

• Inflammation of uveal tracts of the eye , cranial nerve involvement,submandibular sublingual and lacrimal gland involvement .

• Often presence of chronic low grade fever .

• Symptoms :• Lassitude

• Malaise

• Vague GI disturbances , nausea , vomiting .

• Xerostomia

• Patchy erythema on skin.

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• Enlargement of cervical lymph nodes .

• Lesions – uveoparotitis,conjunctivitis,uveitis , keratitis ,CORNEAL HERPES

• Signs and symptoms disappears in time

while parotid swelling and visualdisturbance may persist

• SEVENTH NERVE PARALYSIS .

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MIDLINE LETHAL GRANULOMA

• IDIOPATHIC PROGRESSIVE DESTRUCTION OF THENOSE ,PARANASAL SINUS ,PALATE ,FACE ANDPHARYNX

• DYSFUNCTION OF IMMUNE MECHANISM

…..GRANULOMA FORMATION • AFFECTED PERSON LACKS RESISTANT TO THE

PROGRESS OF THE DISEASE

• ASSOCIATD WITH NEOPLASTIC ANDINFLAMMATORY DISEASE

• MOST UNUSUAL CONDITION

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CLINICAL FEATURES

• ULCERATION OF PALATE AND NASAL SEPTUM ,STUFFINESS IN

THE NOSE

• PALATAL AND NASAL AND MALAR BONES INVOLVES

• PURULENT DISCHARGE ,PERFORATING SINUS TRACTS

,SLOUGHING OF THE SOFT TISSUES LEAVING A DIRECT

OPENING INTO THE NASOPHARYNX AND ORAL CAVITY

• VASCULAR ALLERGY ,ARTHUS PHENOMENON,PERIARTERITIS

NODOSA ,

• PATIENT ULTIMATELY DIES OF EXHAUSTION OR OF

HAEMORRHAGE IF A LARGE BLOOD VESSE BECOMES ERODED

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Histologic features:

• Extensive necrosis with infiltration of some inflammatory cells

• the formation of occasional new capillaries .

• TREATMENT:

Usually fatal diseases .• Corticosteriod therapy .

• Coupled with antibiotics for secondary infection .

• Some authorities believe that the disease is best treated with

high dose of radaition therapy.

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WEGENER’S GRANULOMATOSIS 

• CLINICAL FEATURES

• INFANTS TO ELDERLY ,MAJORITY IN 4 TH OR 5 TH DECADE OF

THE LIFE

• MALE PREDOMINANCE

• RHINITIS,OTITIS,SINUSITIS

• COUGH,HEMOPTYSIS,FEVER,JOINT PAINS,HAEMORRHAGIC OR

VESICULAR SKIN LESIONS

GRANULOMATOUS LESIONS OF THE LUNG• GLOMERULONEHRITIS …..UREMIA…..TERMINAL RENAL

FAILURE

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Oral manifestations

• Involvement of gingiva strawberrygingivitisulcerations

• Starts from interdental papilla-spreads toperiodontal structures and lead to bone loss ,

tooth mobility .• Hyperplastic gingivitis(Israelson et al)

• Ulceration of palate due to extension of diseasefrom nose.

• Spontaneous exfoliation of teeth and failure of healing after removal of tooth.

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STRAWBERRY GINGIVITIS

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HISTOLOGIC FEATURES

• MIXED INFLAMMATION AROUND THE BLOOD

VESSELS

• VASCULITIS

• ORAL BIOPSY ….PSEUDOEPITHELIOMATOUS

HYPERPLASIA AND SUBEPITHELIAL ABSCESS

• GINGIVAL LESIONS …SCATTERED GIANT CELLS

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Laboratory findings

• Anemia

• Leukocytosis

• Elevated E.S.R.

• Hyperglobinemia

• Hematuria

Some patients- circulating immune complex.

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TREATMENT

• PREDNISONE

• CYCLOPHOSPHAMIDE

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Chronic granulomatous disease

• Uncommon herediatary CONDITION caused due x

linked mode of tranmission.

• Majority patients are males

• Characterised by severe reccurent infection as aresult of defect of intracellular leukocyte enzyme

formation

• Failure to destroy catalase positive organism.

A VARIANT TRANSMITTED AS AN AUTOSOMAL

RECESSIVE CHARACTERISTIC

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CLINICAL FEATURES

CLINICAL FEATURES

INFECTION FROM INFANCY …..LUNG

,LIVER,SPEEN,BONE,ECZEMATOUS LESIONS ON

THE FACE ,LEADING TO NECROSIS AND

GRANULOMA FORMATION

ABSCESS ,SEPTICAEMIA

,PNEUMONIA,PERICARDITIS ,MENINGITIS,OSTEOMYLELITIS

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Oral manifestation

• Diffused stomatitis with or without solitary or

multiple ulcerations.

• benign migratory glossitis

• Enamel hyperplasia in very rare cases

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Histologic features

• Small granulomas with mononuclear

histocytes

• Multiple inulated giant cells

• Central necrosis with polymorphonuclear

leukocyte may also be present.

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Diagnosis and treatment

• Diagnosis:- neutrophil function test

• Treatment :- vigorous treatment of infection

Angioedema (angioneurotic edema

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Angioedema (angioneurotic edema,

Quincke’s edema)

• Diffused erythematous swelling of skin mucosa and submucosal connective tissue.,

• Results in death due to GI or respiratory tractinvolvement.

• Pathogenesis:-

1] allergic angioedema (due to mast cell degradation)

2] associated with use of ACE inhibitors

3]activation of complement pathway• Presence of high level of antigen antibody complex

• Grossly elevated peripheral blood eosinophillic count.

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Clinical features

• Soft,non tender,diffuse edematous,solitary ormultiple

• Lips ,chin,eyes,tongue,pharynx,larynx,hands,arms,legs,genitals

and buttocks• Enlargement usually resloves within 24 to 72 hrs

• Git symptons include pain ,vomitting,waterydiarrhoea

• Perioral or periorbital oedema

• Skin colour normal or slightly pink

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TREATMENT

Antihisatmines

Laryngeal involvement ….intramuscular

epinephrine

Iv corticosteroids

C1 – inh deficiency respond to intubation and

tracheotomy

Androgens such as danazol ,stanazol for

hereditary and acquired form

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Drug allergy

• IGE MEDIATED REACTIONS …ANTIBODY BINDS

TO THE DRUG THAT IS ALREADY ATTACHED TO

THE CELL SURFACE

• IN NON IMMUNOLOGIC DRUG REACTIONS,DRUGS DIRECTLY AFFECT THE MAST CELLS

WHICH CAUSES RELEASE OF CHEMICAL

MEDIATORS

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Clinical features :

• Skin lesions , arthralgia ,fever,

lymphadenopathy and rarely agranulocytosis .

• Common drugs aspirin , barbiturates ,

chloromphenicol, tetracycline ,penicillin ,streptomycin and sulphonamides .

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treatment

• Antihistamines (cortisone)

• Adrenaline

• Corticosteroids

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Oral manifestation .

• Stomatitis medicamentosa .

• Ulceration, necrosis, hemorrhage , gingivalhyperplasia.

• Altered salivary function .

• Altered taste sensation.

• Allergic reactions erythema multiforme ,

• Negative patch taste .

•Localized erythema and edema .

• Gingiva – necrotizing gingivitis or vincent’s diseases .

• Hairy tongue .

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HAIRY TONGUE

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CONTD

• Intraoral fixed drug reactions

• Lichenoid drug reactions

• Elongation and staining of filiform papillae

,producing a heavy coating of the tongue

• Anaphylactic stomatitis

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Histologic features.

• Non specific patterns .

• Admixture of lymphocytes ,eosinophils and

neutrophils .

• Vacuolar changes of basal layer and individual

necrotic epithelial cells .

• Distinctive annular fluorescence

pattern.(string of pearl’s ). 

• Basal cell cytoplasmic antibody .

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Treatment

• Antihistamines ( cortisone )

• Adrenaline

• Corticosteroids

• Anaphlactic stomatitis …antihistamines

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Contact stomatitis and dermatitis

• Causative agent chemical in nature

• Haptens

• Require conjugation with proteins to become

effective

• Process occurs with the aid of intra epithelial

langerhans cells

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• DENTAL OR COSMETIC PREPARATIONS .

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1. Dentrifrices .

2. Mouth washes .

3. Denture powder .

4. Lipsticks , candy ,cough drops, chewing gum .

• DENTAL MATERIALS :

1. Rubber dam .

2. Vulcanite .

3. Alcrylic .

4. Metal alloy base .

DENTAL THERAUPATIC AGENTS :1. Alcohols

2. Antibiotics

3. Iodides ,phenols

4. Procaine .

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Clinical features

• Stomatitis venenata

• Itching and burning sensation

• Skin becomes rough and dry

• Appearance of erythema

• Vesicle formation

Vesicle rupture …it becomes more severe

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Oral manifestations .

• Mucosa – remarkably inflamed and edematous .

• Bright red gingiva in all quadrants .

• Buccal mucosa – puffy , dark red , revealing ,engorged and

ejected superficial capillaries on closure examination .

• Zone of ulceration – lips .

• Chronic cases – mucosaerythematous , hyperkeratotic

• Scaling , fissuring , or cracking of vermillion lip border.

Contact stomatitis .

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Histologic features

• Intra and inter cellular edema of the

epithelium along with the vesicle formation

within the epithelium or at the basement

membrane• Increased eosinophils

• Lymphocytes and plasma cells

• Engorged and dilated blood vessels

• Connective tissue – edema

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Diagnosis and treatment .

• Diagnosis – patch test

• Treatment- removal of offending material

Contact stomatitis with cinnamon

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Contact stomatitis with cinnamon

flavouring

• Toothpaste –plasma cell gingivitis ,edema

,erythema

• Erythematous mucositis of the buccal mucosa

and tongue ,exfoliative chilitis ,circumoraldermatitis

• Lingual keratosis

• Buccal mucosa – oblong,hyper keratotic

lesions with an erythematous base

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Contact stomatitis .

• Cinnamon oils –flavoring agent .

• Used in ice-cream , soft drinks alcoholic

beverages processed meats ,gum , candy

,tooth paste and mouth washes .

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l f

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Histologic features .

• Acanthotic epithelium with elongated reteridges thinned suprapapillary palates .

• Hyperkeratosis and neutrophil exocytosis is

observed .• Connective tissue exhibits a diffuse chronic

inflammatory infiltrate predominantlyconsisting of lymphocytes .

• Characteristic perivascular infiltration of lymphocytes .

d

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Treatment and prognosis

• Reaction disappears within a week of 

discontinuance of cinnamon products

• Reappears with use of cinnamon products

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Contact stomatitis from chronic oral

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Contact stomatitis from chronic oral

mucosal contact with dental amalgam

• neurotoxicity ,kidney dysfunction, reduced

incompetence, alterations of oral and

intestinal flora , birth defects ,

• Contact lichenoid reactions to amalgam

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B f l

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Because of gloves …. 

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Cli i l d hi t l i l f t

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Clinical and histological features .

• Commonly seen in posterior buccal mucosa,ventral borders of the tongue and gingival cuffsadjacent to subgingival amalgam restorations.

White or ertythematous with or without striae .• Histologically features similar to lichen planus like

hydropic degeneration of basal cell layer .

• Hyperkeratotic or atropic epithelium ,and dense

band- like chronic inflammatory infiltrateconsisting predominantly of lymphocytes areobserved

T t t d i

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Treatment and prognosis .

• Improving oral hygienic ,smoothening,polishing ,and recontouring of the restoration

before adopting aggressive measures .

• Amalgam replaced with a non-metallicrestoration .

P i l d titi

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Perioral dermatitis

• Skin disease of the circum oral area due totartar control,bubble gum ,night creams

,toothpaste, moisturizers

• Topical corticosteroids is inciting agents

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Cli i l f t

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Clinical features

• Pruritis

• Female predominance

• Lesions as papules or papulopustules

• Surface surrounding the vermillion border of 

the lip ,with zone of spared skin immediately

adjacent to the vermillion border .

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Hi t l i f t

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Histologic features

• Rosacea like pattern

• Chronic lymphohistiocytic dermatitis

• Mimicking sarcoidosis

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T t t d i

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Treatment and prognosis .

• topical corticosteroid and prescribing topicalmetronidsazole

• With out topical tetracycline .

• Recurrences are uncommon.

Bibliography

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Bibliography

• Shafer’s textbook of oral pathology

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