Diagnostic Hierarchy for Chronic Headache and OroFacial pain free download

Diagnostic Hierarchy for Chronic Headache and OroFacial pain

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Diagnosis Chart for Oral Mucosal Lesions

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Note on Necrotizing Sialometaplasia

Itis spontaneous condition of an unknown cause usually of the palate in whichlarge area of the surface epithelium underlying connective tissue and all theassociated minor salivary glands become necrotic while the ducts under gosquamous metaplasia. 

Clinicalfeatures:

Usuallythe location is at the junction of the hard and the soft palatebut it may alsobe present at tongue, retromolar pad and the nasal cavity.

NSMis characterized by deep seated ulceration it is punched out

Within its deep crater are the gray granular lobules which represents the necroticminor salivary glands.

Itis 2-3 cm in diameter.

Itis asymptomatic but there may be numbness or burning pain.

Histopathology:

Inthe palatal epithelium there is no zone of ulceration which replaced by fibringranulation tissue.

Thelobules of minor salivary glands undergo coagulation necrosis.

Therescattered neurophils and foamy histocytes present in zone of necrosis.

Treatment:

Notreatment is required once the diagnosis is confirmed by histologicalexamination .

Theulcer area heals by its self with in 1-3 months.

Necrotizing Sialometaplasia

Necrotizing Sialometaplasia

Notes on Sialolithiasis-Clinical features, Investigations, Histopathology and Treatment

Sialolithiasis

Thereis presence of one or more round or oval calcified structures in the duct ofthe major or minor salivary glands( salivary stones)

Howthe stone is formed:

Itis assumed that mucin proteins and desquamated ductal epithelial cells form asmall nidus on which the calcium salts are precipitated, this nidus then allowsconcentric lamellar crystallizations to occur and thus sialolith increases insize as a layer by layer gets deposited on it

Clinicalfeatures of sialolithiasis:

About80%of sialolith affects the major salivary glands and there is more predilectionsfor the submandibular gland.

Stonesare rare in children the average age is the 4^th decade with no sex preference.

Theyare asymptomatic discovered on dental radiographs.

Ifsymptomatic the chief complains are pain and swelling . Swelling is results asthere is ductal dilatation caused by the ductal blockade.

Thepain is described as pulling drawing or stinging.

SialolithiasisInvestigations:

Panoramicradiograph.

Ultrasound imaging

orsailography

Histopathologyof sialolithiasis:

Stone: On gross examination moststones are yellow or white in colour. they may be round to oval

  - some of the stones are nodular

  - after decalcification the stone showsconcentric rings as of the annual rings of a tree trunk

   -The stone is acellular and amorphous innature and may contain microbial colonies.

Ducts: the ductal lining thatsurrounds sialolith shows variety of reactive changes.

   - there is squamous and mucus cell

     metaplasia and changes to stratifiedsquamous epithelium with numerous mucous goblet cells

Sialolithiasistreatment:

• Manyof the major salivary gland sialoliths can be removed by manipulation of thestone through major duct orifice
• Whenmanipulation fails then a surgical cut is made into the main duct
• Intriangular, or multiple stones and long standing obstructions removal of thestone and sialadenectomy is done.

Notes on Mucocele and Mucous Retention cyst-Etiology,Clinical Features,Differential Diagnosis and Treatment

Salivary glands react to injury or obstruction by undergoing atrophic degeneration and necrosis with replacement of the parenchyma byinflammatory cells and ultimately fibrous scar formation

Mucocele

It is a tissue swelling composed of pooled mucus thatescapes into the connective tissue from several excretory ducts

Mucocele

Whensalivary duct is severed the acinar cells will continue to secrete saliva intothe severed duct.

Atthe site of the cut/severance the secretory product escape into the connectivetissue forming a pool of mucus that distends the surrounding tissue.

Etiology:

Minorglands of the lip are most prone to severance as a result of injury or bitingthe mucosa.

Intraoral minor salivary can also be effected as result of some irritation as well.

Clinicalfeatures

Mostlyencountered in children and young adults.

Twothird of the mucoceles occur in the 3^rd decade of life.

Bothmales and females are effected equally.

Site:mucosal surface of the lower lip

              buccal mucosa

              floor the mouth

              ventral of the tongue and palate

Clinicalappearance of the mococele depends on its location within the submucosa

Moresuperficial zones of mucous extravasations presents a fluctuant mass withbluish translucent appearance.

Patientusually feels the mucocele and the fluctuation in its size

Painis quite rare .

Initiallythe mucocels are well circumscribed but with repeated truma they become nodular,more diffuse and firm on palpation.

Themucoceles have finely vascularized and distended, appearance often referred toas frogs belly that’s why they are also called Ranulas

Whenpart of this ranula is deep seated in to the sumental or submandibular spacethen the term used is the” Plunging Ranula”

Differentialdiagnosis

• Mucoepidermoidcarcinoma
• Cavernoushemangeoma (when there is hemorrhage)
• Blistersseen in some bullous and desqumative disease.

Histopathology:

Underlyingpool of mucin distends the sarface epithelium.

Themucin is walled of by the rim of granulation tissue or in long standing casesby condensed collagen.

Anepithelial lining is lacking

Themucinous material  basophilic oracidophillic and contains  neutrophilsand large oval foam cells the histocytes .

Thebase of the mucocele will reveal feeder duct.

Longstanding mucoceles will show acinar degeneration with fibrosis and minimalinflammation .

Treatment:

Minorsalivary gland mucocele will not resolve on its own it must be surgicallyexcised.

Tominimize the chances of recurrence the feeder gland should also be removed.

Postsurgical parasthesia might occur when the branches of the mental nerve aresevered

Surgical Removal of Mucocele-Video

Mucusretention cyst

Itis a swelling caused by an obstruction of a salivary gland excretory ductresulting in an epithelial lining cavity containing mucus. Mucus retention cystis sometimes also referred as Sialocyst

Themucus retention cyst is lined by epithelium and rarely occur in the majorsalivary gland, when they do occur they are multiple i.e. poly cystic diseaseof the parotid gland

Clinicalfeatures:

Encounteredin adults from 3^rd -5^th decade.

Thelesion is painless and fluctuant and at times bluish in appearance.

Site:parotid cysts are located in the   superficial lobe as fluctuant well defined mass.

    -with in the oral cavity the floor of themouth is the most common place.

    -this is followed by the lip and the buccalmucosa

Histopathology:

Theepithelium of the cyst is stratified cuboidal or columnar duct like epithelium.

Thecytoplasm in the of these cells is either clear or eosinophlic and my show somefeatures mucous differentiation

70%of these cyst are unilocular rest of the 30% have multilocular pattern.

 

Treatment:

Simpleexcision is the treatment of choice with caution of rupturing the cystic sacs.

Recurrenceis rare.

Howeverdamage to the adjacent gland may result in a mucocele formation.

Common Vesiculobullous Diseases Etiology,Clinical Presentation,Microscopic findings,Diagnosis,Differential diagnosis and Treatment

Epidermolysis Bullosa

Etiology

• A diverse group ofpredominantly cutaneous, but also mucosal, mechanobullous diseases

• Inherited form:autosomal dominant or recessive patterns may occur

• Acquired form(acquisita): autoimmune from autoantibodies (immunoglobulin G [IgG]) to typeVII collagen deposited within the basement membrane zone and upper dermis orlamina propria

Clinical Presentation

• Variable, dependingupon the specific form of many subtypes recognized

• Mucosal lesionsrange in severity from mild to debilitating, depending on subtype:

• Inherited forms havewide range of oral mucosal involvement, with most severe form (autosomalrecessive, dermolytic) also demonstrating enamel hypoplasia and caries

• Acquisita form withmucous membrane pemphigoid variant shows oral and conjunctivalerosions/blisters

• Mucosal involvementabsent in several variants

• Scarring andstricture formation common in severe recessive forms

• Mucosa is oftenfriable, but it may be severely blistered, eroded, or ulcerated.

• Loss of oralanatomic landmarks may follow severe scarring (eg, tongue mucosa may becomesmooth and atrophic with episodes of blistering and scarring).

• Obliteration ofvestibules, reduction of oral opening, ankyloglossia

• Scarring can beassociated with atrophy and leukoplakia, with increased risk for squamous cellcarcinoma development.

Microscopic Findings

• Bullae vary inlocation depending upon the form that is present:

• Intraepithelial innonscarring forms

• Atepithelial–connective tissue junction in dystrophic forms

•Subepithelial/intradermal in scarring forms

• Ultrastructuralfindings are as follows:

• Intraepithelialforms associated with defective cytokeratin groups

• Junctional formsassociated with defective anchoring filaments at hemidesmosomal sites(epithelial–connective tissue junction)

• Dermal typesdemonstrate anchoring fibril or collagen destruction.

Diagnosis

• Distribution oflesions

• Family history

• Microscopicevaluation

• Ultrastructuralevaluation

• Immunohistochemicalevaluation of basement membrane zone using specific labeled antibodies asmarkers for site of blister formation

Differential Diagnosis

• Varies with specificform

• Generally includesthe following:

• Bullous pemphigoid

• Mucous membrane(cicatricial) pemphigoid

• Erosive lichenplanus

• Dermatitisherpetiformis

• Porphyria cutaneatarda

• Erythema multiforme

• Bullous impetigo

• Kindler syndrome

• Ritter’s disease

Treatment

• Acquisita form:

• Some recent successwith colchicine and dapsone

• Immunosuppressiveagents including azathioprine, methotrexate, and cyclosporine may be effective

• Acquisita andinherited forms:

• Avoidance of trauma

• Dental preventionstrategies including extra-soft brushes, daily topical fluoride applications,dietary counseling

Prognosis

• Widely variabledepending on subtype

Erythema Multiforme

Etiology

• Many cases precededby infection with herpes simplex; less often with Mycoplasma pneumoniae or other organisms

• May be related todrug consumption, including sulfonamides, other antibiotics, analgesics, phenolphthalein-containinglaxatives, barbiturates

• Another trigger maybe radiation therapy.

• Essentially animmunologically mediated reactive process, possibly related to circulatingimmune complexes

Clinical Presentation

• Acute onset ofmultiple, painful, shallow ulcers and erosions with irregular margins

• Early mucosallesions are macular, erythematous, and occasionally bullous.

• May affect oral mucosaand skin synchronously or metachronously

• Lips most commonlyaffected with eroded, crusted, and hemorrhagic lesions (serosanguinous exudate)known as Stevens-Johnson syndrome when severe

• Predilection foryoung adults

• As many as one-halfof oral cases have associated erythematous to bullous skin lesions.

• Target or iris skinlesions may be noted over extremities.

• Genital and ocularlesions may occur.

• Usuallyself-limiting; 2- to 4-week course

• Recurrence iscommon.

Diagnosis

• Appearance

• Rapid onset

• Multiple siteinvolvement in one-half of cases

• Biopsy results oftenhelpful, but not always diagnostic

Differential Diagnosis

• Viral infection, inparticular, acute herpetic gingivostomatitis (Note: Erythema multiforme rarelyaffects the gingiva.)

• Pemphigus vulgaris

• Major aphthousulcers

• Erosive lichenplanus

• Mucous membrane(cicatricial) pemphigoid

Treatment

• Mild (minor) form:symptomatic/supportive treatment with adequate hydration, liquid diet, analgesics,topical corticosteroid agents

• Severe (major) form:systemic corticosteroids, parenteral fluid replacement, antipyretics

• If evidence of anantecedent viral infection or trigger exists, systemic antiviral drugs during thedisease or as a prophylactic measure may help.

• See “Therapeutics”section for details.

Prognosis

• Generally excellent

• Recurrences common

 

Hand-Foot-and-MouthDisease

Etiology

• A very commonenterovirus infection (coxsackievirus A10 or A16), which may occur in mild epidemicproportion, chiefly in children

• Incubation period isshort, usually less than 1 week

Clinical Presentation

• Oral mucosal lesionswith focal herpes simplex–like appearance, usually involving nonkeratinizedtissue (soft palate, floor of mouth, labial-buccal mucosa)

• Accompanying palmar,plantar, and digital lesions are deeply seated, vesicular, and erythematous

• Short course withmild symptoms

Diagnosis

• Concomitant oral andcutaneous lesions

• Skin lesionscommonly involve hands and feet.

• Skin lesions mayinvolve buttocks.

• Antibody-titerincrease measured between acute and recovery phases

Differential Diagnosis

• Herpangina

• Herpes simplexinfection

• Acute lymphonodularpharyngitis

Treatment

• Symptomatictreatment only

• Patient should becautioned against the use of aspirin to manage fever.

Prognosis

• Excellent

• Lifelong immunity,but it is strain specific

Herpangina

Etiology

• Most often bymembers of coxsackievirus group A (7, 9, 10, and 16) or group B (1–5)

• Occasionally due toechovirus 9 or 17

Clinical Presentation

• Incubation period of5 to 9 days

• Acute onset

• Usually endemic inyoung children; usually occurs in summer

• Often subclinical

• Posterior oralcavity, tonsillar pillars involved

• Macular erythematousareas precede short-lived vesicular eruption, followed by superficialulceration

• Accompanied bypharyngitis, dysphagia, fever, malaise, headache, lymphadenitis, and vomiting

• Self-limitingcourse, usually under 2 weeks

Diagnosis

• Other viralillnesses to be ruled out or separated

• Course, time ofyear, location of lesions, contact with known infected individual

Differential Diagnosis

• Hand-foot-and-mouthdisease

• Varicella

• Acute herpeticgingivostomatitis

Treatment

• Soft diet

• Hydration

• Antipyretics

• Chlorhexidine rinses

• Compounded mouthrinses

Prognosis

• Excellent

Herpetic Stomatitis:Primary

Etiology

• Herpes simplex virus(HSV)

• Over 95% of oral primary herpes due to HSV-1

• Physical contact ismode of transmission

Clinical Presentation

• 88% of populationexperience subclinical infection or mild transient symptoms

• Most cases occur inthose between 0.5 and 5 years of age.

• Incubation period ofup to 2 weeks

• Abrupt onset inthose with low or absent antibody to HSV-1

• Fever, anorexia,lymphadenopathy, headache, in addition to oral ulcers

• Coalescing, grouped,pinhead-sized vesicles that ulcerate

• Ulcers show ayellow, fibrinous base with an erythematous halo

• Both keratinized andnonkeratinized mucosa affected

• Gingival tissue withedema, intense erythema, pain, and tenderness

• Lips, perioral skinmay be involved

• 7- to 14-day course

Diagnosis

• Usually by clinicalpresentation and pattern of involvement

• Cytology preparationto demonstrate multinucleate virusinfected giant epithelial cells

• Biopsy results ofintact macular area show intraepithelial vesicles or early virus-inducedepithelial (cytopathic) changes

• Viral culture orpolymerase chain reaction (PCR) examination of blister fluid or scraping frombase of erosion

Differential Diagnosis

• Herpangina

• Hand-foot-and-mouthdisease

• Varicella

• Herpes zoster(shingles)

• Erythema multiforme(typically no gingival lesions)

Treatment

• Soft diet and hydration

• Antipyretics (avoidaspirin)

• Chlorhexidine rinses

• Systemic antiviralagents (acyclovir, valacyclovir) if early in course or in immunocompromisedpatients

• Compounded mouthrinse

Prognosis

• Excellent inimmunocompetent host

• Remission/latentphase in nearly all those affected who have adequate antibody titers

Impetigo

Etiology

• Cutaneous bacterialinfection: Streptococcus and Staphylococcus species

• Is spread throughdirect contact

• Highly contagious

Clinical Presentation

• Honey-colored,perioral crusts preceded by vesicles

• Flaccid bullae lesscommon (bullous impetigo)

Diagnosis

• Clinical features

• Culture of organism(usually group A, â-hemolyticstreptococci or group II Staphylococcusaureus)

• Herpes simplex(recurrent)

• Exfoliativecheilitis

• Drug eruptions

• Othervesiculobullous diseases

Treatment

• Topical antibiotics(mupirocin, clindamycin)

• Systemic antibiotics

Prognosis

• Excellent

• Rarely,poststreptococcal glomerulonephritis may develop.

Mucous MembranePemphigoid

Etiology

• Autoimmune; triggerunknown

• Autoantibodiesdirected against basement membrane zone antigens

Clinical Presentation

• Vesicles and bullae(short lived) followed by ulceration

• Multiple intraoralsites (occasionally gingiva only)

• Usually in olderadults

• 2:1 femalepredilection

• Ocular lesions notedin one-third of cases

• Proclivity forscarring in ocular, laryngeal, nasopharyngeal, and oropharyngeal tissues

Microscopic Findings        

• Subepithelial cleftformation

• Linear pattern IgGand complement 3 (C3) along basement membrane zone; less commonly IgA

• Directimmunofluorescence examination positive in 80% of cases

• Indirectimmunofluorescence examination usually negative

• Immunoreactantsdeposited in lamina lucida in most patients

Diagnosis

• Biopsy

• Direct immunofluorescentexamination

Differential Diagnosis

• Pemphigus vulgaris

• Erythema multiforme

• Erosive lichen planus

• Lupus erythematosus

• Epidermolysis bullosa acquisita

Treatment

• Topical corticosteroids

• Systemic prednisone,azathioprine, or cyclophosphamide

•Tetracycline/niacinamide

• Dapsone

• See “Therapeutics”section for details.

Prognosis

• Morbidity related tomucosal scarring (oropharyngeal, nasopharyngeal, laryngeal, ocular, genital)

• Management oftendifficult due to variable response to corticosteroids

• Management oftenrequires multiple specialists working in concert (dental, dermatology,ophthalmology, otolaryngology)

Paraneoplastic Pemphigus

Etiology

• Autoimmune,triggered by malignant or benign tumors

• Autoantibodiesdirected against a variety of epidermal antigens including desmogleins 3 and 1,desmoplakins I and II, and other desmosomal antigens, as well as basementmembrane zone antigens

Clinical Presentation

• Short-lived vesiclesand bullae followed by erosion and ulceration; resembles oral pemphigus

• Multiple oral sites

• Severe hemorrhagic,crusted erosive cheilitis

• Painful lesions

• Cutaneous lesionsare polymorphous; may resemble lichen planus, erythema multiforme, or bullouspemphigoid

• Underlying neoplasmssuch as non-Hodgkin’s lymphoma, leukemia, thymoma, spindle cell neoplasms,Waldenström’s macroglobulinemia, and Castleman’s disease

Microscopic Findings

• Suprabasilaracantholysis, keratinocyte necrosis, and vacuolar interface inflammation

• Directimmunofluorescent testing is positive for epithelial cell surface deposition ofIgG and C3 and a lichenoid tissue reaction interface deposition pattern

• Indirectimmunofluorescent testing is positive for epithelial cell surface IgGantibodies

• Special testing withmouse and rat bladder, cardiac muscle, and liver may demonstrate paraneoplasticpemphigus antibodies that bind to simple columnar and transitional epithelia

Diagnosis

• Biopsy of skin ormucosa

• Directimmunofluorescent examination of skin or mucosa

• Indirectimmunofluorescent examination of sera including special substrates

Differential Diagnosis

• Pemphigus vulgaris

• Erythema multiforme

• Stevens-Johnsonsyndrome

• Mucous membrane(cicatricial) pemphigoid

• Erosive oral lichenplanus

Treatment

• Identification ofconcurrent malignancy

• Immunosuppressivetherapy

Prognosis

• Good with excisionof benign neoplasms

• Grave, usuallyfatal, with malignancies

• Management is verychallenging.

Pemphigus Vulgaris

Etiology

• An autoimmunedisease where antibodies are directed toward the desmosome-related proteinsdesmoglein 3 or desmoglein 1

• A drug-induced formexists with less specificity in terms of immunologic features, clinicalpresentation, and histopathology

Clinical Presentation

• Over 50% of casesdevelop oral lesions as the initial manifestation

• Oral lesions developin 70% of cases

• Painful, shallowirregular ulcers with friable adjacent mucosa

• Nonkeratinized sites(buccal, floor, ventral tongue) often are initial sites affected

• Lateral shearingforce on uninvolved skin or mucosa can produce a surface slough or inducevesicle formation (Nikolsky sign)

Microscopic Findings

• Separation orclefting of suprabasal from basal layer of epithelium

• Intact basal layerof surface epithelium

• Vesicle forms atsite of epithelial split

• Nonadherent spinouscells float in blister fluid (Tzanck cells)

• Directimmunofluorescence examination positive in all cases

• IgG localization tointercellular spaces of epithelium

• C3 localization tointercellular spaces in 80% of cases

• IgA localization tointercellular spaces in 30% of cases

• Indirectimmunofluorescence examination positive in 80% of cases

• General correlationwith severity of clinical disease

Diagnosis

• Clinical appearance

• Mucosalmanifestations

• Direct/indirectimmunofluorescent studies

Differential Diagnosis

• Mucous membrane(cicatricial) pemphigoid

• Erythema multiforme

• Erosive lichenplanus

• Drug reaction

• Paraneoplasticpemphigus

Treatment

• Systemicimmunosuppression

• Prednisone, azathioprine,mycophenolate mofetil, cyclophosphamide

• Plasmapheresis plusimmunosuppression

• IVIg for somerecalcitrant cases

• See “Therapeutics”section for details.

Prognosis

• Guarded

• Approximately a 5%mortality rate secondary to long-term systemic corticosteroid–relatedcomplications

Recurrent HerpeticStomatitis: Secondary

Etiology

• Herpes simplex virus

• Reactivation oflatent virus

Clinical Presentation

• Prodrome oftingling, burning, or pain at site of recurrence

• Multiple, grouped,fragile vesicles that ulcerate and coalesce

• Most common onvermilion border of lips or adjacent skin

• Intraoralrecurrences characteristically on hard palate or attached gingiva (masticatorymucosa)

• In immunocompromisedpatients, lesions may occur in any oral site and are more severe (herpeticgeometric glossitis).

Diagnosis

• Characteristicclinical presentation and history

• Viral culture or PCRexamination of blister fluid or scraping from base of erosion

• Cytologic smear

• Directimmunofluorescence examination of smear

Differential Diagnosis

• Erythema multiforme

• Herpes zoster(shingles)

• Herpangina

• Hand-foot-and-mouthdisease

Treatment

• Acyclovir orvalacyclovir early in prodrome

• Supportive

• Acyclovir may beused for prophylaxis for seropositive transplant patients

• Ganciclovir may beused for human immunodeficiency virus (HIV)-positive patients, especially thoseco-infected with cytomegalovirus.

• For recurrent herpeslabialis, see “Therapeutics” section.

Prognosis

• Excellent

• Healing withoutscarring within 10 to 14 days

• Protracted healingin HIV-positive patients

Stevens-JohnsonSyndrome

Etiology

 • A complex mucocutaneousdisease affecting two or more mucosal sites simultaneously

• Most common trigger:antecedent recurrent herpes simplex infection

• Infection with Mycoplasma also may serve as a trigger.

• Medications mayserve as initiators in some cases.

• Sometimes referredto as “erythema multiforme major”

Clinical Presentation

• Labial vermilion andanterior portion of oral cavity usually affected initially

• Early phase ismacular followed by erosion, sloughing, and painful ulceration

• Lip ulcers appearcrusted and hemorrhagic.

• Pseudomembrane;foul-smelling presentation as bacterial colonization supervenes

• Posterior oralcavity and oropharyngeal involvement leads to odynophagia, sialorrhea, drooling

• Eye (conjunctival)involvement may occur.

• Genital involvementmay occur.

• Cutaneousinvolvement may become bullous.

• Iris or targetlesions are characteristic on skin.

Microscopic Findings

• Subepithelialseparation with basal cell liquefaction

• Intraepithelialneutrophils

• Epithelial andconnective tissue edema

• Perivascularlymphocytic infiltrate

Diagnosis

• Usually made onclinical grounds

• Histopathology isnot diagnostic.

Differential Diagnosis

• Pemphigus vulgaris

• Paraneoplasticpemphigus

• Mucous membrane(cicatricial) pemphigoid

• Bullous pemphigoid

• Acute herpeticgingivostomatitis

• Stomatitismedicamentosa

Treatment

• Hydration and localsymptomatic measures

• Topical compoundedoral rinses

• Systemiccorticosteroid use controversial

• Recurrent, virallyassociated cases may be reduced in frequency with use of daily, low-doseantiviral prophylactic therapy (acyclovir, famciclovir, valacyclovir).

• May requireadmission to hospital burn unit

Prognosis

• Good; self-limitingusually

• Recurrences notuncommon

Varicella and HerpesZoster

Etiology

• Primary and recurrent formsdue to varicella-zoster virus (VZV)

• Primary VZV (chickenpox): achildhood exanthem

• Secondary (recurrent) VZV(herpes zoster/shingles) infection: most common in elderly or immunocompromisedadults

Clinical Presentation

• Varicella(chickenpox)

• Fever, headache,malaise, and pharyngitis with a 2-week

incubation

• Skin with widespreadvesicular eruption

• Oral mucosa withshort-lived vesicles that rupture forming shallow, defined ulcers

• Herpes zoster(shingles)

• Unilateral, dermatomal, grouped vesicular eruption of skin and/or oral mucosa

• Vesicles maycoalesce prior to ulceration and crusting.

• Lesions are painful.

• Prodromal symptomsalong affected dermatome may occur.

• Pain, paresthesia,burning, tingling

• Postherpetic painmay be severe.

Diagnosis

• Clinical appearanceand symptoms

• Cytologic smear withcytopathic effect present (multinucleated giant cells)

• Viral culture or PCRexamination of blister fluid or scraping from base of erosion

• Serologic evaluationof VZV antibody

• Biopsy with directfluorescent examination using fluoresceinlabeled VZV antibody

Differential Diagnosis

• Primary herpessimplex/acute herpetic gingivostomatitis

• Recurrent intraoralherpes simplex

• Pemphigus vulgaris

• Mucous membrane(cicatricial) pemphigoid

Treatment

• Symptomaticmanagement in primary infection

• Antiviral drugs(especially acyclovir) in immunocompromised patients or patients with extensivedisease

• Systemiccorticosteroids may be used to help control/prevent postherpetic neuralgia.

• Pain control toprevent “CNS imprinting”

Prognosis

• Generally good

• Recurrences morelikely in immunosuppressed patients