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Spongiotic and psoriasiform reaction pattern Boštjan Luzar Institute of Pathology Medical Faculty, Ljubljana, Slovenia

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Spongiotic and psoriasiform reactionpattern

Boštjan LuzarInstitute of Pathology

Medical Faculty, Ljubljana, Slovenia

Spongiotic and psoriasiformreaction pattern

• Dynamic prosess• Different changes as the lesions evolve• Distinguishing clinical subtypes on histological

features frequently NOT possible• Patterns can overlap

– Some entities can have a variety of patterns(spongiotic and psoriasiform)

• Epidermis and dermis

Spongiotic reaction pattern

Spongiotic reaction pattern- Definition -

• Intraepidermal andintercellular edema(spongiosis)Widened

intercellularspaces Elongation of

intercellelarbridges

EARLY

Spongiotic reaction pattern

• Spongiosis Microscopic foci Vesicles Bullae DE juction

separation Crusting

• Exocytosis Lymphocytes Neutrophils Eosinophils

LATER

Pathogenesis of spongiosis

• Increased permeability of superficial vascularplexus– Immunological reactions– Direct damage– Unknown causes

• Increased hydrostatic pressure• Osmotic gradient towards the epidermis

Three phases of spongiotic dermatitis

• Acute• Subacute• Chronic

! There is a continuum of changes andhistological features frequently overlap

Acute spongiotic dermatitis- Changes in the epidermis -

• Stratum corneum retains normal basket-weave pattern

• Palor of keratinocytes• No acanthosis• Spongiosis

– Microvesicles

Acute spongiotic dermatitis

Acute spongiotic dermatitis- Changes in the dermis -

• Edema of the papillary dermis• Dermal perivascular inflammatory cell

infiltrate is variable Lymphocytes EosinophilsNeutrophils

Subacute spongiotic dermatitis

• Reactive changes of the epidermis Acanthosis (overlap with psoriasiform

pattern) Parakeratosis

• Granular layer may be diminished• Less spongiosis• Less dermal edema• Variable inflammation in the dermis, often

with eosinophils

Chronic spongiotic dermatitis

• Hyperkeratosis• Parakeratosis (with/without)• Acanthosis• No/little spongiosis• Granular layer thickened, irregular• Dermal inflammation mild• Dermal fibrosis can be present

Chronic spongiotic dermatitis

Conditions featuring spongiosis

• Eczema dermatitis family• Stasis dermatitis• Pityriasis rosea• Infections• Insect bite reaction• Polymorphous eruption of pregnancy• Erythema multiforme• Papular acrodermatitis of childhood• ....

Eczematous dermatitis = Eczema

• Clinical term• Group of disorders• Similar clinical features Moist Papules and plaques Vesicles Crust scale Erythematous base

• Similar histological features Spongiosis

• Frequently have different etiologies

Eczema- Background -

• Insufficiently distinct to reliably separate them onhistological grounds alone, clinical data vital

Spongiotic dermatitis, consistent with eczema

• Clinicians can subclassify on the basis of clinicalpresentation, history and possibly additional tests(e.g. allergic or irritant contact dermatitis, ...)

Eczematous dermatitis- Variants -

• Endogeneous– Atopic– Seborrheic– Discoid

(nummular)– Hand eczema– Autosensitization

(id) reaction

• Exogeneous– Contact– Infective– Asteatotic

Hand eczema(dyshidrotic eczema, pompholyx,

palmoplantar eczema)

Hand eczema (palmoplantar eczema)

• Recurrent pruritic vesiculareruption- Palms (70%)- Soles (10%)- Palms and soles (20%)- Digits (volar part, sides)

• Vesicles appear as smallpale papules

• Scaling, cracking• F>M

Hand eczema (palmoplantar eczema)- Pathogenesis -

• Idiopatic– Patients frequently have atopy– Majority of cases

• Allergic contact dermatitis– Drugs, shover gels, food, ...– Significant proportions

• Id-reactions

Hand eczema (palmoplantar eczema)

• Important to exclude dermatophyte infection(PAS stain)– ! The presence of neutrophils in the stratum

corneum

Contact dermatitis

Contact dermatitis

• Allergic Type IV hypersensitivity Exposure to specific antigen Poison ivy, latex, nickel, rubber, ...

• IrritantDirect damage of the epidermis 80% of the occupational skin diseasesDetergents, solvents, acids, alkalis, ...

Contact dermatitis- Clinical presentation -

• Erythematous plaues, papules and sometimesvesicles

• Distribution and shape of the lesion cansuggest etiology

Allergic contact dermatitis

Langerhans cell microabscesses

Eosinophilic granulocytescan be

scarce or absentin contact dermatitis.

Irritant contact dermatitis- Histological features

• Changes depend on the concentration of theoffending agent

• Pallor and ballooning of keratinocytes in theupper dermis

• Necroses of keratinocytes in variable numbers• Exocytosis of neutrophils in the area(s) of

ballooning and necrosis of keratinocytes

Discoid dermatitis(nummular eczema)

Discoid dermatitis (nummular eczema)- Clinical features -

• Single/multiple pruritic lesions• Usually starts as tiny papules or

papulovesicles– Confluence of lesions– Grouping in the shape of coins

• Surface wheeping and/or crusted• Margins usually flat

Discoid dermatitis (nummular eczema)- Clinical features -

• Sites of predilection– Lower legs– Forearms (extensor)– Dorsum of hands

• Two peak ages of onset– Young women– Middle aged adults

• Chronic course withremissions and relapses

Nummular dermatitis- Pathogenesis -

• Poorly understood• Related to atopy• As a consequence of allergy to

– Nickel– Cobalt– Chromate

• Can follow exposure to irritants– Soap, acid, alkalis

Nummular dermatitis- Histology -

• Acute/subacute/chronic spongiotic dermatitis• Progressive psoriasiform hyperplasia of the

epidermis, not as uniform as in allergic contactdermatitis

• Scale crust frequent• Dermal infiltrate contains lymphocytes,

occasional neutrophils, eosinophils andplasma cells

‘Specific’ forms of spongiotic dermatitis

• Stasis dermatitis• Pityriasis rosea• Vesicular dermatophytosis

! ALWAYS CORRELATE WITH CLINICAL HISTORY

Stasis (varicose) dermatitis

• Middle aged and older patients• Impaired venous return from lower limbs• Medial aspects of lower leg / ankle• Clinical presentation

- Oedema with shiny or erythematousappearance

- Dry, scaly, crusted erythematous orbrawnish discolorations

• Often around stasis ulcer(s)

Stasis (varicose) dermatitis

• Spongiosis and acanthosis• Lobular vascular proliferation

– Can be prominent with formation of papules• Hemosiderin

– Abundant, throughout the dermis• Fibrosis

– prominent in long-standing lesions• Inflammation (L, MF, PL)• Erythrocyte extravasation

Pityriasis rosea

Pityriasis rosea

• Acute self limited disease• F>M• 15-55 years (about 75% of patients)• Seasonal variations• Recurrent disease in < 5%

Pityriasis rosea

• Single red scalyplaque = heraldpatch

• Usually on the trunk• Increases in size

over 48 hours (2-10cm)

• Systemic symptomscan also be present

Pityriasis rosea

• Secondaryincubation periodof 7-14 days

• Generalizederuption oferythematousscaly lesions

• Chest, abdomen,thighs, arms, back

• Cause unknown

Pityriasis rosea- Histology -

• Subacute/chronic spongiotic dermatitis• Focal hyperkeratosis• (multi)focal parakeratosis• Slight irregular acanthosis• Vesiculation rare• Superficial perivascular mononuclear

inflammatory cell infiltrate• Extravasation of erythrocytes

!Neutrophils in the cornified layer are not a

feature of pityriasis rosea*

Consider guttate psoriasis*

Exclude infection

Spongiotic dermatitis- Secondary changes-

• Frequently becomes infected• Dramatic change in histopathologyMarked acute inflammationDevelopment of pustules

• Subcorneal• Intraepidermal• Subepidermal

• Additional stain(s) necessary

Psoriasiform reaction pattern

Psoriasiform reaction pattern

• Epidermalhyperplasia(acanthosis)

• Uniform andmarkedly enlargedrete ridges

Psoriasiform reaction pattern

• Psoriasis• Reiter’s syndrome• Pityriasis rubra pilaris• Pityriasis rosea• Lichen simplex chronicus• Psoriasiform drug eruptions• Subacute/chronic spongiotic dermatitis• Necrolytic migratory erythema• ....

Psoriasis vulgarisis

the prototype ofpsoriasiform dermatitis

Psoriasis vulgaris• Classic features Sharply demarcated erythematous plaques Silvery scaly surface

• Sites of predilection– Scalp– Extensor surfaces– Lower back– Periumbilical– Nails (pitting, distal onycholysis, ...)

• Granular layerabsent

Psoriasis vulgaris- Histology -

• Uniform acanthosis• Parakeratosis (prominent, confluent)• Diminished/absent granular layer• Collections of neutrophils in the epidermis• Thinning of suprapapillary plates• Papillary dermal vesselsDilated, congested Turtous

Eosinophilsare typically

ABSENTin psoriasis

If present, consider psoriasis-likeeczematous process, drug eruption, ...

*Classic psoriasis not difficult to

recognize*

Rarely biopsied*

Variants of psoriasis can be challenging

Evolving psoriasis- Histology -

• Epidermal changes– Mild initial spongiosis– Mild acanthosis– Focal parakeratosis– Mild lymphocyte exocytosis

• Dermal changes– Dilatation and congestion of superficial

vascular plexus– Mild perivascular lymphocytic infiltrate

Evolving psoriasis

Gutate psoriasis• Rapid onset of

numerous smallplaques and papules(0.5-1.5 cm)

• Upper trunk, proximalextremities

• Young patients• Often history of

antecedent pharyngitis(streptococcal)

Guttate psoriasis - histology

Histological features overlap with those ofevolving disease

Guttate psoriasis• Acanthosis much less marked• Parakeratosis FocalNeutrophils

• Focal loss/diminution of granular cell layer• Mild spongiosis• Superficial dermal inflammation

– Neutrophilic granulocytes, lymphocytes– No eosinophils!

Guttate psoriasis

Pustular psoriasis - generalized

• Fever of several daysduration

• Sudden appearance ofsterile pustules (2-3mm)

• Erythematous skin –progression toerythroderma

• Recurrent episodes offever and pustules

Pustular psoriasis - generalized

• Predisposing conditions– Infections (bacterial, viral)– Withdrawal of systemic steroid therapy– Drugs– Pregnancy– Hypocalaemia– Sunlight / phototherapy– Emotional stress– ...

Pustular psoriasis

A characteristichistological feature is

formation ofmacropustule(s)

Pustular psoriasis

• Large collections of neutrophils withinepidermis and/or stratum corneum

• Granular layerNormal Partially diminised

• No significant acanthosis due to the rapiddevelopment

Pustular psoriasis – dif. dg.

• Infection (fungi)Additional stains (PAS, ...)

• Generalized exentematous pustulosisHistory of new medications Eosinophis!!!

Pityriasis rubra pilaris

Pityriasis rubra pilaris

• Rare disease• Small follicular papules

(trunk)– Central keratin plug

• Erythema– Perifollicular

erythema– Confluent– Large expanding

plaques

Pityriasis rubra pilaris

• Islands of sparedskin

• Erythema hasorange-yellow tint

• Palmoplantarkeratoderma

Pityriasis rubra pilaris –non follicular lesions

• Checkerboard parakeratosis (alternating orthoand parakeratosis in horizontal/verticalfashion)

• Focal/confluent hypergranulosis• Marked uniform acanthosis• Broad rete ridges• Thick suprapapillary plates• Narrow dermal papillae

Pityriasis rubra pilaris

‘Shoulder parakeratosis’

Pityriasis rubrapilaris

• Follicular plugging

Pityriasis rubra pilaris

Can be confusedwith

psoriasison histology.

Pityriasis rubra pilaris

1. Lacks neutrophils in stratum corneumor epidermis

2. No suprapapillar plate thinning3. Granular layer not diminished

Pityriasis rubra pilaris - beware

1. Biopsies from early lesions can beinconclusive

2. Biopsies from follicular papules non-specific

Lichen simplex chronicus and prurigo nodularis

• Related entities• Result of persistent rubbing or scratching• Pruritic scaly plaques• Pruritic nodules• Ulceration secondary to excoriation

Lichen simplex chronicus and prurigo nodularis

Onlyon areas

that patientcan

reach

Lichen simplex chronicus and prurigo nodularis

Nape of the neckShin

ForearmsDorsal feet

Perianal / genital areas

Lichen simplex chronicus

• Prominent hyperkeratosis• Psoriasiform hyperplasia• Focal parakeratosis• Hypergranulosis

Lichen simplex chronicus

Fibrosis of papillary dermis characterised byvertically oriented

thick collagen fibres(vertical streaking)

Lichen simplex chronicus

Prurigo nodularis

• Pseudo-epitheliomatoushyperplasia

• Extension into hairfollicle

Spongiotic and psoriasiform reaction pattern- Conclusions -

• Dynamic prosess• Different changes as the lesions evolve• Distinguishing clinical subtypes on histological

features frequently NOT possible• Patterns can overlap• Clinico-pathological correlation crucial