Clinics in Dermatology (2007) 25, 524–528

The histopathologic spectrum of psoriasis

Michael Murphy, MD, Philip Kerr, MD, Jane M. Grant-Kels, MD⁎
Division of Dermatopathology, Department of Dermatology, University of Connecticut Health Center, Farmington, CT 06030

Abstract Psoriasis is the prototype of a group of cutaneous disorders (psoriasiform dermatitides) that
show psoriasiform epidermal hyperplasia, defined as regular elongation of the rete ridges with
preservation of the rete ridge–dermal papillae pattern. Depending on whether the lesion is early or
resolving, psoriasiform epidermal changes may be subtle or prominent. Other histologic clues to the
diagnosis of psoriasis include more dilated and tortuous papillary blood vessels, neutrophils within the
epidermis associated with spongiosis (spongiform pustules), neutrophils beneath the cornified layer
(subcorneal pustules), neutrophils within the cornified and parakeratotic horn, hypogranulosis, and more
keratinocytic mitotic figures above the basal cell layer.
© 2007 Elsevier Inc. All rights reserved.

Psoriasis vulgaris clinicopathologic correlation has, over the years, furthered

Psoriasis is a chronic relapsing erythematosquamous
dermatitis affecting 2% of the US population and is
characterized by abnormal keratinocytic hyperproliferation
resulting in thickening of the epidermis (producing well-
circumscribed clinical plaques) and stratum corneum
(producing scale).1-4 In its classic presentation (psoriasis
vulgaris), the disease presents as well-circumscribed reddish
and scaly papules and plaques typically on the elbows,
knees, and scalp, in addition to other cutaneous sites. In this
form, the disease is usually easy to diagnose on clinical
features alone, and skin biopsy for histopathologic review is
typically not performed or required. However, microscopic
analysis of skin biopsy specimens can be useful not only to
confirm the diagnosis of psoriasis in classic and clinically
atypical variants but also to correlate the clinical signs and
symptoms with histopathologic changes. In addition,
⁎ Corresponding author. Dowling South, MC 6230, 263 Farmington
Ave, Farmington, CT 06030.
E-mail address: grant@nso1.uchc.edu (J.M. Grant-Kels).
our understanding of the pathophysiology of this disease.
As a consequence of the course of remissions and
exacerbations of this disease, the histopathologic findings
in psoriasis vary with the age of the lesions.1-4 The earliest
changes can be nonspecific, with a preponderance of
dermal changes, including a sparse superficial perivascular
T-lymphocytic infiltrate. This is followed by the development
of dilated and slightly tortuous blood vessels within dermal
papillae, mild dermal edema, and minimal spongiosis with
rare T-lymphocyte and/or neutrophil exocytosis (Fig. 1). (The
term exocytosis refers to the extension of inflammatory cells
into the epidermis.) Of note is that intradermal T lymphocytes
are predominantly CD4 positive, whereas intraepidermal
T lymphocytes are predominantly CD8 positive.
The subsequent papular/early plaque stage shows slight
psoriasiform (regular) epidermal hyperplasia, with greater
neutrophil exocytosis and small mounds of parakeratosis
containing neutrophils, in addition to the cited changes
identified in earlier lesions (Fig. 2). The inflammatory
infiltrate in the dermis at this stage is usually composed of
lymphocytes, histiocytes, and neutrophils, in addition to
extravasated red blood cells.

0738-081X/$ – see front matter © 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.clindermatol.2007.08.005
Histopathologic spectrum of psoriasis
Fig. 1 Early stage: Frames A to D show sparse superficial
perivascular lymphocytic infiltrates with minimal spongiosis and
extension of lymphocytes into the epidermis (exocytosis).
Fully developed clinical plaques show marked epidermal
hyperplasia with characteristic features, including (a) regular
elongation of epidermal rete ridges, (b) rete ridges with
characteristic bulbous enlargement of their tips or “clubbing”
(i.e., widening of the deeper portion of the rete; in addition,
some rete ridges are fused with adjacent ones), (c) reciprocal
elongation of intervening dermal papillae containing dilated
and tortuous capillaries and fine fibrillary collagen, and
(d) thinning of the epidermis that lies immediately above the
dermal papillae (“suprapapillary plate thinning”; this thin-
ning predominantly affects the granular and spinous layers).
In addition, there is pallor of the superficial layers of the
Fig. 2 Papular stage: (A) Slight epidermal hyperplasia with
mounds of parakeratosis (arrow), minimal spongiosis, lymphocyte
exocytosis, and superficial perivascular lymphocytic infiltrate
with vascular ectasias; (B) superficial dermal vascular ectasias;
(C) single neutrophil exocytosis (arrows); and (D) mounds of
parakeratosis containing neutrophils (Munro's microabscess) and
subjacent hypogranulosis.
525
Fig. 3 Plaque stage: Frames A and B show regular elongation of
epidermal rete ridges with characteristic bulbous enlargement of
their tips or clubbing (some rete ridges are fused with adjacent ones)
and reciprocal elongation of intervening dermal papillae containing
dilated tortuous capillaries and fine fibrillary collagen, with
thinning of the epidermis above the dermal papillae (suprapapillary
plate thinning; the latter thinning predominantly affects the granular
and spinous layers). In Frame C, there is pallor of the superficial
layers of the epidermis, and spongiosis is minimal or absent. There
is marked hyperkeratosis, often composed of alternating orthoker-
atosis and horizontally confluent (but vertically intermittent)
parakeratosis. In addition, there is hypogranulosis subjacent to
areas of parakeratosis. Frame D shows dilated tortuous capillaries
with dermal papillae. Frame E shows increased mitotic activity
within the suprabasal layer.
epidermis, and spongiosis is minimal or absent (Fig. 3).
There is marked hyperkeratosis, often composed of alternat-
ing orthokeratosis and horizontally confluent (but vertically
intermittent) parakeratosis, suggesting that epidermal growth
activity fluctuates in these lesions. There is hypogranulosis
subjacent to areas of parakeratosis. Collections of neutro-
phils within the parakeratosis (Munro's microabscesses) are
present in most cases (∼75%) and less commonly within the
spinous layer (spongiform pustules of Kogoj). The latter
types are smaller than those seen in the pustular variants of
psoriasis, as subsequently described. Spongiform pustules of
Kogoj are formed by the migration of neutrophils from the
papillary capillaries, via the thinned suprapapillary plates
(termed squirting papillae), with aggregation of neutrophils
beneath the stratum corneum and in the upper malpighian
layer between degenerating and thinned keratinocytes
(Fig. 4). Subsequently, the keratinocytes at the center of
the pustule degenerate with the formation of a large single
cavity surrounded by a rim of thinned keratinocytes. As
neutrophils migrate upward into the overlying stratum
corneum, they become pyknotic and form Munro's micro-
abscesses, which are typically located above dermal papillae.
A sparse superficial dermal perivascular lymphocytic
inflammatory infiltrate with occasional neutrophils is
typically present. Plasma cells are not prominent, except in
526
Fig. 4 Frames A to C show spongiform pustules of Kogoj formed
by the aggregation of neutrophils beneath the stratum corneum and
in the upper malpighian layer between degenerating and thinned
keratinocytes (thin arrow). Subsequently, the keratinocytes at the
center of the pustule degenerate with the formation of a large single
cavity surrounded by a rim of thinned keratinocytes. As neutrophils
migrate upward into the overlying stratum corneum, they become
pyknotic and form a Munro's microabscess (thick arrow).
lesions from mucosal sites and in the case of patients with
HIV infection. It should be noted that these histopathologic
features are not always identified, even in biopsy specimens
from “classic” clinical lesions of psoriasis.
The epidermal thickening may affect any or all layers of
the epidermis and is caused by increased keratinocyte
proliferation, reflecting the increased mitotic activity within
the basal and suprabasal layers.5,6 As compared with normal
skin, psoriatic lesions show up to 27 times the mitotic
activity, a 12-fold decrease in the cell cycle time of basal and
suprabasal keratinocytes, and a greater than 7-fold increase
in the epidermis turnover time (∼7 days in psoriatic skin vs
∼56 days in normal skin). There is also an increase in the
apoptotic rate, in concert with a reduction in bcl-2 (an
antiapoptotic protein) expression in basal cells. In psoriatic
skin, basal keratinocytes maintain expression of K5 and K14
(the keratins typical of basal keratinocytes in normal skin),
whereas K1 and K10 (the keratins typical of suprabasal cells
M. Murphy et al.
in normal skin) are replaced by so-called hyperproliferation-
associated keratins K6 and K16, in addition to K17.7
Resolving or treated plaques of psoriasis initially show
progressive reduction in the presence of neutrophils within
the stratum corneum and parakeratosis, with reformation of
the granular zone and orthokeratosis. The epidermal
hyperplastic changes resolve later. There may be residual
mild superficial dermal fibrosis with persistence of papillary
dermal capillary dilatation and tortuosity, as the only
histopathologic clues to this disease.
There are variants of psoriasis that have different clinical
appearances and variations in their histopathologic find-
ings.1-4 Because of the atypical clinical features that differ
from those of classic psoriasis vulgaris as previously
described, skin biopsy with microscopic analysis is more
commonly performed for a definitive histopathologic
diagnosis and/or to exclude other clinical mimics.
Guttate (eruptive) psoriasis
Guttate psoriasis, a variant more common in children, is
often associated with antecedent oropharyngeal streptococ-
cal infection. The disease is mediated by T lymphocytes
specific for group A β-hemolytic streptococcal antigens.
Patients with guttate psoriasis show small (1-5 mm)
erythematous papules with fine scale over the upper trunk
and proximal extremities. Lesions of guttate psoriasis show
histologic features similar to those of papular lesions,
although (a) there is less epidermal hyperplasia without
significant elongation of the rete ridges, (b) the granular zone
may be diminished but rarely absent, (c) there are greater
inflammatory infiltrates, particularly neutrophilic compo-
nents, and (d) there is often “normal” orthokeratosis
overlying the parakeratosis containing neutrophils (reflecting
the sudden onset of this variant).
Pustular psoriasis
Pustular psoriasis is a rare manifestation of this disease
characterized by widespread sterile pustules that may occur in
a variety of clinical settings of psoriasis, including (a)
pustular psoriasis of Barber, in which pustules are localized to
the palms and/or soles and often accompanied by classic
plaque-type psoriasis at other sites; (b) pustular psoriasis of
von Zumbusch, a generalized form of pustular psoriasis with
systemic signs and symptoms (fever, anemia, and leukocy-
tosis) and often precipitated by systemic drugs; (c) pustular
psoriasis of pregnancy (impetigo herpetiformis); and (d)
superimposed on classic plaque-type psoriatic lesions. The
predominant diagnostic and histopathologic feature is the
presence of intraepidermal pustules (spongiform pustules of
Kogoj) at different stages of evolution. These pustules are
Histopathologic spectrum of psoriasis
larger than those seen in other variants of psoriasis and are
therefore clinically apparent. Similar to other variants, the
neutrophils of the spongiform pustule eventually migrate into
the stratum corneum and assume the appearance of a Munro
microabscess. In acute pustular psoriasis, the histopathologic
features are not typical of those seen in psoriasis vulgaris
because the neutrophil exocytosis occurs before the time
necessary to produce the typical epidermal hyperplastic
changes. When pustules occur within typical plaques of
psoriasis, the other histopathologic features found can reflect
psoriasis vulgaris at any stage of development.
Erythrodermic psoriasis
Generalized erythroderma (redness and scaling) affecting
the entire skin surface occurs in up to 2% of patients with
psoriasis, often precipitated by a prior systemic infection or
therapy (including withdrawal of potent topical or systemic
steroids and withdrawal of a systemic therapy, such as
methotrexate, secondary to phototoxicity or secondary to an
irritant contact dermatitis caused by topical tar therapy).
Erythroderma can be a clinical presentation secondary to a
variety of diseases. Therefore, a new patient presenting with
erythroderma requires multiple biopsies to determine the
underlying etiology. In approximately 20% of patients with
erythrodermic psoriasis, the underlying cause can be
attributed to psoriasis.
Erythrodermic psoriasis lesions typically show an absent
stratum corneum (resulting in a lesser degree of the classic
clinically evident micaceous scaling), with more prominent
dilatation of superficial dermal blood vessels, in addition
to the histologic features of early psoriatic lesions, as
previously described.
Other variants
Less common psoriatic lesions include the following:
(a) geographic variant, with linear, annular, figurate, and
polycyclic subtypes; (b) ostraceous variant, with markedly
thickened laminated stratum corneum as compared with
topical lesions; (c) rupial lesions, with marked parakeratotic
scales containing numerous neutrophils, sera, and bacteria;
and (d) follicular variant, with perivascular and peri-
follicular inflammatory infiltrates, follicular plugging, and
midostial parakeratosis.
In addition, there are regional variations in the histo-
pathologic features of psoriasis. For example, psoriasis can
involve mucosal sites, including the vulva and the glan penis
(more commonly in uncircumcised men). Mucosal involve-
ment often elicits less epidermal hyperplasia and scaling as
compared with other cutaneous sites, but spongiosis can be
more prominent. Scalp involvement often shows more
significant plaque formation (caused by marked epidermal
527
hyperplasia). Hair loss is not usually associated with
psoriasis and, if noted, is most often a result of telogen
effluvium. Sebopsoriasis is a term used for clinical lesions
on the scalp that demonstrate features of psoriasis and
seborrheic dermatitis. Clinically, the lesions of seborrheic
dermatitis tend to be yellow-red with greasier scales than
noted in classic psoriasis. Histologically, seborrheic derma-
titis demonstrates irregular acanthosis, spongiosis, super-
ficial perivascular and perifollicular predominantly
lymphocytic infiltrates, and focal parakeratosis particularly
at the lips of follicular ostia. Neutrophils within the epidermis
and parakeratotic horn are not usually noted in seborrheic
dermatitis unassociated with psoriasis.
Nails
Fingernails are involved in up to 50% of patients with skin
lesions of psoriasis, whereas toenails are involved in up to
35% of patients with skin lesions of psoriasis and adjacent nail
involvement (fingernails or toenails) in up to 80% of patients
with psoriatic arthropathy. Nail involvement is the only
manifestation in 10% of patients. Psoriasis may involve any
part of the nail unit, including the nail plate/matrix, nail bed,
hyponychium, and/or the nail folds.8 Clinical lesions include
pitting, discoloration, onycholysis, subungual hyperkeratosis,
nail grooving, splinter hemorrhages, and/or complete nail loss.
The characteristic histologic feature is the foci of parakeratosis
within the nail plate that correlate with the clinical features of
nail roughness and leukonychia. The shedding of these foci of
parakeratosis gives rise to the clinical pitting of the nail plate.
The “oil spots” (yellow-brown discolorations under the nail
plate) are a result of involvement of the nail bed (psoriasiform
onychitis) by the typical changes of psoriasis as seen at other
cutaneous sites: elongation of dermal papillae with dilated and
tortuous capillaries, focal hypogranulosis, hyperkeratosis with
parakeratosis, and Munro's microabscesses. The distal nail
onycholysis is caused by a split between the hyponychium and
the foci of neutrophils and parakeratosis within the overlying
nail plate. Splinter hemorrhages are caused by extravasation of
erythrocytes from the superficial tortuous fragile blood
vessels. Although routine histology with hematoxylin-eosin
stain is the gold standard for the histologic diagnosis of nail
disease, it is important that periodic acid–Schiff stain and/or
Gomori methenamine silver stain also be performed in all
cases to rule out a fungal nail infection (onychomycosis),
which can have clinical and histologic features similar to those
of psoriatic nail disease.
Clinicopathologic correlation
The plaque elevation in psoriasis vulgaris lesions is
caused primarily by the epidermal hyperplasia and elonga-
tion of rete ridges and to a lesser extent by the subjacent
528
dermal edema and inflammatory infiltrate. The fine silvery
scale is a result of the confluent parakeratosis. The
combination of superficial dermal capillaries and overlying
suprapapillary epidermal thinning is responsible for the
erythematous appearance of psoriatic lesion and the Auspitz
sign (pinpoint bleeding points on removal of the scale).
Differential diagnosis
The histologic features that are most useful in the
histopathologic diagnosis of psoriasis are (a) Munro's
microabscesses (collections of neutrophils within the para-
keratosis), (b) spongiform pustules of Kogoj (neutrophils
within the spinous layer), and (c) dilatation of papillary
dermal capillaries with overlying thinning of the suprapa-
pillary epidermis. However, the “classic” histopathologic
features of psoriasis are often not seen because clinicians
rarely perform biopsy on skin lesions that show the typical
clinical features of psoriasis. Many biopsy specimens of
suspected psoriatic lesions show only focal diagnostic
features and/or overlapping features with other cutaneous
inflammatory disorders. A definitive diagnosis of psoriasis
often requires multiple sections through the tissue specimen
(to identify focal changes), additional special stains, and
clinicopathologic correlation. Although the presence of
neutrophils within the superficial epidermis and/or paraker-
atosis is highly diagnostic of subtypes of psoriasis, this
feature also raises the differential diagnosis of bacterial
impetigo, pustular fungal infections (dermatophytosis and
candidiasis), subcorneal pustular dermatosis of Sneddon-
Wilkinson, transient neonatal pustular melanosis, pustular
drug eruptions, and Reiter's disease. Therefore, additional
Gram, periodic acid–Schiff, and/or Gomori methenamine
silver stains are important to exclude infectious microorgan-
isms. Other features of psoriasis, such as epidermal hyper-
plasia with elongation of rete ridges (“psoriasiform”),
parakeratosis, and mild spongiosis, can be seen in chronic
eczematous dermatitides (e.g., irritant/allergic contact der-
matitis, atopic dermatitis, and nummular dermatitis) and
pityriasis rubra pilaris. In chronic eczematous dermatitis, the
elongation of rete ridges is not typically as regular as that in
psoriasis, and the spongiosis is often more marked and is a
diagnostic histopathologic feature in this condition. Eosino-
phils, which are common in allergic contact dermatitis, are
not typically seen in lesions of psoriasis but may be seen in
partially treated lesions (i.e., psoriasis with superimposed
allergic contact dermatitis secondary to topical therapy).
Lesions of seborrheic dermatitis may be difficult to dis-
M. Murphy et al.
tinguish from psoriasis. Perifollicular parakeratosis, in
addition to the changes of chronic eczematous dermatitis
outlined, would favor seborrheic dermatitis. In addition, if
psoriatic plaques have been previously rubbed, the histo-
pathologic features of the primary psoriatic lesion may be
masked or obscured by features of lichen simplex chronicus
(hypergranulosis, thickening of suprapapillary epidermis,
and vertically oriented fibrosis of the superficial dermis).
Pityriasis rubra pilaris can often be differentiated from
psoriasis by the presence of a thicker suprapapillary
epidermis, broader and shorter rete ridges, perifollicular
parakeratosis, and alternating zones of orthokeratosis and
parakeratosis in vertical and horizontal directions. Of note is
that the latter feature may be seen in psoriasis as a
consequence of episodic activity, indicating the dynamic
nature of this disease. Guttate psoriasis can show overlapping
histologic features with small plaque parapsoriasis and
pityriasis rosea. The presence of ectatic and tortuous blood
vessels within dermal papillae and neutrophils within the
stratum corneum supports a diagnosis of guttate psoriasis
over the other 2 disease entities.
In conclusion, although classic psoriasis is often straight-
forward to diagnose clinically and histopathologically,
psoriasiform dermatoses are a complex group of skin
diseases that can be secondary to various underlying diseases
and triggers. Multiple punch biopsies over time may be
required to establish the definitive diagnosis.
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