Identification of Basic Patterns - Skin - Perivascular Dermatitis

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Identification of Basic Patterns: Skin: Perivascular Dermatitis
See Figs. 5.16 A&B, 5.17 A&B, 5.18 A&B, 5.19 A&B, 5.20 A&B, 5.21 A&B, and 5.22 A&B
Figure 5.16: A. Perivascular dermatitis, perivascular only, superficial. B. Perivascular dermatitis,

perivascular only, superficial and deep.
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Figure 5.17: A. Perivascular dermatitis, perivascular and interstitial, superficial. B. Perivascular dermatitis,
perivascular and interstitial, superficial and deep.
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Figure 5.18: A. Interface dermatitis, vacuolar, superficial. B. Interface dermatitis, vacuolar, superficial and
deep.
Figure 5.19: A. Interface dermatitis, lichenoid, superficial. B. Interface dermatitis, lichenoid, superficial and
deep.
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Figure 5.20: A. Ballooning dermatitis, superficial. B. Ballooning dermatitis, superficial and deep.
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Figure 5.21: A. Spongiotic dermatitis, superficial. B. Spongiotic dermatitis, superficial and deep.
Figure 5.22: A. Psoriasiform dermatitis, superficial. B. Psoriasiform dermatitis, superficial and deep.
Of the seven essential patterns of inflammatory diseases in the skin appreciable at scanning magnification,
perivascular dermatitis is the most common by far. It is the one that microscopists encounter most often in the
routine practice of surgical pathology and in the specialized practice of dermatopathology. Most of the common
inflammatory diseases of the skin are perivascular dermatitides, among those being allergic contact dermatitis,
nummular dermatitis, dyshidrotic dermatitis, psoriasis, lichen planus, pityriasis rosea, seborrheic dermatitis, and
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dermatophytosis, and most of those present themselves, at a minimum, with infiltrates made up of lymphocytes
positioned around venules of the superficial plexus.
When viewed at scanning power, a perivascular dermatitis is identified by the presence of inflammatory cells around
venules situated either in the upper part of the reticular dermis, i.e., around those of the superficial plexus, or in both
the upper and lower parts of the reticular dermis, i.e., around venules of the superficial and deep vascular plexuses
(see Fig. 5.16). By doing away with the distinction, artificially, between "superficial perivascular dermatitis" and
"superficial and deep perivascular dermatitis," a microscopist no longer is compelled to grapple with which of the two
categories is applicable when a particular infiltrate of inflammatory cells resides somewhere in between "superficial"
and "deep" (Fig. 5.23A), as surely is the case at times, or is impelled to wrestle with the issue of which category is
the proper one when a particular infiltrate is recognized to be overwhelmingly "superficial," but, nonetheless, a few
inflammatory cells are spied "deep," as certainly occurs on occasion. Moreover, it is undeniable that a condition
which presents itself conventionally as an infiltrate situated both "superficial and deep," such as lupus tumidus (Fig.
5.23 B&C), may, episodically, be "superficial" only, and one that typically is positioned "superficial" only, such as
allergic contact dermatitis (Fig. 5.24 A–C), is "superficial and deep." An infiltrate of inflammatory cells may be
confined to the zone immediately around venules (perivascular only) or it may involve, too, the interstitium of the
reticular dermis (perivascular and interstitial) (see Fig. 5.17), the inflammatory cells then being insinuated between
bundles of collagen. When, at scanning magnification, a superficial and deep perivascular infiltrate of lymphocytes is
decidedly "bottom heavy," it is likely to be a manifestation of a lymphoma, rather than of a dermatitis.
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Figure 5.23: A. Perivascular dermatitis, superficial. B&C. Lupus tumidus. As a rule, the infiltrate of
lymphocytes in lupus tumidus, that distinctive expression of discoid lupus erythematosus characterized by
abundant mucin in the reticular dermis but no changes at the dermoepidermal interface or in the epidermis,
is both superficial and deep, but in this example, the infiltrate is superficial only.
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Figure 5.24: A. Perivascular dermatitis, superficial and deep (slight deep). B&C. Allergic contact dermatitis.
As a rule, the infiltrate of lymphocytes in this particular type of spongiotic dermatitis is superficial only, but
in the example shown here, the infiltrate is deep as well as superficial.
Once a pattern of perivascular dermatitis has been identified, it is necessary then to make a judgment about whether
the epidermis, including the junction between it and the dermis (dermoepidermal interface), is affected by the
process, i.e., whether or not any changes at all also are present in the epidermis. If the epidermis is spared, the
pattern is either "perivascular dermatitis only" or "perivascular and interstitial dermatitis only" (see Figs. 5.16 and
5.17); if the epidermis is affected, the pattern may be one in which the dermoepidermal interface is obscured
("interface dermatitis") (see Figs. 5.18 and 5.19), spinous cells are ballooned ("ballooning dermatitis") (see Fig.
5.20), spongiosis is discernible ("spongiotic dermatitis") (see Fig. 5.21), or psoriasiform acanthosis is apparent
("psoriasiform dermatitis") (see Fig. 5.22). Not uncommonly, more than one of those four patterns is evident
concurrently, for example, interface dermatitis and spongiotic dermatitis together in a drug eruption, and spongiotic
dermatitis and psoriasiform dermatitis together in allergic contact dermatitis or nummular dermatitis.
"Perivascular dermatitis only" and "perivascular and interstitial dermatitis only" (see Figs. 5.16 and 5.17) are the
patterns most vexing to those whose task it is to interpret inflammatory diseases in the skin by means of
conventional microscopy. In former times, those were the patterns to which histopathologists were most apt to
surrender abjectly in frustration, "signing them out" in those days, uninformatively, as "chronic nonspecific dermatitis."
By utilizing the algorithmic method recommended here, not only does it become possible for many perivascular
dermatitides to be diagnosed with specificity, but it becomes a reality that, in most instances, is achievable. Ideally,
every diagnosis of "perivascular dermatitis only" and "perivascular and interstitial dermatitis only" should be delivered
in language used in the usual discourse of dermatologists, e.g., vitiligo, Schamberg's disease, and urticaria.
Realistically, however, there are, without doubt, situations in which a specific diagnosis simply cannot be made, e.g.,
a "perivascular dermatitis only" that consists entirely of lymphocytes and exhibits no other ancillary findings. In that
situation, a note should be appended to a diagnosis rendered descriptively ("sparse perivascular dermatitis of
lymphocytes"), that addendum being designed to inform a clinician of authentic considerations in the differential
diagnosis, in the particular example just given the best possibilities being viral exanthem and morbilliform drug
eruption.
A microscopist should not be outwitted by dermatophytic hyphae that play "hide and seek." Although in most cases,
those hyphae are identifiable readily as they repose in cornified cells of surface and infundibular epidermis, inner
sheath, and hair shaft in sections stained conventionally with hematoxylin and eosin, on occasion, they seem to be in
cognito, eluding as they do detection with that "routine" stain, but being revealed strikingly by specialized stains, such
as periodic-Schiff and silver methenamine. In actuality, however, if dermatophytes are demonstrable by application
of a "special stain," they must be visualizable, too, in sections stained by hematoxylin and eosin, and then subjected
to scrutiny with dogged intensity.
A microscopist must take cognizance of the difference between "perivascular dermatitis only" on one hand and
"perivascular and interstitial dermatitis only" on the other; those different patterns direct a histopathologist to
consideration diagnostically of different diseases. For example, at scanning magnification, a perivascular infiltrate
composed of lymphocytes accompanied by few, if any, extravasated erythrocytes signifies certain morbilliform drug
eruptions and certain viral exanthems, a perivascular and interstitial infiltrate of lymphocytes joined by erythrocytes
extravasated in number indicates Schamberg's disease (Fig. 5.25 A&B), and a perivascular and interstitial infiltrate of
lymphocytes unaccompanied by extruded red blood cells telegraphs likelihood of a patch of mycosis fungoides (Fig.
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5.26 A&B). In the case of Schamberg's disease, the extrusion of erythrocytes into the dermis follows on compromise
of the wall of small vessels secondary to the combined effects of the inflammatory process itself and of stasis; there
is no justification for the assertion that Schamberg's disease is a "capillaritis" (there is no such thing in the skin as a
vasculitis of capillaries, the vessels affected most often by far in true vasculitis being venules). Schamberg's disease
is not a vasculitis and, moreover, most examples of that persistent pigmented purpuric dermatitis met with clinically
do not qualify truly as an eruption, the lesions appearing slowly over time. As a parenthesis, it merits mention that the
persistent pigmented purpuric dermatitides named eponymically for Schamberg, Gougerot and Blum, and Doucas
and Kapetanakis are mere variations on a single theme pathologic. That is true also for the example known as
Majocchi's, although the latter differs from the others by being characterized by a single attribute clinical, to wit,
annularity of purpuric lesions.
Figure 5.25: A&B. Diagnosis with specificity. A superficial perivascular and interstitial infiltrate of
lymphocytes accompanied by extravasated erythrocytes is diagnostic of Schamberg's disease.
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Figure 5.26: A&B. Diagnosis with specificity. A superficial perivascular and interstitial infiltrate of
lymphocytes devoid of erythrocytes extravasated in the reticular dermis and joined by wiry bundles of
collagen in haphazard array in the papillary dermis equates to the patch/subtle plaque stage of mycosis
fungoides.
A perivascular and interstitial infiltrate in which lymphocytes and a few eosinophils are present around venules and
eosinophils are scattered in the interstitium should call to mind pruritic urticarial papules and plaques of pregnancy
(PUPPP) (Fig. 5.27 A&B) on one hand and a drug eruption made up of macules and papules on the other (Fig. 5.28
A&B). Sometimes PUPPP is accompanied by subtle spongiosis. A "nibble" by a timid insect also is characterized by
a perivascular and interstitial infiltrate containing eosinophils, and lymphocytes, the eosinophils being by themselves
in the interstitium, and even though the infiltrate is superficial (in contrast to that brought about by the "bite" of a more
plucky, voracious insect, which not only is superficial and deep, but may extend into the subcutaneous fat), it displays
a wedge shape, the apex of which is directed toward the subcutis (Fig. 5.29 A&B). In some perivascular and
interstitial dermatitides, neutrophils predominate in the interstitium. That is the case for some examples of urtica (Fig.
5.30 A&B) (in other examples, eosinophils are preponderant in the interstitium), which is very common, for most
examples of erysipelas (a phlegmonous dermatitis), which is uncommon, and in all examples of evolving cutis laxa
(Fig. 5.31 A&B) (in which the polymorphonuclear leukocytes are aligned along elastic fibers, those structures
eventually being destroyed by the effects of lysosomal enzymes), which is very rare. Neutrophils, along with
lymphocytes, plasma cells, and eosinophils, are encountered at times in the interstitium of the reticular dermis of
lesions of morphea at an early stage of that process (Fig. 5.32 A&B).
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Figure 5.27: A&B. Diagnosis with near specificity. A perivascular and interstitial infiltrate of lymphocytes
especially around venules and eosinophils mostly in the interstitium is indicative of pruritic urticarial
papules and plaques of pregnancy.
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Figure 5.28: A&B. Diagnosis with near specificity. A perivascular and interstitial infiltrate of lymphocytes
and eosinophils may be encountered in one type of drug eruption.
Figure 5.29: A&B. Diagnosis with specificity. A moderately dense, subtly wedge-shaped infiltrate of
lymphocytes and numerous eosinophils in the upper part of the dermis represents a response to an assault
by a timid arthropod.
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Figure 5.30: A&B. Diagnosis with specificity. An infiltrate of lymphocytes and neutrophils around venules,
and neutrophils scattered in the interstitium is typical of urtica.
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Figure 5.31: A&B. Diagnosis with specificity. Neutrophils distributed particularly along the course of elastic
fibers in the reticular dermis is diagnostic of cutis laxa.
Figure 5.32: A&B. Diagnosis with specificity. A "bottom-heavy" perivascular and interstitial mixed-cell
infiltrate, made up of lymphocytes, plasma cells, eosinophils, and, sometimes, a sprinkling of neutrophils, is
characteristic of morphea at a stage so early in the process that collagen bundles are not yet crowded and
thickened, although the tinctorial quality of them has changed.
A perivascular and interstitial infiltrate in which epithelioid histiocytes predominate in the interstitium and lymphocytes
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surround venules is met with in granuloma annulare (Fig. 5.33 A&B). When the histiocytes are accompanied by
neutrophils and eosinophils, as well as by lymphocytes and plasma cells, and especially when that infiltrate is
"bottom heavy," sometimes affecting septa in the subcutaneous fat, the diagnosis is interstitial granulomatous
dermatitis with arthritis. In some lesions of nephrogenic fibrosing dermopathy at an early stage of that process (Fig.
5.34 A&B), plump oval monomorphous fibrocytes in number are splayed between bundles of collagen in the reticular
dermis in a manner reminiscent of histiocytes in the interstitial expression of granuloma annulare. In nephrogenic
fibrosing dermopathy, however, the changes are diffuse, not focal, and never are there discrete zones in which a
palisade has been formed by the mesenchymal cells.
Figure 5.33: A&B. Diagnosis with specificity. A perivascular infiltrate of lymphocytes joined by epithelioid
histiocytes insinuated between bundles of collagen in the reticular dermis is characteristic of granuloma
annulare.
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Figure 5.34: A&B. Diagnosis with specificity. Fibrocytes splayed between collagen bundles throughout the
reticular dermis in the near absence of a perivascular infiltrate signals a stage in the evolution of
nephrogenic fibrosing dermopathy.
Some proliferations termed hyperplasias and hamartomas may, at scanning magnification, be mistaken for a
"perivascular" or "perivascular and interstitial" dermatitis, the former being exemplified by a patch of Kaposi's
sarcoma (Fig. 5.35 A&B) and the latter by a superficial type of congenital melanocytic nevus marked by
angiocentricity of cells of the nevus (Fig. 5.36 A&B), the so-called nevus cells really being abnormal melanocytes.
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Figure 5.35: A&B. Simulation of an inflammatory disease. A perivascular lymphoplasmacytic infiltrate, such
as this, could be misconstrued as that of a dermatitis, e.g., erythema migrans. In fact, the proliferation of
thin-walled vessels, some of them around pre-existing venules, is typical of the macule/patch stage of
Kaposi's sarcoma, a hyperplasia in the sense that term was used in classic pathology; when herpesvirus is
withdrawn, the proliferation involutes.
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Figure 5.36: A&B. Simulation of an inflammatory disease. At first glance at scanning magnification, the
infiltrate pictured here could be misinterpreted as that of a perivascular dermatitis, e.g., erythema
figuratum. In fact, the cells distributed in angiocentric and adnexocentric fashion are abnormal melanocytes
of a congenital nevus.
Before proceeding to perivascular dermatitis in which the epidermis is affected also, it is worthwhile to devote a few
lines to the subject of "acuteness" of inflammatory diseases of the skin. One such sign is erythrocytes extravasated
in the upper part of the dermis and another is edema in the papillary dermis, as evidenced there by pallor.
Erythrocytes extravasated in the upper part of the dermis are expected in all inflammatory diseases in the process of
erupting, e.g., psoriasis of guttate type (Fig. 5.37 A&B), pityriasis rosea "daughter" lesions (Fig. 5.38 A&B), lichen
planus (Fig. 5.39 A&B), erythema multiforme (Fig. 5.40 A&B), and Mucha-Habermann disease (Fig. 5.41 A&B), to
give but five of many examples, the red blood cells being sent flying into tissue consequent to dilation rapidly of
venules and capillaries of the superficial plexus.
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Figure 5.37: A&B. Erythrocytes extravasated in an eruption, a sign of acuteness. Eruptive psoriasis,
characterized by mounds of scale-crust that house neutrophils at the summit of them, is affiliated,
consistently, with erythrocytes extravasated in the upper part of the dermis and, often, in the epidermis.
Figure 5.38: A&B. Erythrocytes extravasated in an eruption, a sign of acuteness. Eruptive pityriasis rosea,
in addition to being typified by spongiosis and mounds of parakeratosis, is accompanied invariably by
erythrocytes extravasated in the papillary dermis and, at times, in the epidermis.
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Figure 5.39: A&B. Erythrocytes extravasated in an eruption, a sign of acuteness. Eruptive lichen planus, in
addition to displaying features typical, is associated with erythrocytes extravasated in the upper part of the
dermis.
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Figure 5.40: A&B. Erythrocytes extravasated in an eruption, a sign of acuteness. Eruptive erythema
multiforme, in addition to exhibiting attributes typical of that condition at an early stage of it, is
accompanied, repeatedly, by erythrocytes extravasated in the upper part of the dermis and, at times, in the
epidermis.
Figure 5.41: A&B. Erythrocytes extravasated in an eruption, a sign of acuteness. Eruptive Mucha-
Habermann disease shows interface changes of the vacuolar type, among them being individual necrotic
keratocytes in the context of a normal cornified layer and many red blood cells extravasated in the upper
part of the dermis and in the epidermis.
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Sometimes edema of the papillary dermis is so intense that it verges on subepidermal vesiculation, a situation that
presents itself most often on glabrous skin in polymorphous light eruption (for perivascular mostly) (Fig. 5.42 A&B)
and in a response to the "bite" of an insect (for perivascular and interstitial) (Fig. 5.43 A&B), but also in Mucha-
Habermann disease (Fig. 5.44 A&B), dermatophytosis (Fig. 5.45 A&B) and Sweet's syndrome (Fig. 5.46 A&B) (and
its sometimes lookalike pyoderma gangrenosum) (Fig. 5.47 A&B), and that expresses itself most often on, or near,
volar skin in pernio (which tends to be perivascular mostly) (Fig. 5.48 A&B), a manifestation usually of lupus
erythematosus. What seems at first blush to be extensive edema of a thickened papillary dermis in lichen sclerosus
et atrophicus often is paleness conveyed by fibrillary bundles of collagen (Fig. 5.49 A&B).
Figure 5.42: A&B. Extensive edema in the papillary dermis, a sign of acuteness. Intense edema of the
papillary dermis in polymorphous light eruption is found only during the crescendo of that process.
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Figure 5.43: A&B. Extensive edema in the papillary dermis, a sign of acuteness. Striking edema of the
papillary dermis occurs commonly in response to the "bite" of an insect.
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Figure 5.44: A&B. Extensive edema in the papillary dermis, a sign of acuteness. Formidable edema of the
papillary dermis is expected at an early stage of a florid eruption of Mucha-Habermann disease.
Figure 5.45: A&B. Extensive edema in the papillary dermis, a sign of acuteness. Marked edema of the
papillary dermis may be a manifestation of dermatophytosis, hyphae in this section of tissue being present
in large number in the inner sheath of a follicle.
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Figure 5.46: A&B. Extensive edema in the papillary dermis, a sign of acuteness. Extraordinary edema of the
papillary dermis is typical of Sweet's syndrome during an early stage of it.
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Figure 5.47: A&B. Extensive edema in the papillary dermis, a sign of acuteness. Inordinate edema of the
papillary dermis in pyoderma gangrenosum during an early phase of it, that condition often being
indistinguishable histopathologically from Sweet's syndrome.
Figure 5.48: A&B. Extensive edema in the papillary dermis, a sign of acuteness. Remarkable edema of the
papillary dermis at the outset of pernio, a manifestation of lupus erythematosus.
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Figure 5.49: A&B. Simulation of extensive edema in the papillary dermis. The pallor in the upper part of the
dermis of lichen sclerosus et atrophicus, a superficial expression of morphea, usually is not a manifestation
of edema, but a representation of delicate bundles of collagen separated widely from one another in a
decidedly thickened papillary dermis.
Certain malignant neoplastic diseases erupt in the manner of an inflammatory disease and, not surprisingly, they
simulate the eruptive phase of some inflammatory disorders, histopathologically and clinically. For example,
lymphomatoid papulosis (Fig. 5.50 A&B), a lymphoma, often resembles pityriasis lichenoides et varioliformis acuta
and, like that florid inflammatory process, is affiliated, at the beginning of it, with extravasated erythrocytes, edema
of the papillary dermis, and neutrophils in mounds of parakeratosis. Acute myelogenous leukemia (Fig. 5.51 A&B)
may be associated with a perivascular and interstitial infiltrate reminiscent of that of certain drug eruptions, and
Letterer-Siewe disease (Fig. 5.52 A&B) and Hand-Schüller-Christian disease, maladies of Langerhans' cells, also
are joined by a mixed-cell infiltrate of inflammatory cells, lymphocytes, plasma cells, eosinophils and neutrophils
among them, as well as by erythrocytes extravasated in the dermis. By virtue of specific findings cytopathologic,
e.g., atypical lymphocytes in the case of lymphomatoid papulosis, immature myelocytes in myelogenous leukemia,
and aberrant Langerhans' cells in histiocytosis X, the neoplastic process can be differentiated definitively from an
inflammatory one.
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Figure 5.50: A&B. Simulation of an inflammatory disease by a neoplastic process (a lymphoma) affiliated
with a mixed infiltrate of inflammatory cells and edema in the papillary dermis. At first glance at scanning
magnification, changes in lymphomatoid papulosis shown here could be misread as an inflammatory
process, the infiltrate often assuming the shape of a wedge and being made up of inflammatory cells in
addition to neoplastic lymphocytes. The finding of strikingly abnormal lymphocytes enables the condition to
be recognized for the lymphoma it is.
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Figure 5.51: A&B. Simulation of an inflammatory disease by a neoplastic process (a leukemia) associated
with extensive edema in the papillary dermis. Eye catching edema of the papillary dermis may be met with in
acute myelogenous leukemia, as illustrated here.
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Figure 5.52: A&B. Simulation of an inflammatory disease by a neoplastic process (histiocytosis X) marked
by extensive edema in the papillary dermis and a mixed infiltrate of inflammatory cells. At first blush, the
findings shown could be misjudged as those of an inflammatory process because of the edema and the mix
of inflammatory cells, but the presence of numerous abnormal Langerhans' cells compels to Letterer-Siwe
disease.
When, at scanning magnification, a determination is made that a perivascular infiltrate fulfills criteria for "interface
dermatitis," a decision then must be made about whether the type of change at the dermoepidermal junction is
"vacuolar" (a sprinkling of inflammatory cells, usually lymphocytes, in conjunction with vacuolar alteration along that
interface, a combination of findings that contributes to what normally is a sharply delineated junction now appearing
indistinct) (Fig. 5.53 A–C) or "lichenoid" (a bandlike infiltrate of inflammatory cells, usually lymphocytes, that, in
association with vacuolar alteration, tends to obscure the interface) (Fig. 5.54 A–C). A lichenoid infiltrate may be
continuous or discontinuous, that is, patchy (Fig. 5.55 A–C). Irrespective of whether the changes at the
dermoepidermal interface are "vacuolar" or "lichenoid," individual necrotic keratocytes, sometimes few and at other
times numerous in the epidermal basal layer or just above it, often are accompaniments (Fig. 5.56 A&B).
Episodically, clusters of necrotic keratocytes may form at or above the dermoepidermal junction. Very uncommonly,
a lichenoid infiltrate actually spares the interface between dermis and epidermis, a stereotypical example of that
phenomenon being an expression of the lichenoid purpura of Gougerot and Blum (Fig. 5.57 A&B); in that
circumstance, the epidermis largely is unaffected. By proceeding in algorithmic fashion, a specific diagnosis usually
can be reached for interface dermatitides of both "vacuolar" and "lichenoid" types.
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Figure 5.53: A. Interface dermatitis, vacuolar. B&C. Interface dermatitis, vacuolar, of lupus erythematosus.
The vacuoles at the junction of dermis and epidermis in this lesion of discoid lupus erythematosus are
accompanied by a sprinkling of lymphocytes and an occasional necrotic keratocyte, that constellation being
expected in many examples of the disease.
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Figure 5.54: A. Interface dermatitis, lichenoid, continuous (bandlike). B&C. Interface dermatitis, lichenoid,
continuous (bandlike), of lichen planus. The bandlike infiltrate pictured here extends across the entire front
of the upper part of the dermis.
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Figure 5.55: A. Interface dermatosis, lichenoid, discontinuous (patchy). B&C. Interface "dermatitis,"
lichenoid, discontinuous (patchy) of mycosis fungoides. The infiltrate of mycosis fungoides shown here
does not sweep across the entire front of the upper part of the dermis, but is distinctly interrupted. Note
the wiry bundles of collagen in haphazard array and the lymphocytes in a cluster in the epidermis, both
findings being expected in a longstanding patch/subtle plaque of mycosis fungoides.
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Figure 5.56: A&B. Findings encountered often in an interface dermatitis: necrotic keratocytes. In this
example of a vacuolar type of interface dermatitis, namely, dermatomyositis, necrotic keratocytes are
disposed as solitary units and in tiny clusters, especially in the lower part of the epidermis. Changes in the
epidermis such as these also may be met with an interface dermatitis of lichenoid type.
Figure 5.57: A&B. Lichenoid dermatitis with sparing of the dermoepidermal interface. A patchy lichenoid
infiltrate of lymphocytes that spares the dermoepidermal junction largely, but is joined by extravasated
erythrocytes, computes to the lichenoid purpura of Gougerot and Blum.
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As but one example of a sign that identifies with specificity interface dermatitides of the vacuolar type is a thickened
basement membrane of surface and infundibular epidermis (Fig. 5.58 A&B) and, episodically, of eccrine ductal
epithelium (Fig. 5.59 A&B), that strip indicating either discoid lupus erythematosus or dermatomyositis; those two
diseases at times may not be distinguishable from one another by conventional microscopy, but can be differentiated
if the infiltrate of lymphocytes is deep and/or dense, that presentation signifying lupus erythematosus. In addition to a
thickened basement membrane, discoid lupus erythematosus and dermatomyositis have in common a remarkable
tendency to a "smudged" (i.e., blurred) appearance of the dermoepidermal interface (Fig. 5.60 A&B) and to
prominent thinning of the epidermis, particularly in longstanding lesions marked by sclerosis of the uppermost part of
the dermis (Fig. 5.61 A&B). A caricature of the thinned epidermis that occurs in discoid lupus erythematosus is seen
also in dermatomyositis and in that distinctive disorder, a manifestation usually of lupus erythematosus known as
Degos' disease, in which the epidermis can be paper-thin, just as it may be in some manifestations of porokeratosis
(Fig. 5.62 A&B). The findings in the vacuolar type of interface dermatitis, such as that of lupus erythematosus, in
which inflammatory cells, usually lymphocytes, are scattered along the junction of dermis and epidermis (Fig. 5.63
A&B) are very different from those of flat or very slightly elevated lesions of mycosis fungoides in which lymphocytes
disposed as solitary units are positioned, in loci, smack in the basal layer of the epidermis itself (Fig. 5.64 A&B).
Those differences are crucial to distinguishing an inflammatory disease from the neoplastic (lymphomatous) one.
Figure 5.58: A&B. Diagnosis with specificity of an interface dermatitis: a thickened basement membrane.
The strikingly thickened basement membrane situated between the altered dermis and the thinned
epidermis is indicative here of discoid lupus erythematosus. A change in the basement membrane identical
to this may be seen in dermatomyositis.
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Figure 5.59: A&B. Diagnosis with specificity of an interface dermatitis: a thickened basement membrane. A
decidedly thickened basement membrane beneath surface epidermis and along an eccrine duct is typical of
a longstanding lesion of discoid lupus erythematosus, pictured here, and of dermatomyositis, and may be
present not only beneath surface epidermis, but along infundibular epidermis.
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Figure 5.60: A&B. Diagnosis with specificity of an interface dermatitis: a smudged appearance of the
dermoepidermal interface. The finding pictured at the interface is typical of lupus erythematosus and of
dermatomyositis.
Figure 5.61: A&B. Diagnosis with specificity of an interface dermatitis: a strikingly thinned epidermis. The
interface dermatitis of vacuolar type of lupus erythematosus illustrated here, and of dermatomyositis, may
be associated with a markedly thinned epidermis.
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Figure 5.62: A&B. An example of an extraordinarily thinned epidermis: porokeratosis, disseminated

superficial actinic type. The epidermis in the center of this lesion of disseminated superficial actinic
porokeratosis, the cornoid lamella being a signature for every type of porokeratosis, is paper-thin, a
circumstance also encountered episodically in discoid lupus erythematosus, in particular the expression of
it known as Degos' disease, and, at times, in dermatomyositis.
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Figure 5.63: A&B. An example of lymphocytes in conjunction with vacuoles at the dermoepidermal junction
of an interface dermatitis: lupus erythematosus. Lymphocytes, in company with vacuoles, are present at
the junction of dermis and epidermis in most interface dermatitides of the vacuolar type, lupus
erythematosus being a representative example.
Figure 5.64: A&B. Lymphocytes in the epidermal basal layer: mycosis fungoides, patch/subtle plaque stage.
In contrast to the situation in the vacuolar type of interface dermatitis, lymphocytes in a flattish lesion of
mycosis fungoides are present in the basal layer itself, and they are unaccompanied by vacuoles at the
interface. Note also the elongated mound of parakeratosis that so often graces a flat lesion of mycosis
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fungoides.
Episodically, lichenoid dermatitides may resemble closely one another histopathologically, but despite the similarities,
a precise diagnosis still can be made with confidence by paying heed to criteria that enable distinctions to be made
among them. For example, it is possible by virtue of notation of perceivable differences to diagnose with specificity
lichen planus (Fig. 5.65 A&B), lichen planus-like drug eruption (Fig. 5.66 A&B), lichenoid photodermatitis, lichenoid
discoid lupus erythematosus (Fig. 5.67 A&B), lichenoid purpura (Fig. 5.68 A&B), lichen striatus (Fig. 5.69 A&B),
acrodermatitis chronica atrophicans (Fig. 5.70 A&B), lichen planus-like keratosis (Fig. 5.71 A&B), porokeratosis (Fig.
5.72 A&B), mycosis fungoides (Fig. 5.73 A&B), and Bowen's disease (Fig. 5.74 A&B) when that latter superficial
carcinoma is obscured largely by a lichenoid infiltrate of lymphocytes.
Figure 5.65: A&B. Lichenoid dermatitis, lichen planus. The bandlike infiltrate of lymphocytes in lichen planus
cuts a swath across the upper part of the dermis.
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Figure 5.66: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid drug eruption differs from true
lichen planus by absence of characteristic changes in the epidermis, seen particularly well on the right of
the photomicrograph shown at scanning magnification, and the presence of numerous eosinophils in the
upper part of the reticular dermis.
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Figure 5.67: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid dermatitis, to wit, lichenoid discoid
lupus erythematosus, differs from lichen planus in several respects, not the least of which is the presence
of a distinctly thickened basement membrane at the interface of dermis and surface epidermis.
Figure 5.68: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid dermatitis, namely, that of the
lichenoid purpura of Gougerot and Blum, differs from lichen planus by absence of wedge-shaped
hypergranulosis and jagged acanthosis, and presence of numerous erythrocytes extravasated in the
papillary dermis and epidermis.
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Figure 5.69: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid dermatitis, that is, lichen striatus,
differs from authentic lichen planus in several ways, among those being the striking adnexocentricity, in
particular, eccrocentricity, of lymphocytes.
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Figure 5.70: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid dermatitis made up mostly of
plasma cells is typical of acrodermatitis chronica atrophicans.
Figure 5.71: A&B. Lichenoid infiltrate, not a dermatitis. This is not a dermatitis, but a benign neoplasm, i.e.,
a lichen planus-like keratosis, which differs from lichen planus by absence of wedge-shaped
hypergranulosis in repeatable intervals and the presence of parakeratosis. What is designated "lichen
planus-like keratosis" actually is a solar lentigo in the process of undergoing involution consequent to the
effects on it of products of lymphocytes.
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Figure 5.72: A&B. Lichenoid infiltrate, not a dermatitis. This process, namely, disseminated superficial
porokeratosis, characterized at this stage of its chronological course by a patchy lichenoid infiltrate of
lymphocytes, differs from lichen planus by distinct columns of parakeratosis, i.e., cornoid lamellae,
oriented, as often is the case, at a tangent. Unlike an authentic inflammatory disease, porokeratosis never
disappears.
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Figure 5.73: A&B. Lichenoid infiltrate, not a dermatitis. This lichenoid infiltrate is not that of a dermatitis, but
of a lymphoma, namely, mycosis fungoides, it differing from lichen planus in several ways, the most
important for diagnosis being the presence of lymphocytes accompanied by paltry spongiosis in the
spinous zone of the epidermis.
Figure 5.74: A&B. Lichenoid infiltrate, not a dermatitis. This lichenoid infiltrate is a response to a malignant
neoplasm, i.e., Bowen's disease, which is one expression of superficial squamous-cell carcinoma. The
strikingly abnormal pagetoid keratocytes in the spinous zone are characteristic of one presentation of
Bowen's disease. As a general principle, superficial malignant neoplasms in skin tend to be associated, to
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variable extent, with infiltrates of lymphocytes.
Of the manifold manifestations histopathologic of drug eruptions, those corresponding to each of the eight basic
patterns, the most common by far is interface dermatitis, it being of both the vacuolar and the lichenoid types. One
clue to diagnosis of a lichenoid drug eruption, in contradistinction to authentic lichen planus, is a constellation of
epidermal changes, namely, clusters of necrotic keratocytes, thinning of the granular zone, and loci of parakeratosis
(Figs. 5.75 A&B, 5.76 A&B, and 5.77 A&B).
Figure 5.75: A&B. Lichenoid dermatitis, not lichen planus. This particular lichenoid drug eruption, induced
by gold, differs from lichen planus by the presence of many clusters of necrotic keratocytes, a thinned
epidermis, no wedge-shaped hypergranulosis, and a basket-weave quality of the stratum corneum.
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Figure 5.76: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid drug eruption differs from lichen
planus by virtue of necrotic keratocytes in extraordinary number, many of them arranged in clusters, in the
lower part of the epidermis, a granular zone thinned focally, and parakeratosis.
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Figure 5.77: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid drug eruption differs from lichen
planus by the vast number of necrotic keratocytes, many of them arranged in clusters, a granular zone
thinned focally, absence of wedge-shaped hypergranulosis in repeatable fashion, and a cornified layer with
a basket-weave pattern.
A lichenoid infiltrate made up mostly of plasma cells is characteristic of a stage in the evolution of acrodermatitis
chronica atrophicans (Fig. 5.78 A&B), of plasma cells and histiocytes in secondary syphilis (Fig. 5.79 A&B), and of
histiocytes mostly in a particular manifestation of sarcoidosis. An immunoperoxidase stain specific for the spirochete
of Treponema pallidum allows that causative agent to be revealed in all its splendor (Fig. 5.80 A&B).
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Figure 5.78: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid mixed-cell infiltrate, replete with
plasma cells, is affiliated with coarse bundles of collagen in the upper part of the dermis and a thinned
epidermis, the findings being characteristic of a longstanding lesion of acrodermatitis chronica atrophicans.
Figure 5.79: A&B. Lichenoid dermatitis, not lichen planus. This lichenoid mixed-cell infiltrate made up mostly
of plasma cells and histiocytes obscures the dermoepidermal interface of an epidermis, which is thinned
focally and parakeratotic, findings typical of secondary syphilis.
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Figure 5.80: A&B. Confirmation of a diagnosis of secondary syphilis. The spirochetal cause of this patchy
lichenoid infiltrate of lymphocytes, plasma cells, and histiocytes is established, indubitably, by an
immunoperoxidase stain specific for Treponema pallidum. As a general principle, a histopathologist should
refrain from issuing a diagnosis, unequivocally, of syphilis in sections stained conventionally by
hematoxylin and eosin.
Reflection on two examples of "lichenoid dermatitis" just mentioned, to wit, acrodermatitis chronica atrophicans and
secondary syphilis, compels to the recognition that the bandlike infiltrate in those two conditions not only is different
from that of lichen planus by virtue of the composition of inflammatory cells themselves (plasma cells being invariable
in those two infectious diseases, rarely being present in true lichen planus (see Figs. 5.54 B&C and 5.65 A&B), but
by the width of the band itself; as a rule, the lichenoid infiltrate in lichen planus is not as wide as that of
acrodermatitis chronica atrophicans and secondary syphilis, infiltrates in the latter two extending well into the
reticular dermis (Fig. 5.81 A&B). In short, "lichenoid" as used in this work designates a bandlike infiltrate situated
immediately beneath the epidermis, one that may extend for only a short distance below the papillary dermis but, at
times, extending well into the upper part of the reticular dermis.
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Figure 5.81: A&B. Location of the lichenoid infiltrate of secondary syphilis. The infiltrate composed largely
of plasma cells extends from immediately beneath the epidermis well into the reticular dermis, considerably
below that of the usual band of lymphocytes in lichen planus. The pattern of the infiltrate pictured here
illustrates how subjective are judgments made about patterns such as "lichenoid," "nodular," and "diffuse."
Of course, there are instances when a particular lichenoid dermatitis defies efforts, no matter how valiant, to
decipher it diagnostically. That situation, as always is the case when uncertainty prevails, calls for a diagnosis
descriptive and a note that seeks to inform the managing clinician of possibilities, realistically, in differential
diagnosis. In such circumstances, it is advisable for a histopathologist to request a clinician to apprise of the
sequence of the disease as it plays out over time, the hope being that an accurate diagnosis can be reached one
day as a consequence of summation of clinical features, histopathologic findings, and biologic course. Even better in
an endeavor to expedite the process of coming to a diagnosis with precision, especially if the histopathologist also is
a dermatologist and if the clinician and patient are receptive, is viewing the lesions in vivo, i.e., "in the flesh," grossly,
by the same person who "read" the sections of tissue, i.e., the dermatohistopathologist (a term meant here as
generic for any colleague who is engaged seriously in diagnosis by conventional microscopy of diseases of the skin).
That exercise in clinicopathologic correlation enhances greatly the chance of coming to an accurate diagnosis with
specificity.
When, at scanning power, a perivascular dermatitis is seen to be joined by ballooned keratocytes in the spinous zone
of the epidermis, the pattern is designated "ballooning dermatitis" (Fig. 5.82A). Ballooning may occur as the only
change in an epidermis, as at a very early stage in infection by the virus of herpes (Fig. 5.82 B&C), or in company
with interface changes, as in erythema multiforme and fixed drug eruption (Fig. 5.83 A&B), in association with
spongiosis, as in prurigo pigmentosa (Fig. 5.84 A&B), and in conjunction with acantholysis, as in a fully developed
lesion of infection by herpesvirus. Several other viral diseases are typified by ballooning so striking that it is destined
to eventuate in vesiculation intraepidermal, e.g., vaccinia, variola, and hand-foot-and-mouth disease. Ballooning en
route to vesiculation progresses through a stage in which the distorted epidermis assumes a netlike configuration, a
pattern referred to as reticular alteration and one that is associated, invariably, with necrosis of keratocytes in the
zone of epidermis affected (Fig. 5.85 A&B). It should be noted, however, that severe ballooning of spinous cells may
lead to necrosis of individual keratocytes in the absence of reticular alteration (Fig. 5.86 A&B). When necrosis
secondary to ballooning is extensive, especially that which progresses to striking reticular alteration, it no longer may
be possible to detect nuclear changes diagnostic of infection by herpesvirus, such as steel gray nuclei and
"margination" of nucleoplasm, i.e., accentuation of nucleoplasm at the periphery of the nucleus, the findings late at
that stage being indistinguishable from those at a comparable stage of erythema multiforme, fixed drug eruption, and
Mucha-Habermann disease (Fig. 5.87 A&B).
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Figure 5.82: A. Ballooning. B&C. Ballooning in infection by herpesvirus. Known also as "intracellular
edema," ballooning, as the name denotes, pertains to cytoplasm that appears to be increased substantially
and of pale hue. It may be the most striking change in an epidermis, as is the case here in this lesion early
in the course of infection by herpesvirus, which also sports binucleate and multinucleate spinous cells.
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Figure 5.83: A&B. Ballooning in conjunction with necrotic keratocytes in an interface dermatitis: fixed drug
eruption. Markedly ballooned cytoplasm of keratocytes eventuates in necrosis, as shown. Lymphocytes are
present in association with vacuolar alteration at the dermoepidermal junction and in the zone of ballooned
keratocytes. Most examples of fixed drug eruption show interface changes of vacuolar type, but here they
are of lichenoid type.
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Figure 5.84: A&B. Ballooning in conjunction with spongiosis: prurigo pigmentosa. The occurrence, jointly,
of ballooning and spongiosis is common in prurigo pigmentosa, depicted here and characterized, too, by
neutrophils in the edematous papillary dermis and in the epidermis.
Figure 5.85: A&B. Ballooning eventuating in reticular alteration and necrosis of keratocytes en masse:
erythema multiforme. Extensive ballooning, as pictured in this lesion of erythema multiforme, results,
always, in necrosis of individual keratocytes affected. Inevitable equally is necrosis en masse in a zone of
reticular alteration, that distinctive pattern coming into being as a consequence of rupture of ballooned
keratocytes, as was the situation here.
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Figure 5.86: A&B. Ballooning as an antecedent to necrosis: erythema multiforme. Ballooning, if severe,
leads inexorably to necrosis of keratocytes without proceeding necessarily to reticular alteration, as is the
situation here in this example of erythema multiforme.
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Figure 5.87: A&B. Ballooning eventuating in reticular alteration and necrosis of keratocytes en masse:
Mucha-Habermann disease. Severe ballooning of keratocytes results, invariably, in reticular alteration,
every instance of which is associated with necrosis of all of the keratocytes affected, as is the situation in
this lesion of Mucha-Habermann disease.
When, at scanning magnification, a perivascular dermatitis is seen to be affiliated with a focus, or with foci, of
spongiosis, the pattern is termed "spongiotic dermatitis" (Fig. 5.88A). In the vast majority of instances, spongiosis is
mediated by lymphocytes (Fig. 5.88 B&C), but, on occasion, it is brought into being by eosinophils (Fig. 5.89 A&B)
and, episodically, by neutrophils (Fig. 5.90 A&B). Although more than a score of spongiotic dermatitides have been
identified, two sets of them are sampled by biopsy often, the diseases in each of those sets being indistinguishable
histopathologically from one another. A duo is represented by the "identical twins" pityriasis rosea and erythema
annulare centrifugum (Fig. 5.91 A&B) and a foursome by the lookalikes allergic contact dermatitis/nummular
dermatitis (Fig. 5.92 A&B), dyshidrotic dermatitis/id reaction (Fig. 5.93 A&B). At times, however, it may be
exceedingly difficult to distinguish a particular example of pityriasis rosea from one of nummular dermatitis (Fig. 5.94
A&B). Because spongiosis is one of many patterns in an epithelium that superficial fungi are able to induce (Fig. 5.95
A&B), the cornified layer of a spongiotic dermatitis should be inspected critically, as a routine, for hyphae of
dermatophytosis (Fig. 5.96 A–D), those organisms having a predilection for orthokeratotic cells and an aversion to
both parakeratotic ones and serum, their favorite haunt being at the interface between a zone of altered cornification,
e.g., parakeratosis, and the normal stratum corneum above it ("sandwich sign") (Fig. 5.97 A&B). The same caveat
applies to the findings of neutrophils in the epidermis (and, at times, the upper part of the dermis): A stratum
corneum of a section of tissue so affected should be searched scrupulously for the presence of dermatophytes.
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Figure 5.88: A. Spongiosis. B&C. Spongiosis mediated by lymphocytes in allergic contact dermatitis. Known
also as "intercellular edema," spongiosis may be the dominant change in an epidermis, as in this lesion of
allergic contact dermatitis where lymphocytes were responsible for bringing spongiosis into being.
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Figure 5.89: A&B. Spongiosis mediated by eosinophils: allergic contact dermatitis. Spongiosis in this
instance is seen to eventuate in vesiculation, eosinophils, and to a lesser extent, lymphocytes, being
responsibly for these changes in this example of allergic contact dermatitis.
Figure 5.90: A&B. Spongiosis mediated by neutrophils: prurigo pigmentosa. Uncommonly, neutrophils are
vehicles to induction of spongiosis, as in this example of prurigo pigmentosa where, in foci, spongiosis has
eventuated in tiny spongiotic vesicles. If, however, neutrophils are present in larger numbers in an
epidermis, what may have begun as spongiosis ends, inevitably, as pustulation.
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Figure 5.91: A&B. Lookalikes histopathologic: pityriasis rosea and erythema annulare centrifugum. The
spongiotic dermatitis accompanied by small mounds of parakeratosis is typical of pityriasis rosea; changes
identical to these may be seen in erythema annulare centrifugum.
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Figure 5.92: A&B. Lookalikes histopathologic: allergic contact dermatitis and nummular dermatitis. This
spongiotic dermatitis on glabrous skin is either allergic contact dermatitis or nummular dermatitis, the two
being indistinguishable from one another histopathologically.
Figure 5.93: A&B. Lookalikes histopathologic: allergic contact dermatitis, nummular dermatitis, dyshidrotic
dermatitis, and "id" reaction. This spongiotic dermatitis on volar skin could be any one of four "conditions"
that look like one another histopathologically, but usually are distinguishable readily clinically. In this
instance, the patient had dyshidrotic dermatitis.
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Figure 5.94: A&B. Differential diagnosis of a spongiotic dermatitis: pityriasis rosea versus nummular
dermatitis. Sometimes it is exceedingly difficult to decide this issue on the basis of findings microscopic
alone. Clues here to the diagnosis of nummular dermatitis are edema of the papillary dermis, extent of
acanthosis, and amount of serum in the scale-crusts.
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Figure 5.95: A&B. Diagnosis with specificity of a spongiotic dermatitis: dermatophytosis. These changes
were brought into being by the effects of dermatophytes situated in the stratum corneum, hyphae being
identifiable at high magnification. A clue to the diagnosis is marked edema in some dermal papillae.
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Figure 5.96: A–D. Diagnosis with specificity of a spongiotic dermatitis: dermatophytosis. This spongiotic
dermatitis was brought about by dermatophytes that reside in the stratum corneum. A clue to the diagnosis
is the presence of neutrophils in a mound of parakeratosis. The hyphae are seen better in the sections
stained by periodic acid Schiff (PAS).
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Figure 5.97: A&B. "Sandwich sign" of dermatophytosis. Dermatophytic fungi often are detected best at the
interface between parakeratosis and orthokeratosis, that clue being known as the "sandwich sign."
A spongiotic dermatitis may progress to become a spongiotic psoriasiform dermatitis and then a psoriasiform
dermatitis before restitutio ad integrum (Fig. 5.98 A&B). During the stages marked by spongiosis, lesions may be
topped either by scale-crusts (parakeratosis with serum in variable amount) (Fig. 5.99) or by scale (parakeratosis
alone) (Fig. 5.100).
Figure 5.98: A&B. Chronological sequence of one type of spongiotic dermatitis: nummular dermatitis. What
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begins as spongiotic dermatitis, as in this example of nummular dermatitis, tends to proceed to spongiotic
psoriasiform dermatitis and, eventually, to psoriasiform dermatitis devoid of spongiosis.
Figure 5.99: Scale-crusts. Two scale-crusts, that term co-opted from clinical dermatology for purposes
histopathologic, the one on the left consisting mostly of serum enveloped by parakeratosis, the one on the
right mostly of parakeratosis that houses globules of serum, are indications that definitive spongiosis was
present earlier at this site.
Figure 5.100: Scales. Mounds of parakeratosis devoid of serum is manifested clinically as scale, that term
being employed by us for findings histopathologic as well as clinical. From changes such as these, it may
be inferred that a tad of spongiosis was present earlier at this site, it being too negligible to have
contributed discernible serum to the mounds of parakeratosis pictured.
Episodically, lymphocytes in foci of spongiosis induced by hyphae of dermatophytosis may be numerous and larger
than usual, a circumstance that may seduce a microscopist into misperceiving a fungal disease as lymphomatoid
papulosis or mycosis fungoides, a pitfall that is avoided by spying the offending organisms in the cornified layer.
Another trap to be reckoned with is spongiotic simulation of "Pautrier's microabscesses" of mycosis fungoides. The
changes in the epidermis in both the spongiotic simulator and the "real thing" are focal, discrete, and associated with
mononuclear cells, but in a true spongiotic simulator (Fig. 5.101 A&B), the roundish cluster of cells consists mostly of
keratocytes (often still displaying intercellular bridges) and Langerhans' cells, in company with a sprinkling of small
lymphocytes and, at times, evidence of serum, whereas in an authentic roundish collection of Pautrier (Fig. 5.102
A&B), nearly all the cells are abnormal lymphocytes, packed together tightly and unaccompanied by serum.
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Figure 5.101: A&B. Spongiotic simulation of "Pautrier's microabscesses": spongiotic simulators of

collections ("microabscesses") of Pautrier in this lesion of Giamatti-Crosti disease consist of foci of
spongiosis that are made up mostly of keratocytes, but also of Langerhans' cells and lymphocytes, in
contrast to that attributed wrongly to Pautrier, which is composed nearly entirely of abnormal lymphocytes
of mycosis fungoides.
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Figure 5.102: A&B. "Pautrier's microabscesses." Collections of Pautrier differ from spongiotic simulators of
them by being composed, virtually entirely, of abnormal lymphocytes of a lymphoma. The term is wrong on
both counts: Darier, not Pautrier, was the first to call attention to it and the collections are not abscesses,
being made up as they are of lymphocytes, not neutrophils.
Lymphocytes in an "interface dermatitis" do not come to a halt abruptly when they arrive at the junction between
dermis and epidermis; some of them actually enter the spinous zone where they evoke spongiosis. For that reason,
a hint of spongiosis may be noted in "interface dermatitides" such as erythema multiforme, Mucha-Habermann
disease, certain viral exanthems, certain drug eruptions (Fig. 5.103 A&B), and, rarely, even in secondary syphilis
(Fig. 5.104 A&B). Of course spongiosis, albeit negligible, may occur in flattish lesions of mycosis fungoides (Fig.
5.105 A&B), lymphocytes being present there as solitary units in the spinous zone. Usually, however, the individual
lymphocytes, few and often far between, in the epidermis of mycosis fungoides fail to induce any spongiosis, or very
little of it; that phenomenon of seeming inertness of dispersed lymphocytes should call to mind the possibility likely of
mycosis fungoides (Fig. 5.106 A&B).
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Figure 5.103: A&B. Spongiosis in conjunction with vacuolar alteration: drug eruption. A spongiotic
dermatitis with parakeratosis that is joined by interface dermatitis of the vacuolar type should call to mind
the likelihood of a drug eruption, which is the diagnosis here.
Figure 5.104: A&B. Spongiosis in conjunction with a lichenoid infiltrate: secondary syphilis. When
lymphocytes in a lichenoid dermatitis, here composed mostly of plasma cells in secondary syphilis, enter
the spinous zone, as they do episodically, spongiosis also is induced.
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Figure 5.105: A&B. Spongiosis in a neoplastic process: mycosis fungoides. When lymphocytes pepper an
epidermis, even in a lymphoma such as that manifestation of mycosis fungoides designated pagetoid
reticulosis (Woringer-Kolopp disease) shown here, some spongiosis is inevitable, although only a tiny
fraction of what would have been induced by lymphocytes of an inflammatory disease.
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Figure 5.106: A&B. Lymphocytes in an epidermis virtually devoid of spongiosis: mycosis fungoides.
Numerous lymphocytes scattered in an acanthotic epidermis nearly bereft of spongiosis is characteristic of
a patch/subtle plaque of mycosis fungoides. In contrast, a few lymphocytes scattered in an epidermis of an
inflammatory disease, such as allergic contact dermatitis, bring about prominent spongiosis and even
spongiotic vesiculation.
Spongiosis within infundibular epidermis is crucial to diagnosis of an uncommon condition known as disseminate and
recurrent infundibulofolliculitis, and it is a feature, too, of the common conditions seborrheic dermatitis (Fig. 5.107
A&B), rosacea and variants of it, namely, perioral and periocular dermatitis, and some responses to the "bite" of an
insect, that critter homing to infundibula that offer a delicacy, namely, sebaceous secretion, which is made more
aromatic and more savory by the effects on it of the mite Demodex, the yeast Pityrosporum, and the bacteria
Staphylococci and Corynebacteria.
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Figure 5.107: A&B. Spongiosis in both infundibular and surface epidermis: seborrheic dermatitis.
Spongiosis is present not only in the acanthotic surface epidermis that boasts mounds of parakeratosis,
but in infundibular epidermis, too, findings diagnostic of seborrheic dermatitis.
When a perivascular dermatitis is coupled with psoriasiform acanthosis, the pattern is termed "psoriasiform
dermatitis" (Fig. 5.108A). For purposes of the method utilized here, psoriasiform refers to epidermal changes like
those in a fully developed lesion of psoriasis (Fig. 5.108 B&C), i.e., one in which epidermal rete ridges are distinctly
elongated and the precipitously sinuous pattern formed by them and dermal papillae is maintained. Conceptually,
however, the pattern of a lesion of eruptive (guttate) psoriasis (Fig. 5.109 A&B) is just as psoriasiform as that of a
plaque of psoriasis, but for us in regard to purposes pedagogical, the guttate is not the stereotype of psoriasiform; a
fully formed plaque is. In this context, when rete ridges are of equal length, the psoriasiform acanthosis is termed
"even" (see Fig. 5.108 B&C) (and usually signifies psoriasis) and when they are not of uniform length, it is called
"uneven" (Fig. 5.110 A&B) (and generally indicates a condition other than psoriasis, such as chronic allergic contact
dermatitis/nummular dermatitis or dermatophytosis). Other distinctive signs enable a microscopist to differentiate the
more common psoriasiform dermatitides one from another, e.g., psoriasis, chronic allergic contact dermatitis and
chronic nummular dermatitis, lichen simplex chronicus (which, in actuality, is not a true inflammatory disease, the
inflammatory cells present there being called forth by energetic, persistent rubbing), and pityriasis rubra pilaris.
Except for the finding of hyphae in the cornified layer, dermatophytosis, at every stage of its course chronologically,
may be indistinguishable from psoriasis. A clue to diagnosis of the psoriasiform dermatitis of psoriatic erythroderma
is the disparity between the thickness of the viable epidermis and the thinness of the stratum corneum, only a few
parakeratotic cells still being in place, the vast majority of them having been desquamated as a consequence of the
exfoliative process.
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Figure 5.108: A. Psoriasiform dermatitis. B&C. Fully developed psoriasis as the prototype of psoriasiform
dermatitis. The model for psoriasiform dermatitis is a fully developed lesion of psoriasis, shown here. Note
the dramatic pin-hair turn undulations between thin rete ridges of even length and thin dermal papillae, the
latter housing a dilated tortuous capillary that spirals to very near the base of a thinned suprapapillary
plate.
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Figure 5.109: A&B. Guttate psoriasis, conceptually, is as psoriasiform as is a plaque of psoriasis. Eruptive
(guttate) psoriasis is characterized by slight acanthosis and mounds of parakeratosis with neutrophils at
their summit, the mounds pictured here being staggered beneath the original cornified layer with its
basket-weave configuration. In theory, this particular manifestation of psoriasis is just as "psoriasiform" as
the prototype of psoriasis depicted in Figure 5.108.
Figure 5.110: A&B. Psoriasiform dermatitis, uneven. The psoriasiform acanthosis is uneven because rete
ridges are of uneven length (and breadth). Hyphae in the cornified layer establish this psoriasiform
dermatitis as that of dermatophytosis.
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As a rule, psoriasiform dermatitides are affiliated with abnormalities in cornification that take the form usually of
parakeratosis that, not uncommonly, is joined by orthokeratosis. That combination of ortho- and parakeratosis
assumes a variety of patterns that are helpful in coming to diagnosis with specificity, such as broad tiers of
parakeratosis that alternate with less dramatic tiers of orthokeratosis, both of them in horizontal array, in psoriasis
(Fig. 5.111), and small "squares" of parakeratosis that alternate with "squares" of orthokeratosis in both horizontal
and vertical arrangement in pityriasis rubra pilaris (Fig. 5.112). The psoriasiform dermatitis of seborrheic dermatitis is
typified by mounds of parakeratosis or of scale-crust situated at the lips of ostia of infundibula (Fig. 5.113).
Figure 5.111: Findings in the cornified layer specific for psoriasis. Alternation of parakeratosis with
orthokeratosis, in vertical and periodic fashion, throughout a thickened stratum corneum is specific for
psoriasis.
Figure 5.112: Findings in the cornified layer specific for pityriasis rubra pilaris. The alternation of
orthokeratosis and parakeratosis, vertically and horizontally, is characteristic of pityriasis rubra pilaris.
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Figure 5.113: Findings in the cornified layer specific for seborrheic dermatitis. Mounds of scale-crust at the
lips of an infundibular ostium are typical of seborrheic dermatitis.
A person with a disposition to psoriasis genetically is susceptible to induction of a Koebner (isomorphic) phenomenon
wherein a lesion of psoriasis may be brought forth by trauma to the skin of different kinds, and that is what seems to
happen histopathologically when an eruption, such as that of graft-versus-host reaction (Fig. 5.114 A&B) or a
neoplastic process, such as a subtle plaque of mycosis fungoides (Fig. 5.115 A&B) occurs in a patient with a
psoriatic diathesis. In addition to telltale signs of the primary process, for example, mycosis fungoides characterized
by lymphocytes in dermal papillae, in the basal layer in loci, and in the spinous zone in company with scant
spongiosis, there are typical findings of psoriasis, such as edema of dermal papillae, long, thin rete ridges of rather
equal length, decrease in the width of the granular zone focally, and parakeratosis (Fig. 5.116 A&B); sometimes
mounds of parakeratosis are staggered in the cornified layer, the summit of the mounds often being chock full of
neutrophils.
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Figure 5.114: A&B. Koebnerization: psoriasis by graft-versus-host disease. Two different pathologic
processes are at play, concurrently, namely, graft-vs-host reaction evidenced by numerous necrotic
keratocytes, and psoriasis, which was brought into being presumably as a Koebner phenomenon in
response to the "trauma" inflicted on the skin by the graft-vs-host reaction. The presumption is based on
the assumption that the patient afflicted is a psoriatic genetically.
Figure 5.115: A&B. Koebnerization: psoriasis by mycosis fungoides. Two different processes are engaged
concurrently here, namely, mycosis fungoides, evidenced by numerous lymphocytes at the summit of
dermal papillae and in a spinous zone that exhibits scant spongiosis, and psoriasis, all of the findings of
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which are apparent at scanning magnification. The infiltrate of mycosis fungoides served to induce
psoriasis in a patient psoriatic genetically.
Figure 5.116: A&B. Koebnerization: psoriasis by mycosis fungoides. The findings pictured could be
misconstrued as those of psoriasis alone, but the patchy lichenoid infiltrate and numerous lymphocytes in
dermal papillae and in the spinous zone, in conjunction with paltry spongiosis, are indicative of mycosis
fungoides that induced findings of psoriasis in a patient who is a psoriatic genetically.
As already has been stated, more than one pattern of perivascular dermatitis may be discerned in a single section of
tissue, the associations met with most often being spongiotic, lichenoid, and psoriasiform. Even at scanning power, a
histopathologist is able to recognize easily the combinations of spongiotic lichenoid dermatitis (Fig. 5.117A),
spongiotic psoriasiform dermatitis (Fig. 5.117B), spongiotic psoriasiform lichenoid dermatitis (Fig. 5.117C), and
psoriasiform lichenoid dermatitis (Fig. 5.117D). Each of those combinations of patterns has importance because
each is a beacon for consideration diagnostically of certain diseases. Spongiotic and vacuolar changes together (and
even ballooning, too) are observed episodically in lesions of erythema multiforme, fixed drug eruption (Fig. 5.118
A&B), and Mucha-Habermann disease at an early stage of those conditions, but, as a rule, the dominant changes in
each of those three inflammatory diseases are found at the interface between epidermis and dermis; for that reason
they are regarded, for purposes of this algorithmic method predicated on pattern analysis, as interface dermatitides.
Spongiotic and lichenoid changes together are witnessed often in bullous pemphigoid at the urticarial stage of that
disease, the patchy bandlike infiltrate being composed of lymphocytes and many eosinophils (Fig. 5.119 A&B). In
spongiotic lichenoid dermatitis, as is the case in spongiotic vacuolar dermatitis, two different patterns are at play
simultaneously. But no matter in regard to coming to a diagnosis with specificity; the method advanced here also
permits the correct diagnosis to be reached through the routes algorithmically of spongiotic and ballooning dermatitis.
Curiously, hardly ever does a microscopist note a psoriasiform-vacuolar pattern and when, rarely, that is seen,
vacuoles in company with a sprinkling of lymphocytes are noticeable both at the base of rete ridges and along the
sides of them, as well as at suprapapillary plates (Fig. 5.120 A&B). Because that particular pattern, sometimes
joined by spongiosis, is so exceptional, when it is encountered, the culprit proves usually to be a drug given
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systemically.
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Figure 5.117: Combinations of patterns. A. Spongiotic lichenoid. B. Spongiotic psoriasiform. C. Spongiotic

psoriasiform lichenoid. D. Psoriasiform lichenoid.
Figure 5.118: A&B. Combination of patterns: interface and spongiotic in a fixed drug eruption. A
combination of interface (vacuolar) and spongiotic dermatitis is expected in some lesions of fixed drug
eruption at an early stage of that process. At times, those two patterns may be joined by ballooning. Other
evidences of acuteness in this lesion are neutrophils in the dermis, individual necrotic keratocytes, and a
stratum corneum still unaffected by that which transpired beneath it.
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Figure 5.119: A&B. Combination of patterns: interface and spongiotic in an urticarial lesion of bullous
pemphigoid. The presence of numerous eosinophils in conjunction with lymphocytes in a bandlike infiltrate,
in the context of this particular set of patterns, to wit, patchy lichenoid and spongiotic, establishes the
diagnosis as bullous pemphigoid.
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Figure 5.120: A&B. Psoriasiform vacuolar pattern, a rarity: drug eruption. A psoriasiform vacuolar pattern is
unusual and should call to mind the likelihood of a drug eruption, as was the case here. The numerous red
blood cells extravasated in the papillary dermis and the epidermis, in conjunction with a cornified layer still
normal, are indications of how explosive was this eruption.
Once a pattern of "perivascular dermatitis" (perivascular only, perivascular and interstitial only, interface, ballooning,
spongiotic, and psoriasiform) or a combination of the subdivisions (spongiotic lichenoid, spongiotic psoriasiform,
spongiotic psoriasiform lichenoid, and psoriasiform lichenoid) has been identified, a microscopist must proceed to
determine the composition, exactly, of the infiltrate, i.e., lymphocytes alone (Fig. 5.121 A&B) or a mixture of cells. A
mixed-cell infiltrate refers to any combination of lymphocytes, plasma cells, histiocytes, neutrophils, and eosinophils
(Fig. 5.122 A&B). The combinations and permutations of those cells also have importance for diagnosis. In the
category of perivascular and interstitial dermatitis only, for example, neutrophils and eosinophils are dominant in
urtica (Fig. 5.123 A&B), whereas lymphocytes and eosinophils predominate in a response to the assault by an
arthropod (Fig. 5.124 A&B). Even in urtica, however, some lymphocytes are positioned around venules, just as is the
case for those round cells in nearly all infiltrates made up of a mix of cells.
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Figure 5.121: A&B. "Lymphocytic infiltrate": a description generic. A perivascular dermatitis that is
"superficial and deep" and made up almost entirely of lymphocytes is designated, for purposes of
succinctness, "lymphocytic infiltrate." That distinctive pattern may be brought into being in polymorphous
light eruption, erythema figuratum, and the tumid expression of lupus erythematosus, the latter being
distinguishable from the others by the presence in abundance of mucin between bundles of collagen in the
reticular dermis.
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Figure 5.122: A&B. A mixed-cell infiltrate of an inflammatory disease: granuloma faciale/erythema elevatum
diutinum. A nodular mixed-cell infiltrate composed of neutrophils, nuclear "dust" of neutrophils,
eosinophils, lymphocytes, and plasma cells is characteristic of granuloma faciale/erythema elevatum
diutinum at a stage in the evolution of it.
Figure 5.123: A&B. A mixed-cell infiltrate of an inflammatory disease: urtica. A perivascular and interstitial
mixed-cell infiltrate made up mostly of neutrophils and eosinophils is typical of urtica at a fully developed
stage of it.
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Figure 5.124: A&B. A mixed-cell infiltrate of an inflammatory disease: assault by an arthropod. A

perivascular and interstitial mixed-cell infiltrate that consists of lymphocytes and numerous eosinophils is
indicative of a response to an assault by an arthropod.
Atypical lymphocytes in a mixed infiltrate of inflammatory cells are seen in one of the presentations of lymphomatoid
papulosis (Fig. 5.125 A&B), a lymphoma of CD30 type, whereas atypical lymphocytes in company with small
lymphocytes are observed episodically in an infiltrate induced by herpesvirus, yet accompanied by epidermal and
adnexal epithelium that fails to exhibit any of the nuclear or cytoplasmic changes characteristic of that infectious
process (Fig. 5.126 A&B). A monomorphous infiltrate of atypical lymphocytes signifies lymphoma (Fig. 5.127 A&B)
and a monomorphous infiltrate of mast cells indicates urticaria pigmentosa (Fig. 5.128 A&B), a benign neoplastic
process known also as mastocytosis.
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Figure 5.125: A&B. A mixed-cell infiltrate of a neoplastic disease: lymphomatoid papulosis. A perivascular
mixed-cell infiltrate composed predominantly of atypical lymphocytes, but also of small lymphocytes and
scattered neutrophils is that of lymphomatoid papulosis, a CD30 lymphoma.
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Figure 5.126: A&B. A mixed-cell infiltrate containing atypical lymphocytes in an inflammatory disease:
infection by herpesvirus. A moderately dense perivascular mixed-cell infiltrate made up mostly of atypical
lymphocytes, but also of small lymphocytes, is expected in one presentation of infection by herpesvirus in
which none of the cytopathologic changes epithelial, neither nuclear nor cytoplasmic, of that infection are
evident.
Figure 5.127: A&B. A monomorphous infiltrate in a neoplastic disease: lymphoma. An infiltrate made up
nearly entirely of atypical lymphocytes is that of lymphoma.
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Figure 5.128: A&B. A monomorphous infiltrate in a neoplastic disease: urticaria pigmentosa. An infiltrate
composed entirely of mast cells is that of urticaria pigmentosa (mastocytosis).
Where, precisely, cells of an infiltrate of an inflammatory disease are situated in regard to venules and the
interstitium, how dense is the infiltrate, and what cells constitute the infiltrate are helpful in determining where a
particular lesion is in the course of the "life" of it. For example, early in urtica, lymphocytes, neutrophils, and
eosinophils are found only around venules (Fig. 5.129 A&B), whereas later, neutrophils and mostly eosinophils are
scattered in the interstitium (Fig. 5.130 A&B), lymphocytes then being predominant around venules. Near the end,
neutrophils and eosinophils disappear, leaving as residuum a sparse infiltrate of lymphocytes perivascularly (Fig.
5.131 A&B).
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Figure 5.129: A&B. The life of a lesion: urtica, early. At an early stage of urtica, lymphocytes, neutrophils,
and eosinophils are huddled around venules.
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Figure 5.130: A&B. The life of a lesion: urtica, fully developed. At a fully developed stage of urtica,
neutrophils and eosinophils are scattered in the interstitium.
Figure 5.131: A&B. The life of a lesion: urtica, late. At a late stage of urtica, lymphocytes, alone (or joined by
a residual eosinophil), are present around venules.
The status of the stratum corneum is informative in regard to the duration of a particular "perivascular dermatitis with
epidermal changes" (interface, ballooning, spongiotic, and psoriasiform), i.e., from the time of inception of a lesion to
the moment of biopsy of it. For example, if in an inflammatory process, such as psoriasis, the cornified layer is
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perfectly normal, it may be inferred that the lesion is but a few days old. If, however, the original cornified layer is
separated from the viable epidermis by a few mounds of parakeratosis, then the process may be intuited to be more
than a week old. If, in exaggeration, the original cornified layer is removed far from the viable epidermis by numerous
mounds of parakeratosis in stepladder array, then it may be concluded, rightly, that the lesion is at least two weeks
old. Similar judgments may be made about Mucha-Habermann disease during the first two weeks in the life of a
lesion of it (Figs. 5.132 A&B, 5.133 A&B, and 5.134 A&B). In short, where, precisely, the cornified layer is situated
vis-à-vis the viable epidermis permits inferences to be drawn about where, approximately, a particular eruption
happens to be in the expected chronological course of it. Not surprisingly, by the time a lesion of Mucha-Habermann
disease is of several weeks duration, it has assumed a very different appearance in regard to the epidermis and
particularly to the cornified layer, the latter exhibiting no parakeratosis in mounds staggered, but rather an occasional
mound in what otherwise is orthokeratosis (Fig. 5.135 A&B). The status of the upper part of the viable epidermis,
namely, the uppermost part of the spinous zone and the entire granular zone, also may be informative in regard to
the duration of a particular type of "perivascular dermatitis with epidermal changes," the quintessential example of
that being the progression of pallor at those sites in the group of "deficiency diseases," that is, acrodermatitis
enteropathica, necrolytic migratory erythema, pellagra, Hartnup's disease, kwashiorkor, and maple syrup disease. In
the course of but a few days, pallor in the upper part of the viable epidermis (Fig. 5.136 A&B) increases dramatically
as the keratocytes affected become ballooned increasingly and the number of them, in width, increases, too (Fig.
5.137 A&B), at times even eventuating in intraepidermal vesiculation (Fig. 5.138 A&B). Concurrent with those findings
are ones in the stratum corneum, that layer progressing from being decorated by a thin band of parakeratosis (see
Fig. 5.136 A&B) to a formidable scale-crust (see Fig. 5.138 A&B). The changes are accompanied by an influx of
neutrophils into the epidermis, so great at times that spongiform pustules come into being.
Figure 5.132: A&B. Significance of a normal cornified layer for determining the age of an inflammatory
process very early in its course. At an early stage of this interface dermatitis, to wit, Mucha-Habermann
disease, the stratum corneum still is normal. A lesion such as this one is but a few days old.
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Figure 5.133: A&B. Significance of parakeratosis at the base of a normal cornified layer for judging the age
of an inflammatory process rather early in its course. At a stage of this interface dermatitis, namely, "acute"
Mucha-Habermann disease, later chronologically than that shown in Figure 5.132, the original normal
stratum corneum is present still, but at the base of it are some mounds of parakeratosis. This lesion is
about nine days old.
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Figure 5.134: A&B. Significance of an original normal cornified layer about to be shed by the effects of
ever-increasing scale-crust beneath it for assessing the age of an inflammatory process somewhat early in
its course. At a stage of Mucha-Habermann disease, still later than that shown in Figure 5.133, a large
scale-crust is situated beneath the original stratum corneum. This lesion can be inferred to be about two
weeks old.
Figure 5.135: A&B. The character of the cornified layer as an indication of the age of a lesion. The cornified
layer of this example of Mucha-Habermann disease is devoid of neutrophils and of mounds of parakeratosis
staggered, exhibiting instead orthokeratosis punctuated only episodically by a mound of parakeratosis.
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This lesion can be told to be at least several weeks old, it representing slow evolution, moving at the pace
of a tortoise (chronica), not of a hare (acuta).
Figure 5.136: A&B. Pallor of epidermal cells in a deficiency disease (acrodermatitis enteropathica), early.
Keratocytes in the uppermost part of the spinous zone and in the granular zone of the slightly acanthotic
epidermis are pale and covered by a broad thin band of parakeratosis.
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Figure 5.137: A&B. Pallor of epidermal cells in a deficiency disease (necrolytic migratory erythema), fully
developed. Keratocytes in the upper half of the spinous zone and in the granular zone of an acanthotic
epidermis are pale and clear because they are so extraordinarily swollen. Beneath the original cornified
layer, recognizable by its basket-weave appearance, can be seen the very beginning of formation of what
will be scale-crust.
Figure 5.138: A&B. Pallor of epidermal cells of a deficiency disease (acrodermatitis enteropathica), late.
Keratocytes throughout much of the markedly acanthotic epidermis are mostly clear because they are
swollen almost to the point of bursting, some of them already having ruptured to initiate what will be an
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intraepidermal blister. The lesion is topped by a formidable scale-crust.
Also instructive in regard to the duration of a particular lesion of an inflammatory process is the position, precisely, of
melanophages in the upper part of the dermis and whether or not they are accompanied by any other changes. For
example, if melanophages alone are present just beneath the epidermis (Fig. 5.139 A&B), it may be inferred that that
lesion of postinflammatory pigmentary alteration has come into being relatively recently, whereas if melanophages
are present near the base of the papillary dermis, the lesion must be one of longer standing (Fig. 5.140 A&B). If, for
example, melanophages are stationed in the upper part of the papillary dermis of an active lesion of fixed drug
eruption, it may be supposed that that distinctive eruption had occurred only once before at that very site, but if in the
context of all the findings histopathologic of fixed drug eruption, melanophages are found throughout the papillary
dermis and even in the upper part of the reticular dermis (Fig. 5.141 A&B), it may be intuited that the eruption has
developed repeatedly at that same site.
Figure 5.139: A&B. Significance of melanophages situated high in the papillary dermis in regard to
determining how long ago a particular lesion had been "active." When melanophages that represent
post-inflammatory pigmentary alteration reside just beneath the epidermis, it may be inferred that the
inflammatory process was "active" not too long ago.
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Figure 5.140: A&B. Significance of melanophages situated in the upper part of the reticular dermis in regard
to assessing how long ago a particular lesion had been "active." When melanophages indicative of
post-inflammatory pigmentary alteration are distributed around venules of the superficial plexus, as shown
here, it may be inferred that the initiating inflammatory process was "active" many months, if not years,
ago.
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Figure 5.141: A&B. Depth of melanophages as an indication of the history of a lesion of a fixed drug
eruption. Melanophages around venules of the superficial plexus of a fixed drug eruption, now in
efflorescence in the form of a distinctive interface dermatitis, are testimony to that eruption having
occurred previously, and more than once, at this very site.
In conclusion, by summation of the (1) pattern formed by infiltrates of inflammatory cells, (2) changes at the
dermoepidermal interface and in the epidermis, and (3) character of the inflammatory cells themselves, a
microscopist can "home in" on diagnosis of a particular perivascular dermatitis.
Infiltrates of some neoplastic diseases may assume patterns just like those of inflammatory diseases, the exemplar
of that being flat or very slightly elevated lesions of the lymphoma, mycosis fungoides, patches and subtle plaques of
which being known in times past as small- and large-plaque parapsoriasis. Those lesions often simulate inflammatory
diseases whose pattern is lichenoid, spongiotic, psoriasiform, or a combination of them, chief among those
combinations being spongiotic lichenoid, spongiotic psoriasiform lichenoid, and psoriasiform lichenoid, lymphocytes
being preponderant in all of those patterns. Whenever any of the patterns just mentioned are confronted in the
context of an infiltrate made up almost entirely of lymphocytes, the possibility of mycosis fungoides must be
entertained seriously. Signs confirmatory of that lymphoma, which manifests itself in a remarkably protean fashion
morphologically (both histopathologically and clinically), are wiry bundles of collagen in haphazard array (Fig. 5.142
A&B) in zones of patchy lichenoid infiltration (those bundles sometimes being more eye-catching than changes in the
epidermis), "stuffing" of dermal papillae by lymphocytes (Fig. 5.143 A&B), lymphocytes aligned as solitary units in
loci of the epidermal basal layer (Fig. 5.144 A&B), "peppering" of the spinous zone, in foci, by lymphocytes in
company with scant, if any, spongiosis (Fig. 5.145 A&B) (an exaggeration of that phenomenon being "pagetoid
reticulosis" [Fig. 5.146 A&B]), lymphocytes in the epidermis at times being much larger than lymphocytes in the
dermis (Fig. 5.147 A&B) and, episodically, lymphocytes in the granular zone and/or cornified layer (see Fig. 5.143
A&B), a situation usually not met with in a spongiotic dermatitis. Commonly, one or more incipient clusters of
lymphocytes are present in the viable epidermis (Fig. 5.148 A&B) and, uncommonly, small collections of lymphocytes
even are found in the non-viable cornified layer (see Fig. 5.143 A&B); commonly, patches and subtle plaques of
mycosis fungoides are decorated by elongated mounds of parakeratosis (Fig. 5.149 A&B), some of them punctuated
at times by a tad of serum, but practically never by a dollop of that homogeneous pink material. That being so,
plentiful serum in scale-crusts is a boon in differentiating some lesions of nummular dermatitis from mycosis
fungoides. It cannot be emphasized too firmly that "Pautrier's microabscesses" (see Fig. 5.102 A&B) —a misnomer
on both scores—are not requisite for diagnosis of flat and slightly elevated lesions of mycosis fungoides. In fact, only
rarely are those collections of lymphocytes found in patches and plaques of that lymphoma; tiny clusters are the rule,
if any collections of lymphocytes are present at all (Fig. 5.150 A&B). Episodically, lymphocytes as solitary units may
be present in an epidermis of a persistent pigmented purpuric dermatitis (Schamberg's, Gougerot/Blum, and
Doucas/Kapetenakis) that displays little spongiosis in association with those round cells (Fig. 5.151 A&B). The finding
of erythrocytes extravasated in the upper part of the dermis, and even in the epidermis, and/or siderophages
enables the inflammatory process to be distinguished from mycosis fungoides, to which it is not at all related. On
occasion, the infiltrate of lymphocytes in a patch of mycosis fungoides, that flat lesion having been designated in the
past either "large-plaque parapsoriasis" or "small-plaque parapsoriasis," is pathetically scant, but, even then, subtle
changes in the epidermis enable the correct diagnosis to be made, in the vast majority of instances, with assurance.
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Figure 5.142: A&B. Significance of wiry bundles of collagen in haphazard array in the papillary dermis in
regard to duration of a particular lichenoid infiltrate. Wiry bundles of collagen in conjunction with a patchy
lichenoid infiltrate of lymphocytes are encountered often in the patch/subtle plaque stage of mycosis
fungoides, as shown here, those bundles being a sign of the infiltrate having been present for many
months, probably years.
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Figure 5.143: A&B. "Stuffed derma sign" of mycosis fungoides. Dermal papillae stuffed with lymphocytes
are a finding common in subtle plaques of mycosis fungoides. At scanning magnification it is possible to
see that many papillae are filled by lymphocytes. At high magnification, lymphocytes as solitary units and in
tiny collections are apparent in the epidermis.
Figure 5.144: A&B. The importance of lymphocytes aligned, in loci, in the epidermal basal layer for
diagnosis of a macule/patch of mycosis fungoides. Lymphocytes disposed as solitary units in the basal
layer of the epidermis, if only in a small locus, such as illustrated here, are virtually diagnostic of a flat
lesion of mycosis fungoides.
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Figure 5.145: A&B. "Dolly Parton sign" of mycosis fungoides. The disparity between an epidermis peppered
by lymphocytes and paltry spongiosis in company with them, i.e., too much for too little, is indicative of
mycosis fungoides.
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Figure 5.146: A&B. Exaggeration of epidermotropism of lymphocytes in mycosis fungoides. A caricature of

the changes in Figure 5.145 is met with in "pagetoid reticulosis," known also as "Woringer-Kolopp disease,"
that particular expression of mycosis fungoides being typified by lymphocytes in profusion in an epidermis
that displays piddling spongiosis. Note the solitary lymphocytes in the cornified layer.
Figure 5.147: A&B. Lymphocytes in the epidermis larger than those in the dermis in mycosis fungoides.
Unique among cutaneous diseases is the phenomenon in mycosis fungoides of lymphocytes in the
epidermis being considerably larger than lymphocytes in the dermis, that happening been witnessed only
episodically.
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Figure 5.148: A&B. The irrelevance of "Pautrier's microabscesses" to diagnosis of flat and slightly elevated
lesions of mycosis fungoides. Despite trumpetings in the past of "Pautrier's microabscesses" being
requisite for diagnosis of mycosis fungoides, in reality, lymphocytes in the epidermis of patches and subtle
plaques of that disease are disposed mostly as solitary units and much less often in tiny clusters.
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Figure 5.149: A&B. The importance of elongated mounds of parakeratosis as a clue to diagnosis of flat or
slightly elevated lesions of mycosis fungoides. Elongated mounds of parakeratosis, especially in the
context of a slightly acanthotic epidermis that houses scattered lymphocytes in the near absence of
spongiosis, are an evidence in favor of mycosis fungoides.
Figure 5.150: A&B. Tiny collections of abnormal lymphocytes in mycosis fungoides. So incipient may be
clusters of abnormal lymphocytes in an epidermis of mycosis fungoides that discrete collections of them
have yet to form. The collections surely are not abscesses (made up as they are of lymphocytes, not
neutrophils), and they certainly were not described by Pautrier (they were called to his attention by Darier).
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Figure 5.151: A&B. Schamberg's disease as a simulator of mycosis fungoides. Although in foci within the
epidermis scattered lymphocytes are affiliated with scant spongiosis, findings suggestive highly of mycosis
fungoides, the presence of erythrocytes extravasated there in number and in the upper part of the dermis
exclude that condition from consideration. Schamberg's disease is unrelated to mycosis fungoides.
Although, at long last, dermatologists and dermatopathologists now acknowledge that "large-plaque parapsoriasis" is
mycosis fungoides, the vast majority of colleagues, including the authors of every textbook, continue to affirm that
"small-plaque parapsoriasis," that is, digitate and guttate dermatosis, is not mycosis fungoides, despite the fact that
clinically, histopathologically, and biologically (the lesions tend to persist and enlarge slowly, not involuting in the
absence of treatment as is the rule for inflammatory diseases) it fulfills criteria for mycosis fungoides.
Macules and papules of urticaria pigmentosa, especially as that disease presents itself as telangiectasia macularis
eruptiva perstans (Fig. 5.152 A&B), may mimic inflammatory conditions whose pattern is perivascular and interstitial;
what, at first glance, seems to be an infiltrate of inflammatory cells, on inspection closely turns out to be made up
mostly of neoplastic mast cells. Microscopists must be alert exquisitely to the trap posed by each of the mimics
neoplastic of inflammatory diseases of the skin.
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Figure 5.152: A&B. Mastocytosis as a simulator of a perivascular and interstitial dermatitis. A

monomorphous infiltrate of small mononuclear cells scattered among telangiectatic vessels could be
misconstrued as changes of an inflammatory process, but when those mononuclear cells are noted to be
mast cells, as is the situation here, the diagnosis is telangiectasia macularis eruptiva perstans, one of
several distinctive manifestations of urticaria pigmentosa.
Before ending this discussion of the "new" category of "perivascular dermatitis," a warning is in order. Although it
usually matters not a whit whether a histopathologist begins the algorithm as "superficial" or "superficial and deep,"
"perivascular" (or "perivascular and interstitial") sufficing, in actuality, there are, a few exceptions to that "rule," and
they must be fastened in neurons indelibly. A few inflammatory diseases, in nearly every instance of them, are
typified by an infiltrate that is wholly superficial, the three most representative of that constellation already having
been alluded to, namely, some viral exanthems (like Fifth's disease), some morbilliform drug eruptions, and vitiligo.
Tinea versicolor also is affiliated invariably with an infiltrate that is superficial only, that infectious inflammatory
disease being recognizable readily for what it is by the presence in the stratum corneum of hyphae and spores
whose appearance is distinctive. In analogy, some inflammatory diseases nearly always have infiltrates that are both
superficial and deep, the three best examples being polymorphous light eruption, erythema figuratum, and tumid
lupus erythematosus. Exceptions do occur, as in the rare expression of lupus tumidus in which the infiltrate of
lymphocytes is superficial only (see Fig. 5.23 B&C).
A few inflammatory diseases that are perivascular (and often interstitial) may be "bottom heavy" because they are
associated with panniculitis, examples of that phenomenon being witnessed in morphea, lupus profundus, and
necrobiosis lipoidica. A dramatic presentation of a "bottom heavy" infiltrate of lymphocytes occurs in alopecia areata
in which follicles are all in late catagen (Fig. 5.153 A–C), the deep perivascular infiltrate of lymphocytes marking sites
where a follicular papilla was stationed prior to its ascent behind the ever-shrinking inferior segment of a follicle in
catagen. When a biopsy of erythema nodosum fails to deliver subcutaneous fat, all that a microscopist may observe
is a rather sparse, superficial and deep, perivascular infiltrate of lymphocytes. As was remarked on earlier, a
markedly "bottom-heavy" infiltrate of lymphocytes almost always indicates a lymphoma, that infiltrate extending well
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into the subcutaneous fat (Fig. 5.154 A&B), or a leukemia (Fig. 5.155 A&B).
Figure 5.153 : A. "Bottom-heavy" infiltrate. B&C. "Bottom-heavy" infiltrate of lymphocytes confined to the
dermis as a clue to an inflammatory disease, to wit, alopecia areata. A rare example of a perivascular
dermatitis positioned deep but not superficial ("bottom-heavy") is alopecia areata. A "deep" perivascular
dermatitis, that is, lymphocytes only around venules of the deep plexus, in company with follicles all in
catagen, is diagnostic of alopecia areata. Prior to involution of the follicles, then in anagen, lymphocytes
enveloped the bulb of them, and those inflammatory cells remained behind, especially in perivascular locale,
as the withering follicles ascended. When a "bottom-heavy" infiltrate of lymphocytes extends well into the
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subcutaneous fat, the diagnosis likely is lymphoma.
Figure 5.154: A&B. "Bottom-heavy" infiltrate of lymphocytes in the dermis and subcutaneous fat as a clue
to lymphoma. A "bottom-heavy" infiltrate in which lymphocytes monopolize and that extends into the
subcutis is likely to be that of a B-cell lymphoma, as was the case here. At this moment in evolution, nuclei
of lymphocytes may not be strikingly abnormal. That being so, at this juncture the silhouette of the infiltrate
is more important for diagnosis than attributes cytopathologic of it.
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Figure 5.155: A&B. "Bottom-heavy" infiltrate of lymphocytes as a clue to leukemia. Although the infiltrate
shown is only slightly "bottom-heavy," that is sufficient, especially in the context of its being perivascular
and interstitial and the mononuclear cells being distinctly abnormal, to consider seriously a diagnosis of
leukemia, the patient in this instance having one of myelomonocytic type. The many erythrocytes
extravasated are an accompaniment of the leukemic process.
In three distinctive diseases, a perivascular infiltrate, usually one that is both superficial and deep, assumes a wedge
shape, the apex of which points toward the subcutaneous fat. Those three are a response to the "bite" of an insect
(Fig. 5.156), Mucha-Habermann disease when acute (Fig. 5.157), and lymphomatoid papulosis (Fig. 5.158); the first
two are inflammatory diseases and the last is a lymphoma that may be misinterpreted as an inflammatory disease
because, not uncommonly, the infiltrate consists of small lymphocytes, plasma cells, eosinophils, and neutrophils,
and the papillary dermis displays edema prominently; in such a setting, the presence of strikingly abnormal
lymphocytes, some of them often being in mitosis, permits a diagnosis of lymphomatoid papulosis to be issued
straightforwardly. And so, too, it is for diagnosis with specificity of the other two diseases whose dermal infiltrates
take on the shape of a wedge; by assessing aspects of architectural pattern and attributes of cells that make up the
infiltrate, a diagnosis can be rendered unambiguously.
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Figure 5.156: Wedge-shaped infiltrate of an "insect bite."
Figure 5.157: Wedge-shaped infiltrate of Mucha-Habermann disease.
Figure 5.158: Wedge-shaped infiltrate of lymphomatoid papulosis.
No small number of "perivascular dermatitides" are maddeningly pruritic, Grover's disease, a perivascular dermatitis
affiliated with acantholytic cells and sometimes with spongiosis, when it is joined by numerous eosinophils being the
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most notorious of them, it is inevitable that often they are complicated by signs of forceful rubbing and agitated
scratching (Figs. 5.159 A&B and 5.160 A&B). Vigorous rubbing engaged in persistently may take one of two forms,
namely, (1) marked compact orthokeratosis, hypergranulosis, and acanthosis resembling that of volar skin but that
resides above a dermis that sports folliculosebaceous units (Fig. 5.161 A&B) and (2) a papillary dermis thickened
greatly by coarse bundles of collagen in vertical streaks oriented perpendicular to the skin surface (Fig. 5.162 A&B),
in addition to compact orthokeratosis, hypergranulosis, and uneven acanthosis of infundibular epidermis especially.
Both of those expressions are termed "lichen simplex chronicus" when the lesion is a plaque and prurigo nodularis
(more accurately designated prurigo papularis) when the lesion created is a papule (Figs. 5.163 A&B and 5.164
A&B). A papule that is brought about by the effects of both rubbing and scratching energetically is termed a "picker's
nodule" (Fig. 5.165 A&B). Scratching wildly may initiate a variety of changes in the skin, among those being signs of
impetiginization in the form of clumps of bacteria in scale-crusts (Fig. 5.166 A&B), ragged necrosis of the upper part
of the viable epidermis (Fig. 5.167 A&B), erosions, ulcerations (Fig. 5.168 A&B), crusts, fibrin in subepidermal loci
(Fig. 5.169 A&B), and fibrosis in discrete, narrow foci in the uppermost part of the dermis when nails are dug deeper
(Fig. 5.170 A&B).
Figure 5.159: A&B. A discrete, but distinct, sign of excoriation: necrosis in a tiny locus of epidermis.
Grover's disease, an inflammatory process characterized by focal acantholytic dyskeratosis, is pruritic in
general but especially when eosinophils are numerous, as is the case here. The focus of epidermal
necrosis, evident by keratocytes being eosinophilic, is a sure sign that this lesion has been scratched
animatedly.
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Figure 5.160: A&B. A sign of unbearable pruritus: ulcer secondary to excoriation. This lesion of Grover's
disease, typified by a tiny suprabasilar cleft above which are incipient acantholytic cells, must have been
maddeningly pruritic because the ulcer covered by crust shown here is evidence of scratching furiously.
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Figure 5.161: A&B. The "hairy palm sign" of lichen simplex chronicus. One form of lichen simplex
chronicus, a condition brought into being by the effects of rubbing, to and fro, vigorously and persistently,
is characterized by an epidermis that resembles that of volar skin, i.e., corneocytes arranged compactly in a
stratum corneum thickened markedly, a prominent granular zone, and acanthosis, but because those
findings are present in a setting of folliculosebaceous units, structures that never are found on volar skin
(except in bulldogs), the changes must have been wrought by forceful rubbing and for long.
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Figure 5.162: A&B. Coarse collagen bundles in vertical streaks: a sign of lichen simplex chronicus. A
papillary dermis thickened greatly by coarse bundles of collagen arranged in vertical streaks, those
changes being affiliated invariably with acanthosis, hypergranulosis, and hyperkeratosis, is evidence,
incontrovertibly, of lichen simplex chronicus. The pseudocarcinomatous changes consequent to
proliferation of infundibular and eccrine ductal keratocytes also are secondary to the effects of intense
rubbing.
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Figure 5.163: A&B. An analogue of lichen simplex chronicus: prurigo nodularis (papularis). This papule
produced by rubbing hard a discrete locus of skin for many months, if not years, is characterized by
compact orthokeratosis, prominent wedge-shaped hypergranulosis, proliferation of infundibular and eccrine
ductal epithelium, and a papillary dermis thickened greatly by coarse bundles of collagen arrayed in streaks
vertical.
Figure 5.164: A&B. A miniature of prurigo nodularis: prurigo papularis. This papule produced by rubbing a
discrete locus of skin forcefully for long is a miniature of that shown in Figure 5.163.
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Figure 5.165: A&B. A combination of "prurigo nodularis" and "neurotic excoriation": picker's nodule. What
is called "picker's nodule" combines findings of "prurigo nodularis" and "neurotic excoriation," to wit,
lesions brought into being by the effects in a discrete locus of both rubbing and scratching, the latter
evidenced by erosion and ulceration. Pseudocarcinomatous proliferations are consequent to the trauma
externally.
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Figure 5.166: A&B. Picker's nodule, impetiginized. This lesion came into being by virtue, foremost, of
forceful prolonged rubbing of this site but also by wild excoriation of it intermittently, that having been
complicated by impetiginization evidenced by clumps of bacteria, seen here as basophilic-staining clusters
in serum that constitutes much of the scale-crust. The pustule in the epidermis is a response to the
bacteria.
Figure 5.167: A&B. Distinctive signs of injury from outside the skin (scratching): necrosis in the upper part
of the epidermis. Necrosis, evidenced by karyolysis especially, in the upper half of the viable epidermis is a
result of external injury, in this instance in the form of scratching furiously, so uncontrollably that an ulcer,
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seen at the left side of the photomicrograph "shot" at scanning magnification, was produced.
Figure 5.168: A&B. Distinctive signs of injury from outside the skin (scratching): erosion and ulceration. An
erosion and ulceration covered by crust are secondary to damage inflicted externally.
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Figure 5.169: A&B. A distinctive sign of injury from outside the skin (scratching): fibrin beneath the
epidermis. Fibrin situated immediately beneath the epidermis is a sure sign that the trauma responsible was
delivered from outside the skin.
Figure 5.170: A&B. A distinctive sign of skin having been scratched furiously: a narrow scar in a discrete
locus beneath the epidermis. The discrete, thin scar just below an altered epidermis covered by scale-crust
bears testimony to a superficial ulcer secondary to excoriation wildly having been present at this site.
In contrast to necrosis of keratocytes in the upper part of the epidermis secondary to the effects of injury external
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("outside in"), as occurs most often secondary to scratching, but also in phototoxic dermatitis (Fig. 5.171 A&B),
necrosis of keratocytes in the lower part of the epidermis signifies injury from within the skin itself ("inside out") as
follows often on the influences of lymphocytes distributed along the dermoepidermal junction of "interface
dermatitides" of either "vacuolar" or "lichenoid" types, as exemplified by erythema multiforme (Fig. 5.172 A&B) and
lichen planus (Fig. 5.173 A&B), respectively. Not surprisingly, the stratum corneum is not altered by injuries from the
"outside" sustained instantly, no matter how severe, such as from a burn of any kind, the damage occurring rapidly
and the effects of it thereby taking a toll only on cells that are viable.
Figure 5.171: A&B. A distinctive sign of injury from outside the skin (rays of ultraviolet light): ballooned and
necrotic keratocytes in clusters in the upper part of the epidermis especially. Clusters of ballooned,
necrotic keratocytes in the upper part of the viable epidermis are typical of phototoxic dermatitis and its
lookalike, namely, a sunburn.
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Figure 5.172: A&B. A distinctive sign of injury from within the skin (interface dermatitis, vacuolar): necrotic
keratocytes in the lower part of the epidermis especially. Necrotic keratocytes in the lower portion of the
epidermis are a consequence of damage wreaked by factors in the skin, in this instance from products of
lymphocytes of erythema multiforme.
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Figure 5.173: A&B. A distinctive sign of injury from within the skin (interface dermatitis, lichenoid): necrotic
keratocytes in the lower part of the epidermis especially. The necrotic keratocytes disposed as solitary
units and in clusters in the lower part of the epidermis were brought into being by the effects of products of
lymphocytes in lichen planus.
The presence of a normal stratum corneum is an exceedingly helpful guidepost for enabling a histopathologist to
determine whether keratocytes with a small dark (pyknotic) nucleus and eosinophilic cytoplasm are neurotic (having
died rapidly) or dyskeratotic (having died slowly as a consequence of cornification abnormally), those two types of
cells of very different character being look-alikes morphologically. Almost always, the stratum corneum above
dyskeratotic cells as punctuated by parakeratosis, in contrast to that above necrotic cells, which tends to be normal,
but, if abnormal displays scale-crust, not simply parakeratosis alone. The crust consists largely of serum, which
derives from changes of spongiosis and/or ballooning that sometimes accompany necrotic keratocytes in a disorder
such as Mucha-Habermann disease.
Nowhere in this work are necrotic keratocytes referred to as "apoptotic cells"; apoptosis, typified as it is by pyknosis
and karyorrhexis, fulfills criteria for necrosis. Utilizing the five essential patterns of perivascular dermatitis and
subdivisions of them, the following algorithm can be constructed:
ALGORITHM: Perivascular Dermatitis
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Identification of Basic Patterns - Skin - Perivascular Dermatitis

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Identification of Basic Patterns: Skin: Perivascular Dermatitis

Figure 5.16: A. Perivascular dermatitis, perivascular only, superficial. B. Perivascular dermatitis,

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Figure 5.62: A&B. An example of an extraordinarily thinned epidermis: porokeratosis, disseminated

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variable extent, with infiltrates of lymphocytes.

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