I read the program this week and saw that I was giving a “dermpath review” but actually, I was asked to talk specifically about how to interpret pathology reports in biopsies for dermatitis—A BIG SUBJECT!
So I want to let you know ahead of time that will make a copy of my Powerpoint presentation available both on our CTA website and with the conference materials
I have no disclosures to make.
So I am going to start with biopsy techniques to optimize the pathologic diagnosis, including bxs for alopecia and direct immunofluorescence
Then I will move on to how we dermatopathologists evaluate a bx for dermatitis
And hopefully, you will get an idea of how important the clinicopathologic correlation is diagnosing a dermatitis
INTRO First lets talk about who we dermatopathologists are! (read above) …..
I really hate to say this in some ways, since I practiced general surgical pathology as well as dermatopathology for many years, but most general surgical pathologists don’t get very good DP training. DP has it’s own terminology that most general surgical pathologists have not been trained in—for example, in almost every organ except the skin, when you see neutrophils in a biopsy, it’s called “acute inflammation” and when you see lymphocytes, it’s called “chronic inflammation”—these terms are really meaningless in DP, as plenty of acute processes can be purely lymphocytic and plenty or chronic processes can be neutrophlic (read) For best results—use a dermatopathologist!! (Even if it’s not me! )
Last point—bx off steroids—we will get to that in a bit
This is what a skin biopsy looks like in 3 dimensions---I am showing it to you to emphasize the point that you need to think about where the disease process is when you do your bx so that you can sample the areas we need to see under the microscope to make a dx
When the bx arrives in our lab it is sectioned into smaller slices vertically (this is called “grossing”), then processed overnite in formalin. The next day a histotech comes in and embeds the slices in paraffin wax and uses a microtome to make even thinner slices which are laid onto glass slides and stained with hemotoxalin and eosin to make the “H&E” slide
(GO SLOW) This is the final product—what I really look at all day—the skin in 2 dimensions--this is what a routine H&E stained skin bx looks like at very low power
(point out on normal structures-- different levels-sc, epi, dermis, SQ, hair follicles, sebaceous glands, sweat/eccrine glands)
A little closer up--( AGAIN POINT OUT ) stratum corneum, epidermis, basal layer, keratinocytes, basal layer, dermis, dermal papillae, vessels, inflammation.
H&E-- hematoxalin-blue/purple and eosin-pink/red
We need to look at the entire thickness of dermis when evaluating a biopsy for an inflammatory process. When that process involves the subcutis, there is often necrosis of adipocytes which get left behind by a punch biopsy—so wedge or incisional bx optimal. For vesicles and bullae, its important to keep them intact and for us to look at the adjacent skin
Dermatitis on acral sites and the elbow/knee tend to have a different appearance histologically—an example is psoriasis, which may be very spongiotic at these sites-so if your differential diagnosis is between an eczematous or spongiotic dermatitis and psx, you are likely to get a dx of “psoriasiform spongiotic” or just “psoriasiform” dermatitis back with a comment about how we can’t tell the difference at these sites btw the 2 diseases.
Any lesions with secondary change or which have been treated will also complicate histologic diagnosis.
Now lets move on to bxs for alopecia—I have some rules for you to remember
A 4mm punch is the best size to use for a couple of reasons—the first is that there are standards based on a 4mm punch for hair density and the second is that we need a certain amount of tissue to look at both in terms of the number of hairs and the technicalities of grossing the tissue. We need the SQ fat because that is where the hair bulbs are. For Asian or straight hair look for angle of the hair shaft. For black or African American hair—go straight in at 90 degrees. (read the rest)
Most of time, we can make diagnosis with just one bx if properly processed
Hairs are normally miniaturized and cycle faster in the hairline, which are critical criteria for us in the differential diagnosis of most non-scarring alopecia (eg AA, CTE, MPHL or FPHL) so avoid the hairline if possible
We routinely get a clinical hx of “hair loss” we need more info—maybe you don’t even have a clinical ddx but try to tell us these things-(read)–especially whether diffuse or patchy in non-scarring alopecia. I can’t stress enough how important the clinical is for us-- especially whether diffuse or patchy in non-scarring alopecia.
I don’t want to make a shameless plug for our lab, BUT we are lucky enough to have Janet Roberts and Nisha Desai here in Portland, dermatologists who specialize in alopecia, and use our lab for their biopsies, so we see several a day, where most dermatopathologists might see a less than a handful a month. It’s really important to use a lab with experience handling these biopsies—they are technically challenging to gross in—and, furthermore, many DPs don’t get good training or see a large enough # of these biopsies to get good at them. Remember--2% of all skin bxs are for hair loss—there is significant psychological suffering in these pts and they want to be taken seriously—with that in mind, we put a picture and a detailed microscopic description in each alopecia report, so that Dr Roberts, for instance, can show her pts the report
Let me give you a visual on this--For alopecia bxs in our lab, we us the “Hovert” technique—that is, we shave off the top of the punch biopsy and section it like a routine bx---vertically--so we can see any epidermal change there might be but then the remainder of the punch bx we section transversely so we can see all the hair follicles in the biopsy rather than just the few we would see in vertical sectioning-- allowing for a much more precise diagnosis –but again, it takes very skilled lab personnel to do this to a punch bx. This is a properly sectioned biopsy for alopecia—nice round follicles looking up at you and we are able to see all the follicles in the bx—hopefully you can see blue rim of fibrosis and lymphocytes around 3 of these follicles…this is LPP
This is an alopecia bx which has been tangentially sectioned—making it difficult to evaluate all the follicles. How many follicles are in this biopsy? Do some of these connect?
Proper horizontal sectioning is very important for bxs of BOTH diffuse and scarring hair loss as not all the follicles are affected uniformly in diseases which cause alopecia and we need to see ALL of the follicles in the biopsy
Of note—this is also LPP –we hold out for 2-3 follicles for with perifollicular fibrosis to dx LPP, as a single Pf scar could be an acneiform lesion. I think there are 3 follicles in this bx affected but not sure if looking at different follicles in all these foci
Now on to another special type of bx—for DIF— this is the guide we have on our CTA website which we have b/c we do a relatively high volume of DIFs—we average 3-4/day—and we run all of them “STAT” so the clinicians can get their reports back within 24-48hrs to help with treatment decisions.( DON’T READ LIST except last 2 points) I just want to point our last two points here (read) Once a bx is in formalin, we cannot perform DIF on it—another bx is needed—also, we need to freeze the tissue within 5 days to preserve the antigens we are looking at with this test.
Remember—you cannot make a diagnosis of an immunobullous disease without direct immunofluorescence studies!! For example, probably the most common disease we dx on DIF is bullous pemphigoid and it can be mimicked clinically and histologically by non-immunobullous dzs such as bullous arthropod bites and bullous drug eruptions.
INTRO For DIF bxs, we freeze the tissue so we can apply a panel of antibodies tagged with a fluorochrome to a panel of immunoglobulins (IgA, IgG and IgM) , complement and fibrinogen which we look at with specialized microscope and I want to note here that it is not always a purely positive or negative test—it requires some expertise to interpret Here is an example of a biopsy of bullous pemphigoid—this is a picture of + C3/complement deposition in a linear pattern at the dermal-epidermal junction (point out epi, dermis, BM, collagen with autofluorescence)
As these flourochromes quickly fade with time, we take a picture of these positive tests for documentation and put them in the pathology report
Some more important points about DIF bxs
Now let’s move on to looking at routine H&E (hemotoylin and eosin) stained slides, which is how we make the vast majority of our diagnoses. We can’t talk about the histopathologic diagnosis of skin disease without talking about Bernard Ackerman, who died in 2008, one of the founding fathers of modern dermatopathology
INTRO Ackerman published a book in 1978 called “the Histopathologic Diagnosis of Skin Disease” that helped introduce the concept of “pattern diagnosis” in DP- which is the examination of a slide at scanning magnification and analysis of the silhouette of lesion rather than of its cells, and, by using these patterns, one could use algorithms to generate a differential diagnosis and arrive at a specific diagnosis (but eventually you have to look at the cells!)
Intro These patterns-in one form or another- are memorized by every dermatopathologist in training. I don’t expect you to read this but let me just point out--On the left side is the type (if any) of epidermal change seen in a biopsy—and ,on the right, is the pattern of inflammation in the dermis and/or subcutis…farther to the right are the type of cell in the inflammatory cell infiltrate and any other particular features which lead you to a ddx on the far right side—makes it look easy doesn’t it?
INTRO—Of course, the terminology has evolved somewhat since Ackerman published his book and these next two slides are a similar way of organizing pattern diagnoses adapted from Dr David Weedon’s textbook, simply called “SKIN PATHOLOGY” which is the main textbook used by practicing dermatopathogists today
These are the major “buzzwords” you are likely to see in the diagnostic line of your patients path reports! (read list)
END Keep in mind—these are not entirely specific patterns but they can help us start narrowing the ddx down. Patterns can be mixed and these combinations or “constellation of histologic features” can also prompt certain ddxs—some are even diagnostic. Today I don’t have time to go through all of these reaction patterns in detail, so I am going to concentrate on the first 3 today, which are the most common and all relate to epidermal change: spongiotic, lichenoid/interface and psoriasiform dermatitis. As I discussed with Kim this week, I would be happy to give an additional lecture in a similar format at a later date on the last 3 reaction patterns listed here.
Once we have decided on the major type of epidermal change, we look next at the distribution pattern of inflammation in the dermis…and, of course, these patterns are often mixed as well
Point out “interstitial” is dermis between vessels and other dermal structures and “adnexal” is the hair follicles and the eccrine/sweat glands
Intro Lastly, we look at what cell types are in the inflammatory infiltrate and these are the major inflammatory cell types we see in the skin in dermatitis
I am going to show you some pictures of each cell type and how they can be clues to the dx for us –remember these are CLUES—not hard and fast rules—and I am not going to list of all the diseases which can have these cells
Lets start with eosinophils—these cells have a very distinctive appearance on H&E staining—bilobed nucleus with lots of red-pink granules (“eosin loving”) in the cytoplasm. All of their functions are not worked out yet but we do know that they are the effector cells for killing helminths and for causing tissue damage in hypersensitivity reactions. Of course, they are notorious for being involved in drug reactions, but—not all drug reactions have eosinophils.
Next are neutrophils stain a “neutral” pink. Normally, neutrophils contain a nucleus divided into 2–5 lobes—they are primarily phagocytes (engulfing bacteria, immune complexes and damaged tissue) but also secrete lots of different enzymes which help them in their role against invading micro-organisms—they are highly motile and show up within minutes at the site of trauma and are therefore the hallmark of acute inflammation
However, neuts are also involved in dermatoses such as psx, DH and neutrophilic dermatoses—in these diseases their role is less well understood)
Plasma cells are large lymphocytes with a characteristic appearance--they have an eccentric nucleus with a characteristic “clock face” look to the chromatin—they are terminally differentiated B cells able to produce large volumes of antibody with specificity to a particular antigen. They may be a prominent component of the inflammatory infiltrate in both dermatoses and neoplastic conditions. They are not normally present in skin, with the exception of scalp and skin near mucous membranes. When we see them elsewhere, we think about syphillis and these other diseases (read)
I just want to mention again that, if this seems like a lot of information, this talk will be available to you on-line and with Kim with the other course materials
The histiocyte is a tissue macrophage (which means it mainly eats things) or a dendritic cell and they are part of the mononuclear phagocyte arm of the immune system. These are cells with ovoid nuclei, small nucleoli and abundant pinkish cytoplasm (point out) They can be multinucleate, especially when they are engulfing things (like foreign material)
Of note--Some DPs use the term “granulomatous” when there are large numbers of histiocytes, others reserve it for when there are multinucleate giant cells and/or groups of histiocytes forming granulomas. These details should be in the microscopic description.
Lastly are the mast cell—ovoid nuclei, lots of pale blue cytoplasm—”fried egg” appearance. Mast cells are immune system cells which contain many granules rich in histamine and heparin. Although best known for their role in allergy and anaphylaxis, mast cells play an important protective role as well, being intimately involved in wound healing and defense against pathogens. They show up to just about any party (ie can be found in any dermatitis), but when we see large numbers, we think of mastocytosis.
A lymphocyte is any of 3 types of white blood cell in our immune system. They include natural killer cells (NK cells) (which function in cell-mediated, cytotoxic innate immunity), T cells (for cell-mediated, cytotoxic adaptive immunity), and B cells (for humoral, antibody-driven adaptive immunity). They are the main type of cell found in lymph, which prompted the name lymphocyte.
Last point—this topic is a whole lecture in and of itself—suffice it to say that it requires at least a basic panel of immunostains to look at how many B or T cells are present (large numbers of B cells are abnormal in the skin) and if they have have lost expression of normal lymphocyte markers or are aberrantly expressing certain markers
INTRO So now I want to move back to the major tissue reaction patterns—starting with spongiotic dermatitis.
Just want to point out that in DP, “psoriasiform dermatitis” does not mean that it’s necessarily psoriasis, just that there is hyperplasia or thickening of the epidermis with fairly regular elongation of the rete (point out rete, epi etc)
When we see a spongiotic dermatitis with mostly lymphocytes, either in the dermis or epidermis, the major ddx is (read) All of these can look identical under the microscope, especially these first 4
END Spongiosis is a reaction pattern not a definitive diagnosis! I try to tailor my line diagnosis as much as possible to get you into a specific ddx, but sometimes it is just not possible and I use it more as a descriptor—but I make sure to explain myself in the comment.
How can we DPs narrow down the diagnosis from this long list of diseases which can look so similar histologically?
And I just want to note that please call your DP is you have any questions about a report—we can’t operate in a vacuum and we really appreciate clinical follow up.
So I want to emphasize at this juncture why it is important to biopsy patients off treatment—especially in spongiotic dermatitis--it changes the histology so we cannot make an accurate diagnosis
INTRO While MF is a cutaneous T cell lymphoma and not a true spongiotic dermatitis, I want to say a few words about it, as it is not uncommonly in the clinical differential of a chronic eczematous dermatitis. Bx off steroids—really impt in MF—steroids will mute epidermotropism (lymphocytes migrating into epidermis--one of the key fx we look for for dx) It’s very important to get multiple biopsies to make this dx, as MF histology can vary from lesion to lesion in same patient, and, if we can show the same T cell clone in both bxs by molecular methods (T cell receptor gene re-arrangement), this is a very strong vote for MF. Remember—MF is a clinico-pathologic diagnosis, it’s an indolent disease in it’s early stages and it is better to under rather than over diagnosis it—don’t worry if you don’t get it the first time around in it’s early stages.
Lets get back to spongiosis—there are 4 major subtypes, each with it’s own ddx, and I will use these terms in the line diagnosis when they are present for that reason. I am going to discuss the first three, as the miliarial spongiosis group ddx is really just the three types of miliaria, which are rarely biopsied.
Theses are the major diseases we think about when we see neutrophilic spongiosis—I am going to not dwell on these but have included them for your reference—note--the last one—impetiginization, is probably the most common situation in which we see it
As you can see, there are the usual suspects on this list also in the ddx of uncomplicated, lymphocytic spongiotic dermatitis
BUT we really start thinking of these other diseases when we see eosinophilic spongiosis so I will use this term on the diagnostic line and make sure to mention these other diseases in the comment
Although you an see some degree of follicular spongiosis in disease characterized by epidermal spongiosis, when you see predominantly spongiosis of the follicular epithelium you have a MUCH narrower ddx--Atopic dermatitis most common dx when fc spong is seen
INTRO Lets move on to the next most common reaction pattern we diagnosis: lichenoid/interface dermatitis, which is basically an immune attack on the basal layer of the epidermis causing basal layer cell death and/or vacuolar change (read next two points on slide)
When uncomplicated by other patterns, this is the major ddx in lichenoid/interface pattern—It’s a big list!
Like spongiotic dermatitis, interface/lichenoid dermatitis can be divided into subtypes—(read list)-in the interest of time I am just going to show you one example of each types
This is an example of “acute” lichenoid-interface dermatitis—this is erythema multiforme/toxic epidermolytic necrosis spectrum (point out features)
Note—mostly epidermal basal layer death and vacuolar change—very few lymphocytes in the dermis.
LP-like lichenoid/interface dermatitis- the prototype of a lichenoid dermatitis with prominent basal epidermal keratinocyte death “colloid bodies” (point out). Note the “band-like” infiltrate of lymphocytes in the dermis—this is a histologic feature which also defines “lichenoid” in the minds of most dermatopathologists. This could also be a picture of an LPLK or any of the variants of LP or even a picture of the epidermis in lupus though! As I said before, many of the diseases in this lichenoid/interface category can show a spectrum of changes. The key is the other features in the biopsy and the clinical history.
This is the 3rd type—”Psoriasiform lichenoid” (point out fx)--the example here is secondary syphillis- note the lichenoid infiltrate contains many plasma cells (clue to dx but not always there)
Lastly—the other end of the spectrum—LE--- the prototype of a chronic interface dermatitis—there is cell death but also very prominent vacuolar change. Note that, like the acute interface, there is a very sparse inflammatory cell infiltrate in the dermis compared to the “band-like” or “lichenoid” inflammatory infiltrate in the previous photo. The reason it’s not acute EM like is that there is epidermal atrophy (thinning)—the result of chronicity. You may notice the eosinophils here—this is drug induced LE!
I don’t have time to go into more detail today for all of the diseases in the lichenoid/interface ddx, but I just wanted to show you an example of how, once we identify the major reaction pattern in the epidermis, we put it all together with the pattern of the infiltrate in the dermis—this example is of bx of lupus showing the full constellation of histologic features needed for the diagnosis. Even if the DIF studies are negative, this constellation of features is diagnostic. However, not all cases show the full complement of features, and, in those cases, clinical correlation and DIF studies can help if positive…..As an aside you have to have epidermal change to have a + DIF, so a DIF in tumid lupus will not help you with the dx; also, a + DIF in lupus (which is also called the lupus band test) should always be interpreted with clinical and H&E bx findings, as it may be present in chronic light exposed skin
So I am just briefly going to describe one last reaction pattern—psoriasiform dermatitis--this example is psoriasis (point out histology)
Again, there is a relatively big list for the ddx—note that although this category is “psoriasiform dermatitis” we are really describing a reaction pattern and there are diseases which are not actually dermatitis on this list (eg SCIS).
We don’t really divide these into subtypes as we do with spongiotic and lichenoid/interface dermatitis but we go straight to the stratum corneum and the dermis to see if we can find other clues to the ddx (such as scabetic mite parts or fungal hyphae in the s. corneum, plasma cells in syphillis or atypical lymphocytes showing migration into the epidermis for MF). Notice MF was on the spongiotic and the lichenoid ddx lists and here it again!
So that is all I have time for today…Again, thanks for inviting me to speak today. As I mentioned before, a copy of this presentation will be on our website, and Kim Sanders also has a copy. Also, if you are interested in having me talk again on the rest of the tissue reaction patterns or expand on any of the other topics I touched on today, please let Kim know. And, if any of you would like to stop by and see what we do at the lab, we would be happy to have you visit.
Interpretation of Pathology Reports in Biopsies for Dermatitis
INTEPRETATION OF PATHOLOGY
REPORTS IN BIOPSIES FOR
Jessica Spies, MD
CTA Lab, Portland, OR
• Biopsy techniques– how to optimize
• Dermatitis--how DPs evaluate biopsies
• Terminology – “buzz words” in DP
• Clinicopathologic nature of diagnosing
• DP fellowships--accept physicians from both
pathology and dermatology residencies
• DP training is required in both residencies
• DP training refined in fellowship—50% DP +
50% clinical derm for path trainees, 50%
general pathology for derm trainees
General surgical pathologists
• DP training/expertise varies widely!
• Most will not use terminology I will describe
today (eg “acute” and “chronic” inflammation
terminology does not always apply in DP)
• For best results, use a dermatopathologist!
When you are sent a patient from a primary care
physician with a biopsy report you don’t
– Have your DP review the biopsy
– Remember: PCP may not have performed the
– Rebiopsy patient (off treatment 2 weeks)
Evaluating a skin biopsy
“Top to bottom approach” mainly: type of
epidermal change + type of dermal infiltrate
• Punch not shave biopsy for dermatitis!
• Wedge or incisional bx with a scalpel biopsy if
ruling out a subcutaneous process/panniculitis
• Vesicles and bullae should be removed with
scalpel, to avoid shearing off the blister
Biopsy sites to avoid if possible
• Acral sites
• Center of alopetic patch
• Excoriated lesions (delay bx if no primary
• Treated lesions
• 4MM PUNCH aligned parallel to hair shaft to include
• At ANGLE in Asians and whites, 90 DEGREES in blacks
• One punch—in KEY area—i.e. perifollicular
erythema, active border in scarring alopecia,
positive hair pull test site
• Avoid the hairline unless only site of hair loss!
(where follicles are normally miniaturized and cycle
Include as much clinical history and description
of the lesions as possible
– Shedding? If so, acute or chronic?
– Pattern of hair loss: diffuse or patchy?
– Location of bx!
– Perifollicular erythema or hyperkeratosis
• Use lab with experience in alopecia biopsies!!
• Incorrectly processed specimen unlikely to
yield a diagnosis
• Experience with alopecia varies widely
between DPs (just like in dermatology) –due
to critical mass factor
• New patient previously evaluated for alopecia
without definitive pathology? Biopsy again!
Biopsy for DIF
• Pemphigus and pemphigoid groups: perilesional skin or
• Dermatitis herpetiformis: normal appearing skin 0.5-1.0 cm
away from lesion
• Collagen vascular disease: involved areas of skin such as
• Vasculitis: active/erythematous border of a new lesion;
optimally lesions between 18-24 hours old
• Porphyria cutanea tarda: involved skin.
• Avoid old lesions, ulcers and blisters (false +/-)
• Submit in Michel’s media not formalin (frozen within 5 days)
• Include an H&E biopsy if possible!! DIF testing
has pitfalls and artifacts which can be avoided
if we can correlate with H&E bx
• Clinical history important for us
• DIF another infrequently performed test
• Experience with DIF varies greatly between
• “Pattern diagnosis”-- the examination of a
slide at scanning magnification and analysis of
the silhouette (or architecture) of lesion
rather than of its individual cells
• Although this is used by DPs to some extent in
tumor diagnoses, it is most useful in the
evaluation of biopsies for dermatitis
Example of one of
charts for pattern
Major tissue reaction patterns
• Spongiotic (epidermal intercellular edema)
• Lichenoid/interface (basal cell damage)
• Psoriasiform (regular epidermal hyperplasia)
• Vesiculobullous (blister within or beneath
• Granulomatous (chronic granulomatous)
• Vasculopathic (pathologic changes in
cutaneous blood vessels)
Patterns of inflammation
• Superficial dermal
• Superficial and deep dermal
• Perivascular and/or interstitial
• Perifollicular and/or periadnexal
• Involvement of subcutis
• In epidermis---BP, PV,
• In dermis---all of above
+ urticarial or “dermal”
• Not all drug reactions
• Unusual for collagen
vascular disease (drug
induced LE exception)
• In dermis---
DH, bullous LE, LAD,
• In epidermis--
AGEP, P. foliaceous,
• Normal in scalp,
• Syphillis doesn’t
always have plasma
• AKA macrophages,
• Large numbers—
think infection, esp
if neutrophils too
• Can form
sarcoidosis (dx of
• Basic inflammatory cell
found in all types of
• NK cells, T cells, and B cells
• Cannot distinguish
between types without
• Dense infiltrates—
oma, cutaneous and
systemic lymphomas (IHC
which may progress to
hyperplasia when chronic
When lymphocytic, major ddx is
– allergic/contact dermatitis
– atopic dermatitis
– nummular dermatitis
– id reaction (rare)
– dermatophytosis (PAS-D stain)
– seborrheic dermatitis (scalp and face)
However…you may also see spongiosis
• Arthropod bites
• Spongiotic drug
• Pityriasis rosea
• Light reactions
• Neoplastic infiltrates
• Many others..
The clinical history!
• All DP is clinicopathologic!!
• The more information you give us, the more
specific we can be in our diagnosis
• Some diseases have a unique, diagnostic
histology while others have a large degree of
overlap with other diseases
• A good dermatopathologist tries to narrow
the differential diagnosis for you.
Biopsy of spongiotic/eczematous
Stop topical and systemic immunosuppression
for 2 weeks prior to the biopsy if possible
– Mutes epidermal spongiosis
– Kills lymphocytes
• Biopsy off steroids after 2 weeks
• Multiple bxs (one container OK)--more definitive
diagnosis by histologic and molecular methods
(same T cell clone > 1 bx)
• “Spongiotic dermatitis”? call your DP and/or do
additional bxs if rash evolves and/or you suspect
• Remember: MF is a clinicopathologic diagnosis --
early (patch) stage, is very indolent—better to
under rather than overdiagnosis it.
More specific types of spongiosis
• Neutrophilic spongiosis
• Eosinophilic spongiosis
• Follicular spongiosis
• Miliarial spongiosis
= neutrophils in
epidermis + some
degree of spongiosis
• Key feature = epidermal basal layer damage—
cell death +/- basal layer vacuolar change
• Terminology confusing-- some use “interface
dermatitis” alone when there vacuolar change
predominating or “lichenoid dermatitis” when
cell death and/or a band-like dermal lymphocytic
• Most often used together as most diseases with
this pattern will have some of both features
• Lichen planus and it’s variants
• Lichen niditus
• Lichen striatus
• Lichenoid and fixed drug eruptions
• Erythema multiforme
• Lupus and it’s variants
• Pityriasis lichenoides
• Viral reactions
• Paraneoplastic pemphigus
• Pigmented purpuric dermatitis
• Mycosis fungoides
• Secondary syphillis
• Lichen sclerosus
• Many other, less common diseases
• Acute or “EM like”
• “LP like”
• Psoriasiform lichenoid
• Atrophic or “LE like”
Acute or “EM like” --epidermal basal cell death
and little other epidermal change
“Lichen planus like” --prominent cell death,
band like lymphocytic dermal infiltrate
Atrophic or “LE like”-prominent vacuolar change
+ epidermal atrophy
• Superficial and deep
• Rare if any eosinophils
• Increased dermal mucin
deposition (colloidal iron
• Newly published criteria:
increased numbers of
presenting cells in
• DIF studies may or may
not be + (50-90%)
regular elongation of
• Psoriasis and its variants
• Subacute spongiotic dermatitis
• Lichen simplex chronicus
• Chronic candidiasis and tinea
• Mycosis fungoides
• Norweigan scabies
• Secondary syphillis
• Some deficiency states (pellagra, acrodermatitis enteropathica)
• Bowen’s disease (squamous cell carcinoma in situ)
• Lamellar ichthyosis
• Other rare diseases such as Reiter’s syndrome, AIDS associated
Jessica Spies, Curtis Thompson and Andrea
Chakrapani (all Board certified