A histologic review of 27 patients with lichen

planopilaris
Yasmeen K. Tandon,a,* Najwa Somani, MD,b,c,* Nathaniel C. Cevasco, MD,b and Wilma F. Bergfeld, MDb,c
Rootstown and Cleveland, Ohio

Background: Lichen planopilaris (LPP) is a potential trichologic emergency that can result in permanent
scarring alopecia. Histopathology is a key component of the diagnostic work-up.

Objective: To identify the key histologic features that characterize LPP in order to facilitate diagnosis,
ultimately leading to improved patient outcomes.

Methods: Scalp biopsy specimens from 27 confirmed cases of LPP were reviewed in a blinded fashion to
determine diagnostically helpful histologic features.

Results: Absence of arrector pili muscles and sebaceous glands, a perivascular and perifollicular
lymphocytic infiltrate in the reticular dermis and mucinous perifollicular fibroplasia within the upper
dermis with absence of interfollicular mucin, and superficial perifollicular wedge-shaped scarring were
characterizing features.

Limitations: Sample size was limited, given that biopsy specimens were taken from lesions at varying
stages of evolution and findings vary with disease stage.

Conclusions: This study confirms many previously reported histologic features and highlights new character-
izing features of mucinous perifollicular fibroplasia. ( J Am Acad Dermatol 2008;59:91-8.)

INTRODUCTION
Cicatricial alopecias are a group of disorders in
which follicular units are replaced by fibrous tissue,
resulting in progressive and permanent scarring hair
loss.1 Several underlying disease processes may
eventuate in scarring alopecia. These underlying
diseases may be diagnosed both clinically and his-
tologically in their early stages; however, in late
stages only nonspecific scarring is evident.2
Key diagnostic features present in all forms of
cicatricial alopecia include both visual loss of follic-
ular ostia and destruction of the hair follicles and
sebaceous glands on histopathologic examination.
From the Faculty of Medicine, North Eastern Ohio Universities
Colleges of Medicine and Pharmacy, Rootstowna and the De-
partments of Dermatologyb and Dermatopathology,c Cleveland
Clinic.
*Ms Tandon and Dr Somani share first authorship of this article.
Funding sources: None.
Conflicts of interest: None declared.
Reprint requests: Wilma F. Bergfeld, MD, FACP, 9500 Euclid Ave,
A61, Cleveland, OH 44195. E-mail: bergfew@ccf.org.
0190-9622/$34.00
ª 2008 by the American Academy of Dermatology, Inc.
doi:10.1016/j.jaad.2008.03.007
Abbreviations used:
DLE: discoid lupus erythematosus
LPP: lichen planopilaris
NAHRS: North American Hair Research Society
This can result from primary processes in which
inflammation is directly targeted at the hair follicle or
from secondary processes in which follicular de-
struction results from an inflammatory process that
secondarily extends to the hair follicle, resulting in its
destruction.3,4
According to the North American Hair Research
Society (NAHRS), the primary cicatricial alopecias
are categorized according to the predominant in-
flammatory cell type: lymphocytic, neutrophilic, or
mixed infiltrates. The lymphocytic group consists of
chronic cutaneous lupus erythematosus, classic
pseudopelade (Brocq), lichen planopilaris (LPP),
central centrifugal cicatricial alopecia, alopecia mu-
cinosa, and keratosis follicularis spinulosa decalvans.
The neutrophilic group is comprised of folliculitis
decalvans and dissecting cellulitis. Folliculitis (acne)
keloidalis, folliculitis (acne) necrotica, and erosive
pustular dermatosis are characterized by a mixed

91
92 Tandon et al
Table I. Proposed NAHRS working classification of
primary cicatricial alopecia*
Lymphocytic
Keratosis follicularis spinulosa decalvans
Chronic CLE
LPP
Classic LPP
Frontal fibrosing alopecia
Graham-Little syndrome
Alopecia mucinosa
Classic pseudopelade (Brocq)
Central centrifugal cicatricial alopecia
Neutrophilic
Folliculitis decalvans
Dissecting cellulitis/folliculitis
Mixed
Folliculitis (acne) keloidalis
Folliculitis (acne) necrotica
Erosive pustular dermatosis
CLE, Cutaneous lupus erythematosus; LPP, lichen planopilaris;
NAHRS, North American Hair Research Society.
*From Olsen et al.5
inflammatory infiltrate consisting of lymphocytes,
plasma cells, and/or neutrophils5 (Table I).
Historically, LPP was first described by Pringle in
1895 as classic lichen planus in conjunction with
spinous follicular papules.6,7 Terminology including
‘‘follicular lichen planus of the scalp’’ and ‘‘folliculitis
decalvans et atrophicus’’ has been employed in the
previous literature.8 LPP can be subdivided into 3
variants: classic LPP, frontal fibrosing alopecia, and
Graham-Little syndrome.9 LPP is seen most often in
adults and, in contrast to lichen planus, it more com-
monly affects women.7 The mean age at onset is 52
years.7 The clinical course is chronic and progressive.
The clinical hallmark of active disease is the
presence of erythematous or violaceous papules
associated with perifollicular collarettes of
scale4,8,10,11 and a positive pull test for anagen
hairs.12 Disease activity is greater at the periphery
of the alopecic patch, which contrasts with the
predominantly central activity seen with discoid
lupus erythematosus (DLE).3,13 Associated symp-
toms include moderate to severe scalp pruritus and
dysesthesia (pain, discomfort, and burning). Lesions
are classically multifocal and may eventually merge
to produce large areas of hair loss.14 Smooth bare
hypopigmented patches lacking follicular ostia char-
acterize the chronic end stages.12 Other common
presenting symptoms include hair loss and scalp
tenderness.10 Sites of predilection are the frontocen-
tral scalp and crown.15 Typical lichen planus involv-
ing nonfollicular skin, nails, and mucous membranes
is seen in 50% of cases8 (Table II).
J AM ACAD DERMATOL
JULY 2008
Table II. Clinical features of LPP
d Pruritus
d Discomfort/burning
d Scalp tenderness
d Shedding and hair loss
d Perifollicular erythema and collarettes of scale
d Spinous follicular hyperkeratosis
d Papules (violaceous to brown)
d Lack of follicular orifices, resulting in smooth white
patches
d Positive pull test for anagen hair
d Classic lichen planus on nonehair-bearing skin, mucous
membranes, and nails in 50% of cases
LPP, Lichen planopilaris.
Cicatricial alopecias are considered a trichologic
emergency. Early diagnosis and institution of treat-
ment are paramount and can prevent permanent hair
loss. Clinical features of LPP often overlap with those
of other cicatricial alopecias, necessitating histologic
evaluation in order to arrive at the correct diagnosis.
There are certain histologic features that are unique
to LPP. The purpose of this study was to examine
biopsy specimens of known cases of LPP to identify
the key histologic features that characterize this
entity, such that an earlier and accurate diagnosis
can be made with the ultimate goal of improving
patient outcomes.
Although transverse (horizontal) sections are
recommended and preferred by some investigators
for evaluation of alopecias histologically since they
allow visualization of as many follicular units as
possible and at multiple levels,5,16 a recent study
found vertical sections to be superior to transverse
sections alone.17 Vertical sections have the advan-
tage of providing visualization of the overall reaction
pattern and of the superficial dermis and dermoepi-
dermal junction. Vertical sections are used at our
institution for technical reasons and because of the
preferences of our dermatopathologists. They typi-
cally provide sufficient histologic detail that, together
with appropriate clinical correlation, allows accurate
diagnosis.
METHODS
A retrospective review of patients’ medical rec-
ords and pathology reports was conducted after
receiving Institutional Review Board approval. Five
separate searches of the pathology database were
conducted for cases seen between 1992 and 2003. To
be included in the study, patients had to be seen at
least once by a Cleveland Clinic physician with at
least one biopsy specimen taken of the lesion in
question. Search terms included (1) alopecia not
otherwise specified, (2) lupus, (3) inflammatory
J AM ACAD DERMATOL Tandon et al 93
VOLUME 59, NUMBER 1

Table III. Patient demographics* Table IV. Clinical findings*

Median Findings No. (%) (N = 29)
Category No. (%) Mean 6 SD (range)
Type of alopecia
Total No. of patients 29 LPP 20 (69)
Age (y) at diagnosis 49 6 13 50 (24-70) Frontal fibrosing alopecia 1 (3)
Duration (mo) of disease 43 6 37 36 (4-180) Graham-Little syndrome 0 (0)
Men 2 (7) Nonspecific 8 (28)
Age at diagnosis 37 6 18 37 (24-49) Site of disease
Duration (mo) of disease 48 6 17 48 (36-60) Parietal 26 (90)
Women 27 (93) Frontal 15 (52)
Age at diagnosis 50 6 12 50 (30-70) Occipital 15 (52)
Duration (mo) of disease 42 6 38 36 (4-180) Temporal 6 (21)
Race Eyebrows 3 (10)
Caucasian 17 (59) Facial beard 0 (0)
African American 9 (31) Extent of disease (%)
Other 3 (10) 1-25 0 (0)
26-50 8 (28)
SD, Standard deviation.
52-75 13 (45)
*From Cevasco et al.9
76-100 8 (28)
Signs/symptoms
alopecia, (4) cicatricial scarring alopecia, and (5) Follicular hyperkeratosis 20 (69)
lichen planus/LPP. A total of 55 pathology reports out Pruritus 19 (66)
of a total of 604 were identified as possible LPP. In a Perifollicular erythema 18 (62)
previous study,9 clinicopathological review by 3 Pain 16 (55)
independent reviewers revealed that 29 of these Burning 6 (21)
Other (bleeding) 1 (3)
cases were consistent with LPP. It was necessary that
Lichen planus involvement
both the clinical and pathology reports indicated
Total No. of patients affected 8 (28)
LPP. Hair-bearing areas (axilla, groin) 6 (21)
From the medical records, data including demo- Mucous membranes (oral, genital) 4 (14)
graphics, duration of disease, site and extent of Other hair-bearing areas (legs, arms) 3 (10)
disease, signs and symptoms, and presence or ab- Nails 1 (3)
sence of associated lichen planus was extracted Glabrous skin 1 (3)
(Tables III and IV). The duration of disease was
defined as the time between the initial diagnosis of *From Cevasco et al.9
LPP made by the dermatologist and the date the
patient was last seen in clinic. The ‘‘extent of disease’’ RESULTS
was adapted from Dr Olsen’s guidelines.18 LPP was Clinical findings
further broken down into its 3 variants: LPP, Graham- In this study, 20 patients were retrospectively
Little syndrome, and frontal fibrosing alopecia. The diagnosed as having classic LPP, one as having
article by Kossard, Lee, and Wilkinson19 on post- frontal fibrosing alopecia, and 8 were labeled as
menopausal frontal fibrosing alopecia and the article ‘‘nonspecific’’ because they did not fit into a single
by Whiting2 entitled ‘‘Cicatricial Alopecia: Clinico- category of LPP. Common findings included follicu-
pathological Findings’’ were used to assign patients lar hyperkeratosis, pruritus, scalp pain, and perifol-
to a specific category of LPP. licular erythema. The majority of patients had patchy
Of the 29 cases of LPP, two biopsies were omitted hair loss on the parietal scalp and experienced a 51%
from review because of inadequate slide prepara- to 75% extent of disease in that area. Associated
tion. The biopsy specimens were vertically sectioned lichen planus was present in 8 cases; it was most
and examined with hematoxylin-eosin and elastic commonly seen in hair-bearing areas of the body,
stains. The glass slides from each biopsy were such as the axilla and groin9 (see Table IV).
reviewed blindly by a dermatopathologist with ex-
pertise in hair disorders (W. F. B.) and graded
according to the modified version of the Histologic findings
‘‘Pathology Evaluation for Cicatricial Alopecia’’ de- A blinded review of the 27 scalp biopsies was
veloped by the NAHRS.5 The data were then com- performed. Each biopsy specimen was stained with
piled and a statistical analysis was performed to H&E and elastic stains (Verhoffevan Gieson). The
determine histologic features that characterize LPP. following findings were characteristic of LPP (Fig 1, A
94 Tandon et al
Fig 1. A, Representative punch biopsy specimen of LPP
demonstrates reduced follicular units and absent seba-
ceous glands. Superficial and deep perivascular and per-
ifollicular infiltrate around isthmic bulge region with mild
epidermal hyperplasia and follicular hyperkeratosis are
seen. B, Lymphocytic inflammation in peri-isthmic region
produces interface changes with basal vacuolization and
colloid bodies. C, Perifollicular scar and wedge-shaped
perifollicular loss of elastic staining is present in superficial
dermis. (A and B, Hematoxylin-eosin stain; C, Verhoffe
van Gieson stain. Original magnifications: A, 340; B and
C, 3100.)
and B): markedly reduced hair density (67%), ab-
sence of vellus hair (89%), and absence of abnormal
inner root sheath desquamation (96%) (Table V).
Reduction (59%) or complete absence (19%) of
J AM ACAD DERMATOL
JULY 2008
Table V. Histologic features of the hair follicle in
LPP
Findings No. (%) (N = 27)
Terminal hair density
Normal or mild reduction 0 (0)
Moderate reduction 7 (26)
Marked reduction 18 (67)
Absent 2 (7)
Vellus hair density
Present
Normal 1 (4)
Increased 2 (7)
Decreased 0 (0)
Absent 24 (89)
Abnormal inner root sheath desquamation
Present 1 (4)
Absent 26 (96)
arrector pili muscle, and reduction (30%) or com-
plete absence (70%) of sebaceous glands of involved
follicles were also characteristic (Table VI). There
were no significant epidermal changes. The most
prominent patterns of follicular involvement were
lichenoid (22%) and spongiotic (15%) (see Table VI).
Other characteristics included lymphocytic, primar-
ily perifollicular (70%) and perivascular (93%), in-
flammation. Perivascular lymphocytic inflammation
within the reticular dermis was present in 81% of
cases (Table VII). Perifollicular hyalinization of the
stroma was prominent in both the upper (44%) and
lower dermis (70%) and within the follicular tract
(74%). Mucinous perifollicular fibroplasia (37%) was
present in the upper dermis; however, mucin was
absent in the interfollicular dermis (74%). Loss of
elastic staining revealed superficial perifollicular
wedge-shaped scarring and perifollicular scarring
as predominant patterns (Fig 1, C and Table VIII).
DISCUSSION
Because of the symptomatic nature of the condi-
tion and the enlarging areas of permanent alopecia,
which are difficult to camouflage, patients with LPP
frequently have disturbances in psychosocial inter-
actions and self-perception.20 Immediate and ag-
gressive therapy that reduces the inflammation and
protects the follicle and sebaceous glands from
destruction is needed if the hair follicle is to survive
the inflammatory assault. The goal of this clinico-
pathologic review is to delineate the histologic fea-
tures that will aid the clinician in making an accurate
diagnosis so that early treatment can be initiated.
LPP is most accurately diagnosed through a com-
bination of clinical, histologic, and immunofluores-
cence findings. Many of our findings confirm those
J AM ACAD DERMATOL Tandon et al 95
VOLUME 59, NUMBER 1

Table VI. Epithelial and adnexal structure changes Table VII. Severity, type, and site of inflammation
No. (%) (N = 27) Findings No. (%) (N = 27)
Adnexal structure changes Severity
Arrector pili muscle Absent 1 (4)
Normal 6 (22) Mild 15 (55)
Reduced 16 (59) Moderate 10 (32)
Absent 5 (19) Severe 1 (4)
Sebaceous glands Type
Normal 0 (0) Lymphocytic 26 (96)
Reduced 8 (30) Site
Absent 19 (70) Dermal
Epithelial changes Papillary 4 (15)
Epidermal involvement Reticular (perivascular)* 22 (81)
Absent 20 (74) Follicular
Lichenoid 2 (7) Anagen 20 (74)
Vacuolar 1 (4) Catagen 2 (7)
Spongiosis 0 (0) Telogen 1 (4)
Other: Hyperplasia 4 (15) Interfollicular
Follicular involvement Interstitial 1 (4)
Absent 10 (44) Perifollicular 19 (70)
Lichenoid 6 (22) Perivascular 25 (93)
Vacuolar 2 (7) Subcutaneous 0 (0)
Spongiosis 4 (15)
Other: Tufted 1 (4) *Modified criterion from Olsen et al.5
Cysts 1 (4)
No follicle present 3 (11)
of other studies, the predominantly lymphocytic
Epidermal keratin
infiltrate was centered around the follicle and vas-
Parakeratosis 4 (15)
Hyperkeratosis 1 (4) culature. Perifollicular inflammation was present in
Follicular plugging 3 (11) only 70% of cases. Although interface change involv-
ing the follicle is a commonly relied upon diagnostic
feature, this finding may be absent in later ‘‘burned
out’’ cases. In 81% of the cases the lymphocytic
reported in other studies. Specifically, these include infiltrate extended to involve vasculature in the
marked reduction of terminal hair, complete absence reticular dermis (see Fig 1, A).
of vellus hair, and reduced or absent arrector pili Stromal changes can be diagnostically helpful.
muscles and sebaceous glands.2,10,12 Interestingly, Stromal hyalinization within both the upper and
epidermal changes were absent in 74% of cases and lower areas of the dermis as well as within the
therefore were not diagnostically helpful. Specific follicular fibrous tract was a common finding. A
epidermal features evaluated included lichenoid, novel characterizing feature was the mucinous per-
vacuolar, or spongiotic changes (absent in 44%), ifollicular fibroplasia in the upper dermis. In contrast
hyperkeratosis (present in 4%), parakeratosis (pre- to DLE, interfollicular mucin was characteristically
sent in 15%), and follicular plugging (present in absent in the majority (74%) of our cases.
11%). Although follicular plugging has been re- Furthermore, similar to findings reported by Elston
ported as a helpful feature,8 this was not a helpful et al,22 elastic staining highlighted a superficial per-
finding in our study and may reflect the latter stages ifollicular wedge-shaped scar in the majority (60%)
at which the disease underwent biopsy. The hyper- of our patients. Perifollicular scarring was also very
granulosis in LPP forms a collar in the epidermis common (41%).
around the opening of the affected infundibulum21 The origin of LPP is unknown.2 Drugs, infectious
and is often only found there, in contrast to classic organisms, genetic factors, and immunologic abnor-
lichen planus. Infundibular dilatation is also malities are all thought to be possible inciting
observed.21 agents.23-25 The inflammatory infiltrate in LPP ex-
The degree of inflammation present in each case tends in a band-like pattern along the follicular
was highly dependent on which stage (active or end epithelium and involves the bulge region of the
stage) the lesion was in when the biopsy was hair follicle. It is within the bulge region that the
performed. In the majority of our cases, only a mild follicle stem cells, which give rise to the lower and
inflammatory infiltrate was seen. Similar to findings upper portions of the hair follicle and the epidermis,
96 Tandon et al J AM ACAD DERMATOL
JULY 2008

Table VIII. Histologic changes to the fibrous and Table IX. Histologic features of LPP
interstitial tissue in LPP
Follicular
No. (%) Vacuolar degeneration of basal outer root sheath
Findings (N = 27) epithelium
Fibrous tissue Vacuolar degeneration of basement membrane of
Perifollicular fibrosis follicle
Upper dermis (above bulge) Perifollicular lymphocytic infiltrate
Absent 1 (4) Perivascular lymphocytic infiltrate
Concentric lamellar fibroplasia 3 (11) Perifollicular fibrosis
Mucinous fibroplasia 10 (37) Reduction/absence of sebaceous gland
Hyalinization 12 (44) Reduction/absence of arrector pili muscles
Lower dermis (below bulge) Follicular plugging
Absent 6 (22) Superficial perifollicular wedge-shaped scar with elastic
Concentric lamellar fibroplasia 0 (0) stain
Mucinous fibroplasia 1 (4) Perifollicular scar with elastic stain
Hyalinization 19 (70) Epidermal
Follicular tract Parakeratosis
Absent 2 (7) Hyperkeratosis
Fibrovascular 7 (26) Hypergranulosis35
Hyalinized 20 (74) Vacuolar degeneration of basal keratinocytes35
Mucinous/elastotic fibroplasia 2 (7) Vacuolar degeneration of basal membrane35
Interstitial tissue Interfollicular
Interfollicular mucin Absence of dermal mucin
Absent 20 (74) Mucinous fibroplasia in upper dermis
Mild 4 (15) Hyalinization of upper and lower dermis
Moderate 1 (4)
Possible mucin 2 (7)
Elastic fiber pattern
Normal 1 (4) encircled by a basophilic fibrous stroma. Sebaceous
Perifollicular scar 11 (41) glands and arrector pili muscles are reduced or
Superficial perifollicular wedge shaped 16 (60) absent.10 Additional findings that characterize LPP
Diffuse scar (involving interfollicular dermis) 6 (22) histologically include hypergranulosis, hyperkerato-
sis, destruction of the basement membrane, and
degeneration of basal keratinocytes.35 The loss of
elastic fibers along with hair appendages eventually
are found.26,27 Mobini, Tam, and Kamino28 also have results in loss of volume and depression or atrophy
shown a decrease to absence of labeling with Ki-67, a of the affected scalp with superficial perifollicular
proliferative marker, within the bulge area in LPP. wedge-shaped scarring that has displaced the
This finding supports the potential role that hair superior portion of the follicle (area of the bulge)11
follicle stem cell damage plays in the pathogenesis of (Table IX).
LPP. The hair loses potential for regrowth when the LPP can be difficult to distinguish from other
stem cells in the bulge region are destroyed. The hair scarring alopecias and, in particular, DLE.
enters the catagen stage and ultimately involutes Histologically, DLE can be distinguished from LPP
with end-stage fibrotic tracts and scarring alopecia. by several features. In LPP, the lymphocytic infiltrate
As with other forms of cicatricial alopecia, histo- is only superficial, whereas in DLE, the lymphocytic
logically, LPP evolves through a progressive series of infiltrate involves both the deep and superficial
changes.7 Early stages are characterized by follicular vasculature as well as other adnexal structures,
plugging and a perifollicular infiltrate29 involving the such as eccrine glands.4,35 In DLE the basement
bulge and the infundibulum with vacuolar degener- membrane is thickened and there is an increase in
ation of the basal layer and scattered colloid bod- mucin that, unlike LPP, is often within the interfol-
ies.8,30-33 The inferior segment of the follicle and the licular reticular dermis. Telangiectases, dermal
interfollicular dermis is usually not involved.7 As the sclerosis, and focal thinning of the epidermis are
condition progresses, perifollicular fibrosis is very also distinctive.35 In both entities, there is vacuolar
prominent; however, inflammation may be minimal degeneration of the basal layer of the epidermis and
with the loss of distinctive lichenoid changes.34 follicle.4 Direct immunofluorescence antibody stain-
Fibrosis is in the form of longitudinal tracts present ing in DLE shows deposition of one or multiple of the
at the sites of former follicles.3 The isthmus is immunoglobulins IgG, IgA, IgM, and complement
J AM ACAD DERMATOL
VOLUME 59, NUMBER 1
Table X. Differences between LPP and DLE
LPP
Absence of peri-eccrine infiltrate4
Perifollicular/perivascular lymphocytic infiltrate in
infundibulum
Shaggy fibrinogen deposition along BMZ and
globular deposits of IgM and IgA on direct
immunofluorescence8,31,46
BMZ, Basement membrane zone; DLE, discoid lupus erythematosus; LPP, lichen planopilaris.
C3 in a granular pattern along the basement mem-
brane zone. Immunoreactivity for fibrinogen is often
found in the same distribution36-45(Table X46). By
contrast, direct immunofluorescence in LPP may
show immunoreactivity for fibrinogen in a ‘‘shaggy’’
pattern along the basement membrane zone.46
Globular nonspecific IgM and IgA deposition may
also be seen.8,31 Immunoreactivity for IgG and IgA in
a linear pattern along the follicular basement mem-
brane has been reported in a small case series,
although this may reflect an unrelated disease pro-
cess and is discordant with immunofluorescence
patterns reported elsewhere for lichen planus and
LPP.46
Treatment of LPP is imperfect and at times may not
change the ultimate outcome.12 However, treatment
ameliorates symptoms and slows or arrests the pro-
gression of permanent hair loss if initiated in the
early stages.12 After exclusion of a drug-related
etiology, commonly prescribed therapies include
the use of class I or II, high-potency topical steroids
such as clobetasol propionate or intralesional triam-
cinolone.2 High-potency topical corticosteroids in
combination with oral prednisone (30-40 mg/d),
taken for at least 3 months with a gradual taper,
seems to be the most successful at controlling
symptoms and arresting hair loss.8 Additional treat-
ment options that may be employed include topical
tacrolimus, antimalarial agents, isotretinoin, and cy-
closporine; more recently, mycophenolate mofetil
has been described.2,10,47 While topical high-po-
tency and intralesional corticosteroids remain the
mainstay for treatment of LPP, the use of oral tetra-
cycline (1 g/d) may be more beneficial than once
thought.9 Biotin, multivitamins, and ketoconazole
shampoo are also commonly prescribed.9
This study confirmed many of the histologic
findings that have been previously reported on
LPP. Our study highlights a new characterizing fea-
ture of mucinous perifollicular fibroplasia within the
upper dermis, which was seen in 37% of our cases. In
addition, 81% of cases demonstrated lymphocytic
perivascular inflammation in the reticular dermis,
which contrasts with the typically superficial
Tandon et al 97
DLE
Presence of peri-eccrine infiltrate4
Deep and superficial lymphocytic inflammatory
infiltrate35
Granular deposits along dermoepidermal junction
predominantly of IgG, IgM, and C3. Fibrinogen is
often found in the same distribution.36-45
perivascular and perifollicular lymphocytic infiltrate
reported in other studies. Ultimately, the histologic
features vary greatly depending on the stage at which
the biopsy specimen is taken (active or end stage).
The end-stages of many cicatricial alopecias can
appear identical, necessitating a comprehensive re-
view of each patient that takes into account the
clinical and histologic features as well as the immu-
nofluorescence findings.
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