Case Report
White Sponge Nevus, a Rare but Important Entity
Austin N. Belknap , Indraneel Bhattacharyya *, Mohammed N. Islam and Donald M. Cohen






Citation: Belknap, A.N.;
Bhattacharyya, I.; Islam, M.N.;
Cohen, D.M. White Sponge Nevus, a
Rare but Important Entity. Oral 2021,
1, 307–312. https://doi.org/10.3390/
oral1040030
Academic Editor: Omar Kujan
Received: 17 August 2021
Accepted: 15 October 2021
Published: 22 October 2021
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4.0/).
Oral 2021, 1, 307–312. https://doi.org/10.3390/oral1040030
Department of Oral and Maxillofacial Diagnostic Sciences, University of Florida College of Dentistry,
1395 Center Drive, Gainesville, FL 32610, USA
* Correspondence: ibhattacharyya@dental.ufl.edu
Abstract: White sponge nevus (WSN) is an uncommon, hereditary benign keratinization defect that
primarily affects the oral mucosa and occasionally, though rarely, the skin or other mucosal sites,
such as the nose, esophagus and anogenital area. Sporadic cases of vaginal WSN have been reported.
In the oral cavity, the buccal mucosa is prominently affected. Lesions have been reported at birth
but are more commonly noted later during adolescent years. We present three cases of WSN with a
discussion of the clinical appearance and histopathology, along with a brief review of the literature.
Keywords: white sponge nevus; leukoplakia; oral pathology
1. Introduction
White sponge nevus (WSN) is a rare, autosomal dominant disorder that primarily
affects the oral mucosa [1]. It is a benign genodermatosis characterized by high penetrance
and wide variability [2]. The first WSN case was reported in 1909 by Hyde and Cannon,
who published a detailed report in 1935 [3]. The genetic transmission involves mutations in
the cytokeratin 4 and cytokeratin 13 genes, which cause a defect in the normal keratinization
of the mucosa. This defect causes keratin instability and results in hyperkeratotic lesions
on non-keratinized epithelial surfaces [4].
The onset is usually before 20 years of age, with both sexes affected equally [5].
Clinically, WSN is characterized by symmetric, white, thickened, corrugated, asymptomatic
plaques located predominately on the oral mucosa [2]. The condition most commonly
affects the buccal mucosa bilaterally, followed by the lips, alveolar ridges and the floor of
the mouth [6]. The expression of WSN is variable, with the size of the plaques varying
from patient to patient, and the distribution can change with time [7]. Unlike leukoedema,
the white coloration does not diminish or disappear when the mucosa is stretched.
Differentiating WSN from other malignant, reactive, familial and congenital disorders
is important. The diagnosis of WSN is often solely based on the distinct clinical presentation
and subsequent biopsy of the mucosal lesions, which is usually unnecessary. However,
since the oral manifestations of WSN may clinically resemble other white lesions, a biopsy
followed by microscopic evaluation often provides a definitive diagnosis [8]. In this report,
we contribute three additional cases to the literature that were clinically and microscopically
consistent with WSN.
2. Case Report
The three WSN cases were received as incisional biopsies at the University of Florida
Oral Diagnostic Biopsy Service for microscopic examination. Table 1 presents the summary
of the clinical findings for the three cases.
In comparison, all three cases had similar oral clinical appearance and location; however,
the patient for case one additionally reported lesions bilaterally on the lateral/ventral tongue.
As seen in Figures 1–3, all lesions clinically appeared as corrugated, white plaques with a
spongy texture. All three cases reported similar lesions in some other family members.
https://www.mdpi.com/journal/oral
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Table 1. Demographics, clinical locations and duration reported for 3 cases of WSN.
Table 1. Demographics, clinical locations and duration reported for 3 cases of WSN.
Family Extra-Oral
CaseAge Age
Case Sex
Sex Intra-Oral Intra-Oral
LocationsLocations
Family History Extra-Oral Lesions Duration
Duration
History Lesions
Bilateral buccal mucosa
Bilateral buccal mucosaYes
1 1 48 48
F F Yes No
No 8+years
8+ years
Bilateral ventral tongue
Bilateral ventral tongue
2 2 63 63
F Bilateral
F buccal
Bilateral buccal mucosaYes
mucosa Yes No
No 10+years
10+ years
3 3 18 18
M Bilateral
M buccal mucosa
Bilateral buccal mucosaYes Yes No
No 1+years
1+ years

In comparison, all three cases had similar oral clinical appearance and location; how-
2.1. Case 1
ever, the patient for case one additionally reported lesions bilaterally on the lateral/ventral
A healthy
tongue. As seen48-year-old white
in Figures 1–3, allfemale
lesionspresented with bilateral,
clinically appeared slightly thickened
as corrugated, white
white plaques
lesions of the buccal mucosa and tongue (Figure 1). She stated that the lesions
with a spongy texture. All three cases reported similar lesions in some other family mem- were
asymptomatic,
bers. but she occasionally traumatized the affected areas while chewing. She
recalled her father and nephew having similar lesions but reported that their lesions were
much
2.1. smaller
Case 1 and discrete compared to hers. The patient was aware of her father’s WSN
diagnosis but still requested a biopsy for verification.
A healthy 48-year-old white female presented with bilateral, slightly thickened white
lesions
2.2. Caseof2 the buccal mucosa and tongue (Figure 1). She stated that the lesions were
asymptomatic, but she occasionally traumatized the affected areas while chewing. She
A 63-year-old healthy white female, presented with widespread, bilateral, corrugated
recalled her father and nephew having similar lesions but reported that their lesions were
and slightly stippled white lesions on the buccal mucosa (Figure 2). She also reported her
much smaller and discrete compared to hers. The patient was aware of her father’s WSN
family history, stating that her brother and possibly her father had similar lesions of the
diagnosis
oral cavity.but still requested a biopsy for verification.

Figure
Figure 1. Intra-oral photographs
1. Intra-oral photographs of
of lesions
lesions of
of Case
Case 11 that
that clinically
clinically appeared
appeared as
as corrugated,
corrugated, white
white plaques
plaques with
with aa spongy
spongy
texture of: (a) right buccal mucosa, (b) right ventral-lateral tongue and (c) left buccal
buccal mucosa.
mucosa.

2.3. Case
2.2. Case 23
An63-year-old
A 18-year-oldhealthy
Native-American malepresented
white female, presentedwith
withwidespread,
bilateral, thickened,
bilateral,asymp-
corru-
gated and slightly stippled white lesions on the buccal mucosa (Figure 2).off.
tomatic, white corrugated plaques of the buccal mucosa, which did not rub She(Figure 3).
also re-
The clinician
ported reported
her family that the
history, patient
stating thathad
her poor oraland
brother hygiene. Theher
possibly clinician
fatherwho
had performed
similar le-
the biopsy
sions of thealso
oralconsidered
cavity. candidiasis in the differential diagnosis. The patient reported a
family history of diagnosis of WSN in several family members. Details of the family history
could not be obtained, as the patient was lost to follow-up after the initial visit.
Oral 2021,
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2021, 1, 309
3

Figure 2. Intra-oral photographs of Case 2 that were widespread, corrugated and slightly stippled
white lesions of the: (a) right buccal mucosa and (b) left buccal mucosa.

2.3. Case 3
An 18-year-old Native-American male presented with bilateral, thickened, asympto-
matic, white corrugated plaques of the buccal mucosa, which did not rub off. (Figure 3).
The clinician reported that the patient had poor oral hygiene. The clinician who performed
the biopsy also considered candidiasis in the differential diagnosis. The patient reported
a family history of diagnosis of WSN in several family members. Details of the family
Figure 2.
Figure Intra-oralphotographs
2. Intra-oral photographsof ofCase
Case22 that
that were
were widespread,
widespread, corrugated
corrugated and
and slightly
slightly stippled
stippled
history could not be obtained, as the patient was lost to follow-up after the initial visit.
white lesions of the: (a) right buccal mucosa and (b) left buccal mucosa.
white lesions of the: (a) right buccal mucosa and (b) left buccal mucosa.

2.3. Case 3
An 18-year-old Native-American male presented with bilateral, thickened, asympto-
matic, white corrugated plaques of the buccal mucosa, which did not rub off. (Figure 3).
The clinician reported that the patient had poor oral hygiene. The clinician who performed
the biopsy also considered candidiasis in the differential diagnosis. The patient reported
a family history of diagnosis of WSN in several family members. Details of the family
history could not be obtained, as the patient was lost to follow-up after the initial visit.

Figure
Figure 3.
3. Intra-oral
Intra-oral photographs
photographs of of Case
Case 33 that
that were
were symptomatic,
symptomatic, thickened,
thickened, bilateral
bilateral white
white corru-
corru-
gated plaque lesions of: (a) right posterior buccal mucosa and (b) left posterior buccal mucosa.
gated plaque lesions of: (a) right posterior buccal mucosa and (b) left posterior buccal mucosa.

Discussion
3. Discussion
WSN is aa rare,
rare,hereditary
hereditarydisorder
disorderthat
thataffects approximately
affects approximately oneone
in 200,000 people
in 200,000 [9].
people
WSN
[9]. is inherited
WSN as as
is inherited an an
autosomal
autosomal dominant
dominanttraittraitthat
thatexhibits
exhibitsan
anirregular
irregular penetrance
and variable expressivity [10]. Interestingly, all three of our patients had at least one or
more family members affected, which correlates with other published cases [4,10,11]. The
onset of WSN is usually in infancy or childhood, and the disease reaches its peak in early
Figure 3. Intra-oral
adulthood, photographs
with the durationof ofCase 3 that were
the disease symptomatic,
course thickened,[5].
largely unknown bilateral white corru-
gated plaque lesions of: (a) right posterior buccal mucosa and (b) left posterior buccal mucosa.
WSN is a benign condition resulting in defects in keratinization of the surface mucosa,
predominately the oral mucosa [12]. Less frequently reported mucosal sites involved
3. Discussion
include nasal, esophageal, and genital mucosa. None of our three patients reported
WSN is aofrare,
involvement hereditary
extraoral sites. disorder that affects approximately one in 200,000 people
[9]. WSN is inherited as an autosomal dominant trait that exhibits an irregular penetrance
 and variable expressivity [10]. Interestingly, all three of our patients had at least one or
more family members affected, which correlates with other published cases [4,10,11]. The
onset of WSN is usually in infancy or childhood, and the disease reaches its peak in early
adulthood, with the duration of the disease course largely unknown [5].
WSN is a benign condition resulting in defects in keratinization of the surface mu-
Oral 2021, 1 cosa, predominately the oral mucosa [12]. Less frequently reported mucosal sites involved 310

include nasal, esophageal, and genital mucosa. None of our three patients reported in-
volvement of extraoral sites.
Keratins are
Keratins are aa family
family of of around
around 30 30 proteins
proteins that
that are
are classified
classified asas type
type II and
and type
type II
II
and are differentially expressed according to the tissue of origin and cell contents. WSN
and are differentially expressed according to the tissue of origin and cell contents. WSN
typicallyaffects
typically affectsthetheepithelium
epitheliumthat that covers
covers mucosal
mucosal surfaces,
surfaces, particularly
particularly the the
oraloral cavity
cavity and
and the anogenital region. These surfaces express type II keratin 4
the anogenital region. These surfaces express type II keratin 4 and type I keratin 13. WSNand type I keratin 13.
WSN
is is attributed
attributed to point tomutations
point mutations in the
in the gene gene for
coding coding for cytokeratin
cytokeratin 4 and/or4 cytokeratin
and/or cy-
tokeratin
13 [13]. 13 [13].
The microscopic
The microscopic findings
findings of of WSN
WSN are are characteristic,
characteristic, but
butnot
notentirely
entirelypathognomonic.
pathognomonic.
All three cases presented here had almost identical histopathologic findings
All three cases presented here had almost identical histopathologic findings that
that correlate
correlate
with published literature. As seen in Figure 4, microscopic examination
with published literature. As seen in Figure 4, microscopic examination revealed hyperker- revealed hyper-
keratotic stratified squamous epithelium surfaced by a severely
atotic stratified squamous epithelium surfaced by a severely thickened layer of parakeratin. thickened layer of
parakeratin.
The The surfaceis
surface epithelium epithelium
edematous is edematous
and contains and contains numerous
numerous superficialsuperficial ker-
keratohyaline
atohyaline
granules granules
(Figure 4c). (Figure
Extensive 4c).vacuolization
Extensive vacuolization of the suprabasilar
of the suprabasilar keratinocytes keratinocytes
is seen. The
is seen. The characteristic
characteristic dyskeratotic
dyskeratotic cells, cells, which dense
which demonstrate demonstrate denseeosinophilic
perinuclear perinuclearconden-
eosin-
ophilic condensation of the cytoplasm and perinuclear keratinization,
sation of the cytoplasm and perinuclear keratinization, are prominent [14]. This feature are prominent [14].
This feature is unique to WSN and is attributed to the ultrastructural
is unique to WSN and is attributed to the ultrastructural concentration of tonofilaments concentration of
tonofilaments
around the nucleus. around the nucleus.

Figure4.4. Photomicrographs
Figure Photomicrographs from
from hematoxylin
hematoxylin and
andeosin
eosin(H&E)
(H&E)stained
stainedfrom
fromthe
theleft
leftbuccal
buccalmucosa
mucosasample of of
sample Case 2
Case
demonstrating: (a) a low power view (magnification 10×) (b): numerous dyskeratotic cells with dense perinuclear
2 demonstrating: (a) a low power view (magnification 10×) (b): numerous dyskeratotic cells with dense perinuclear eosino-
philic condensation and perinuclear keratinization (magnification 40×) (c) a higher power view (magnification 20×).
eosinophilic condensation and perinuclear keratinization (magnification 40×) (c) a higher power view (magnification 20×).

Clinically, WSN
Clinically, WSN hashas aa similar
similar appearance
appearance to to aa spectrum
spectrum of of disorders
disorders and
and processes
processes
that present with diffuse white plaques of the oral mucosa. When classifying leukoplakic
that present with diffuse white plaques of the oral mucosa. When classifying leukoplakic
lesions on
lesions on clinical
clinical appearance,
appearance,four fourclinical
clinicaltypes of of
types leukoplakia
leukoplakia have been
have identified:
been (1)
identified:
homogenous,
(1) homogenous, (2)(2)
speckled,
speckled, (3)(3)
white
whiteandandredredpatches
patchesandand(4)
(4)verrucous
verrucous[2,15].
[2,15]. Figure
Figure 55
illustrates the common benign clinical differential diagnosis list of leukoplakic lesions
illustrates the common benign clinical differential diagnosis list of leukoplakic lesions
based on
based on if
if the
the lesion
lesion can
can or
or cannot
cannot be be scraped
scraped off.
off. All
All lesions
lesions that
that cannot
cannotbe bescraped
scrapedoff,
off,
which includes
which includes WSN,
WSN, are
are clinically
clinically classified
classified asas homogeneous
homogeneous leukoplakic
leukoplakic lesions.
lesions. These
These
homogeneous white
homogeneous white plaques
plaques have
have nono red
red segments
segments but but have
have aa fine,
fine, white,
white, grainy
grainy texture
texture
or a more mottled, rough appearance. Additionally, these lesions are considered low-risk
and during the evaluation period, an effort to identify the etiologic factor is key.
Oral 2021, 1, FOR PEER REVIEW 5

Oral 2021, 1 311

or a more mottled, rough appearance. Additionally, these lesions are considered low-risk
and during the evaluation period, an effort to identify the etiologic factor is key.

Figure 5. Common
Figure 5. Commonbenign leukoplakic
benign leukoplakiclesions of the
lesions oral
of the mucosa.
oral mucosa.These benign
These white
benign lesions
white have
lesions have
been categorized based if the lesion can or cannot be scraped off [2].
been categorized based if the lesion can or cannot be scraped off [2].

A top
A topconsideration
consideration in in
thethedifferential diagnosis
differential diagnosis is hereditary
is hereditary benign
benign intraepithelial
intraepithelial
dyskeratosis
dyskeratosis (HBID).
(HBID). However,
However, HBIDHBIDis even a rarer
is even disorder
a rarer disorder thatthatcan bebe
can excluded
excluded duedueto to
thethe
absence
absence of bilateral
of bilateral limbal
limbalconjunctival
conjunctival plaques
plaques andanda lack of of
a lack a genetic
a genetic link to to
link a triracial
a triracial
isolate from
isolate fromNorth
North Carolina
Carolina [13]. Leukoplakia
[13]. Leukoplakia cancan
also be be
also considered
considered in in
thethe differential,
differential,
especially
especially proliferative
proliferativeverrucous
verrucousleukoplakia However,PVL
leukoplakia (PVL). However, PVLtypically
typically presents
presents with
sharply
with sharplydefined
definedmargins,
margins,in comparison
in comparison to the
to indistinct
the indistinctborders of WSN
borders of WSN[16]. [16].
Also,Also,
PVL is
PVLa disease of elderly
is a disease females
of elderly and isand
females usually progressive.
is usually Darier’s
progressive. disease
Darier’s (DD) is
disease another
(DD) is
important
another consideration
important in thein
consideration differential diagnosis,
the differential especially
diagnosis, in theincase
especially theof theofsecond
case the
patient,
second due to
patient, due thetostippled or cobblestone
the stippled appearance
or cobblestone of theofbuccal
appearance mucosa.
the buccal However,
mucosa. How-the
lackthe
ever, of lack
nail and skin
of nail andabnormalities, which are
skin abnormalities, characteristic
which of DD, makes
are characteristic of DD,this makesdiagnosis
this
untenable.
diagnosis Similar to
untenable. DD, dyskeratosis
Similar congenitacongenita
to DD, dyskeratosis and pachyonychia congenitacongenita
and pachyonychia can present
canwith multi-surface
present white oral
with multi-surface white lesions, but alsobut
oral lesions, display nail and
also display nailskin
and abnormalities
skin abnormal-[4].
Pseudomembranous candidiasis was considered as a diagnosis
ities [4]. Pseudomembranous candidiasis was considered as a diagnosis for patient for patient three,three,
but the
but the white lesions found in Candidiasis typically can be wiped off and the lack of re- to
white lesions found in Candidiasis typically can be wiped off and the lack of response
antifungals
sponse would also
to antifungals would rulealso
it out.
rule it out.
WSN WSN is considered
is considered toto
bebe a completelybenign
a completely benignand andharmless
harmlesscondition
conditionwith with nono poten-
potential
for malignant transformation [11]. Patients have reported minor
tial for malignant transformation [11]. Patients have reported minor symptoms of discom- symptoms of discomfort
fortasas
a result
a resultofofaltered
altered texture
textureof ofthethe
oral mucosa
oral mucosa and esthetic
and concerns.
esthetic concerns. Usually,
Usually, there is no
there
treatment required for WSN. Treatment with beta-carotene, various
is no treatment required for WSN. Treatment with beta-carotene, various antibiotics (pen- antibiotics (penicillin,
azithromycin,
icillin, azithromycin, etc.),etc.),
antihistamines,
antihistamines, tetracycline mouth
tetracycline rinses,
mouth local application
rinses, local application of retinoic
of
retinoic acid, laser ablation and surgical resection have all been tried to reduce the extent of
acid, laser ablation and surgical resection have all been tried to reduce the extent
of WSN
WSN lesions,
lesions, as as reported
reported in in the
theliterature,
literature,butbutwithout
withoutmuch muchsuccess
success[17].[17].NoneNone of of
thethe
cases reported here received any treatment and the patients were
cases reported here received any treatment and the patients were reassured of the benign reassured of the benign
character of their lesions.
character of their lesions.
4. Conclusions
4. Conclusions
We present three cases of WSN, with all cases reporting familial involvement. WSN
is aWe present
rare three cases
and benign of WSN,
condition with all
resulting cases
from reporting
a genetic familial
defect involvement.
in keratinization WSN
that most
is acommonly
rare and benign condition resulting from a genetic defect in keratinization that
affects the oral mucosa. Clinicians should be cognizant of WSN when presentedmost
with a characteristic clinical appearance involving multiple sites of the oral cavity in order
to avoid misdiagnosis and unnecessary treatment. The condition can be diagnosed on the
Oral 2021, 1 312

basis of clinical presentation alone on most occasions, and a biopsy is required only for
confirmation of the diagnosis, in cases of unusual features or in the presence of risk factors.

Author Contributions: A.N.B., I.B., M.N.I. and D.M.C. were responsible for the reviewing and
editing of the manuscript, with A.N.B. writing the original manuscript draft. All authors have read
and agreed to the published version of the manuscript.
Funding: This research received no external funding.
Informed Consent Statement: Informed consent was obtained from two of the subjects involved in
the study. One patient’s consent was waived due to the lack of follow-up.
Acknowledgments: The Robert N. Levenson and Grace B. Dunlevy Oral Pathology Research Fund.
Conflicts of Interest: The authors declare no conflict of interest. The acknowledged funders had no
role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of
the manuscript; or in the decision to publish the results.

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