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Chronic lingual papulosis: new, independent entity or “mature”
form of transient lingual papillitis?
Jerry E. Bouquot, DDS, MSD, FICD, FACD,
a
Shawn S. Adibi, DDS,
b
and Maga Sanchez, MD,
c
Houston, Texas
UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER
Objective. Several acute, usually pediatric variants of edematous, symptomatic fungiform lingual papillitis have been reported
since the 1990s, most notably transient lingual papillitis (TLP); but no chronic forms have been mentioned. Is there a chronic
counterpart, akin to the older palatal examples of inflammatory papillary hyperplasia? The objective of this study was to
clinicopathologically characterize a previously unreported entity with clustered, chronic fibrous papules (nonsyndromic) of
the tongue.
Methods. Cases were collected from clinics in 2 dental schools.
Results. Five women and 4 men were identified with multiple, moderately firm, slightly pedunculated, normally colored
masses clustered at the tip of the tongue (n ⫽4), covering the dorsal surface (n ⫽4) or on the lateral border (n ⫽1); 2
showed several erythematous or edematous papules (similar to TLP) admixed with fibrous papules. Patient ages ranged from
31 to 62 years (average 49) and all lesions had been present for many years. All lesions were asymptomatic except for the
lateral border lesion, which presented with a burning sensation and mild tenderness (disappeared with antifungal
medication). Five cases were associated with mouth breathing or a tongue-thrust habit; 4 were associated with geographic
tongue or fissured tongue. Four papules were biopsied. All were composed of dense, avascular fibrous tissue with no or very
few inflammatory cells; one showed focal mild neovascularity and edema. The lesion appeared to represent altered filiform
papillae, more so than fungiform papillae.
Conclusions. Chronic lingual papulosis (CLP) is an innocuous entity represented by focal or diffuse enlargement of numerous
lingual papillae, primarily the filiform papillae. It appears to usually have an adult onset and most likely represents papillary
reaction to very low-grade, chronic irritation or desiccation. Some cases with childhood onset, however, seem to be
variations of normal anatomy. No treatment or biopsy is required, but a number of systemic disorders and syndromes must be
ruled out before applying the CLP diagnosis. (Oral Surg Oral Med Oral Pathol Oral Radiol 2012;113:111-117)
Transient lingual papillitis (TLP), initially reported
by Whitaker et al. in 1996, is a common acute
inflammatory enlargement of fungiform papillae.
1,2
It has an abrupt onset, with 1 or more edematous,
erythematous 2- to 3-mm masses developing over 1-
to 3-hours, sometimes “instantly.” Affected papillae
may become pustular, but even without pus, TLP is
accompanied by moderate-to-severe pain and tender-
ness, often with considerable thermal sensitivity as
well. The pain spontaneously resolves after 1 to 4
days and the papillae return to normal with minimal
risk of recurrence.
1,3-11
The etiology of TLP is un-
clear but appears to be multifactorial. Suggested
causes include acute thermal injury (i.e., coffee, tea,
soup, tobacco smoke), acute mechanical trauma,
chronic mechanical trauma (tongue-thrust habit), hy-
persensitivity to food or candy or oral hygiene prod-
ucts, contact or airborne toxins (photocopier’s pap-
illitis), unidentified infections (local), atopic disease,
and hormonal changes (in women).
1-8
Association
with benign migratory glossitis has been reported.
1
The infective variant seems to follow a viral or
“strep-mouth” pattern, may involve filiform papillae
as well, is typically pediatric in presentation, is ap-
parently contagious, and is associated with fever and
other signs of upper respiratory infection or strep
throat.
3,7
A common myth represents TLP, especially
the single, exquisitely painful papilla, as resulting
from the telling of a lie. This potential etiology has
not been thoroughly researched but “lie bumps” or
“liar’s bumps” are often so painful, albeit transient,
that affected persons clip them off with a nail clipper
to obtain relief.
12
No long-term (years) variant of
TLP has been reported, but we herein present a series
of cases of multiple, sometimes generalized, asymp-
tomatic enlargement of lingual papillae with a
chronic duration.
CASES
Nine cases were derived from the authors’ patient pan-
els (Table I). Of these, 5 (56%) were in women. Patient
a
Chair, Department of Diagnostic & Biomedical Sciences, School of
Dentistry, University of Texas Health Science Center.
b
Assistant Professor, Department of Diagnostic & Biomedical Sciences,
School of Dentistry, University of Texas Health Science Center.
c
Postdoctoral Fellow, Department of Diagnostic & Biomedical Sciences,
School of Dentistry, University of Texas Health Science Center.
Received for publication Jun 2, 2011; returned for revision Sep 14,
2011; accepted for publication Sep 19, 2011.
© 2012 Elsevier Inc. All rights reserved.
2212-4403/$ - see front matter
doi:10.1016/j.tripleo.2011.09.003
Vol. 113 No. 1 January 2012
111
ages at diagnosis ranged from 31.0 to 62.0 years, with
an average of 49.2 years. No common underlying sys-
temic disease or medication was identified, although 2
patients were on thyroid replacement therapy and 2
were taking hypertensive medication. Lingual changes
predated medications in all cases. All lesions (Figures
1-6) had been present for many years, often decades,
with at least 3 being present since childhood. No patient
could remember precisely when the tongue changes
began, however, and none had noticed change over
time. All but one of the tongues were asymptomatic and
no patient could remember ever experiencing the ex-
quisite pain of TLP. The single symptomatic case in our
series was a lateral border lesion with a burning sensa-
tion and mild tenderness, both of which disappeared
with topical antifungal medication (Figure 6). No pa-
tient presented with dysgeusia, hypogeusia, xerostomia,
or halitosis.
The papules showed 2 patterns: focal and diffuse
(generalized). Focal aggregates of papules were usually
found at the tip of the tongue (n ⫽4), but one was
along the lateral border (Figure 6). Diffuse lesions (n ⫽
4) presented as generalized, scattered papules covering
most of the dorsal surface (Figure 1); one of these was
unilateral. Individual papules were pedunculated,
slightly more firm than normal, varying in size from 2
to 5 mm, and were of normal color or were slightly
erythematous. Occasional cases showed much larger
individual papules among the smaller, more uniform
ones (Figure 6); it is not clear whether these represent
Table I. Summary of 9 affected patients
Gender
Age at
diagnosis,
y Clinical presentation and biopsy results, if biopsy was performed Tongue/Oral abnormalities and habits
M* 31 Figure 1. Diffuse involvement of dorsum, bilaterally: papules of
uniform size.
None
M* 62 Figures 2 and 7. Diffuse involvement of dorsum, bilaterally:
considerable variation in size of papules; some papules look
pale. Biopsy: dense fibrous tissue and mild hyperkeratosis.
Fissured tongue
†
F54Figure 3. Tip of tongue: uniform papules surrounded by
geographic tongue.
Geographic tongue
†
; fissured tongue
M53Figure 4. Tip of tongue: papules uniform in size and extending
onto dorsum; some are slightly “edematous”; lateral tongue
crenations.
Mouth breather; nasal obstruction;
tongue-thrust habit; macroglossia
F38Figure 5. Tip of tongue: multiple, asymptomatic, moderately firm,
slightly pedunculated uniform papules. Biopsy: avascular fibrous
tissue with a few subepithelial lymphocytes; small surface
projection of granulation tissue.
Mouth breather; anterior open bite;
white-coated tongue
F53Figures 6 and 8. Lateral border and left dorsum of tongue: some
papules with mild erythema or translucency; mild burning
sensation (disappeared with antifungal prescription); crenations
on lingual borders and with an irritation fibromalike mass.
Biopsy: dense fibrosis, mild chronic subepithelial inflammation;
taste buds in epithelium.
Tongue rubbing against sharp premolars;
fissured tongue
†
; candidiasis
F 46 Tip of tongue: moderate involvement with extension onto dorsum;
papules are somewhat irregular in size.
None
M 47 Diffuse involvement of dorsum: uniform sized papules of normal
color. Biopsy: dense fibrous tissue with a small number of
dilated subepithelial capillaries.
Tongue-thrust habit; mouth breather;
geographic tongue
F* 59 Diffuse involvement of dorsum, bilaterally; associated with fissured
tongue; papules of uniform size.
Mouth breathing; anterior open bite;
fissured tongue
†
All tongue changes had been present for many years in each patient. No systemic or syndromic diseases were associated.
M, male; F, female.
*Childhood onset.
†Geographic or fissured tongue was in the area of chronic lingual papulosis.
Figure 1. Diffuse, bilateral involvement of most lingual pa-
pillae. Some papules have a mild semitranslucent appearance.
ORAL AND MAXILLOFACIAL PATHOLOGY OOOO
112 Bouquot et al. January 2012
a variant of chronic lingual papulosis (CLP) or a simple
combination of several entities (e.g., CLP and irritation
fibroma). Some appeared somewhat translucent, pre-
sumably from a thin excess of surface keratin, possibly
from mild subepithelial edema. Filiform papillae
seemed to be primarily affected, but occasional fungi-
form papillae were involved.
Four papules were biopsied. All were composed of
dense, avascular fibrous tissue with no or very few
inflammatory cells (Figure 7), essentially indistinguish-
able from an irritation fibroma. One papule had a small
secondary surface projection with dilated capillaries,
fibroplasias, and focal edem (i.e., granulation tissue),
whereas another was hyperkeratotic. The largest papule
(see arrow in Figure 6) looked histopathologically like
an inflamed irritation fibroma, but it was an obvious
fungiform papilla, because taste buds could be seen in
the epithelium (Figure 8).
Etiologies could not be definitively established,
but additional tongue changes were seen in all but 2
cases, and 4 (44%) cases were associated with mouth
breathing, tongue-thrust habit, or both. Two of these
showed only tongue tip involvement, whereas 2 had
diffuse papulosis of the entire dorsum. Four patients
had fissured tongue, all with fissures intimately ad-
mixed with the CLP. Two cases of CLP also had
geographic tongue. One of these was physically as-
sociated with CLP (Figure 3), but the “moveable”
nature of geographic tongue is such that close con-
tacts at other points in time may or may not have
occurred.
None of the patients demonstrated a smooth tongue
or hairy tongue, but one had a mild coated tongue with
Figure 2. Diffuse, bilateral involvement of much of the dor-
sal surface, with considerable variation in size of papules and
with some papules showing mild pallor from hyperkeratosis
(inset). Fissured tongue is admixed with the papulosis. Arrow
points to biopsied mass (see Figure 7).
Figure 3. Tip of tongue shows diffuse enlargement of most
papillae, with some showing a somewhat transparent appear-
ance. Papules are located primarily within an area of geo-
graphic tongue, with white streaking at borders of the
papulosis.
Figure 4. Most papillae of the tip of the tongue are en-
larged and some seem slightly edematous. Papules extend
onto the anterior dorsum and crenations are seen on the
lateral borders.
Figure 5. Mild involvement of the tip of the tongue in a
mouth breather. The dorsum shows mild white-coated
tongue, which is not evident in the papulosis. The patient
has mild geographic and fissured tongue (not shown).
(Courtesy of Dr. Edward Halusic, Greensburg, PA; with
permission.)
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Volume 113, Number 1 Bouquot et al. 113
loss of coating in the area of CLP (Figure 5). Two cases
had no lingual abnormalities except the CLP.
DISCUSSION
We suggest the name “chronic lingual papulosis” for
this previously unreported entity. CLP appears typi-
cally to be a fibrous hyperplastic response of filiform
and sometimes fungiform papillae to mild mechanical
irritation, low-grade, long-term inflammation or
chronic desiccation. Although TLP has a papulokera-
totic variant, which may persist for several weeks or
months, CLP does not appear to represent this or any
other form of chronic TLP.
4
CLP duration is far too
long, is not associated with change over time, and,
moreover, none of our patients had ever painful TLP.
To clarify the CLP diagnosis: it is characterized by
multiple (dozens, at least) asymptomatic, normal-col-
ored, enlarged lingual papillae, composed microscopi-
cally of dense fibrous tissue with few, if any, inflam-
matory cells. The abnormality may have an adult or
childhood onset, perhaps with different etiologic fac-
tors at work, and the papules may be clustered or
generalized.
Although all but 2 of our cases exhibited other lin-
gual pathoses, these did not seem necessary for CLP
development, as no secondary condition was constantly
associated and many were not physically close to the
area of CLP involvement. The most-often associated
condition, fissured tongue, at first seems a likely can-
didate for CLP etiology, but we have no means by
which to determine which came first in our patients
and, more significantly, not all cases demonstrated fis-
suring.
Adult-onset CLP is, perhaps, most similar to in-
flammatory papillary hyperplasia beneath a denture
(i.e., a disease that starts with edematous, usually
asymptomatic or mildly symptomatic hard papules
that become more and more fibrotic and less edem-
atous or acutely inflamed over time). We can only
speculate on this pathophysiology, of course, as none
of our patients could remember an early phase with
edematous or erythematous papules. Confirmation
might be found in the presence of sporadic erythem-
atous papules (Figures 3 and 5) and the occasional
mild chronic inflammatory changes seen microscop-
ically (Figure 8), although this is far from conclusive
evidence.
Childhood-onset CLP (Figure 1) is possibly devel-
opmental rather than inflammatory and it might,
Figure 6. Unilateral involvement of dorsum and border of
tongue. Clinically classic irritation fibroma look-alike le-
sion (arrow) is seen in otherwise generalized enlargement
of lingual papillae. Biopsy of the “fibroma” is shown in
Figure 8.
Figure 7. Biopsy from Figure 2. The papule is composed of
dense, rather avascular fibrous tissue with a few chronic
inflammatory cells beneath the epithelium. Surface epithe-
lium is not atrophic and shows a thickened surface layer of
parakeratin. (Magnification ⫻100; H&E stain.)
Figure 8. Biopsy of large papule from Figure 6 shows the
greatest number of chronic inflammatory cells of all biopsied
papules; there is also mild angiogenesis. This papule appears
to represent an enlarged fungiform papilla with taste buds
(arrows, inset). (Magnification ⫻200; H&E stain.)
ORAL AND MAXILLOFACIAL PATHOLOGY OOOO
114 Bouquot et al. January 2012
therefore, be logical to refer to the childhood-onset
cases as “congenital CLP” or “developmental CLP.”
Unfortunately, none of our patients could shed light
on the exact time or manner of onset, and potential
etiologic associations, such as mouth breathing and
fissured tongue, are also seen in children. Until an
investigation of childhood cases clarifies this point,
we prefer the CLP diagnosis to be based entirely on
Table II. Disorders associated with multiple nodules or papules of the tongue
13-30
Observed papillary
change Specific/suspected etiology Comment
Fungiform hyperplasia,
with filiform
depapillation
Cyclosporin therapy (e.g.,
transplantation)
Called “lingual fungiform papillary hypertrophy”; may be associated with gingival
hyperplasia
Strep mouth* Acute infection by hemolytic streptococci, usually with strep throat; like scarlet
fever tongue (strawberry tongue, raspberry tongue), but with no skin rash; acute
onset, oral and pharyngeal pain, 1-wk duration
Scurvy (hypovitaminosis C) Eventually entire tongue enlarges; also with gingival hyperplasia and palatal edema
Familial dysautonomia Also called Riley-Day syndrome; an inherited autonomic neuropathy with
widespread autonomic and sensory nerve dysfunction, including insensitivity to
pain and misinterpretation of taste and heat-input signals
Guttate psoriasis* Prominent fungiform papillae in a smooth lingual dorsum; tear-drop–shaped
erythematous and keratotic psoriasiform skin lesions; usually in persons ⬍30
years of age
Fungiform hyperplasia,
without filiform
depapillation
Cyclosporin therapy Usually the filiform papillae are atrophied
Normal-sized fungiform
papillae, with filiform
depapillation
Anemia, candidiasis,
chemotherapy, AIDS
Atrophic glossitis; fibrous fungiform hyperplasia with otherwise smooth dorsal
surface; may also show angular cheilosis (anemia, candidiasis)
Guttate psoriasis Called psoriasiform fungiform hypertrophy
Kawasaki disease Strawberry tongue
Papillomatosis Epidermal nevus syndrome Pigmented verruciform plaques of the skin, central nervous system abnormalities,
mental deficiencies, seizures; oral mucosa papules may be numerous and
clustered
Bowenoid papulosis Small granular surface change in erythroplakia; microscopically, severe dysplasia or
carcinoma in situ
Acanthosis nigricans Brown hyperkeratotic skin papules; gastrointestinal and gastrointestinal adenomas
and adenocarcinomas; tongue appears “shaggy” from papillary hypertrophy, as do
the lips
Ichthyosis hystrix Hyperkeratosis of skin (defective keratinocyte sloughing); pebbled oral mucosal
surfaces, usually unilateral; skin nevi, called nevus unius lateris, may be seen
without the ichthyosis disorder (see epidermal nevus syndrome)
Supernumerary
fungiform papillae
Supertasters Normal fungiform size; increased risk of burning tongue, orofacial pain
Lymphoid/foliate
papilla hyperplasia
Hyperplastic lingual tonsil Chronic enlargement of lingual tonsils (posterior lateral border) from responding to
repeat infections; not seen on the dorsum; also called foliate papillitis
Lymphoid papillitis Ulcerated nodules, with malignant-appearing lymphoid stroma; skin nodules also
Nodules and papules of
tongue (not papillae)
Nodular median rhomboid
glossitis
Sessile fibrous nodules on depapillated region of the glossitis; posterior dorsum,
midline
Neurofibromatosis Benign nerve tumors or fibrous nodules of any oral surface, but especially the
tongue
Tuberous sclerosis Inherited disorder with seizures, mental deficiency, angiofibromas; irregular fibrous
growths of gingiva, lips, and tongue
Amyloidosis Irregular-sized nodules and papules represent infiltration of amyloid beneath the
epithelium; slow onset (months or weeks)
Lipoid proteinosis Inherited lysosomal storage disease with numerous nodular infiltrates of skin and
mucous membranes; tongue becomes less mobile over time; lingual dorsum
becomes depapillated, with papillae replaced by disease nodules and papules
Leprosy Especially in lepromatous type (masses called lepromas); multiple granulomatous
masses of the tongue and face, with eventual ulceration
Cowden syndrome Multiple hamartomas of skin and mucous membranes; numerous oral fibromas,
especially of the tongue, lips, and gingiva
Enlarged circumvallated
papillae
Hypertrophied
circumvallated papillae
Variation of normal anatomy; papillae are uniformly enlarged, perhaps as much as
twice normal size
*No actual enlargement of papillae, but fungiform papillae are not lost and so appear to be more prominent because they are no longer admixed
with filiform papillae.
OOOO ORIGINAL ARTICLE
Volume 113, Number 1 Bouquot et al. 115
the clinical presentation, not the age of onset or
possible etiologies. In this regard, the reader is re-
minded that CLP is, by definition, not associated
with any of the numerous systemic diseases or syn-
dromes presenting with multiple lingual papules or
nodules (Table II).
13-30
How problematic is CLP to good oral or physical
health? It appears to be innocuous in its biological
behavior and requires no treatment, unless secondarily
infected by Candida in the furrows surrounding the
papules. Our understanding of this is not, of course,
based on long-term follow-up, but rather on the un-
eventful presence of CLP in our patients for many
years, usually decades, before diagnosis.
We consider this entity to require clinical diagnosis
only; biopsy should not be required unless the enlarged
papillae appear atypical (Figure 6), possibly represent-
ing a separate or superimposed lesion. In addition, we
believe CLP to be relatively common, even though we
present only 9 cases. Throughout the many years of our
collective practice experience, we have seen similarly
affected tongues with relative frequency. Our cases,
however, represent only a convenience sample selected
because of good documentation and representation of
the entire spectrum of CLP; a valid prevalence rate is
not available.
Along a similar line, oral pathology biopsy services
receive tissue samples of “hyperplastic lingual papilla”
with some frequency. This does not provide a CLP
diagnosis because the surgeon typically does not pro-
vide information relative to additional similar lingual
masses in the patient.
Mucosal changes without names are extremely
rare in oral pathology, especially for such an obvious
surface alteration. We have no explanation for the
fact that this supposedly common entity has not been
previously reported. Perhaps the present report will
stimulate more significant pathoetiologic investiga-
tion, because, after all, such investigations are done
only on named entities.
CONCLUSIONS
CLP is an innocuous lesion represented by focal or
diffuse fibrous enlargement of numerous lingual papil-
lae, primarily the filiform papillae. It appears to usually
have an adult onset and most likely represents papillary
reaction to very low-grade, chronic irritation or desic-
cation. Some cases with childhood onset, however, may
be developmental in nature. No treatment or biopsy is
required, but a number of systemic disorders and syn-
dromes must be ruled out before applying the CLP
diagnosis.
REFERENCES
1. Whitaker SB, Krupa JJ 3rd, Singh BB. Transient lingual papil-
litis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
1996;82:441-5.
2. Neville B, Damm D, Allen C, Bouquot J. Oral and maxillofacial
pathology. 3rd ed. Philadelphia: W. B. Saunders; 2008.
3. Lacour JP, Perrin C. Eruptive familial lingual papillitis: a new
entity? Pediatr Dermatol 1997;14:13-6.
4. Flaitz CM, Chavarria C. Painful tongue lesions associated with a
food allergy. Pediatr Dent 2001;23:506-7.
5. Brannon RB, Flaitz CM. Transient lingual papillitis: a papulok-
eratotic variant. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 2003;96:187-91.
6. Galun E, Rubinow A. Photocopier’s papillitis. Lancet 1989;
2:929.
7. Roux O, Lacour JP, Paediatricians of the Region var-Côte d’azur.
Eruptive lingual papillitis with household transmission: a pro-
spective clinical study. Br J Dermatol 2004;150:299-303.
8. Marks R, Scarff CE, Yap LM, Verlinden V, Jolley D, Campbell
J. Fungiform papillary glossitis: atopic disease in the mouth? Br J
Dermatol 2005;153:740-5.
9. Chaudhry SI, Buchanan JA, Boulter A, Hodgson TA, Porter SR,
Campbell J. Fungiform papillary glossitis: a ‘new’ diagnosis or a
‘misdiagnosis’? Br J Dermatol 2005;153:740-5.
10. Noonan V, Kemp S, Gallagher G, Kabani S. Transient lingual
papillitis. J Mass Dent Soc 2008;57:39.
11. Giunta JL. Transient lingual papillitis: case reports. J Mass Dent
Soc 2009;58:26-7.
12. Anonymous. Lie Bumps. Available at: http://en.wikipedia.org/
wik/Special:Search?search⫽lie⫹bump%2C⫽tongue&go⫽Go. Ac-
cessed March 17, 2011.
13. Simpson HE. Lymphoid hyperplasia in foliate papillitis. J Oral
Surg Anesth Hosp Dent Serv 1964;22:209-14.
14. Stankler L, Kerr NW. Prominent fungiform papillae in guttate
psoriasis. Br J Oral Maxillofac Surg 1984;22:123-8.
15. Gorlin RJ, Cohen MM, Levin LS. Syndromes of the head and
neck. 3rd ed. Oxford, England: Oxford Press; 1990.
16. Menni S, Beretta D, Piccinno R, Ghio L. Cutaneous and oral
lesions in 32 children after renal transplantation. Pediatr Derma-
tol 1991;8:194-8.
17. Shapiro SD, Abramovitch K, Van Dis ML, Skoczylas LJ, Lan-
glais RP, Jorgenson RJ, et al. Neurofibromatosis: oral and radio-
graphic manifestations. Oral Surg Oral Med Oral Pathol 1984;
58:493-8.
18. Di Felice R, Lombardi T. Foliate papillitis occurring in a child:
a case report. Ann Dent 1993;52:17-8.
19. Silverberg NB, Singh A, Echt AF, Laude TA. Lingual fungiform
papillae with cyclosporin A. Lancet 1996;348:967.
20. Kato NMD, Tomita Y, Yoshida K, Hisai H. Involvement of the
tongue by lymphomatoid papulosis. Am J Dermatopathol 1998;
20:522-6.
21. Sciubba J, Said-Al-Naief N, Fantasia J. Critical review of lym-
phomatoid papulosis of the oral cavity with case report. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90:195-204.
22. Essick GK, Chopra A, Guest S, McGlone F. Lingual tactile acuity,
taste perception, and the density and diameter of fungiform papillae
in female subjects. Physiol Behav 2003;80:289-302.
23. Purohit-Sheth TS, Carr WW. Oral allergy syndrome (pollen–
food allergy syndrome). Allergy Asthma Proc 2005;26:229-30.
24. Chimenos Küstner E, Pascual Cruz M, Pinol Dansis C, Vinals
Iglesias H, Rodríguez de Rivera Campillo ME, López López J.
Lepromatous leprosy: a review and case report. Med Oral Patol
Oral Cir Bucal 2006;11:E474-9.
25. Martins MD, Russo MP, Lemos JB, Fernandes KP, Bussadori
SK, Corrêa CT, et al. Orofacial lesions in treated southeast
ORAL AND MAXILLOFACIAL PATHOLOGY OOOO
116 Bouquot et al. January 2012
Brazilian leprosy patients: a cross-sectional study. Oral Dis
2007;13:270-3.
26. Sparling JD, Hong CH, Brahim JS, Moss J, Darling TN. Oral
findings in 58 adults with tuberous sclerosis complex. J Am Acad
Dermatol 2007;56:786-90.
27. Lier GC, Mrowietz U, Wolfart M, Warnke PH, Wiltfang J,
Springer IN. Psoriasis of the tongue. J Craniomaxillofac Surg
2009;37:51-3.
28. Cengiz MI, Wang HL, Yıldız L. Oral involvement in a case of
AA amyloidosis: a case report. J Med Case Rep 2010;4:200.
29. Maltos AL, da Silva LL, Bernardes Junior AG, Portari GV, da
Cunha DF. Scurvy in a patient with AIDS: case report. Rev Soc
Bras Med Trop 2011; 44:122-3.
30. Haberland-Carrodeguas C, Allen CM, Lovas JG, Hicks J, Flaitz
CM, Carlos R, et al. Review of linear epidermal nevus with oral
mucosal involvement—series of five new cases. Oral Dis
2008;14:131-7.
Reprint requests:
Jerry E. Bouquot, DDS, MSD
Chair, Department of Diagnostic & Biomedical Sciences
Room 3.094b
University of Texas School of Dentistry at Houston
6516 M. D. Anderson Blvd.
Houston, TX 77030
jerry.bouquot@uth.tmc.edu
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Volume 113, Number 1 Bouquot et al. 117