applied

sciences
Review
The Pseudolesions of the Oral Mucosa: Differential
Diagnosis and Related Systemic Conditions
Fedora della Vella 1, * , Dorina Lauritano 2 , Carlo Lajolo 3 , Alberta Lucchese 4 ,
Dario Di Stasio 4 , Maria Contaldo 4 , Rosario Serpico 4 and Massimo Petruzzi 1, *
1 Interdisciplinary Department of Medicine, University of Bari “Aldo Moro”, 70124 Bari, Italy
2 School of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy;
dorina.lauritano@unimib.it
3 Department of Head and Neck, Oral Surgery and Implantology Unit, University Cattolica del Sacro Cuore,
00168 Rome, Italy; carlo.lajolo@unicatt.it
4 Multidisciplinary Department of Medical-Surgical and Dental Specialties, University of Campania “Luigi
Vanvitelli”, 80138 Naples, Italy; alberta.lucchese@unicampania.it (A.L.);
dario.distasio@unicampania.it (D.D.S.); maria.contaldo@gmail.com (M.C.);
rosario.serpico@unicampania.it (R.S.)
* Correspondence: dellavellaf@gmail.com (F.d.V.); massimo.petruzzi@uniba.it (M.P.);
Tel.: +39-0805478388 (F.d.V.)




Received: 7 May 2019; Accepted: 10 June 2019; Published: 13 June 2019


Abstract: Pseudolesions are defined as physiological or paraphysiological changes of the oral normal
anatomy that can easily be misdiagnosed for pathological conditions such as potentially malignant
lesions, infective and immune diseases, or neoplasms. Pseudolesions do not require treatment and a
surgical or pharmacological approach can constitute an overtreatment indeed. This review aims to
describe the most common pseudolesions of oral soft tissues, their possible differential diagnosis and
eventual related systemic diseases or syndromes. The pseudolesions frequently observed in clinical
practice and reported in literature include Fordyce granules, leukoedema, geographic tongue, fissured
tongue, sublingual varices, lingual fimbriae, vallate papillae, white and black hairy tongue, Steno’s
duct hypertrophy, lingual tonsil, white sponge nevus, racial gingival pigmentation, lingual thyroid,
and eruptive cyst. They could be misdiagnosed as oral potential malignant disorders, candidiasis,
Human Papilloma Virus (HPV)-related affections, oral autoimmune diseases, or benign and malignant
tumors. In some cases, pseudolesions feature in a syndromic panel, for example, fissured tongue in
Melkersson–Rosenthal syndrome. It is strictly fundamental for dentists to know and to distinguish
oral pseudolesions from pathological conditions, in order to avoid overtreatment.

Keywords: oral pseudolesion; geographic tongue; Fordyce granules; differential diagnosis

1. Introduction
Oral lesions are characterized by tissue alterations, associated with cytological and histological
changes [1]. They can be determined by traumatic, infective, immune, potentially neoplastic, and
neoplastic (benign or malignant) processes that affect the oral mucosa with different clinical appearance,
onset time, and intensity. Generally, dentists point out oral lesions noting changes in size, surface
morphology, and/or color of an oral mucosal area compared to the surrounding healthy mucosa [2].
Pseudolesions are instead normal oral anatomical structures or paraphysiologic changes of the
oral mucosa with no pathological significance that on routine oral examination may be misdiagnosed
as pathological alterations [3].

Appl. Sci. 2019, 9, 2412; doi:10.3390/app9122412 www.mdpi.com/journal/applsci

Appl. Sci. 2019, 9, 2412 2 of 8

Pseudolesions can trick not only the patient, causing apprehension and cancer phobia, but also
the clinician. A surgical or medical approach to these conditions is not only useless but can result in
overtreatment procedures.
Some of these pseudolesions can simulate oral potentially malignant lesions, vascular
abnormalities, infective and autoimmune diseases, or neoplasms. Their identification is important in
order to establish a correct differential diagnosis from oral diseases and to avoid inappropriate medical
or surgical treatments. In fact, pseudolesions do not require any treatment or therapy [4].
The aim of this review is to illustrate the most common oral pseudolesions, their possible
differential diagnosis, and their eventual association with syndromes and systemic diseases.

2. Fordyce Granules
Small yellow
Appl. Sci. 2017, 7, x“dust-like” bilateral granules disseminated on the oral mucosa are usually4 observed
FOR PEER REVIEW of 8

in about 80% of individuals. They are ectopic sebaceous glands with no pathological significance [5].
soft palate or apprehension due to its unpleasant appearance. It may predispose mycotic infections.
The lips edges, the vestibular mucosa, and the retromolar area are the most involved oral sites
The pseudolesion’s appearance can be mistaken for candidiasis. It is useful to recommend smoking
(Figure 1A). Fordyce granules do not give any symptoms, except for a rough mucous sensation.
suspension, accurate oral hygiene, and lingual brushing to facilitate debris and keratin excess
They removal
are often[24].mistaken for a fungal infection or lichen planus papules. No treatment is needed.

Figure 1. (A) Fordyce granules; (B) leukoedema; (C) gingival pigmentation; (D) geographic tongue;
Figure 1. (A) Fordyce granules; (B) leukoedema; (C) gingival pigmentation; (D) geographic tongue;
(E) fissured tongue; (F) black hairy tongue.
(E) fissured tongue; (F) black hairy tongue.
9. Hyperplasia of Lingual Fimbriae
Lingual fimbriae are normal anatomical structures that appear as small filiform flanges on the
ventral surface of the tongue at the sides of the frenulum (Figure 2A). If hyperplastic, lingual fimbriae
can easily induce diagnostic errors, in fact they are usually confused with squamous papillomas or
warts [17].
Appl. Sci. 2019, 9, 2412 3 of 8

Interestingly, an association between Lynch syndrome (non-polyposic colorectal carcinoma

syndrome) and the Fordyce granules seems to exist, explainable by the activation of a pathway
responsible both for the development of neoplasia and the activation of the sebaceous glands [6].
Careful observation of Fordyce granules, especially located in lower gingival and vestibular
mucosa, may be feasible to identify families potentially affected by non-polyposic colorectal
carcinoma syndrome.

3. Leukoedema
It is characterized by an opalescent white appearance of the vestibular and buccal mucosa
(Figure 1B). The causes are unknown. It is very common in black people (90% of individuals) while
rarely found in Caucasians. It is not considered a lesion, but a variation of the normal anatomy of
the oral mucosa due to intra- and extracellular imbibition [7]. Leukoedema is always bilateral, and it
characteristically disappears when the cheek is stretched only to reappear after releasing the mucosa
(diascopic phenomenon); this makes it well distinguishable from leukoplakia or morsicatio buccarum.
Leukoedema does not require any treatment [8].

4. White Sponge Nevus

It is a rare genodermatosis affecting 1:200,000 people [9], transmitted by an autosomal dominant
character with high penetrance. It has been shown to be related to keratin defects, because of mutations
in the genes encoding mucosal-specific keratins K4 and K13. It looks like a white plaque with velvety
or villous appearance, localized on the vestibular mucosa of both sides. The lesion often extends to
the tongue, the mouth floor, and the oropharynx mucosa, in some cases genital mucosae are also
involved [10]. It can resemble a proliferative leukoplakia or a hyperkeratosic oral lichen planus. It may
need surgical removal in case of oral discomfort [11]. There is only one case reporting an association
between white sponge nevus and ectrodactyly–ectodermal dysplasia–clefting (EEC) syndrome [12].

5. Physiologic (Ethnic/Racial) Gingival Pigmentation

Physiologic pigmentation develops during the first two decades of life. Pigmentation is
asymptomatic and no treatment is required except for aesthetic concerns. Moreover, color variation
may be uniform, unilateral, bilateral, mottled, macular, or blotched and may either involve the
gingival papillae alone, or extend throughout the gingiva and into other oral tissues [13]. Physiologic
pigmentation clinically appears as multifocal or diffuse, with variable prevalence in different ethnic
groups. It is common in African, Asian, and Mediterranean populations, and it is due to an increased
melanocyte activity rather than due to a greater number of melanocytes. Attached gingiva is the most
common site of such pigmentation (Figure 1C) [14].
It can easily be misdiagnosed as melanosis, smoking pigmentation, or melanoma, which generally
appear as localized mucosal stains; although, in the case of pigmentation due to trauma and smoking,
the anamnestic data and the oral sites involved, can be suggestive of their etiology. Gingival and oral
pigmentations are also typical of some systemic syndromes, such as Addison’s disease, Peutz–Jeghers,
McCune–Albright, and Laugier–Hunziker disease [15–17].

6. Geographic Tongue (Migrant Glossitis, Migrant Erythema)

It is a benign condition usually observed on the dorsal tongue mucosa (rarely on other oral
mucosal sites). It is reported in 1–3% of the healthy population with no difference between females and
males. All ages are affected. The etiopathogenesis remains completely unknown. Hypersensitivity to
foods or to other substances has been hypothesized but never definitively demonstrated. Diabetes,
psoriasis, and hormonal changes are described as possibly associated with this condition.
The turnover mechanism that regulates physiological tongue desquamation is probably impaired,
causing the persistence of hypermature areas (the white ones) concurrent with atrophic and hypomature
areas (the red ones).
Appl. Sci. 2019, 9, 2412 4 of 8

A typical whitish border surrounds the erythematous area (Figure 1D). The lesions spontaneously
regress and then reappear after days or weeks. In several cases, geographic tongue is asymptomatic
while in some patients it causes burning and discomfort linked to acid, hot, or spicy food ingestion.
It can be a source of cancer phobia. It is important to reassure the patient about the absolute benignity
of the lesion [18].
This pseudolesion aspect can be misdiagnosed as erythematous candidiasis, erythema multiforme,
atrophic erosive lichen planus, and vesiculosus-bullous diseases. Psoriasis, allergy and atopy, diabetes,
hypertension, tobacco use, and psychological factors are reported to be associated with geographic
tongue [19]. In case of burning sensation and/or soreness affecting the patients’ quality of life, topical
steroids can be prescribed.

7. Fissured Tongue (Scrotal Tongue)

The fissured tongue is a very common condition, affecting about 2–5% of the population, especially
adults. It probably has a hereditary background, and it can develop at any age.
The tongue dorsal surface and the margins show depth fissures of variable dimension and
depth [20]. Some patients show one deep central fissure only, in other cases, numerous radial fissures,
similar to the cerebral sulci or scrotum or walnut husks, radiate from the tongue surface (Figure 1E).
The fissured tongue is often associated with the geographic tongue; in this case, superficial areas
of erythema surrounded by whitish borders are accompanied by the fissures. The fissured tongue
is generally asymptomatic, although in some patients it may cause burning or pain due to spicy
and/or acid food intake [21]. Fissures facilitate food stagnation and the proliferation of bacterial and
mycotic flora. Together with lip numbness and facial paralysis, fissured tongue is part of the triad
of Melkersson–Rosenthal syndrome (orofacial granulomatosis), and it frequently occurs in patients
affected by Down syndrome [22].

8. White and Black Hairy Tongue

White hairy tongue is characterized by a marked hypertrophy of the filiform papillae on the
dorsal surface of the tongue. Pathogenesis is probably linked to excessive keratin production by the
tongue epithelium. Other possible etiological factors include excessive smoking, poor oral hygiene,
and dysbiosis of oral microflora [23]. This condition is often observed after a prolonged antibiotic
therapy. A thick layer of keratin and filiform papillae covers the tongue, giving it a whitish and
dried aspect. If present, the black color is due to the production of bacterial pigments or, in smokers,
the deposition of nicotinic derivatives (Figure 1F). Some patients complain of a tickling sensation
to the soft palate or apprehension due to its unpleasant appearance. It may predispose mycotic
infections. The pseudolesion’s appearance can be mistaken for candidiasis. It is useful to recommend
smoking suspension, accurate oral hygiene, and lingual brushing to facilitate debris and keratin excess
removal [24].

9. Hyperplasia of Lingual Fimbriae

Lingual fimbriae are normal anatomical structures that appear as small filiform flanges on the
ventral surface of the tongue at the sides of the frenulum (Figure 2A). If hyperplastic, lingual fimbriae
can easily induce diagnostic errors, in fact they are usually confused with squamous papillomas or
warts [17].
Appl. Sci. 2019, 9, 2412 5 of 8
Appl. Sci. 2017, 7, x FOR PEER REVIEW 6 of 8

Figure (A)
2. 2.
Figure Lingual
(A) Lingualfimbriae;
fimbriae;(B)
(B)Steno’s
Steno’s duct
duct orifice hyperplasia;(C)
orifice hyperplasia; (C)lingual
lingualthyroid
thyroid(endoscopic
(endoscopic
picture); (D)(D)
picture); sublingual
sublingualvarices;
varices;(E)
(E)eruptive
eruptivecyst;
cyst; (F)
(F) vallate papillae;
papillae;(G)
(G)lingual
lingualtonsil.
tonsil.

10.16.
Steno’s Duct Orifice Hyperplasia
Conclusions
The parotid
The gland duct,
embryogenetic also calledofSteno’s
development the oralduct,
and ends
facialin the oral
tissues cavity
is quite on the buccal
complex, and, inmucosa,
most
facing the vestibular surface of the first or second upper molar. A hyperplasia
cases, it is responsible for simple variations in normal healthy oral anatomy. of the Steno orifice for
traumatic or infective
These variationscauses
could can occur. Itfor
be mistaken becomes enlarged,
pathologies and beassuming
a cause the appearance
of concern of a minute
for individuals
fibroma (Figure
referring 2B).dentists.
to their Failure to recognize
Dentists the reassure
should glandular anatomical
their structure
patient about could cause
the absolute uselessofbiopsy
benignity the
with damage
observed to the glandular
pseudolesions structures
avoiding [25]. diagnostic procedure.
any surgical

11.Author
Lingual Thyroid Conceptualization, F.d.V. and M.P., investigation, F.d.V and M.P., resources, R.S., D.D.S
Contributions:
and A.L., data curation, F.d.V. and M.P., validation, M.C., C.L. and D.L., writing-original draft preparation, F.d.V
ItM.P,
and is due to the persistence
writing-review of ectopic
and editing, thyroid
A.L., D.L., D.D.S.tissue in the
and M.C., posteriorC.L.
visualization, portion of the
and D.L., lingual surface
supervision, R.S.,
(Figure 2C). It is an embryogenetic anomaly caused
D.L. and M.P, project administration M.P., R.S. and C.L. by a defective migration of the thyroid gland from
the primitive pharyngeal cavity to its normal anatomical position [26]. If asymptomatic, the lingual
Appl. Sci. 2019, 9, 2412 6 of 8

thyroid does not require any treatment; when necessary, therapy is based on the administration of
thyroid hormones for suppressive purposes. Surgical ablation or radioactive iodine is reserved for cases
that are not responsive to medical therapy [27]. Rare cases of association between hyperthyroidism
and lingual thyroid are reported [28]. Dermoid cyst, tongue neoplasms, and lymphatic malformations
can be considered in differential diagnosis; radionuclide scanning is necessary to confirm the presence
of ectopic thyroidal tissue [29].

12. Sublingual Varices

Sublingual varices are clinically evident as small enlarged veins on the anterior ventral surface
of the tongue (Figure 2D). They are related to the aging process and hence to collagen elastic fiber
degeneration and weakening of the venous wall. In fact, the prevalence of sublingual varices increases
with age, reported in up to 60% of elderly patients, in both sexes, and in different population groups.
They might be mistaken for Osler–Weber–Rendu syndrome or hereditary hemorrhagic telangiectasia
or multiple hemangiomas. Hypertension, cardiovascular diseases, smoking, and dental wearing are
described as associated with sublingual varices [30].

13. Eruption Cysts

Eruption cysts are benign, odontogenic developmental cysts associated with a primary or, more
often, permanent tooth in the eruptive phase. Clinically, the cyst appears as a soft bluish gingival
mass on the alveolar ridge overlying the crown of an erupting tooth (Figure 2E). They are usually
asymptomatic, and the related teeth erupt without any complications in approximately two months.
The incisive and molar areas are frequently involved [31]. Its aspect can simulate a hemangioma.
Nomura et al. reported multiple eruption cysts in a four-year-old boy with Menkes kinky hair
disease in treatment with an anticonvulsant [32].

14. Vallate Papillae

Vallate papillae are physiological anatomical structures located on the back of the tongue surface
along the sulcus terminalis (Figure 2F). They are usually 8 or up to 12, round with a small central pitting
where the lingual Von Ebner’s salivary gland ducts end. All papillae protrude about 2 mm above the
lingual mucosa, but in some individuals, they can appear more prominent and pronounced; this can be
due to subjective constitution, responsive hypertrophy to irritative triggers (such as gastroesophageal
reflux), or a generalized atrophy of the dorsal tongue [33–35].

15. Lingual Tonsils

Lingual tonsils are collections of lymphoid tissue placed at the back of the tongue, one on either
side, often associated with foliate papillae (Figure 2G). They take part in the formation of Waldeyer’s
ring. They are less prone to be infected compared to other pharyngeal tonsils, thanks to the presence of
mucous tongue glands secreting into the crypts. These structures can become especially visible in case
of hypertrophy, that can often occur in mouth breathers and in patients affected by gastroesophageal
reflux [36,37]. Due to their localization, they are frequently misdiagnosed as oral carcinoma or
benign neoplasms.

16. Conclusions
The embryogenetic development of the oral and facial tissues is quite complex, and, in most cases,
it is responsible for simple variations in normal healthy oral anatomy.
These variations could be mistaken for pathologies and be a cause of concern for individuals
referring to their dentists. Dentists should reassure their patient about the absolute benignity of the
observed pseudolesions avoiding any surgical diagnostic procedure.
Appl. Sci. 2019, 9, 2412 7 of 8

Author Contributions: Conceptualization, F.d.V. and M.P., investigation, F.d.V and M.P., resources, R.S., D.D.S
and A.L., data curation, F.d.V. and M.P., validation, M.C., C.L. and D.L., writing-original draft preparation, F.d.V
and M.P, writing-review and editing, A.L., D.L., D.D.S. and M.C., visualization, C.L. and D.L., supervision, R.S.,
D.L. and M.P, project administration M.P., R.S. and C.L.
Funding: The research received no external funding.
Acknowledgments: The authors are grateful to Professor Nicola Antonio Adolfo Quaranta for providing the
lingual thyroid picture and to Niccolò Petruzzi for the eruptive cyst picture.
Conflicts of Interest: The authors declare no conflict of interests.

References
1. National Cancer Institute. Available online: https://www.cancer.gov/ (accessed on 23 April 2019).
2. Gonsalves, W.C.; Chi, A.C.; Neville, B.W. Common oral Lesions: Part I. Superficial Mucosal Lesions.
Am. Fam. Physician 2007, 75, 501–507. [PubMed]
3. Seoane Leston, J.M.; Aguado Santos, A.; Varela-Centelles, P.I.; Vazquez Garcia, J.; Romero, M.A.;
Pias Villamor, L. Oral Mucosa: Variations from Normalcy, Part I. Cutis 2002, 69, 131–134. [PubMed]
4. Leston, J.M.; Santos, A.A.; Varela-Centelles, P.I.; Garcia, J.V.; Romero, M.A.; Villamor, L.P. Oral Mucosa:
Variations from Normalcy, Part II. Cutis 2002, 69, 215–217. [PubMed]
5. Lee, J.H.; Lee, J.H.; Kwon, N.H.; Yu, D.S.; Kim, G.M.; Park, C.J.; Lee, J.D.; Kim, S.Y. Clinicopathologic
Manifestations of Patients with Fordyce’s Spots. Ann. Dermatol. 2012, 24, 103–106. [CrossRef]
6. De Felice, C.; Parrini, S.; Chitano, G.; Gentile, M.; Dipaola, L.; Latini, G. Fordyce Granules and Hereditary
Non-Polyposis Colorectal Cancer Syndrome. Gut 2005, 54, 1279–1282. [CrossRef] [PubMed]
7. Martin, J.L. Leukoedema: A Review of the Literature. J. Natl. Med. Assoc. 1992, 84, 938–940. [PubMed]
8. Felix, D.H.; Luker, J.; Scully, C. Oral Medicine: 6. White Lesions. Dent. Update 2013, 40, 146–148, 150–152,
154. [CrossRef] [PubMed]
9. Shibuya, Y.; Zhang, J.; Yokoo, S.; Umeda, M.; Komori, T. Constitutional Mutation of Keratin 13 Gene in
Familial White Sponge Nevus. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. 2003, 96, 561–565.
[CrossRef]
10. Nichols, G.E.; Cooper, P.H.; Underwood, P.B., Jr.; Greer, K.E. White Sponge Nevus. Obstet. Gynecol. 1990, 6,
545–548. [CrossRef]
11. Lucchese, A.; Favia, G. White Sponge Naevus with Minimal Clinical and Histological Changes: Report of
Three Cases. J. Oral Pathol. Med. 2006, 35, 317–319. [CrossRef]
12. Dalben, G.S.; Cursino, H.A.; Barbosa, B.A.; Costa, B.; Consolaro, A. White Sponge Nevus in a Patient with
EEC Syndrome. Dermatol. Online J. 2010, 16, 7. [PubMed]
13. Tavares, T.S.; Meirelles, D.P.; de Aguiar, M.C.F.; Caldeira, P.C. Pigmented Lesions of the Oral Mucosa:
A Cross-Sectional Study of 458 Histopathological Specimens. Oral Dis. 2018, 24, 1484–1491. [CrossRef]
[PubMed]
14. Attar, N.B.; Gupta, B.; Deshmukh, A.; Shahabe, S.; Zope, S.; Waykole, Y. Pigmentation on Gingiva:
A Diagnostic Dilemma. Int. J. Periodontics Restor. Dent. 2018, 38, 137–140. [CrossRef] [PubMed]
15. Zaki, H.; Sabharwal, A.; Kramer, J.; Aguirre, A. Laugier-Hunziker Syndrome Presenting with Metachronous
Melanoacanthomas. Head Neck Pathol. 2019, 13, 259–267. [CrossRef] [PubMed]
16. Pichard, D.C.; Boyce, A.M.; Collins, M.T.; Cowen, E.W. Oral Pigmentation in McCune-Albright Syndrome.
JAMA Dermatol. 2014, 150, 760–763. [CrossRef] [PubMed]
17. Ficarra, G. Manuale di Patologia e Medicina Orale, 3rd ed.; McGraw-Hill: Milan, Italy, 2006.
18. Pass, B.; Brown, R.S.; Childers, E.L. Geographic Tongue: Literature Review and Case Reports. Dent. Today
2005, 24, 54–56. [PubMed]
19. Dafar, A.; Çevik-Aras, H.; Robledo-Sierra, J.; Mattsson, U.; Jontell, M. Factors Associated with Geographic
Tongue and Fissured Tongue. Acta Odontol. Scand. 2016, 74, 210–216. [CrossRef] [PubMed]
20. Reamy, B.V.; Derby, R.; Bunt, C.W. Common Tongue Conditions in Primary Care. Am. Fam. Physician 2010,
81, 627–634. [PubMed]
21. Canaan, T.J.; Meehan, S.C. Variations of Structure and Appearance of the Oral Mucosa. Dent. Clin. N. Am.
2005, 49, 1–14. [CrossRef]
22. Rees, T.D. Orofacial Granulomatosis and related conditions. Periodontol. 2000 1999, 21, 145–157. [CrossRef]
Appl. Sci. 2019, 9, 2412 8 of 8

23. Gurvits, G.E.; Tan, A. Black Hairy Tongue Syndrome. World J. Gastroenterol. 2014, 20, 10845–10850. [CrossRef]
[PubMed]
24. Sarti, G.M.; Haddy, R.I.; Schaffer, D.; Kihm, J. Black Hairy Tongue. Am. Fam. Physician 1990, 41, 1751–1755.
25. Neuschl, M.; Kluba, S.; Krimmel, M.; Reinert, S. Iatrogenic Transposition of the Parotid Duct into the Maxillary
SINUS after tooth Extraction and Closure of an Oroantral Fistula. A Case Report. J. Craniomaxillofac. Surg.
2010, 38, 538–540. [CrossRef] [PubMed]
26. Turgut, S.; Murat Ozcan, K.; Celikkanat, S.; Katirci, H.; Ozdem, C. Diagnosis and Treatment of Lingual
Thyroid: A Review. Rev. Laryngol. Otol Rhinol. (Bord) 1997, 118, 189–192. [PubMed]
27. Kumar, S.S.; Kumar, D.M.; Thirunavukuarasu, R. Lingual Thyroid-Conservative Management or Surgery?
A Case Report. Indian J. Surg. 2013, 75 (Suppl. 1), 118–119. [CrossRef]
28. Abdallah-Matta, M.P.; Dubarry, P.H.; Pessey, J.J.; Caron, P. Lingual Thyroid and Hyperthyroidism: A New
Case and Review of the Literature. J. Endocrinol. Investig. 2002, 25, 264–267. [CrossRef] [PubMed]
29. Kumar, L.K.; Kurien, N.M.; Jacob, M.M.; Menon, P.V.; Khalam, S.A. Lingual Thyroid. Ann. Maxillofac. Surg.
2015, 5, 104–107.
30. Kovac-Kavcic, M.; Skaleric, U. The Prevalence of Oral Mucosal Lesions in a Population in Ljubljana, Slovenia.
J. Oral Pathol. Med. 2000, 29, 331–335. [CrossRef]
31. Şen-Tunç, E.; Açikel, H.; Sönmez, I.S.; Bayrak, Ş.; Tüloğlu, N. Eruption Cysts: A Series of 66 Cases with
Clinical Features. Med. Oral Patol. Oral Cir. Bucal 2017, 22, 228–232.
32. Nomura, J.; Tagawa, T.; Seki, Y.; Mori, A.; Nakagawa, T.; Sugatani, T. Kinky Hair Disease with Multiple
Eruption Cysts: A Case Report. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. 1996, 82, 537–540.
[CrossRef]
33. Mamede, R.C.; De Mello-Filho, F.V.; Vigário, L.C.; Dantas, R.O. Effect of Gastroesophageal Reflux on
Hypertrophy of the Base of the Tongue. Otolaryngol. Head Neck Surg. 2000, 122, 607–610. [PubMed]
34. Petruzzi, M.; Lucchese, A.; Campus, G.; Crincoli, V.; Lauritano, D.; Baldoni, E. Oral Stigmatic Lesions of
Gastroesophageal Reflux Disease (GERD). Rev. Med. Chil. 2012, 140, 915–918. [CrossRef] [PubMed]
35. Samad, A.; Mohan, N.; Balaji, R.V.; Augustine, D.; Patil, S.G. Oral Manifestations of Plummer-Vinson
Syndrome: A Classic Report with Literature Review. J. Int. Oral Health 2015, 7, 68–71. [PubMed]
36. Harris, M.S.; Rotenberg, B.W.; Roth, K.; Sowerby, L.J. Factors Associated with Lingual Tonsil Hypertrophy in
Canadian Adults. J. Otolaryngol. Head Neck Surg. 2017, 46, 32. [CrossRef] [PubMed]
37. Costello, R.; Prabhu, V.; Whittet, H. Lingual Tonsil: Clinically Applicable Macroscopic Anatomical
Classification System. Clin. Otolaryngol. 2017, 42, 144–147. [CrossRef] [PubMed]

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