J Oral Maxillofac Surg 2009. Morsicatio Mucosae Oris

J Oral Maxillofac Surg
67:140-146, 2009
Morsicatio Mucosae Oris—A Chronic Oral
Frictional Keratosis, Not a Leukoplakia
Sook-Bin Woo, DMD,* and Dorothy Lin†
Purpose: Morsicatio mucosae oris (MMO) presents as white papules and plaques that may resemble
leukoplakia, and are often biopsied. The objective of this study is to document the clinical features and
histopathology of MMO and to reevaluate the prevalence of dysplasia and/or cancer when this frictional
keratosis is removed from the category of leukoplakia.
Materials and Methods: Cases that were submitted to a single laboratory with a provisional diagnosis
of “leukoplakia,” “hyperkeratosis,” or “white lesion” were evaluated.
Results: Fifty-six lesions of MMO from 56 patients were identified out of 584 white lesions. Most cases
occurred in the third to sixth decades of life. Thirty (53.6%) and 18 (32.1%) out of 56 lesions were located
on the lateral tongue and buccal mucosa, respectively. The lesions showed hyperparakeratosis with a
characteristic frayed, shaggy, peeling surface, and acanthosis with insignificant inflammation. When
MMO is removed from the category of leukoplakia, the percentage of true leukoplakia that are dysplastic
or malignant increased by 12.9%.
Conclusions: MMO is a form of chronic oral frictional keratosis that has no malignant potential, and
should be signed out as such and not merely “hyperparakeratosis and acanthosis” so that it can be
removed from the category of leukoplakia where it does not belong.
© 2009 American Association of Oral and Maxillofacial Surgeons
J Oral Maxillofac Surg 67:140-146, 2009
MMO has been reported to occur in young patients
in the second and third decade.3,4 The prevalence has
been estimated at 6% in those under age 12 with an
equal gender distribution,5 4.6% among reform school
students aged 12 to 24 (most were under age 20),3
1.7% among the general population,3 and 1.8% among
patients aged 15 to 19 years.4
These lesions are sometimes distinctive enough for
a diagnosis based on clinical features alone. They
present as whitish gray papules and plaques on the
buccal mucosa and labial mucosa (usually lower),
often associated with leukoedema and a macerated
appearance; 67% to 72% are bilateral (Figs 1A-C).3,4
Loose thread-like keratin shreds, tissue tags, or desquamative areas are often seen on the surface, and
there may be ulcers and erosions.1,4 Lesions are evanescent and may resolve and recur.3,4 Treatment with
protective screening devices is of limited value.1 In
some cases, the surface keratin may be peeled off,
leaving behind normal-appearing mucosa, unlike candidiasis or vesiculobullous conditions (Fig 1D). Their
diffuse, poorly demarcated, peeling, thready appearance usually makes the clinical diagnosis straightforward. However, MMO may sometimes appear as distinct, well-demarcated plaques (Fig 2).
Leukoplakia is defined as “a predominantly white
lesion that cannot be classified as any other definable
lesion.”6,7 The report by Axell et al6 further states that
“white lesions for which a local cause can be identi-
Bite or chewing trauma, usually of the nonkeratinized
mucosa, takes 2 clinical forms. Acute bite trauma is
caused by a sudden usually unintentional injury to the
oral mucosa with a strong masticatory force such as
occurs during eating, and results in a localized painful
traumatic ulcer. However, primary chronic chewing
injuries are white lesions that result from repetitive,
chronic frictional trauma, usually from raking of the
teeth over the mucosa or “nibbling” of the mucosa,
depending on the severity of the habit. These lesions
have been referred to as “pathominia mucosae oris,”
“morsicatio mucosae oris,” “morsicatio buccarum,” or
“morsicatio labiarum,” depending on the location
(morsus ⫽ bite).1,2 These injuries will be referred to
as “morsicatio mucosae oris” or MMO in this study.
*Associate Professor, Harvard School of Dental Medicine, Boston,
MA; and Associate Pathologist, Pathology Services Inc, Cambridge,
MA.
†Dental Student, Harvard School of Dental Medicine, Boston,
MA.
Address correspondence and reprint requests to Dr Woo: Department of Oral Medicine, Infection, and Immunity, Harvard
School of Dental Medicine, Brigham and Women’s Hospital, Boston, MA 02115; e-mail: [email protected]
© 2009 American Association of Oral and Maxillofacial Surgeons
0278-2391/09/6701-0021$34.00/0
doi:10.1016/j.joms.2008.08.040
140
WOO AND LIN
141
FIGURE 1. A, Irregular, shaggy, poorly delineated white papules and plaques of the left buccal mucosa typical for morsicatio mucosae oris.
B, Irregular, shaggy, poorly delineated white papules and plaques of the lower labial mucosa typical for morsicatio mucosae oris. C, Poorly
delineated white plaque on the right lateral tongue typical for morsicatio mucosae oris. D, Plaque can be peeled away leaving behind
painless, normal-appearing mucosa.
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg 2009.
fied should be classified according to the established
cause and not be included among leukoplakias. Examples are frictional lesions, lesions associated with
dental restorations, and lesions associated with cheekbiting.” Findings at a recent workshop further reiterate that leukoplakias are not caused by friction, have
no specific histology, may or may not show dysplasia,
but have an assessable tendency to malignant transformation.8
Leukoplakia is therefore a clinical term to denote a
keratotic lesion of exclusion, and 9% to 34% present
with dysplasia, carcinoma-in-situ (CIS) or invasive
squamous cell carcinoma (SCCA) at the time of
biopsy.9-12 For this study, the term “nondysplastic
leukoplakia” will be used to describe a white lesion
that shows the nonspecific histopathologic features
of “hyperortho- or –parakeratosis, acanthosis with/
out inflammation.”
There have been few published reports of the histopathology of MMO in the medical literature, and
none of these is recent. The objectives of this study
are to: 1) describe the demographic and clinical data
for MMO, 2) describe the distinctive histopathologic
features, and 3) re-evaluate the prevalence of dysplasia, CIS, and invasive SCCA in leukoplakia when MMO
is removed from that category.
142
MORSICATIO MUCOSAE ORIS
Number of cases
20
15
10
5
0
1
2
3
4
5
6
7
Decade of life
FIGURE 3. Age distribution of lesions.
FIGURE 2. Leukoplakia-like lesion of left lateral tongue that on
biopsy, showed morsicatio mucosae oris.
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg
2009.
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg
2009.
Results
CLINICAL DATA
Materials and Methods
All specimens accessioned at by the Harvard School
of Dental Medicine, Boston, MA, through Pathology
Services Incorporated, Cambridge, MA, from January
2001 to December 2003 with a clinical impression of
“leukoplakia,” “white lesion,” or “hyperkeratosis”
were included in this study. Clinical and demographic
data were obtained from the requisition forms. All
cases had been submitted in formalin and 8 micron
tissue sections were cut and stained with hematoxylin-eosin for evaluation. All cases were also stained
with periodic acid-Schiff with diastase digestion.
Table 1. HISTOPATHOLOGIC DIAGNOSIS OF 584
CASES OF CLINICAL LEUKOPLAKIA
Histopathologic Diagnosis
No. of Cases (%)
Benign alveolar ridge keratosis
Lichen planus/lichenoid mucositis
Morsicatio mucosae oris
Papilloma/verruca vulgaris
Candidiasis
Smokeless tobacco keratosis
Nonspecific ulceration
Subtotal
Hyperkeratosis and/or acanthosis
and/or mucositis
Dysplasia/verrucous hyperplasia/CIS
Squamous cell carcinoma
Total
108 (18.5)
88 (15.1)
52 (8.9)
22 (3.8)
15 (2.5)
6 (1.0)
4 (0.7)
295 (50.5)
216 (37.0)
61 (10.4)
12 (2.1)
584 (100.0)
Abbreviation: CIS, carcinoma-in-situ.
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg
2009.
Five hundred eighty-four lesions were identified,
and their diagnoses are presented in Table 1. Portions
of this cohort have been previously reported.13 Fiftytwo patients with MMO were identified with 56 sites
biopsied. Forty-three cases (82.7%) occurred in adults
between the third and sixth decades, with only 3.8%
of lesions in those below age 20 (Fig 3); there is
an approximately 3:1 male predominance. Thirty
(53.6%) and 18 (32.1%) out of 56 lesions were located
on the lateral tongue and buccal mucosa, respectively; 8.9% were on the lower labial mucosa (Table
2). Only 1 case was stated to occur bilaterally on the
buccal mucosa.
Table 2. CLINICAL DATA
No. of cases
M:F
Age
Symptoms
Smoking history
Bite trauma history
Lesion duration
Lesion size
Location (56 sites)
52
2.7:1
14-85 (mean 49, median 49)
2 painful, 50 unstated
7 smokers, 4 nonsmokers, 41
unstated
7 positive history, 45 unstated
7 (⬍6 months), 3 (6-12 months), 3
(⬎1 year), 39 unstated
8 (ⱕ10 mm), 3 (11-20 mm), 1 (⬎20
mm), 43 unstated
30 tongue (28 lateral, 1 ventral, 1
posterior)
18 buccal mucosa
5 labial mucosa (1 lower, 3 midline,
1 unstated)
1 retromolar pad, 1 alveolar ridge
1 unstated
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg
2009.
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WOO AND LIN
FIGURE 4. A, Photomicrograph showing marked shaggy hyperparakeratosis with surface fissures and clefts, acanthosis with ballooned cells, and
insignificant inflammation (H&E, magnification ⫻40). B, Photomicrograph showing marked hyperparakeratosis and acanthosis (H&E, magnification
⫻100). C, Photomicrograph showing the cleavage within the parakeratin that allows the surface to be peeled off leaving behind thickened nonulcerated
mucosa (H&E, magnification ⫻100). D, Photomicrograph showing the fissures and clefts within the thick parakeratin rimmed by bacteria without an
inflammatory response, and ballooned cells (H&E, magnification ⫻200).
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg 2009.
Histologic Features
All cases showed hyperparakeratosis with a shaggy,
“frayed,” or peeling surface with fissures and clefts
within the keratin, and most cases (89.3%) exhibited
surface colonization with bacteria in the absence of
any inflammatory reaction (Figs 4A-D). One case
showed candidal hyphae without evidence of spongiotic pustules or inflammation. All but 3 cases exhibited benign epithelial hyperplasia, and 80.8% of cases
exhibited ballooned cells with intracellular edema
(typical for mild surface trauma such as leukoedema).
A papillary surface configuration was noted in 44.2%
of cases. Inflammatory cells were present in the epithelium in only 1 case and inflammation was minimal
to absent in the connective tissue in 92.9% of cases; 5
cases showed focal ulceration. Reactive epithelial
atypia was noted in 4 cases, always in cases that
showed ulceration or inflammation. There were no
cases of epithelial dysplasia or carcinoma.
Discussion
MMO is a common chronic mucosal frictional keratosis characterized by poorly demarcated, rough,
shaggy, peeling, white papules, and plaques on the
buccal mucosa, lateral border of the tongue, or the
lower labial mucosa, areas that are easily accessible
to, and readily traumatized by, the teeth. It is often
factitial or self-induced, although the patient may not
be conscious of the habit or it may be secondary to a
nocturnal parafunctional habit. Chronic frictional injury of the gingiva or alveolar ridge mucosa, especially
of the retromolar pad, presents as benign alveolar
ridge keratosis (BARK) with different histologic fea-
144
MORSICATIO MUCOSAE ORIS
tures, namely, hyperorthokeratosis and acanthosis
with slight papillomatosis, features identical to friction-induced skin lesions of lichen simplex chronicus.13
Several differences were noted between this study
and previous large studies, all of which were published in the 1970s.3-5
AGE OF OCCURRENCE
This study found that most patients were in the fifth
and sixth decade, whereas previous studies found
that the highest incidence was among those in the
second and third decade. One of those studies was
based on examination of subjects under the age of
12,5 whereas another showed lesions in patients from
the first to the fifth decade, with the highest prevalence in the second decade.4 Another found lesions in reform school children primarily in the
second decade of life.3 Of significance, those studies did not have histopathologic confirmation of the
diagnosis.
SITES OF INVOLVEMENT
None of the previous large studies report involvement of the tongue, only involvement of the buccal
mucosa and labial mucosa.1,3,4 In this study, the
tongue was the most common site biopsied, and
formed 53.6% of all specimens with MMO. This may
be a reflection of the tongue being a high risk site for
dysplasia and oral cancer, so that clinicians tended to
biopsy white lesions at this site, which they feel are
suspicious for leukoplakia, particularly in men who
smoke. Therefore, it may be selection bias that led to
the almost 3:1 male predominance in this series. Because most of the clinical data obtained from the
accession forms were incomplete, it is difficult to
draw conclusions regarding smoking history, bilaterality, or history of trauma.
Although the clinical appearance of MMO is usually
fairly typical, a biopsy is always warranted if the
clinician is not absolutely certain that a white lesion is
an MMO. Some helpful clinical features that distinguish this from leukoplakia are 1) rough, shaggy,
often peeling surface; 2) bilaterality; 3) location on
movable, nonkeratinized mucosa that can be reached
by the teeth; and 4) usually lack of distinct margin or
demarcation of the white area from the surrounding
normal mucosa. A history of a chronic chewing habit
may or may not be elicited. Although proliferative
(verrucous) leukoplakia may be bilateral and sometimes even symmetric, they will often also involve
areas that cannot be reached by the teeth (such as
the gingiva).14,15 In the author’s experience, leukoplakia that is associated with dysplasia including proliferative (verruous) leukoplakia often will have areas
that are clearly demarcated from the adjacent mucosa,
FIGURE 5. Dysplastic leukoplakia of the right lateral tongue (note
sharp demarcation).
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg
2009.
a helpful clinical sign that often, although not always,
distinguishes dysplastic lesions from reactive or inflammatory lesions (Fig 5).
The histopathology has been described in previous
reports as “parakeratosis with surface debris and bacteria, epithelial hyperplasia, swollen epithelial cells,
and scant inflammation with no evidence of dysplasia”1,3,16-18 This is in keeping with what was seen in
this study. The characteristic histopathologic features
of this condition are the following: 1) hyperparakeratosis that may be marked with a shaggy, frayed, fissured, or peeling appearance; hyperorthokeratosis,
although sometimes present, rarely occurs extensively or alone in MMO; 2) surface bacterial colonization is usually but not inevitably present; 3) benign
epithelial hyperplasia with intracellular edema and
ballooning of superficial keratinocytes; 4) insignificant inflammation; and 5) occasionally reactive atypia
if there is ulceration or inflammation. Interestingly,
the mucosa of betel nut chewers may show the same
histopathology.19
WHY IS MMO NOT LEUKOPLAKIA?
At an international symposium of the International Collaborative Group on Oral White Lesions
(ICGOWL) leukoplakia was defined as follows: “a predominantly white lesion that cannot be classified as
any other definable lesion; some lesions will transform to cancer.”6 Therefore, it is only when the clinician has excluded the possibility that the patient has
any other specific white lesion that a clinical diagnosis of leukoplakia can be made (Table 3). The definition specifically excludes lesions caused by friction.
More recently, at a workshop coordinated by the
World Health Organization (WHO) Collaborating Cen-
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WOO AND LIN
Table 3. LESIONS THAT MAY APPEAR WHITE
Developmental
Cannon white sponge nevus
Hereditary benign intraepithelial dyskeratosis
Dyskeratosis congenita
Pachyonychia congenita
Other oral lesions in genodermatoses associated with
dyskeratosis
Inflammatory/reactive
Frictional/factitial
Morsicatio mucosae oris
Benign alveolar ridge keratosis
Mouth-wash induced desquamation
Infectious
Oral viral (hairy) leukoplakia
Candidiasis
Immune-mediated
Lichen planus/lichenoid stomatititis
Chronic graft-versus-host disease
Tobacco-associated
Smokeless tobacco keratosis
Nicotinic stomatitis
Autoimmune
Lupus erythematosus
Others
Nondysplastic leukoplakia
Premalignant and malignant
Dysplastic leukoplakia
Verrucous leukoplakia
Proliferative leukoplakia
Squamous cell carcinoma
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg
2009.
ter for Oral Cancer and Precancer (CCOCP) in the
United Kingdom, leukoplakia was defined as “a white
plaque of questionable risk having excluded (other)
known diseases or disorders that carry no increased
risk for cancer.”8 They further state that this is a
clinical term with no specific histology, may or may
not show dysplasia, but with an assessable tendency
to malignant transformation. They, too, exclude any
lesion caused by friction.
MMO is a primary frictional injury of the oral
mucosa with defined clinical and histopathologic
features, and as such, should be signed out by the
pathologist with this specific moniker or other phrase
indicating its primary frictional character rather
than using the nonspecific diagnosis of “hyperorthoor -parakeratosis, acanthosis and/or chronic inflammation.” It has no malignant potential, and because it is
frictional in nature, must be excluded from lesions of
leukoplakia as defined by the ICGOWL and more
recently by the WHO CCOCP.
More importantly, a nonspecific histopathologic diagnosis causes these lesions to enter the “pool” of all
leukoplakia lesions and dilutes the prevalence of dysplasia, CIS, and SCCA in such leukoplakias. This is not
of mere academic interest but has serious conse-
quences for patient care. In the largest study on leukoplakia,9 all lesions that were keratotic were included and this probably included all primary MMO
and all BARK, a benign frictional keratosis of the
gingiva with characteristic histologic and clinical findings.13 These 2 entities form a substantial portion of
oral white lesions, and they are completely benign
with no malignant potential; they are NOT even nondysplastic leukoplakias. If these 2 groups of frictional
injuries are removed from the pool of leukoplakia, the
prevalence of dysplasia, CIS, and invasive SCCA in
leukoplakia will increase. When the cases of MMO
were removed from this series of 584 of clinical leukoplakia, the percentage of leukoplakias that were
dysplastic/CIS/SCCA rose from 16.3% to 18.4%, an
increase of 12.9%. If we also remove BARK from the
nonspecific “hyperkeratosis with/out acanthosis,” the
percentage of leukoplakias that were dysplastic/CIS/
SCCA rose from 16.3% to 26.3%, an increase of 55.2%
(Table 4).
It is possible, indeed probable, that many of the
white lesions noted in the pivotal study by Waldron
and Shafer9 represented MMO and BARK because the
2 most common sites for white lesions in that study
were the buccal mucosa and the gingiva. MMO in this
study was most commonly found on the buccal mucosa and BARK, which as its name indicates is found
on the gingiva.13 The most common sites for dysplastic leukoplakias are the ventral tongue and floor of
mouth.
Understanding the true nature of leukoplakia may
have been hampered partially by the use of nonspecific histologic diagnosis of many hyperkeratotic lesions. Although some are very well recognized such
Table 4. PREVALENCE OF DYSPLASIA, CIS, AND
CARCINOMA IN WHITE LESIONS
White lesions including MMO and BARK
MMO
BARK
Subtotal
Hyperortho- or -parakeratosis and/or acanthosis
and/or mucositis
Dysplasia/verrucous hyperplasia/CIS
Squamous cell carcinoma
Subtotal
Total
449
52
108
160
216
61
12
73
449
NOTE. % dysplasia/carcinoma if BARK/MMO included as
leukoplakia 73/449 ⫽ 16.3%.
% dysplasia/carcinoma if MMO excluded as leukoplakia
73/449-52 ⫽ 18.4% (% change ⫹12.9%).
% dysplasia/carcinoma if BARK/MMO excluded as leukoplakia 73/449-160 ⫽ 25.3% (% change ⫽ ⫹55.2%).
Abbreviations: MMO, morsicatio mucosae oris; BARK, benign alveolar ridge keratosis; CIS, carcinoma-in-situ.
Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg
2009.
146
as many of the lesions noted in Table 3, the histology
of oral frictional keratoses such as BARK, for example,
has been defined only recently.13 Furthermore, although the histopathologic features of MMO are well
known to many oral and maxillofacial pathologists,
this entity is less well recognized in skin and general
pathology circles, and they are usually given a nonspecific diagnosis of “parakeratosis and acanthosis”
without further interpretation.
Diagnosing MMO as merely “hyperortho- or –parakeratosis with acanthosis” (referred to in many pathology circles as the histologic sign-out), although histologically correct, does not provide an accurate
interpretation of this condition because this is the
same histologic sign-out offered for nondysplastic
leukoplakias. MMO has much more specific histology
than nondysplastic leukoplakias. Smokeless tobacco
keratosis for example, also exhibits “hyperorthoor –parakeratosis and acanthosis,” and although this is
histologically correct, it is more accurate and helpful
to the clinician to diagnose and sign it out as smokeless tobacco keratosis.
In this study, there still remained 216 lesions that
exhibited hyperpara or orthokeratosis that could not
be further classified but were not dysplastic. It may be
helpful to clinicians if the pathologists signing out
such cases add as a descriptor, “likely reactive” at the
end of the microscopic description of “hyperorthoor -parakeratosis, acanthosis, and/or chronic inflammation” for white lesions that appear inflammatory
but that are not at this time, classifiable as a specific
entity. This would be an extension of the recommendation made by ICGOWL that all histopathology reports on biopsies of leukoplakias should include a
statement on the presence or absence of epithelial
dysplasia.6 Such lesions may represent early or healing frictional keratoses (MMO or BARK), some other
yet to be histologically defined lesion caused by mechanical or chemical irritation, or subtle hypersensitivity reaction to topical or systemic substances.
As more and more hyperkeratotic lesions take their
rightful place as completely benign and recognizable
entities with an inflammatory/reactive etiology, research on true leukoplakias can be more focused.
Clinicians play an important role by providing good
clinical data and by working closely with their pathol-
MORSICATIO MUCOSAE ORIS
ogist to arrive at an accurate diagnosis for oral white
lesions.
Acknowledgments
I thank the oral and maxillofacial surgeons, periodontists, oral
medicine specialists and general dentists who submitted these
cases, on which this research is based. I also thank Dr Manal
Al-Sheddi for her help with some of the data management.
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