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Morsicatio Mucosae Oris—A Chronic Oral Frictional Keratosis, Not a Leukoplakia Sook-Bin Woo, DMD,* and Dorothy Lin†

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Morsicatio Mucosae Oris—A Chronic Oral Frictional Keratosis, Not a Leukoplakia Sook-Bin Woo, DMD,* and Dorothy Lin† 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 Bite or chewing trauma, usually of the nonkeratinized MMO has been reported to occur in young patients mucosa, takes 2 clinical forms. Acute bite trauma is in the second and third decade.3,4 The prevalence has caused by a sudden usually unintentional injury to the been estimated at 6% in those under age 12 with an oral mucosa with a strong masticatory force such as equal gender distribution,5 4.6% among reform school occurs during eating, and results in a localized painful students aged 12 to 24 (most were under age 20),3 3 traumatic ulcer. However, primary chronic chewing 1.7% among the general population, and 1.8% among 4 injuries are white lesions that result from repetitive, patients aged 15 to 19 years. chronic frictional trauma, usually from raking of the These lesions are sometimes distinctive enough for teeth over the mucosa or “nibbling” of the mucosa, a diagnosis based on clinical features alone. They depending on the severity of the habit. These lesions present as whitish gray papules and plaques on the have been referred to as “pathominia mucosae oris,” buccal mucosa and labial mucosa (usually lower), often associated with leukoedema and a macerated “morsicatio mucosae oris,” “morsicatio buccarum,” or 3,4 “morsicatio labiarum,” depending on the location appearance; 67% to 72% are bilateral (Figs 1A-C). (morsus ϭ bite).1,2 These injuries will be referred to Loose thread-like keratin shreds, tissue tags, or des- as “morsicatio mucosae oris” or MMO in this study. quamative areas are often seen on the surface, and there may be ulcers and erosions.1,4 Lesions are eva- nescent and may resolve and recur.3,4 Treatment with 1 *Associate Professor, Harvard School of Dental Medicine, Boston, protective screening devices is of limited value. In MA; and Associate Pathologist, Pathology Services Inc, Cambridge, some cases, the surface keratin may be peeled off, MA. leaving behind normal-appearing mucosa, unlike can- †Dental Student, Harvard School of Dental Medicine, Boston, didiasis or vesiculobullous conditions (Fig 1D). Their MA. diffuse, poorly demarcated, peeling, thready appear- Address correspondence and reprint requests to Dr Woo: De- ance usually makes the clinical diagnosis straightfor- partment of Oral Medicine, Infection, and Immunity, Harvard ward. However, MMO may sometimes appear as dis- School of Dental Medicine, Brigham and Women’s Hospital, Bos- tinct, well-demarcated plaques (Fig 2). ton, MA 02115; e-mail: [email protected] Leukoplakia is defined as “a predominantly white © 2009 American Association of Oral and Maxillofacial Surgeons lesion that cannot be classified as any other definable 6,7 6 0278-2391/09/6701-0021$34.00/0 lesion.” The report by Axell et al further states that doi:10.1016/j.joms.2008.08.040 “white lesions for which a local cause can be identi- 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 biopsy.9-12 For this study, the term “nondysplastic cause and not be included among leukoplakias. Ex- leukoplakia” will be used to describe a white lesion amples are frictional lesions, lesions associated with that shows the nonspecific histopathologic features dental restorations, and lesions associated with cheek- of “hyperortho- or –parakeratosis, acanthosis with/ biting.” Findings at a recent workshop further reiter- out inflammation.” ate that leukoplakias are not caused by friction, have There have been few published reports of the his- no specific histology, may or may not show dysplasia, topathology of MMO in the medical literature, and but have an assessable tendency to malignant trans- none of these is recent. The objectives of this study formation.8 are to: 1) describe the demographic and clinical data Leukoplakia is therefore a clinical term to denote a for MMO, 2) describe the distinctive histopathologic keratotic lesion of exclusion, and 9% to 34% present features, and 3) re-evaluate the prevalence of dyspla- with dysplasia, carcinoma-in-situ (CIS) or invasive sia, CIS, and invasive SCCA in leukoplakia when MMO squamous cell carcinoma (SCCA) at the time of is removed from that category. 142 MORSICATIO MUCOSAE ORIS Number of cases 20 15 10 5 0 1234567 Decade of life FIGURE 3. Age distribution of lesions. Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg FIGURE 2. Leukoplakia-like lesion of left lateral tongue that on 2009. biopsy, showed morsicatio mucosae oris. Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg 2009. Results CLINICAL DATA Materials and Methods Five hundred eighty-four lesions were identified, All specimens accessioned at by the Harvard School and their diagnoses are presented in Table 1. Portions 13 of Dental Medicine, Boston, MA, through Pathology of this cohort have been previously reported. Fifty- Services Incorporated, Cambridge, MA, from January two patients with MMO were identified with 56 sites 2001 to December 2003 with a clinical impression of biopsied. Forty-three cases (82.7%) occurred in adults “leukoplakia,” “white lesion,” or “hyperkeratosis” between the third and sixth decades, with only 3.8% were included in this study. Clinical and demographic of lesions in those below age 20 (Fig 3); there is data were obtained from the requisition forms. All an approximately 3:1 male predominance. Thirty cases had been submitted in formalin and 8 micron (53.6%) and 18 (32.1%) out of 56 lesions were located tissue sections were cut and stained with hematoxy- on the lateral tongue and buccal mucosa, respec- lin-eosin for evaluation. All cases were also stained tively; 8.9% were on the lower labial mucosa (Table with periodic acid-Schiff with diastase digestion. 2). Only 1 case was stated to occur bilaterally on the buccal mucosa. Table 2. CLINICAL DATA Table 1. HISTOPATHOLOGIC DIAGNOSIS OF 584 CASES OF CLINICAL LEUKOPLAKIA No. of cases 52 M:F 2.7:1 Histopathologic Diagnosis No. of Cases (%) Age 14-85 (mean 49, median 49) Symptoms 2 painful, 50 unstated Benign alveolar ridge keratosis 108 (18.5) Smoking history 7 smokers, 4 nonsmokers, 41 Lichen planus/lichenoid mucositis 88 (15.1) unstated Morsicatio mucosae oris 52 (8.9) Bite trauma history 7 positive history, 45 unstated Papilloma/verruca vulgaris 22 (3.8) Lesion duration 7 (Ͻ6 months), 3 (6-12 months), 3 Candidiasis 15 (2.5) (Ͼ1 year), 39 unstated Smokeless tobacco keratosis 6 (1.0) Lesion size 8 (Յ10 mm), 3 (11-20 mm), 1 (Ͼ20 Nonspecific ulceration 4 (0.7) mm), 43 unstated Subtotal 295 (50.5) Location (56 sites) 30 tongue (28 lateral, 1 ventral, 1 Hyperkeratosis and/or acanthosis posterior) and/or mucositis 216 (37.0) 18 buccal mucosa Dysplasia/verrucous hyperplasia/CIS 61 (10.4) 5 labial mucosa (1 lower, 3 midline, Squamous cell carcinoma 12 (2.1) 1 unstated) Total 584 (100.0) 1 retromolar pad, 1 alveolar ridge Abbreviation: CIS, carcinoma-in-situ. 1 unstated Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg 2009. 2009. WOO AND LIN 143 FIGURE 4. A, Photomicrograph showing marked shaggy hyperparakeratosis with surface fissures and clefts, acanthosis with ballooned cells, and insignificant inflammation (H&E, magnification ϫ40). B, Photomicrograph showing marked hyperparakeratosis and acanthosis (H&E, magnification ϫ100). C, Photomicrograph showing the cleavage within the parakeratin that allows the surface to be peeled off leaving behind thickened nonulcerated mucosa (H&E, magnification ϫ100). D, Photomicrograph showing the fissures and clefts within the thick parakeratin rimmed by bacteria without an inflammatory response, and ballooned cells (H&E, magnification ϫ200). Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg 2009. Histologic Features showed ulceration or inflammation. There were no All cases showed hyperparakeratosis with a shaggy, cases of epithelial dysplasia or carcinoma. “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 Discussion any inflammatory reaction (Figs 4A-D).
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