J Oral Maxillofac Surg 67:140-146, 2009 Morsicatio Mucosae Oris—A Chronic Oral Frictional , Not a 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 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 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 , 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 /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). One case MMO is a common chronic mucosal frictional ker- showed candidal hyphae without evidence of spon- atosis characterized by poorly demarcated, rough, giotic pustules or inflammation. All but 3 cases exhib- shaggy, peeling, white papules, and plaques on the ited benign epithelial hyperplasia, and 80.8% of cases buccal mucosa, lateral border of the tongue, or the exhibited ballooned cells with intracellular edema lower labial mucosa, areas that are easily accessible (typical for mild surface trauma such as leukoedema). to, and readily traumatized by, the teeth. It is often A papillary surface configuration was noted in 44.2% factitial or self-induced, although the patient may not of cases. Inflammatory cells were present in the epi- be conscious of the habit or it may be secondary to a thelium in only 1 case and inflammation was minimal nocturnal parafunctional habit. Chronic frictional in- to absent in the connective tissue in 92.9% of cases; 5 jury of the gingiva or alveolar ridge mucosa, especially cases showed focal ulceration. Reactive epithelial of the retromolar pad, presents as benign alveolar atypia was noted in 4 cases, always in cases that ridge keratosis (BARK) with different histologic fea- 144 MORSICATIO MUCOSAE ORIS tures, namely, hyperorthokeratosis and acanthosis with slight papillomatosis, features identical to fric- tion-induced skin lesions of lichen simplex chroni- cus.13 Several differences were noted between this study and previous large studies, all of which were pub- lished 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 prev- 4 FIGURE 5. Dysplastic leukoplakia of the right lateral tongue (note alence in the second decade. Another found le- sharp demarcation). sions in reform school children primarily in the Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg 3 second decade of life. Of significance, those stud- 2009. ies did not have histopathologic confirmation of the diagnosis. a helpful clinical sign that often, although not always, SITES OF INVOLVEMENT distinguishes dysplastic lesions from reactive or in- None of the previous large studies report involve- flammatory lesions (Fig 5). ment of the tongue, only involvement of the buccal The histopathology has been described in previous mucosa and labial mucosa.1,3,4 In this study, the reports as “parakeratosis with surface debris and bac- tongue was the most common site biopsied, and teria, epithelial hyperplasia, swollen epithelial cells, formed 53.6% of all specimens with MMO. This may and scant inflammation with no evidence of dyspla- be a reflection of the tongue being a high risk site for sia”1,3,16-18 This is in keeping with what was seen in dysplasia and , so that clinicians tended to this study. The characteristic histopathologic features biopsy white lesions at this site, which they feel are of this condition are the following: 1) hyperparakera- suspicious for leukoplakia, particularly in men who tosis that may be marked with a shaggy, frayed, fis- smoke. Therefore, it may be selection bias that led to sured, or peeling appearance; hyperorthokeratosis, the almost 3:1 male predominance in this series. Be- although sometimes present, rarely occurs exten- cause most of the clinical data obtained from the sively or alone in MMO; 2) surface bacterial coloniza- accession forms were incomplete, it is difficult to tion is usually but not inevitably present; 3) benign draw conclusions regarding smoking history, bilater- epithelial hyperplasia with intracellular edema and ality, or history of trauma. ballooning of superficial keratinocytes; 4) insignifi- Although the clinical appearance of MMO is usually cant inflammation; and 5) occasionally reactive atypia fairly typical, a biopsy is always warranted if the if there is ulceration or inflammation. Interestingly, clinician is not absolutely certain that a white lesion is the mucosa of betel nut chewers may show the same an MMO. Some helpful clinical features that distin- histopathology.19 guish this from leukoplakia are 1) rough, shaggy, often peeling surface; 2) bilaterality; 3) location on WHY IS MMO NOT LEUKOPLAKIA? movable, nonkeratinized mucosa that can be reached At an international symposium of the Interna- by the teeth; and 4) usually lack of distinct margin or tional Collaborative Group on Oral White Lesions demarcation of the white area from the surrounding (ICGOWL) leukoplakia was defined as follows: “a pre- normal mucosa. A history of a chronic chewing habit dominantly white lesion that cannot be classified as may or may not be elicited. Although proliferative any other definable lesion; some lesions will trans- (verrucous) leukoplakia may be bilateral and some- form to cancer.”6 Therefore, it is only when the cli- times even symmetric, they will often also involve nician has excluded the possibility that the patient has areas that cannot be reached by the teeth (such as any other specific white lesion that a clinical diagno- the gingiva).14,15 In the author’s experience, leuko- sis of leukoplakia can be made (Table 3). The defini- plakia that is associated with dysplasia including pro- tion specifically excludes lesions caused by friction. liferative (verruous) leukoplakia often will have areas More recently, at a workshop coordinated by the that are clearly demarcated from the adjacent mucosa, World Health Organization (WHO) Collaborating Cen- WOO AND LIN 145

quences for patient care. In the largest study on leu- Table 3. LESIONS THAT MAY APPEAR WHITE koplakia,9 all lesions that were keratotic were in- Developmental cluded and this probably included all primary MMO Cannon and all BARK, a benign frictional keratosis of the Hereditary benign intraepithelial dyskeratosis gingiva with characteristic histologic and clinical find- Dyskeratosis congenita 13 Pachyonychia congenita ings. These 2 entities form a substantial portion of Other oral lesions in genodermatoses associated with oral white lesions, and they are completely benign dyskeratosis with no malignant potential; they are NOT even non- Inflammatory/reactive dysplastic leukoplakias. If these 2 groups of frictional Frictional/factitial injuries are removed from the pool of leukoplakia, the Morsicatio mucosae oris Benign alveolar ridge keratosis prevalence of dysplasia, CIS, and invasive SCCA in Mouth-wash induced desquamation leukoplakia will increase. When the cases of MMO Infectious were removed from this series of 584 of clinical leu- Oral viral (hairy) leukoplakia koplakia, the percentage of leukoplakias that were Candidiasis dysplastic/CIS/SCCA rose from 16.3% to 18.4%, an Immune-mediated Lichen planus/lichenoid stomatititis increase of 12.9%. If we also remove BARK from the Chronic graft-versus-host disease nonspecific “hyperkeratosis with/out acanthosis,” the Tobacco-associated percentage of leukoplakias that were dysplastic/CIS/ Smokeless tobacco keratosis SCCA rose from 16.3% to 26.3%, an increase of 55.2% Nicotinic (Table 4). Autoimmune It is possible, indeed probable, that many of the Others white lesions noted in the pivotal study by Waldron Nondysplastic leukoplakia and Shafer9 represented MMO and BARK because the Premalignant and malignant 2 most common sites for white lesions in that study Dysplastic leukoplakia were the buccal mucosa and the gingiva. MMO in this Verrucous leukoplakia Proliferative leukoplakia study was most commonly found on the buccal mu- Squamous cell carcinoma cosa and BARK, which as its name indicates is found on the gingiva.13 The most common sites for dysplas- Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg 2009. tic leukoplakias are the ventral tongue and floor of mouth. Understanding the true nature of leukoplakia may ter for Oral Cancer and Precancer (CCOCP) in the have been hampered partially by the use of nonspe- United Kingdom, leukoplakia was defined as “a white cific histologic diagnosis of many hyperkeratotic le- plaque of questionable risk having excluded (other) sions. Although some are very well recognized such 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 Table 4. PREVALENCE OF DYSPLASIA, CIS, AND not show dysplasia, but with an assessable tendency CARCINOMA IN WHITE LESIONS to malignant transformation. They, too, exclude any White lesions including MMO and BARK 449 lesion caused by friction. MMO 52 MMO is a primary frictional injury of the oral BARK 108 mucosa with defined clinical and histopathologic Subtotal 160 features, and as such, should be signed out by the Hyperortho- or -parakeratosis and/or acanthosis and/or mucositis 216 pathologist with this specific moniker or other phrase Dysplasia/verrucous hyperplasia/CIS 61 indicating its primary frictional character rather Squamous cell carcinoma 12 than using the nonspecific diagnosis of “hyperortho- Subtotal 73 or -parakeratosis, acanthosis and/or chronic inflamma- Total 449 tion.” It has no malignant potential, and because it is NOTE. % dysplasia/carcinoma if BARK/MMO included as frictional in nature, must be excluded from lesions of leukoplakia 73/449 ϭ 16.3%. leukoplakia as defined by the ICGOWL and more % dysplasia/carcinoma if MMO excluded as leukoplakia recently by the WHO CCOCP. 73/449-52 ϭ 18.4% (% change ϩ12.9%). More importantly, a nonspecific histopathologic di- % dysplasia/carcinoma if BARK/MMO excluded as leuko- plakia 73/449-160 ϭ 25.3% (% change ϭϩ55.2%). agnosis causes these lesions to enter the “pool” of all Abbreviations: MMO, morsicatio mucosae oris; BARK, be- leukoplakia lesions and dilutes the prevalence of dys- nign alveolar ridge keratosis; CIS, carcinoma-in-situ. plasia, CIS, and SCCA in such leukoplakias. This is not Woo and Lin. Morsicatio Mucosae Oris. J Oral Maxillofac Surg of mere academic interest but has serious conse- 2009. 146 MORSICATIO MUCOSAE ORIS as many of the lesions noted in Table 3, the histology ogist to arrive at an accurate diagnosis for oral white of oral frictional keratoses such as BARK, for example, lesions. 13 has been defined only recently. Furthermore, al- Acknowledgments though the histopathologic features of MMO are well known to many oral and maxillofacial pathologists, I thank the oral and maxillofacial surgeons, periodontists, oral medicine specialists and general dentists who submitted these this entity is less well recognized in skin and general cases, on which this research is based. I also thank Dr Manal pathology circles, and they are usually given a non- Al-Sheddi for her help with some of the data management. specific diagnosis of “parakeratosis and acanthosis” without further interpretation. References Diagnosing MMO as merely “hyperortho- or –para- 1. Hjorting-Hansen E, Holst E: Morsicatio mucosae oris and suctio keratosis with acanthosis” (referred to in many pathol- mucosae oris. Scand J Dent Res 78:492, 1970 ogy circles as the histologic sign-out), although histo- 2. Physical and Chemical Injuries (ed 2). Philadelphia, Elsevier, 2002 logically correct, does not provide an accurate 3. Van-Wyk CW, Staz J, Farman AG: The chewing lesion of the interpretation of this condition because this is the cheeks and : Its features and prevalence among a selected same histologic sign-out offered for nondysplastic group of adolescents. J Dent 5:193, 1977 4. Sewerin I: A clinical and epidemiologic study of morsicatio leukoplakias. MMO has much more specific histology buccarum/labiorum. Scand J Dent Res 79:73, 1971 than nondysplastic leukoplakias. Smokeless tobacco 5. Bessa CF, Santos PJ, Aguiar MC, et al: Prevalence of oral mu- keratosis for example, also exhibits “hyperortho- cosal alterations in children from 0 to 12 years old. J Oral Pathol Med 33:17, 2004 or –parakeratosis and acanthosis,” and although this is 6. Axell T, Pindborg JJ, Smith CJ, et al: Oral white lesions with histologically correct, it is more accurate and helpful special reference to precancerous and tobacco-related lesions: to the clinician to diagnose and sign it out as smoke- Conclusions of an international symposium held in Uppsala, Sweden, May 18-21 1994. International Collaborative Group on less tobacco keratosis. Oral White Lesions. J Oral Pathol Med 25:49, 1996 In this study, there still remained 216 lesions that 7. van der Waal I, Axell T: Oral leukoplakia: A proposal for exhibited hyperpara or orthokeratosis that could not uniform reporting. Oral Oncol 38:521, 2002 8. Warnakulasuriya S, Johnson NW, van der Waal I: Nomenclature be further classified but were not dysplastic. It may be and classification of potentially malignant disorders of the oral helpful to clinicians if the pathologists signing out mucosa. J Oral Pathol Med 36:575, 2007 such cases add as a descriptor, “likely reactive” at the 9. Waldron CA, Shafer WG: Leukoplakia revisited: A clinicopath- ologic study of 3265 oral leukoplakias. Cancer 36:1386, 1975 end of the microscopic description of “hyperortho- 10. Banoczy J, Csiba A: Occurrence of epithelial dysplasia in oral or -parakeratosis, acanthosis, and/or chronic inflam- leukoplakia. Analysis and follow-up study of 12 cases. Oral Surg Oral Med Oral Pathol 42:766, 1976 mation” for white lesions that appear inflammatory 11. Silverman S, Gorsky M, Lozada F: Oral leukoplakia and malig- but that are not at this time, classifiable as a specific nant transformation. Cancer 53:563, 1984 entity. This would be an extension of the recommen- 12. Lumerman H, Freedman P, Kerpel S: Oral epithelial dysplasia and the development of invasive squamous cell carcinoma. dation made by ICGOWL that all histopathology re- Oral Surg Oral Med Oral Pathol Oral Radiol Endod 79:321, 1995 ports on biopsies of leukoplakias should include a 13. Natarajan E, Woo SB: Benign alveolar ridge keratosis (oral statement on the presence or absence of epithelial lichen simplex chronicus): A distinct clinicopathologic entity. 6 J Am Acad Dermatol 58:151, 2008 dysplasia. Such lesions may represent early or heal- 14. Silverman S Jr, Gorsky M: Proliferative verrucous leukoplakia: A ing frictional keratoses (MMO or BARK), some other follow-up study of 54 cases. Oral Surg Oral Med Oral Pathol yet to be histologically defined lesion caused by me- Oral Radiol Endod 84:154, 1997 15. Zakrzewska JM, Lopes V, Speight P, et al: Proliferative verru- chanical or chemical irritation, or subtle hypersensi- cous leukoplakia: A report of ten cases. Oral Surg Oral Med tivity reaction to topical or systemic substances. Oral Pathol Oral Radiol Endod 82:396, 1996 As more and more hyperkeratotic lesions take their 16. Kocsard E, Schwarz L, Stephen BS, et al: Morsicatio buccarum. Br J Dermatol 74:454, 1962 rightful place as completely benign and recognizable 17. Obermayer ME: Cheekbiting (morsicatio buccarum). Arch Der- entities with an inflammatory/reactive etiology, re- matol 90:185, 1964 search on true leukoplakias can be more focused. 18. Glass LF, Maize JC: Morsicatio buccarum et labiorum (excessive cheek and biting). Am J Dermatopathol 13:271, 1991 Clinicians play an important role by providing good 19. Reichart PA, Philipsen HP: Betel chewer’s mucosa—A review. clinical data and by working closely with their pathol- J Oral Pathol Med 27:239, 1998