THE LARGEST DENTAL MEETING/EXHIBITION/CONGRESS IN THE UNITED STATES Leukoplakia and Look-alikes: How to Diﬀern ate and Manage Sook-Bin Woo, D.M.D. Wednesday December 4, 2013 Welcome to the Greater New York Dental Mee ng 6 Days of Educa on Seminars, Hands-on Workshops & Essays Friday - Wednesday th Friday, November 29 12:00 Noon - 4:30 P.M. Saturday, November 30th 8:00 A.M. - 4:30 P.M. Sunday, December 1st - Tuesday, December 3rd 8:00 A.M. - 5:30 P.M. Wednesday, December 4th 8:00 A.M. - 4:30 P.M. 4 Days of Exhibits Exhibit Hall Hours Sunday Sunday, December 1st - Tuesday, December 3rd 9:30 A.M. - 5:30 P.M. Wednesday, December 4th 9:30 A.M. - 5:00 P.M. 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By Dr. Sook-Bin Woo (1) Half Day Seminar (3 hrs); Wednesday, December 4, 2013; 9:00 – 12:00PM Leukoplakia and Look-alikes: How to Differentiate and Manage By Sook-Bin Woo DMD FDSRCS (Edin) Associate Professor, Harvard School of Dental Medicine, Boston BWH website www.partners.org>Brigham and Women’s Hospital>Depts and Services>Surgery>Oral Medicine>For Professionals>For Staff Professionals Provides patient information For oral pathology/radiology/oral medicine symposium in September, email me at [email protected] – 6 CE credits What makes a lesion white? • Thick keratin • Thick epithelium • Altered epithelium - benign • Benign (swelling and edema of cells) • Degeneration of cells (using caustic dentifrices) • Altered epithelium – premalignant and malignant • Pre-cancerous or dysplastic • Cancerous What makes a lesion white? • Are all white lesions leukoplakia (leuko: white; plak: plaque)? • No! Name is misleading History of leukoplakia definition • 1978 (WHO): white patch or plaque that cannot be characterized clinically or pathologically as any other disease • 1984: white patch or plaque that cannot be characterized clinically or pathologically as any other disease and is not associated with any physical or chemical causative agent except use of tobacco History of leukoplakia definition • 1996 (WHO): predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion: some leukoplakias will transform into cancer …… frictional lesions are excluded…..biopsy is mandatory….. Current definition of leukoplakia • 2007 (WHO): White plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer. • It is a clinical term only; modified after histopathologic evaluation. Classification of white lesions By etiology and frequency – questions you ask as clinician – Is this lesion……. • Developmental/congenital/genetic • Reactive • Physical/mechanical trauma • Chemical trauma • Others • • • • Infectious Immune-mediated/autoimmune Pre-neoplastic and Neoplastic Metabolic Defined white lesions that are not leukoplakias • Developmental • • • • • Cannon white sponge nevus Hereditary benign intraepithelial dyskeratosis Oral Darier disease/warty dyskeratoma Dyskeratosis congenita Pachyonychia congenita • Extremely rare Reactive • Reaction to mild local injury – most common • • • • • Leukoedema (eg. smoking) Contact desquamation (eg. Listerine) Smokeless tobacco lesion Nicotinic stomatitis - salivary duct injury Frictional keratoses • Morsicatio mucosae oris • Benign alveolar ridge keratosis • Other frictional keratosis • Hairy tongue • Infectious • Candidiasis • Hairy leukoplakia (EBV-associated) • Immune-mediated • Migratory glossitis • Lichen planus/lichenoid lesions • Autoimmune • Lupus erythematosus • Chronic graft-vs.-host disease • Dysplastic, neoplastic • Leukoplakia (without obvious dysplasia) – keratosis of unknown significance • Dysplastic leukoplakia • Including verrucous leukoplakia • Invasive squamous cell carcinoma Clinical help hint for diagnosis of leukoplakia • Sharply demarcated at least around part of the lesion – suggesting that a CLONE of genetically altered cells have proliferated • Fissuring • Noted in > 90% of cases Leukoedema • Clinical • Variation of normal ? • Associated with very mild topical injury (eg smoking, mouth wash use) • Stretching eliminates appearance • POORLY DEMARCATED • Is this a leukoplakia? Management • Discontinue offending agent (eg. smoking) • Change to milder toothpaste or mouthwash Contact desquamation • Clinical presentation • Delicate, white wisps of tissue with underlying normal mucosa • Culprits – Tartar-control toothpaste, Pro-Health toothpaste, Listerine (21.6-26.9% alcohol) • POORLY DEMARCATED • Is this a leukoplakia? Management • Change to a milder tooth paste or mouthwash Smokeless Tobacco Lesion • Clinical • Grey-white opalescent area with parallel ridges where tobacco is placed • Painless • Cells are edematous like leukoedema • Is this a leukoplakia? Management • Early lesions: Lesions will resolve if remove the irritant – smokeless tobacco – is removed • Late lesions: Once leukoplakia develops, lesions unlikely to resolve and should be removed. • Smokeless tobacco has very low association with cancer unless leukoplakia has developed. • Used for “risk reduction” in some patients Nicotinic stomatitis • Caused by heat especially of pipe smoking, and not by nicotine • See in patients who drink very hot liquids regularly • Appearance caused by inflammation of excretory salivary ducts that open onto the surface • Is this a leukoplakia? Management • Discontinue habit • However, once it is established, difficult to return tissues to normal Morsicatio mucosae oris/Chronic factitial/bite injury • Clinical • Occurs in 1% to 2% of the population • White papules and plaques, shaggy surface, focal erosions, erythema, sometimes ulcerations • POORLY DEMARCATED • Is this a leukoplakia? Management • Reassure patient • No treatment • Bite guards not been shown to be helpful Benign alveolar ridge keratosis (BARK) • Clinical • White plaque on the alveolar ridge, painless, may be rough; poorly demarcated • Often in the area of previously extracted mandibular third molar (wisdom tooth) • POORLY DEMARCATED • Is this a leukoplakia? Management • Reassure patient • No treatment required if retromolar pad • Reline and/or remake denture as necessary. Hairy/coated tongue • Painless, but patient may report stale or foul taste in mouth; gagging • White thick mat on dorsum, may be pigmented • Often a history of antibiotic use and misdiagnosed as candidiasis • No other plaques or papules elsewhere • Is this a leukoplakia? Hairy Tongue • Etiology: • Elongated of filiform papillae because of retention of keratin from • Dehydration, increased mucous and decreased serous (watery saliva) • Smoking • Reduced keratin loss because not eating coarse foods • Idiopathic • Increased chromogenic bacterial growth – green, brown, yellow Management • Get a good history • No treatment is necessary • Hydrate well • Return to eating a healthy diet with fresh fruits and vegetables Candidiasis • Often burning sensation or sensitivity • Pseudomembranous candidiasis (thrush) curdy white papules and plaques on erythematous base • May or may not wipe off • Is this a leukoplakia? Other forms of candidiasis • • • • Erythematous or atrophic candidiasis Angular cheilitis Median rhomboid glossitis Hyperplastic candidiasis Treatment All for 7-10 days • Nystatin 100,000 iu/ml; dispense 300 ml, swish x 3-5 min, and spit out 5 ml (1 teaspoon) QID • Clotrimazole 10 mg troches; suck on one troche QID • Mycolog (mycostatin and triamcinolone) under denture TID, treat denture • Vytone (iodoquinol and hydrocortisone) under denture Compliance is a big issue because of need for multiple doses. • Fluconazole 100 mg QD x 5-7 days for generally healthy patients Hairy leukoplakia • Painless, unless super-imposed candidiasis • Bilateral, symmetric, usually on lateral tongue • Immunocompromised – AIDS, organ transplantation • This is not a TRUE leukoplakia; name is confusing. It is an Epstein Barr virus infection without any malignant potential. Management • • • • Reduce immunosuppression Treat candidiasis if present No specific therapy If HIV/AIDS related, HAART will usually resolve lesions Migratory Glossitis/Stomatitis Geographic tongue • Clinical • 1% to 2% of the population • Tongue dorsum and ventrum has red, bald areas delineated by curving ring-like white lines • May affect other mucosal sites • Is this a leukoplakia? Benign Migratory Glossitis • What to do? • Up to 1/3 of patients are atopic so get a good history • How do you elicit a history of atopy? • Asthma • Eczema • Hayfever • Food Intolerance Does immediate family member have them? Did/do you have these conditions? • Associated with some forms of psoriasis Benign Migratory Glossitis • Treatment and follow-up • No treatment necessary unless severe in which case topical steroids may be used • Topical anesthetics such as 2% viscous lidocaine or diphenhydramine (Benadryl) • Patient education and information Lichen planus • Clinical • • • • • White: keratotic, reticulated, papular Red: erosive, erythematous Yellow: ulcerative If on gingiva, may have gingival-genital syndrome This is not a leukoplakia Etio-pathogenesis • Local causes • Amalgam (used to be called galvanism) • Cinnamic aldehyde (in Tartar control and other toothpastes, chewing gum) • Systemic causes • Medications (esp. anti-hypertensives such as hydrochlorthiazide, allopurinol, sulfasalazine, carbamazepine, statins, TNF alpha inhibitors etc) • Hepatitis C esp. in patients living around Mediterranean • Lupus erythematosus, chronic graft-vs-host disease Autoimmune diseases that are “lichenoid” • Red and white areas of the mucosa, bilaterally symmetric • Hepatitis C • Lupus erythematosus • Chronic graft-vs.-host disease after hematopoietic cell (bone marrow) transplantation Management of lichen planus • If due to hypertensive agents, changing medication not usually helpful – all classes can cause lichenoid reactions Topical steroids • Class I • Clobetasol 0.05% gel • Betamethasone 0.05% • Class II • fluocinonide gel 0.05% Place in stent for 30 min BID if only gingiva involved. • Important to avoid vermilion – cause atrophy with chronic use • Class IV steroid • Kenalog (triamcinolone 0.1%) in Orabase • Dexamethasone (0.1 mg/ml) swish with 5 ml, hold for 3-5 min and spit out • Steroid inhalers eg. fluticasone (Flonase), budesonide (Rhinocort) Treatment of lichen planus • Other topical immunosuppresive agents • Calcineurin-inhibitors • Tacrolimus (0.1% ointment or rinse, swish and spit out) • Intralesional steroid injections • Kenalog-40 (40 mg triamcinolone/ml) • Systemic therapy • Prednisone (1 mg/kg) • Hydroxychloroquin (Plaquenil) Plaque-type lichen planus • Current thinking • If striations are not present, not a sub-type of lichen planus - leukoplakia • If striations are present, may be development of leukoplakia within lichen planus • Must be biopsied and completely removed/ablated • May be associated with malignant transformation in lichen planus Plaque-type lichen planus • Current thinking • If striations are not present, not a sub-type of lichen planus - this is a leukoplakia • If striations are present, may be development of leukoplakia within lichen planus • Must be biopsied and completely removed/ablated • May be associated with malignant transformation in lichen planus Current definition of leukoplakia • 2007 (WHO): White plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer. • It is a clinical term only; modified after histopathologic evaluation. • 1-3% of general population • 50-70% of patients with leukoplakia smoke Occurrence of dysplasia/SCCa • Prior to 2005 • 10-20% of all leukoplakias are dysplasia or carcinoma at the time of biopsy • New data • 40-45% of all leukoplakias are dysplasia or carcinoma at the time of biopsy Occurrence of dysplasia/SCCa • Prior to 2005 • 10-20% of all leukoplakias are dysplasia or carcinoma at the time of biopsy • New data • 40-45% of all leukoplakias are dysplasia or carcinoma at the time of biopsy Leukoplakia • Localized leukoplakia • Homogenous - well-demarcated, fissured • Non-homogenous – not as well-demarcated • speckled (erythroleukoplakia)* • Verrucous* • Nodular* • Proliferative leukoplakia (PL) • Non-homogenous • Verrucous (most common – proliferative verrucous leukoplakia) • Erythroleukoplakia *Non-homogenous forms and PL have a higher association with dysplasia and carcinoma Prognosis • 3-15% transform to invasive squamous cell carcinoma • Non-homogenous leukoplakias more likely to do this • Proliferative leukoplakia show 70-100% transformation to squamous cell carcinoma over time Leukoplakia • Clinical • common sites are tongue, floor of mouth and gingiva • lesions on the floor of mouth, ventral tongue and soft palate have a higher association with dysplasia or carcinoma than other sites (>50%) • Helpful sign – sharp demarcation at least in parts of the lesion Risk factors • Same as with SCCa • • • • • • • • • Cigarette smoking Alcohol use Areca nut use Sunlight (mostly lip) Age Immunosuppression History of previous cancer Family history of cancer HPV (mostly oropharyngeal and tonsillar) Helpful clinical features • Applies mainly to homogenous lesions that can resemble other conditions • Sharp demarcation at least along part of the lesion • Fissuring Be careful! • If you get a diagnosis on a pathology report “Hyperkeratosis, no dysplasia” BE CAREFUL! Verrucous white lesions • Verrucous leukoplakia • White plaque (leukoplakia) that has a rough, warty surface configuration but is not a mass lesion • Proliferative (verrucous) leukoplakia • Verrucous leukoplakia but extensive at one site, or multifocal • Progressive, persistent • Usually female, often gingival • Biopsies show “hyperkeratosis, no dysplasia” • 70-100% develop verrucous or SCCA Pathology report • Hyperkeratosis and epithelial hyperplasia with chronic inflammation, no dysplasia present Check clinical lesion again • Is this “hyperkeratosis” frictional/reactive or not? • If not frictional/reactive, it is a TRUE leukoplakia What does it mean for you? • All true leukoplakias are potentially cancerous lesions. • If just “hyperkeratosis”, re-evaluate the clinical lesion. Re-evaluate the lesion • • • • • • • • Is it at least partially welldemarcated? Has it ever resolved completely? Could it be frictional? If unlikely to be frictional, what can be causing the hyperkeratosis? Early dysplasia? Are there risk factors in patient? Is this a “high risk” site? Is it verrucous? What would you do if this was in your mouth Weigh carefully no treatment vs. treatment • • • • • • Do we know if this will become invasive? Do we know when it will become invasive? How morbid, difficult, expensive is removal? Is the patient healthy and what age? Can we safely watch and see what happens? If we watch with the option to remove it later, have we lost valuable time? Diagnosis: Hyperkeratosis, no dysplasia • Watch • • • • • Get smaller Stay the same Get bigger Change in appearance Change in symptoms • Remove • Is this too morbid? • Easier to follow Management of localized leukoplakia • All dysplastic lesions must be excised, preferably with clear margins. • Even if not dysplastic, conservative or narrow excision should be considered, if no clear etiology is identified. • Wide excision of recurrent lesions It got smaller – NO It stayed the same – NO It got bigger – YES It became nodular – YES It became stiff - YES Some important concepts • Silverman et al. 1985: 16% of “benign hyperkeratosis” became SCCa over time. • Many “benign hyperkeratosis” are already dysplastic genetically. • Why should “benign” hyperkeratosis become invasive carcinoma? Normal-appearing cells on microscopy but hyperkeratotic Normal Normal cell cell Genotypic dysplasia Critical accumulation of genetic mutations Phenotypic Dysplasia: Cytologic Architectural Abnormal-appearing on microscopy Invasive cancer Acceptable risk • What level of risk of cancer development is acceptable to watch a leukoplakia without dysplasia in your mouth? • 1 in 10,000 – acceptable to watch? • 1 in 1000 – acceptable to watch? • 1 in 100 – acceptable to watch? • If we use very conservative numbers, it is 2-3% - 1 in 30. • If we use the high frequency, 16% of benign hyperkeratosis become dysplasia or cancer – 1 in 5 Diagnosis: Hyperkeratosis, acanthosis, non-specific, no dysplasia Re-evaluate for causative factors esp. friction Localized leukoplakia Poorly demarcated Proliferative leukoplakia Well-demarcated Likely frictional Large > 3 cm Small < 3 cm Morsicatio mucosae oris Watch x q 3 mo, rebx q 12 mo. Excise/ablate narrowly; follow q 3 mo No recurrence; follow q 3-6 mo Recurred; excise with 23 mm. margin Benign alveolar ridge keratosis Non-specific reactive No treatment No recurrence; follow q 3-6 mo. Watch, rebiopsy, excise nodular or verrucous area; follow q 3 mo Photodynamic therapy Management of proliferative leukoplakia • Multiple biopsies with close follow-up (every 3-6 months); use of adjunctive tests may or may not be useful • Laser ablation • Chemo-prevention • Photodynamic therapy HPV and oral cancer • Strongly associated with the number of sex partners; 26 vaginal-sex; 6 oral sex (D’Souza 2007) • Mostly male in early 7th decade • Weak to no association with smoking • Mostly oropharyngeal and tonsillar; usually with cervical node metastasis when first diagnosed • Better prognosis even when metastasis has occurred to cervical lymph node (82% vs 57% 3year survival, Ang et al. 2010) HPV-associated dysplastic leukoplakia 20 cases in our laboratory • • • • Mostly males Median age 60 years Most lesions ventral tongue 2/20 became squamous cell carcinoma and 1 recurred HPV leukoplakia • Clinically just a leukoplakia • Histologically specific: HPV apoptotic epithelial dysplasia; high risk HPV positive and always p16 positive • Not sure of prevalence because newly identified. A Case • This 56 year old woman presented with this asymptomatic lesion of the left lateral tongue of unknown duration. • 2 ppd smoker X 40 years • She returns 18 months later after nursing her sister who subsequently died of breast cancer. Take home message • Not all white lesions are leukoplakias • Most white lesions are frictional keratoses on the buccal mucosa, tongue and ridge • ~ 40% of true leukoplakias are dysplastic or cancer at the time of diagnosis • Be careful of the sharply demarcated plaque that has no obvious dysplasia – consider removing it.
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