Lecture 9 - Oral White Lesions.pdf

DENT4008 ORAL MEDICINE White Lesions Assist. Prof. Elif ÇELEBİ School of Dental Medicine Department of Oral and Maxillofacial Radiology [email protected] OUTLINE Leukoedema Leukoplakia Actinic (Solar) Cheilitis Hairy Leukoplakia Proliferative Verrucous Leukoplakia Submucous Fibr...

DENT4008 ORAL MEDICINE White Lesions Assist. Prof. Elif ÇELEBİ School of Dental Medicine Department of Oral and Maxillofacial Radiology [email protected] OUTLINE Leukoedema Leukoplakia Actinic (Solar) Cheilitis Hairy Leukoplakia Proliferative Verrucous Leukoplakia Submucous Fibrosis Lichen Planus Lichenoid Drug Eruptions Oral Candidiasis Frictional Hyperkeratosis Fordyce’s Granules Smokeless Tobacco Keratosis (Snuff Pouch) White Sponge Nevus Oral Candidiasis Oral Candidiasis Leukoedema Etiology • Unknown • Benign; common in general population, with racial clustering in Africans Diagnosis • Clinical recognition is sufficient. Leukoedema Clinical Presentation • Symmetric, asymptomatic • Buccal mucosa involved by graywhite, diffuse, milky surface with an opalescent quality • Wrinkled surface features at rest • White appearance dissappears with stretching of mucosa Leukoedema Differential Diagnosis • Cheek chewing • White sponge nevus • Lichen planus • Candidiasis Prognosis • Excellent, no treatment is required Leukoplakia Etiology • Essentially unknown, although many cases related to use of tobacco Leukoplakia Clinical Presentation • Most occur in the fifth decade and beyond • An idiopathic white (sometimes white-and-red) patch • Most common on lip, gingiva, buccal mucosa • Increased risk of dysplasia or carcinoma when occurring on tongue, floor of mouth, vermilion portion of lip • Clinical subsets include homogeneous, verrucous, speckled, and proliferative verrucous leukoplakia (proliferative form may be multiple and persistent) • Cases may advance or regress unpredictably—reflective of a dynamic process • Progress to dysplasia or malignancy may occur with little or no change in clinical appearance. Leukoplakia Diagnosis • Performance of a biopsy is mandatory after elimination of any suspected causative factors • Multiple biopsies of large lesions are needed to be performed due to microscopic heterogeneity within a single lesion. Leukoplakia Differential Diagnosis Other white lesions • Frictional keratosis • Burn (thermal/chemical) • Hyperplastic candidiasis • Lichen planus Genetic alterations (genodermatoses) • White sponge nevus • Hereditary benign intra-epithelial dyskeratosis • Dyskeratosis Leukoplakia Prognosis • Observation with repeat biopsies to be performed Prevention • Elimination of tobacco use and heavy alcohol consumption • Recurrences may be reduced by systemic retinoid therapy. Hairy Leukoplakia Etiology • Probably due to opportunistic Epstein-Barr virus (EBV) infection of epithelial cells • Usually in an immunocompromised or immunosuppressed host (HIV/AIDS) Hairy Leukoplakia Clinical Presentation • Usually arises on lateral tongue border • Early lesions are fine, white, vertical streaks with an overall corrugated surface • Later lesions may be thickened to be plaque-like • Extensive lesions can involve dorsum of tongue and buccal mucosa • May serve as a pre-AIDS immunodeficiency syndrome) sign (acquired Diagnosis • Incisional biopsy findings show characteristic EBV nuclear inclusions in upper-level keratinocytes Differential Diagnosis • Frictional hyperkeratosis • Lichen planus • Hyperplastic candidiasis Proliferative Verrucous Leukoplakia Etiology • PVL has been suspected to have a viral etiology, although an association has not been confirmed Diagnosis • Based upon appearance, clinical course, and microscopic diagnosis (ie, clinical-pathologic correlation) Proliferative Verrucous Leukoplakia Clinical Presentation • Progressive and persistent • Initially a flat hyperkeratotic to warty surface • Usually encountered in older women, • The lower gingiva is a predilection site. Proliferative Verrucous Leukoplakia Differential Diagnosis • Idiopathic leukoplakia • Oral warts/condyloma • Verrucous/squamous cell carcinoma Prognosis • Progression to carcinoma frequently occurs, usually many years after initial lesion(s) develops. Lichen Planus Etiology • Unknown • Autoimmune T cell–mediated disease targeting basal keratinocytes (antigen unknown) • Lichenoid changes associated with galvanism, graft-versus-host disease (GVHD), certain drugs, contact allergens Lichen Planus Clinical Presentation • Up to 3 to 4% of population have oral lichen planus • 0.5 to 1% of population have cutaneous lichen planus; 50% also have oral lesions (25% with oral lesions have concomitant skin lesions) • White females (60%) • Occurs in fourth to eighth decades Lichen Planus Clinical phenotypes • Reticular (and papular as its close clinical variant). • Erythematous (also referred to as atrophic). • Ulcerative (also referred to as erosive). • Plaque-like. • Bullous—very uncommon and usually associated with one of the other phenotypes. Lichen Planus Oral site frequency: 1. buccal mucosa (most frequent) 2. tongue 3. gingiva 4. lips (least frequent) Bilateral and often symmetric distribution Skin sites: forearm, scalp, genitalia Wickham Lines Desquamative Gingivitis as a Manifestation of Oral Lichen Planus Lichen Planus Diagnosis • Examination of oral mucosa, skin, genitalia • Negative ocular mucosa history; no history of blistering • Use of drugs, galvanism, Graft-versus-host disease to be ruled out • Biopsy • Direct immunofluorescence Lichen Planus Differential Diagnosis • Lichenoid drug eruptions • Lichenoid contact reactions • Lupus erythematosus • Erythema multiforme • Mucous membrane pemphigoid Prognosis • Good prognosis; rare malignant transformation (0.5–3%) • May be cyclic; may last for years/decades • Tends to be chronic Lichenoid Drug Eruptions Etiology • Penicillin, gold, NSAIDs, and sulfonamides are examples of drugs that have been related to the development of OLDEs. Lichenoid Drug Eruptions Clinical Presentation • Predominantly unilateral and present with an ulcerative reaction pattern. • OLDEs are often clinically indistinguishable from OLP with hyperkeratotic striations and an erythematous base. • Most often in buccal mucosa and attached gingiva, but any site may be involved Lichenoid Drug Eruptions Diagnosis • Identification and elimination of causative substance • Biopsy of areas unresponsive to elimination strategy to demonstrate characteristic keratosis and interface inflammation and associated changes Lichenoid Drug Eruptions Differential Diagnosis • Lichen planus • Leukoplakia • Dysplasia/carcinoma Prognosis • Good • Observation while lesions exist Oral Lichenoid Contact Reactions • OLCR is considered to be due to a delayed (contact) hypersensitivity reaction to constituents derived from dental materials. • The majority of patients, but not all, are patch test positive to mercury (Hg), which lends support to OLCR being allergic in nature. • Although Hg is usually considered the primary etiologic factor, other amalgam constituents may also initiate OLCR, and other filling materials such as gold, composites, and glass ionomers may also generate reactions. Smoker’s Palate (Nikotine Stomatitis) • In smoker’s palate, an erythematous irritation is initially seen, and this lesion is followed by a whitish palatal mucosa reflecting a hyperkeratosis. • As part of this lesion, red dots can be observed representing orifices of accessory salivary glands, which can be enlarged and display metaplasia Actinic (Solar) Cheilitis Etiology • Chronic, excessive exposure to solar radiation; ultraviolet spectrum (ranging from 290 to 320 nm) most damaging • May progress to cutaneous actinic keratosis and/or squamous cell carcinoma Actinic (Solar) Cheilitis Clinical Presentation • Vermilion portion of lower lip • Pale irregularly opaque (keratotic) surface with intervening red (atrophic) zones • More advanced lesions are scaly, crusted and/or indurated. • Progression to carcinoma often heralded by persistent ulceration or erosion Diagnosis • Thermal/chemical burn ruled out by history • Chronic ultraviolet light exposure • Biopsy findings Differential Diagnosis • Exfoliative cheilitis • Squamous cell carcinoma Prognosis • Lifelong follow-up • Up to 10% develop into squamous cell carcinoma. • When carcinoma develops, growth tends to be slow and metastasis occurs late; 85 to 90% long-term survival Submucous Fibrosis Etiology • Results from direct mucosal contact with a quid containing areca (betel) nut, tobacco, and other ingredients • Risk of oral squamous cell carcinoma is increased several-fold Submucous Fibrosis Clinical Presentation • Mucosal rigidity, trismus • Sites most often affected: buccal mucosa, soft palate • Leukoplakia of surface with pallor • Deep scarring, epithelial atrophy in cheeks, soft palate Submucous Fibrosis Diagnosis • Appearance • History Prognosis • Irreversible • Treatment consists of local steroid injection and surgical disruption (lysis) of fibrous bands, however, outcomes are generally poor White Sponge Nevus Etiology • Hereditary (autosomal-dominant) disorder of keratinization affecting nonkeratinizing oral, esophageal, and anogenital mucosal epithelium • Point mutations in the keratin 4 and/or 13 genes Epidemiology The clinical appearance usually commences during adolescence, The sex distribution has been reported to be equal. White Sponge Nevus Clinical Presentation • Asymptomatic • Deeply folded, thickened, white mucosa • Buccal mucosa chiefly affected • No functional impairment White Sponge Nevus Diagnosis • Clinical appearance • Family history • Microscopic findings Differential Diagnosis • Idiopathic leukoplakia • Chemical/thermal burn • Chronic low-grade trauma (morsicatio) White Sponge Nevus Treatment • None required • No malignant potential Smokeless Tobacco Keratosis (Snuff Pouch) Etiology • Persistent habit of holding ground tobacco within the mucobuccal vestibule Smokeless Tobacco Keratosis (Snuff Pouch) Clinical Presentation • Usually in men in Western countries • Mucosal pouch with soft, white, fissured appearance • Leathery surface due to chronic tobacco use over many years Smokeless Tobacco Keratosis (Snuff Pouch) Diagnosis • Clinical appearance • Biopsy Differential Diagnosis • Leukoplakia (idiopathic) • Mucosal burn (chemical/thermal) Prognosis • Generally good with tobacco cessation • Malignant transformation to squamous cell carcinoma or verrucous carcinoma Frictional Hyperkeratosis Etiology • Chronic, low-grade biting habit Clinical Presentation • White, keratotic surface • Frictional hyperkeratosis is often seen in edentulous areas of the alveolar ridge, but may also be observed in other parts of the oral mucosa exposed to increased friction or trauma. • Asymptomatic Frictional Hyperkeratosis Diagnosis • Based on clinical features • Biopsy Prognosis • Excellent Differential Diagnosis • Leukoplakia References Michael Glick (ed.); Martin S. Greenberg (ed.); Peter B. Lockhart (ed.); Stephen J. Challacombe (ed.). Burket's Oral Medicine. 13th edition. Wiley-Blackwell. June 2021. ISBN: 9781119597780 Jean M. Bruch; Nathaniel Treister. Clinical Oral Medicine and Pathology: Springer. 2016. Joseph Regezi, James Sciubba, Richard Jordan. Oral Pathology Clinical Pathologic Correlations. 7th Edition. Saunders; 2016 George Laskaris. Color Atlas of Oral Diseases: Diagnosis and Treatment. Thieme Medical Publishers; 4th editon Edward W Odell. Cawson's Essentials of Oral Pathology and Oral Medicine E-Book (9th ed.). Elsevier Health Sciences; May 2017