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RECOGNIZING WHITE LESIONS PART I: Reactive, Idiopathic, Hereditary

RECOGNIZING WHITE LESIONS PART I: Reactive, Idiopathic, Hereditary . David E. Wojtowicz, DDS, MBA. White Lesions . A Lesion Appears WHITE Because Some Material Is Obscuring the Normal PINK or Racial Color. Is the WHITE Material Directly on the Surface?.

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RECOGNIZING WHITE LESIONS PART I: Reactive, Idiopathic, Hereditary

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  1. RECOGNIZING WHITE LESIONS PART I: Reactive, Idiopathic, Hereditary David E. Wojtowicz, DDS, MBA

  2. White Lesions • A Lesion Appears WHITE Because Some Material Is Obscuring the Normal PINK or Racial Color. • Is the WHITE Material Directly on the Surface?

  3. 3 Mechanismsto Achieve White Appearance • Epithelial Thickening • Rough / Does NOT Rub Off • Surface Material • Rough / Does Rub Off • Subepithelial Change • Smooth / Does NOT Rub Off

  4. Six Common Etiologies for White Lesions • Reactive (Snuff) • Idiopathic (Hairy Tongue) • Hereditary (Leukoedema) • Auto-Immune (Lichen Planus) • Infectious (Candidiasis) • Neoplastic (SCC)

  5. 1. Six Reactive White Hyperkeratotic Lesions(These are HYPERKERATOTIC. They Do NOT Rub Off.) a.Snuff Dipper’s Lesion b.Nicotinic Stomatitis c.Chemical Burn d.Linea Alba e.Actinic Cheilitis f.Denture Acanthosis

  6. 1. Six Reactive White Hyperkeratotic Lesions(Do They Rub Off?)a.Snuff Dipper’s Lesion • Wrinkled, Velvety • US & Canada, Lower Carcinogenic Rate • Asia Higher Rate Due to Added Carcinogens • Treatment = Quit Habit, Switch Site

  7. 1. Six Reactive White Lesionsb.Nicotinic Stomatitis • Grey, White and Red on Hard Palate • Pipe and Tobacco Smoking (Heat) • Red Spots, Inflamed Minor Salivary Gland Orifices • Treatment = Quit Smoking

  8. 1. Six Reactive White Hyperkeratotic Lesionsc.Chemical Burn • Caused by Aspirin • Painful • Usually in Molar Region • Treatment = Discontinue Aspirin Use

  9. 1. Six Reactive White Hyperkeratotic Lesionsd.Linea Alba • Most Common White Lesion • White Line @ Occlusal Plane • Bilateral on the Buccal Mucosa • No Treatment Needed

  10. 1. Six Reactive White Hyperkeratotic Lesionse.Actinic Cheilitis • Sun Damage • Lower Lip • Obliteration of Border • Treatment = Avoid Sun, Use Sunblock

  11. 1. Six Reactive White Hyperkeratotic Lesionsf.Denture Acanthosis • Caused by Irritants • Clinical Appearance is Similar to Hyperkeratosis • Thickened Intermediate Cell layer • Elongation of Rete Pegs • Treatment = Avoid Irritants, ie. Ill-fitting Dentures

  12. 2. Two Idiopathic White Hyperkeratotic Lesions • Geographic Tongue • Hairy Tongue

  13. Geographic Tongue(Benign Migratory Glossitis) • White Borders (+/-Hyperkeratotic) • Red Patches of Denuded Filiform Papillae • Common Disorder (1 - 2%), Females, Young Adults • Painfree or . . . • Painful if inflamation is present • Treatment = None, or Topical Anesthetic

  14. Hairy Tongue • Shaggy Matte of Filliform Papillae • Candidiasis Stimulates the Hyperplasia • Coffee, Tea, Tobacco = Black • Treatment = Brush Tongue, Improve Oral Hygiene

  15. 3. Two Hereditary White Hyperkeratotic Lesions • Leukoedema • White Sponge Nevus

  16. Leukoedema • Milky Grey Film • Bilateral Buccal Mucosa, Non-progressive • Disappears When Stretched • More Common in Black Population • Treatment = None Needed

  17. White Sponge Nevus • Rough, Fissured Texture • Symetric, Bilateral Buccal Mucosa • Appears During Childhood, Non-progressive • Autosomal Dominant Transmission

  18. RECOGNIZING WHITE LESIONS II:Auto-Immune, Infectious, Neoplastic David E. Wojtowicz, DDS, MBA

  19. 4. Two Auto-Immune White Hyperkeratotic Lesions • Lichen Planus • Lupus Erythematosus

  20. Lichen Planus • Auto-immune Degeneration of Connective Tissue / Mucosa (Skin) Interface • Middle Age (Rare Before 30) • M = F, Skin Lesions (33%)

  21. Lichen Planus • Reticular (Wickham’s Striae) • Annular • Erosive • Atrophic, Bullous

  22. Lichen Planus • Stress & Thiazide Drugs are Possible Triggers • Differential: Snuff (Stretch) White Sponge (Youth) • Treatment = None if Asymptomatic . . .

  23. Erosive Lichen Planus • Painful • Risk Factor for SCC • Treatment = Biopsy, Steroids, Retinoic Acid

  24. Lupus Erythematosus • Skin Lesions: Butterfly Rash (Sun Exposed Area) • Mucosal Lesions: Rough White Patch • Bordered by Striae, Ulcers, Erythema

  25. Lupus Erythematosus • Systemic: Arthritis, Vasculitis (Renal Failure) • Antinuclear Antibodies (ANA) • Differential: Lichen Planus (Symmetrical & Cutaneous), Leukoedema (Stretch) White Sponge (Youth) • Treatment = Corticosteroids

  26. 5. Three Infectious White Lesions • Candidiasis (DOES & Does NOT Scrape Off) - FIVE Clinical Lesions • Oral Hairy Leukoplakia (Does NOTScrape Off) • Syphilitic Mucous Patch (Does NOTScrape Off)

  27. Candidiasis (Moniliasis) • Acute • Pseudomembraneous (“Thrush”) - White • DOESScrape Off • Atrophic (“Erythematous”) - Red • (Does NOT Scrape Off) • Chronic • Hyperplastic (“Candidal Leukoplakia”) - White • (Does NOT Scrape Off)

  28. Candidiasis • Commensal Organism - Normal Oral Flora • Capable of Opportunistic Infections (Hyphae) • Early Sign of Host Defense Breakdown (Neutropenia) • Risk Factors: Antibiotics, Imunosupression, Diabetes, HIV, Steroids, Nutritional Deficiency, Radiation/Chemo

  29. Candidiasis: Acute Pseudomembraneous • White, Scrapes Off • Underlying Tissue: Erythematous, Hemorrhagic, Pruritic • Newborns & RF (See Previous Item) • Treatment = a. Correct the Predisposing Factorb. Prescribe: Nystatin Vaginal Tablets • Disp: 70 • Use: One Tablet as a Lozenge 5 Times a Day

  30. Candidiasis: Chronic Hyperplastic-Candidal Leukoplakia • Keratotic Plaques or Papules (?Scrape Off?) Against Erythematous Background With Acanthosis • Sites: Labial Commissure, Labial & Buccal Vestibule • Risk Factors: Smoking, Poor Oral Hygiene (Dentures), Xerostomia - These Are Essentially All Chronic Irritants

  31. Candidiasis: Chronic Hyperplastic-Candidal Leukoplakia • Cancer Risk: Biopsy is Mandatory of All Speckled Erythroplakia or Erythroleuko-plakia Because of Increased SCC Risk • Treatment = a. Correct the Predisposing Factorb. Biopsy Lesionc. Prescribe: Nystatin Vaginal Tablets • Disp: 70 • Use: One Tablet as a Lozenge 5 Times a Day

  32. Candidiasis: Three RedChronic Oral Lesions • Angular Cheilitis = Perleche (Red) • Median Rhomboid Glossitis (Red) • Denture Sore Mouth = Atrophic Candidiasis (Red)

  33. Oral Hairy Leukoplakia • Rough, Hyperkeratotic, Patch • Opportunistic E-B Virus • HIV & Immunocompromised • Bilateral, Lateral Borders of the Tongue • Treatment: None or Acylovir • Disp: 60 Capsules • One Cap q.4h. for 5 to 10 days

  34. Syphilitic Mucous Patch • Painless, White, Mucosal Ulcers With . . . • Nonpruritic Skin Rash, Lymphadenopathy • Signs of Secondary Syphilis (T. pallidum)

  35. 6. Four Neoplastic White Lesions • Squamous Cell Carcinoma • Verrucous Carcinoma • Epithelial Dysplasia • Carcinoma in Situ

  36. Squamous Cell Carcinoma (SCC) • 90% of All Oral Malignancies = SCC • Mixed Red & White is Most Likely Presentation • Age: Elderly (40+) Gender: Males (2:1) • Location: Lower Lip, Floor of Mouth, Lateral & Ventral Tongue, Soft Palate

  37. Squamous Cell Carcinoma (SCC) • Uncontrolled Growth • “Up Regulation” of Oncogenes • Kinases & Cyclines Become Overactive • Deactivation of Suppresser Genes (Antioncogenes)

  38. Verrucous Carcinoma • Hyperkeratotic, Exophytic, Papillary • Age: Elderly (60+) Gender: Males (2:1) • Location: Gingiva, Alveolar Ridge, Buccal Mucosa

  39. Epithelial Dysplasia • Premalignanat Changes of Cell & Architecture • Mixed Red & White is Most Likely Presentation • Cell Alterations: Nuclear Changes • Architecture Alterations: Bulbous Rete Pegs

  40. Carcinoma in Situ (CIS) • Entire Thickness (Top to Bottom Change) • Basement Membrane Intact • No Invasion or Change of Connective Tissue

  41. Geriatrics • Proliferative Verrucous Leukoplakia (PVL) • Hyperkeratotic Lesions Mixed Smooth and Warty • Mainly on Edentulous Alveoloar Ridge • Cancer Risk: May Progress to SCC or VC

  42. Risk Factors / Predisposing Factors • Demographic (Age,Gender,Race) • Social (Alcohol, Tobacco, Oral Habits) • Recent History (*Trauma, *Infection, Surgery) (*Especially Chronic) • Medical History (Chronic Disease, Acute Illness, Medications,Treatments) (Especially: Diabetes, Organ Cancer, Antibiotics, Chemo)

  43. 3 Mechanisms: • Surface Material • Rough / Does Rub Off • Epithelial Thickening • Rough / Does NOT Rub Off • Subepithelial Change • Smooth / Does NOT Rub Off • TwoExamples: • Fordyce Granules = Ectopic Sebaceous Glands • Scar: Surgical, Traumatic

  44. Clues to Normal • Bilateral Symmetry • Predictable Locations • Asymptomatic • Independent Finding (no Secondary Features such as redness, swelling) • Increase with Age • Remains Unchanged w/ Treatment

  45. Glossary of Terms • Acanthosis: excessively thickened intermediate cell layer with broad and long rete pegs • Hyperkeratosis: excessively thickened keratin in stratum corneum • Leukoplakia: a white patch on the oral mucosa that cannot be scraped off and cannot be classified as any other disease

  46. Review: Which of the Following Choices Demonstrate Concepts of Differential Diagnosis: • List of Diseases With Similar Manifestations (Yes) • Oral Ulcer (No, monomorphic presentation) • Zinc Deficiency, Trauma, Herpes, Aphthous Lesion as Potential Etiologies for a Single Monomorphic Presentation. (Yes) • Rely Primarily on the Clinical Appearance (No, must include history, risk factors, visual inspection)

  47. List the Seven Primary Clinical Manifestations of Non-dental Lesions • Normal Variation • White • Red (Pigmented or Dark) • Ulceration • Exophytic • Radiographic • Syndrome

  48. List Four Techniques Employed to Investigate the Secondary Clinical Features of Oral Lesions: • Visual Inspection • Palpation • Probing • Patient Awareness

  49. Name at Least Four Visual Features to Inspect for When Examining an Oral Lesion: • Location • Shape & Contours • Size • Solitary/Multiple • Borders • Homogenous/Heterogeneous • Surface Color/Texture • Displacement (of Teeth?)

  50. During Palpation One Can Check For: • Compressible • Tender • Color Change (Blanching) • Mobile / Bound Down • Induration • Probing, Exudate

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