Oral Epithelial Dysplasia Lecture Notes PDF

BDS10014 Oral Epithelial Dysplasia Aims: The aim of this lecture is to detail the histopathological aspects of oral epithelial dysplasia. Objectives: On completion of this lecture, the student should be able to: • Understand the clinical features of the different degrees of oral epithelial dysplas...

BDS10014 Oral Epithelial Dysplasia Aims: The aim of this lecture is to detail the histopathological aspects of oral epithelial dysplasia. Objectives: On completion of this lecture, the student should be able to: • Understand the clinical features of the different degrees of oral epithelial dysplasia and carcinoma-in-situ Oral potentially malignant disorders This is the current preferred term to describe the clinical presentations that carry a risk of cancer development in the oral cavity These lesions include: ▪Dyskeratosis congenita ▪Leukoplakia ▪Smokless tobacoo keratosis ▪Erythroplakia ▪Palatal lesions due to reverse ▪Actinic Cheilosis smoking (Actinic Cheilitis) ▪Chronic candidiasis ▪Oral submucous ▪Lichen planus fibrosis ▪Discoid lupus erythematosus ▪Syphilitic glossitis ▪Actinic keratosis Epithelial Dysplasia Definition •It is a histological term which means abnormal formation of epithelium (or any tissue). •These cytological abnormalities are seen in both malignant and premalignant lesions (How to differentiate between them????) •Dysplasia is usually graded as mild, moderate and severe. •About 5-18% of epithelial dysplasias become malignant. Abnormal mitosis 12 80 80 12 Unequal division Oral Epithelial Dysplasia Architectural changes Cytological changes Irregular epithelial stratification Abnormal variation in nuclear size Loss of polarity of basal cells Abnormal variation in nuclear shape Drop-shaped rete ridges Abnormal variation in cell size Increased number of mitotic figures Abnormal variation in cell shape Abnormally superficial mitoses Increased nuclear-cytoplasmic ratio Premature keratinization in single cells Atypical mitotic figures Keratin pearls within rete pegs Increased number and size of nucleoli Loss of epithelial cell cohesion Hyperchromasia Oral Epithelial Dysplasia Architectural changes Normal Oral Epithelial Dysplasia Normal Loss of polarity of basal cells Bulbous or teardrop shaped rete pegs. Oral Epithelial Dysplasia Individual cell keratinization Cell nest & keratin pearl formation Oral Epithelial Dysplasia Abnormal mitosis [site, rate, shape] Normal mitosis Oral Epithelial Dysplasia Increased number and size of nucleoli Increased nuclear-cytoplasmic ratio Hyperchromasia Abnormal variation in nuclear & cellular size & shape Grading of epithelial dysplasia Dysplasia is usually graded (according to the degree of epithelial involvement): 1. Mild epithelial dysplasia seen in lower 1/3 of the epithelium (alterations limited to the basal and parabasal layers) 2. Moderate epithelial dysplasia involves at least half the epithelium 3. Severe epithelial dysplasia (carcinoma in situ) involves most of the epithelium thickness (top to bottom changes). Grading of epithelial dysplasia Mild dysplasia Mild dysplasia Moderate dysplasia Moderate dysplasia Severe dysplasia Severe dysplasia Etiology Extrinsic factors Intrinsic factors 1. Tobacco (smoked or smokeless) • Cigarette, cigar, pipe smoking is the primary risk factor for oral potentially malignant disorders and oral cancer. This is due to the effect of chemical constituents of tobacco, and its combustion end products (tar) [which are carcinogens] in addition to heat generated by smoking Tobacoo [benzpyrenes & benzanethracene combustion Epoxides [partial oxidation] ❖Nicotine is the addictive agent and is not by itself carcinogenic 2. Alcohol Tobacco and alcohol combination may represent an example of co-carcinogens working synergistically It affects the liver, thus decreasing its efficiency in detoxification of carcinogenic material Alcohol increases permeability of mucosa to carcinogens 3. Actinic radiation Ultraviolet radiation increases risk of actinic cheilitis as well as leukoplakia of the lower lip causing characteristic mutations in the cellular DNA. 4. Chronic infections ▪Several viruses such as HPV. ▪Less commonly, candida albicans & syphilis Candidal leukoplakia Syphilis 5. Nutritional deficiency Iron deficiency anemia especially the severe chronic form known as Plummer- Vinson or Paterson- Kelly syndrome affects the integrity of the epithelium resulting in atrophic oral mucosa which is more susceptible to the effects of extrinsic factors [general malnutrition may cause atrophy of mucosa] . ➢Leukoplakia Definition • This is a clinical term denoting white plaque or patch on oral mucosa that can not be rubbed off and can not be characterized clinically as any other disease”. ❖ The term is strictly a CLINICAL one and does not imply a specific histopathologic tissue alteration. ➢Leukoplakia Clinical features Site: Buccal mucosa and alveolar mucosa. 2.Tongue and lip. 3.Hard and soft palate. 4.Floor of the mouth. 5.Gingiva. Appearance: Lesions usually appear as tough and adherent plaques, slightly raised The surface is irregular, graywhite in colour. Clinical appearance of leukoplakia Mild or thin leukoplakia [soft flat, translucent, grey/white plaques] Thick or fissured leukoplakia [leathery, showing deep fissures Granular or nodular leukoplakia [showing surface irregularities] Verrucous or verruciform leukoplakia [showing surface projections] Proliferative verrucous leukoplakia appear as nodular, papillary or verruciform surface projections Speckled Leukoplakia [showing red patches (erythroplakia ❖Among the clinical variants of leukoplakia, proliferative verrucous leukoplakia and speckled Leukoplakia exhibit higher risk for malignant transformation ❖Proliferative verrucous leukoplakia is a distinct and aggressive form of oral potentially malignant disorder. It is multifocal, has progressive course and high recurrence ❖ Speckled Leukoplakia in which epithelial cells are immature, atrophic and can no longer produce keratin Histological features 1. Intact basement membrane 2. Thickened surface keratin 3. Thickened prickle cell layer (acanthosis) 4. Criteria of epithelial dysplasia [5 to 25 % of the cases show epithelial dysplasia] Treatment ➢ Avoid the causative factors ➢ Excision ➢ Follow up These features masks the underlying vascularity & cause white colour of leukoplakia Clinical differential diagnosis candidiasis [can be rubbed off] chronic cheek biting, frictional keratosis, [chronic trauma] lichen planus white sponge nevus hairy leukoplakia geographic tongue [migratory] ➢Erythroplakia Definition Erythroplakia is a flat red patch that can’t be attributed to any other condition ➢40% of lesions show malignant transformation Clinical features ❑Common sites: floor of mouth, tongue & soft palate ❑Appears as red macule or plaque with well demarcated borders ❑Its texture is soft & velvety ❑Flat or depressed Histological features 1. Severe epithelial dysplasia 2. Intact basement membrane 3. Absence of keratin 4. epithelium is often atrophic so, allows the underlying blood vessels to show through and result in the red appearance Clinical differential diagnosis candidiasis Vascular lesions mucositis Psoriasis (geographic tongue ) ➢Actinic cheilitis (solar cheilitis) Definition A form of cheilitis in which there is accelerated tissue damage of the vermilion of the lips, especially the lower lip, as a result of chronic exposure to sunlight. It occurs more common in ❑older males (above 45) ❑in individuals with a light complexion (fair skin) ❑individuals with outdoor occupations ➢Actinic cheilitis (solar cheilitis) Clinically ❑ The lesion develops so slowly that patients are often unaware of change. There is a history of chronic sun exposure. ❑ There is atrophy, dryness and fissuring of the vermillion border. ❑ The vermilion-skin junction is poorly defined (blurring). ❑ The lip may become scaly and indurated and may be ulcerated ➢Actinic cheilitis (solar cheilitis) Histopathology ❑ Hyperkeratosis. ❑ Atrophy of the epithelium (decrease in thickness of prickle cell layer.) ❑ Varying degrees of epithelial dysplasia may be seen. ❑ Intact basement membrane. ❑ The underlying connective tissue demonstrates a band of amorphous acellular, basophilic change (altered elastin that replaces normal collagen) known as solar (actinic) elastosis. ➢Nicotine Stomatitis Definition Nicotine stomatitis is a common tobacco-related form of keratosis of the hard palate. Etiology ❑It is typically associated with pipe and cigar smoking [little risk of malignant transformation in palate] ❑The combination of tobacco carcinogens and heat is markedly intensified in reverse smoking (lit end positioned inside the mouth), adding a significant risk for malignant conversion ➢Nicotine Stomatitis Clinically ❑The palatal mucosa becomes diffusely gray or white ❑Palatal keratin may be so thickened and impart fissured or dried mud appearance ❑Red dots surrounded by white keratotic rings appear [dots represent inflammation of the salivary gland and its duct] ➢Nicotine Stomatitis Histopathology ❑Epithelial hyperplasia and hyperkeratosis. ❑Inflammatory changes in minor salivary glands. Prognosis ❑It is completely reversible, the palate usually returns normal within 1 or 2 weeks after discontinuation of tobacco habit. ❑Little risk of malignant transformation in palate except for “reverse smokers” ➢Oral submucous fibrosis Definition It is a high risk precancerous condition characterized by chronic progressive scarring of the oral mucosa • Common in Asian communities specially in India Etiology & pathogenesis •Areca nut betel quid chewing [fibrosis is induced by areca nut as it causes disruption of collagen metabolism, epithelial alteration and carcinogenesis result mainly from tobacco] •Ingestion of chilies ➢Oral submucous fibrosis Clinical features ❑ Inability to open the mouth (trismus) ❑ Oral burning sensation ❑ Xerostomia ❑ the mucosa develops marble-like pallor (appear white) with progressive stiffness ❑ Vesicles, petechiae may be seen ❑ Tongue may become immobile, diminished in size and devoid of papillae Histopathological features ❑ Juxta epithelial and submucosal deposition of densely collagenized, hypovascular connective tissue ❑ Chronic inflammatory cells ❑ Signs of epithelial dysplasia are seen in 10 to 15% of cases ❑ Intact basement membrane Prognosis It doesn’t regress with habit cessation Key points ▪ Oral potentially malignant disorders are the clinical presentations that carry a risk of cancer development in the oral cavity ▪ OPMD may show signs of epithelial dysplasia such as leukoplakia and erythroplakia ▪ OPMD may not show signs of epithelial dysplasia such as chronic candidiasis and lichen planus ▪ Signs of epithelial dysplasia are divided into architectural and cytological changes ▪ Nicotine Stomatitis is completely reversible, the palate usually returns normal within 1 or 2 weeks after discontinuation of tobacco habit Aims: The aim of this lecture is to detail the histopathological aspects of oral epithelial dysplasia. Objectives: On completion of this lecture, the student should be able to: • Understand the clinical features of the different degrees of oral epithelial dysplasia and carcinoma-in-situ Reading material: Students are advised to review any relevant teaching provided in the first year. In addition they are advised to read relevant sections of the following texts: • Robinson M et al. Soames’ and Southam’s Oral Pathology. 5th edition. Oxford University Press, 2018 pp 77-84 • Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 299-316 • Gandolfo S, Scully C, Carrozzo M. Oral Medicine, Churchill Livingston, 2006 pp 74 • Felix D, Luker J, Scully C. Oral Medicine: Update for the Dental Team, Dental Update Books 2015 pp 45-48 • Scully C. Oral and Maxillofacial Medicine, Churchill Livingstone 2008 pp 211-224 Thank you