3rd lecture



5-Idiopathic leukoplakia
Defined by the World Health Organization {WHO} as : "A white patch that cannot be characterized clinically or pathologically as any other disease ." N.B. Leuko = white ; plakia = patch

 The term is strictly a clinical one & does not imply a specific histopathologic tissue alteration  The diagnosis depend on the exclusion of other entities that appear white  It is considered a premalignant lesion because : The frequency of transformation into malignancy is greater than the risk associated with normal mucosa Etiology The cause of leukoplakia remains unknown but hypothesis abound {exist} Many cases are related to: 1. Tobacco use 2. Alcohol abuse 3. Chronic irritation 4. Nutritional deficiency 5. Sun light or actinic radiation

Clinical features Age : middle aged & older population Site : may occur anywhere on the oral cavity  Mandibular buccal mucosa account for almost half of the leukoplakias  The floor of the mouth & the ventral surface of the tongue account for a relatively small percentage but they account for the high malignant potential Leukoplakic lesions are classified according to the surface texture into : 1-Homogeneous leukoplakia : • White plaque on a base of uninflammed , normal appearing tissue with smooth or wrinkled surface

2 -Speckled leukoplakia : • White flecks or fine nodules on an atrophic base • It can be regarded as a combination between leukoplakia & erythroplakia • Spekled lesions show dysplasia more than lesions with a homogeneous surface 3- Proliferative verrucous leukoplakia • This type begins as a simple keratosis & eventually becomes verrucous in nature • It is persistent • Multifocal • Has the potential to recur • Some may be associated with HPV • Malignant transformation to verrucous carcinoma or squamous carcinoma has been reported in 15% of the cases

Histopathologic features : Histologic changes varies from hyperkeratosis, dysplasia , & carcinoma in situ to invasive carcinoma 1. Hyperkeratosis :{hyperorthokeratosis or hyperparakeratosis or a combination of both } with or without acanthosis 2. Dysplasia : indicates abnormal epithelium & disordered growth .Dysplasia is graded as mild, moderate & severe • Mild epithelial dysplasia refers to alteration limited to the basal & parabasal layers • Moderate demonstrates involvement from basal layer to mid portion of the prickle cell layer • Severe epithelial dysplasia demonstrates involvement from the basal layer to a level above the midpoint of the epithelium

3. Carcinoma in situ : the most severe dysplasia where abnormalities extend throughout the thickness of the epithelium • Carcinoma in situ spreads in a lateral direction 4. Invasive carcinoma : begins when a focus of epithelial cell invades the lamina propria 1 to 2mm beyond the basal lamina

Features of dysplastic epithelial cells 1) Enlarged nuclei & cells 2) Large &prominent nucleoli 3) Pleomorphic nuclei & cells {abnormally shaped} 4) Increases nuclear cytoplasmic ratio 5) Hyprchromatic nuclei {excessively dark staining nuclei} 6) Dyskeratosis {premature keratinization of individual cells } 7) Increased mitotic activity{excessive number of mitosis } 8) Abnormal mitotic figures{ tripolar or star-shaped Features of dysplastic epithelium which are evident at low power magnification 1)Bulbous or teardrop-shaped rete ridges & basal cells hyperplasia

normal 2) 3) 4) Loss of polarity{lack of progressive maturation towards the surface} Keratin or epithelial pearl {focal, round collections of concentrically layered keratinized cells} Loss of epithelial cell cohesiveness

Differential diagnosis: White lesions which can be removed by a gauze or tongue blade 1. Pseudomembraneous candidiasis 2. Thermal burn 3. Chemical burn 4. White furred tongue White lesions which are not removable 1. Leukoplakia 2. Tobacco keratosis 3. Leukodema 4. Lichen planus 5. Nicotinic stomatitis 6. hairy leukoplakia 7. white spongy nevus White lesions showing bilateral distribution 1. Hereditary conditions 2. Cheek chewing 3. Lichen planus 4. Lupus erythematosus White lesions with cutaneous lesions 1. Lichen panus 2. Lupus erythematosus

Premalignant lesions of the oral mucosa Premalignant lesion is a morphologically altered tissue that has a great risk than normal tissue for malignant transformation Premalignant lesions include : 1. 2. 3. 4. N.B.  Toluidine blue is a stain used to detect the premalignant lesions  It stains the premalignant lesions in blue Idiopathic Leukoplakia Candidal leukoplakia Erythroplakia Oral epithelial atrophy

Definition Erythroplakia is a clinical term that refers to a red patch on the oral mucosa which cannot be attributed, clinically or microscopically, to any other diagnosable disease

Etiology : The causes of this lesion are the same to those of oral cancer  Tobacco has a significant role in the induction of many of these lesions  Alcohol  Nutitional difficiency  And other factors may also have modifying roles

Clinical features Age : between 50 & 70 years Common sites : the floor of the mouth & the ventral surface of the tongue  Bright red plaque of velvety texture  Homogeneous irregular outline  Focal white areas representing keratosis intermingling the red patches speckled leukoplakia Histopathologic features  40% of erythroplakias shows severe dysplastic changes or carcinoma in situ  50% of the cases are squamous carcinoma  A relative reduction in keratin production & relative increase in vascularity account for the red color of these lesions

Differential diagnosis A differential diagnosis should include :  Kaposi s sarcoma  Contact allergic reaction  Vascular malformation Treatment : Surgical excision is the treatment of choice

Oral epithelial atrophy
Conditions which predispose to oral epithelial atrophy 1. Plummer-Vinson syndrome {Patterson-kelly syndrome} 2. Submucous fibrosis

1-Plummer-Vinson syndrome
It is a condition characterized by : 1. Iron deficiency anemia 2. Post-cricoid carcinoma 3. Oral manifestations i. Glossitis &dysphagia ii. Burning sensation in the tongue &oral mucosa iii. Severe angular cheilitis iv. Marked atrophy of the lingual papillae producing smooth red appearance of the dorsal tongue surface

2-Oral submucous fibrosis Etiology :
1. Chronic exposure to chilly peppers 2. Frequent chewing of betel nut 3. Chronic & prolonged deficiency of iron &B-complex vitamin , especially folic acid Such factors alter the oral mucosa & increases the hypersensitivity to many potential irritant such as dietary spices & tobacco with an inflammatory reaction & fibrotic response

Clinical features

1. Age : 20 to40 years 2. Occurring almost exclusively in Indians 3. Site : the soft palate & the buccal mucosa but may extend into the pharynx& oesophagus 4. The affected mucosa loses its resilience & elasticity with resultant trismus & difficulty in eating

Treatment and prognosis Includes elimination of the causative factor Intralesional injections of steroids The primary importance of submucous fibrosis relates to its reported premalignant nature The development of squamous cell carcinoma has been noted in one third of the affected patients

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