Premalignant lesions may expose to a promoting. factor & may be induced to undergo malignant. Carcinoma in situ displays the cytologic features of

Transcription

1 بسم رلاهللا

2 Def. Premalignant lesions may expose to a promoting factor & may be induced to undergo malignant transformation. Carcinoma in situ displays the cytologic features of malignancy without invasion of the basement membrane

3 Premalignant lesions include: 1. Leukoplakia 2. Candidal leukoplakia 3.Erythroplakia 4.Oral Submucous filrosis.

4 Leukoplakia

5 Definition It is a clinical term, and the lesion is defined as a white patch or plaque, firmly attached to the oral mucosa, that cannot be classified as any other disease entity. It is a precancerous lesion

6 Etiology The exact etiology remains unknown. predisposing factors 1.Tobacco 2.Alcohol 3.chronic local friction 4. Candida albicans 5. Human papilloma virus (HPV) 6.biting the cheek 7. rough, uneven teeth 8. dentures (especially if improperly fitted)

7 Clinical classification 1.Homogeneous (common) 2.Nodular leukoplakia 3. speckled (less common) 4. Proliferative verrucous (rare).

8 Clinical Features Site: mainly on buccal mucosa Features: uniformly white plaques Prognosis: Low malignant transformation potential

9

10

11 Features: 1.Small aggregated hemispherical red or white surface alterations 2. red background or substrate Prognosis Stronger risk of dysplasia or malignant potential than in homogeneous leukoplakia

12 Def. Regarded as a combination of or a transition between leukoplakia and erythroplakia. It is less common Clinical Features Site: buccal mucosa, tongue, floor of the mouth, gingiva S&S: 1.white flecks 2. fine nodules on an atrophic erythematous base Prognosis: Stronger malignant potential than homogeneous leukoplakia

13 Def. Diffuse white and /or papillary ( warty ) areas of the oral mucosa resulting from varying degrees of epithelial hyperplasia;has the potential to develop into verrucous carcinoma or well-differentiated.it is the least common type squamous cell carcinoma.

14

15 Prognosis: High risk of intervening dysplasia and carcinoma developing High rate of recurrence and histological progression toward carcinoma

16 epithelial dysplasia

17 Epithelial atrophy Cellular atypia Epithelial dysplasia Carcinoma in situ Reduction in the Atypia is A premalignant change The most severe stage of normal thickness of individual cellular in epithelium epithelial dysplasia, epithelium that changes in characterized by a involving the entire involves less than the dysplastic combination of cellular thickness of the entire thickness of epithelium which and architectural epithelium, with the the epithelium reflect alterations epithelial basement abnormalities in membrane remaining proliferation, intact. maturation, and differentiation of epithelial cells.

18

19

20 1.The histological appearances reflect varying degrees of keratosis 2.Changes in epithelial thickness 3.Epithelial dysplasia 4. Diffuse chronic inflammatory cell infiltration of varying severity in the lamina propria.

21 1. Nuclear and cellular pleomorphism (Nuclei and cells show different size and shape). 2. Increase in the nuclear/cytoplasmic ratio by either area or volume. 3. Nuclear hyperchromatism (Deeply stained Nucleus). 4. Prominent nucleoli. 5. Increased and abnormal mitoses. Mitoses may be increased in number, occur higher up in epithelium than is usual (i.e. away from the basal layer 6. Distributed polarity of the basal cells or loss of cellular orientation (The cells in the basal layer have no definable long axis and the nuclei have no regular polarity. 7. Basal cell hyperplasia. The presence of several layers of cells of basaloid appearance. 8. Drop-shaped rete pegs(the rete pegs are wider at their deeper part than they are more superficially). 9.Irregular epithelial stratification or distributed maturation. The cells no longer show a proper sequence of morphological and maturational changes as they pass from the basal layer to the surface. 10.Abnormal keratinization. Keratinization occurring below the normal keratin layer, either as individual cell keratinization with in the stratum spinosum or as disturbed maturation of groups of cells resulting in the formation of intraepithelial keratin pearls. 11-Loss or reduction of intercellular adhesion (or cohesion). This may be difficult to distinguish from intercellular oedema.

22

23

24

25 Types: 1.Mild epithelial dysplasia 2. Moderate epithelial dysplasia 3.Severe epithelial dysplasia

26 Alterations limited principally to the basal and parabasal layers.

27 Demonstrates involvement from the basal layer to the midportion of the spinous layer.

28 Demonstrates alterations from the basal layer to above midpoint of the epithelium.

29

30

31

32

33 Def. Carcinoma in situ is defined as dysplastic epithelial cells that extend from the basal layer to the surface of the mucosa " top to bottom" change. Histopathology 1.There may or may not be a thin layer of parakeratin on the surface. 2. The epithelium may be hyperplastic or atrophic. 3. the entire thickness of the epithelium is involved 4. No invasion has occurred despite the fact that a typical epithelial- cell look exactly like those of squamous cell carcinoma. 5. Keratin pearl formation is rare in carcinoma in situ and may indicate the presence of a focus of invasive squamous cell carcinoma

34

35

36

37 1.Leukoplakia is generally diagnosed with an oral exam. 2. During a physical exam, your dentist can confirm if the patches are leukoplakia. 3. Other tests may be needed to confirm the cause. 4. Biopsy ( A small tissue sample is sent to a pathologist for diagnosis. The goal is to rule out the possibility of oral cancer). D.D Oral thrush is a yeast infection of the mouth. The patches it causes are usually softer than leukoplakia patches. They may bleed more easily. With treatment, you may be able to prevent future patches from developing.

38 Erythroplakia

39 Erythroplakia Def. Red - patch that cannot be clinically or pathologically diagnosed as any other condition Etiology Clinical features 1.Unknown 2.epithelial dysplasia 3.Carcinoma in situ Age: older men (65-74) years old Site: floor of mouth, tongue, and soft palate S&S: 1. asymptomatic 2. well demarcated erythematous macule 3. plaque with a soft velvety texture. 4. associated with an adjacent leukoplakia ( erythroplakia). Histopathology 1.several epithelial dysplasia 2. carcinoma in situ 3.superficially invasive squamous cell carcinoma. 4.The epithelium shows a lack of keratin production and often is atrophic, but it may be hyperplastic. 5.This lack of keratinization, especially when combined epithelial thinness allows the underlying microvasculature to show through, thereby explaining the red color. 6.The underlying connective tissue often demonstrate chronic inflammation Differential Diagnosis 1.Non specific mucsitis 2. Candidiasis 3. Vascular lesions These lesions may clinically mimic Erythroplakia Biopsy is often required to distinguish between them

40 Oral submucous fibrosis

41 Oral submucous fibrosis Def. It is a chronic progressive, diffuse firm whitish areas of submucosal scarring usually caused by frequent and prolonged contact with betel nut quids,tobacco,or hot chili peppers; lesions have high-risk precancerous condition of the oral mucosa seen primarily on the Indian and in South East Asia. Etiology Clinical features Histopathology 1. tobacco 2. betel nut quids 3. hot chili peppers Site: buccal mucosa retromalar area, and the soft palate Age: young adult S&S:1. inability to open the mouth ( trismus ) 2, mucosal pain associated with spicy food. 3. The jaws may actually be inseparable in the advanced cases. 4. Vesicles, petachiae, melanosis, xerostomia 5. Generalized oral burning sensation are usually the first signs and symptoms. 6. The mucosa in these regions develops a blotchy marblelike pallor and a progressive stiffness of subepithelial tissues. 7. When the tongue is involved, it becomes rather immobile frequently diminished in size and often avoid of papillae. 1.submucosal deposition of extremely dense & a vascular collagenous connective tissue 2. variable numbers of chronic inflammatory cells. 3. Epithelial changes include hyperkeratosis with marked epithelial atrophy. 4. Epithelial dysplasia without carcinoma is found.

42

43

44

45

46

47

48 Chronic hyperplastic candidosis (candidal leukoplakia)

49 Chronic hyperplastic candidosis (candidal leukoplakia) A clinical form of C. albicans infection consisting of white plaques or papules against an erythematous background containing hyphae in the parakeratin layer of the thickened epithelium. Etiology 1.Tobacco 2. Smoking 3. Denture wearing 4. Occlusal friction Clinical features Site: Lesions are seen most frequently on the buccal mucosa to the commissure of the lips S&S: 1. Dense, opaque white patches of irregular thickness and density with a rough or nodular surface 2. They cannot be removed by scraping,but fragments may be detached & identification of hyphae in smears of such material assists in the diagnosis. 3. Speckled leukoplakia (areas fo erythematous mucosa are present within the plaque) 4. Roughly triangular 5. Often bilateral white plaques tapering posteriorly Histopathology.1.Parakeratinized epithelium 2. Markedly hyperplastic and acanthotic epithelium 3. Many of cells in tparakeratinizedd surface of epitheliums separated by oedema 4.Micro-abscesses from numerous neutrophil leucocytes 5. Candidal hyphae invade the parakeratin more or less at right angles to the surface, but never penetrate deeper into the prickle cell layers 6.Acute and chronic inflammatory cells innprickle cell layer 7. Mixed chronic inflammatory cell infiltrate lamina propria) 8. Areas of atrophic epithelium may be present within the lesion and in these areas the superficial layers of candida infected parakeratinnmay be missing which may be responsible for the erythematous appearance seen clinically

50 Thank you