(4) Keratoses and Related Disorders of Oral Mucosa I
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Transcript of (4) Keratoses and Related Disorders of Oral Mucosa I
Dent 355-10Keratoses and Related
Disorders of Oral Mucosa I
IntroductionClassificationDefinition of histopathologic termsHereditary conditionsTraumatic keratosesLeukoplakiaDermatological causes of white patches
Introduction:Normal Oral Mucosa
• Color of normal oral mucosa: vascularity, melanin, epithelial thickness, keratinization.
• Non-keratinized parts.
• Non-keratinized parts.
Introduction: White Patches
• White patches may be due to increased or abnormal production of keratin which appears white in the wet oral environment: they cannot be scraped off.
• Accumulation of debris and desquamated cells on oral mucosa may also result in white areas: can be scraped off.
Etiological Classification of White Oral Lesions
HereditaryOral epithelial nevus
Oral manifestations of other rare
genodermatoses
Leukoedema
TraumaticMechanical (frictional keratosis)
Chemical
Thermal
InfectiveCandidosis:
- acute psuedomembranous
- chronic hyperplastic
- chronic mucocutaneous
Syphilitic leukoplakia
Hairy leukoplakia
IdiopathicLeukoplakia
DermatologicalLichen planus
Lupus erythematosus
NeoplasticCarcinoma in situ
Squamous cell carcinoma
Definition of Histopathological Terms
• Orthokeratosis: superficial keratinized squames are flattened, anucleate, with homogeneous, acidophilic cytoplasm.
• Parakeratosis: superficial keratinized squames are flattened, with homogeneous, acidophilic cytoplasm, but contain pyknotic nuclei.
• Hyperkeratosis: increased thickness of keratin layer.
• Hyperparakeratosis: increased thickness of parakeratin layer.
• Keratosis: keratinization of epithelium that is not normally keratinized.
Definition of Histopathological Terms
• Acanthosis: hyperplasia of prickle cell layer which results in overall increased thickness of epithelium, with broadened, elongated rete ridges.
• Epithelial atrophy: decreased epithelial thickness usually associated with loss of rete ridges.
• Cellular atypia: a group of cellular changes which cytologically characterize dysplasia and which are typically seen in premalignant lesions.
• Epithelial dysplasia: a term describing epithelium when features of cellular atypia are present.
* Atypia refers to cells, while dysplasia refers to the tissue as a whole.
Hereditary Conditions (Genodermatoses): Oral Epithelial Nevus (White Sponge Nevus)
• Autosomal dominant with incomplete penetrance and variable expressivity.
• Mutations in genes coding for keratins 4 & 13.
• Abnormality in desquamation.
• Benign condition with no consequences other than altered appearance of mucosa.
• Any part of oral mucosa may be affected, as well as other mucosal surfaces in the body.
• Edges not well-defined.
• Shaggy or folded appearance.
• May appear in infancy, childhood, or adolescence.
• Histopathology:- Acanthosis.- Hyperparakeratosis.- Intracellular edema of prickle and parakeratinized cell layers.- Pyknotic nuclei impart basketweave appearance.
Hereditary Conditions (Genodermatoses):Leukoedema
• Particularly evident in persons with racial pigmentation of oral mucosa.
• Ethnic and racial clustering suggest hereditary factors.
• Regarded as a variant of normal.
• Presents as a translucent, milky whiteness of the surface of the mucosa with a slightly folded appearance.
• It tends to disappear on stretching.
• Histology:- Acanthosis with broadened rete ridges.- Superficial prickle cells appear vacuolated
and contain glycogen.
Traumatic Keratoses:Mechanical Trauma-Frictional Keratosis
• Acute friction may lead to blistering and ulceration.
• Chronic friction leads to epithelial thickening and hyperkeratinization known as frictional keratosis.
• Frictional keratosis may result from: sharp tooth, chronic cheek biting, prolonged wear of ill-fitting dentures.
• To diagnose frictional keratosis a source of chronic irritation that fits the size and shape of the lesion must be identified. Lesion must resolve upon removal of the source.
• Histopathology: - Hyperkeratosis +/- acanthosis.- There is no dysplasia.
Traumatic Keratoses: Chemical
• Severe chemical insult to oral mucosa produces epithelial necrosis, sloughing & ulceration, e. g. Aspirin burn.
• Low grade, chronic insult is seen in tobacco users, whether it is smoked, chewed, or used as snuff. Also in other chewing habits such as betel nut.
Traumatic Keratoses: Thermal
• Generalized hyperkeratosis is seen is smokers of cigarettes, cigars, and pipes, particularly anterior buccal mucosa, tongue & palate.
• Combination of thermal and chemical factors likely.
• Localized keratosis on lips at site of cigarette may be seen with constant use, also on palate and dorsal tongue in pipe smokers.
Traumatic Keratoses: Thermal-Nicotinic Stomatitis
• A characteristic palatal condition seen in smokers, particularly in pipe smokers.
• Characterized by hyperkeratinized palatal mucosa with a cobblestone appearance, with inflamed orifices of minor salivary gland ducts showing as red dots centrally.
• Condition is reversible upon cessation of smoking and is not considered premalignant.
• However, in smokers, the presence of these conditions indicates the potential for abnormal changes that may be premalignant, therefore the whole mouth should be examined carefully for other lesions.
• Histopathologic Features:- Hyperkaratinized and acanthotic squamous
epithelium.- Mild chronic inflammation of subepithelial
connective tissue and mucous glands.
Leukoplakia
•Leukoplakia = white patch.
•WHO original definition: "a white patch which cannot be characterized clinically
or histopathologically as any other disease."
•Definition slightly modified in 1994 to: "a predominantly white lesion of the oral
mucosa that cannot be characterized as any other definable lesion ."
Leukoplakia
• Leukoplakia is a clinical diagnosis arrived at by exclusion of other white lesions.
• It implies no particular histopathologic change or behavior.
• However, a small percentage are premalignant and some may be invasive carcinomas at presentation.
• It is impossible to predict which lesions are likely to become malignant, but certain clinical and histopathological features are recognized as being associated with an increased risk.
Leukoplakia: Incidence• Worldwide variation from <1%->10%.
• Problems in comparison due to difficulties in standardization of diagnostic criteria.
• Marked variation in incidence, sex, site, and age groups affected between different cultural and ethnic groups, reflecting variations in possible etiological factors.
• Leukoplakias involving ventral tongue and/or FOM (sublingual keratosis) have a higher risk of malignant transformation.
• Previous studies in Western Europe & North America: - predominance in males - generally described as affecting older people- FOM & buccal mucosa mostly affected.
• Recent studies in the same areas indicate that:- M:F ratio is becoming almost equal- incidence in younger adults is increasing- this possibly reflects changes in smoking habits.
Leukoplakia: Clinical Features
• Homogeneous- flat, uniform, predominantly white
plaques- may show shallow cracks/fissures
• Non-homogeneous (including speckled)
- irregular nodular/thickened, sometimes verrucous surface.
- often speckled with areas of erythroplakia.
• Non homogeneous lesions have a worse prognosis.
Leukoplakia: Clinical Features
• Erythroplakia: "a bright red velvety plaque on the oral mucosa which cannot be categorized clinically or pathologically as being due to any other condition".
• Erythroplakia: - may be homogeneous with a well-defined
but irregular outline- or may be intermingled with patches of
leukoplakia (speckled leukoplakia)- histopathologically, erythroplakia may
represent carcinoma-in-situ or invasive carcinoma.
- its development in a previously uniform white lesion is an important clinical sign which may indicate sinister change.
Leukoplakia: Clinical Features
• Clinical features that may indicate malignant change in leukoplakia/erythroplakia:
1. development of erythroplakia in a previously uniform white lesion
2. fixation3. induration4. ulceration5. lymphadenopathy6. bone destruction if it overlies bone7. other clinical features of
malignancy.
Leukoplakia: Etiological Factors
• Leukoplakia is by definition idiopathic, but in some patients, predisposing factors can be identified.
• Etiology is likely to be multifactorial
• Tobacco use is a major factor.
Leukoplakia: Etiological Factors
1. Tobacco
• The most common factor in patients with leukoplakia.
• Higher prevalence of leukoplakia among smokers.
• Prevalence increases with amount of tobacco.
• Distribution of lesions may vary with particular type of habit: cigarettes, bidis, reverse smoking, tobacco chewing, pans, snuff dipping.
• In those patients whose tobacco-associated keratosis regresses on cessation of the habit the lesion should not be classified as leukoplakia.
• Smoked tobacco.
• Smokeless tobacco: areca nut (betel nut), chewing tobacco and snuff.
Leukoplakia: Etiological Factors
2. Alcohol:
No clear evidence for importance as a factor.
Many heavy smokers however are also heavy drinkers.
3. Candida:
• Candidal leukoplakia (chronic hyperplastic candidosis).
• May be associated with idiopathic leukoplakia.
Leukoplakia: Etiological Factors
4. Viruses: • HPV: type 16 & 18, uncertain role.
• EBV: hairy leukoplakia, completely different lesion, no premalignant potential.
5. Oral Epithelial Atrophy:
• Iron deficiency.
• Submucous fibrosis.
• Tertiary syphilis.
• Some vitamin deficiencies.
• Sideropenic dysphagia (Plummer-Vinson syndrome).
Leukoplakia: Etiological Factors
6. Tumor-Suppressor Genes: • Mutations in tumor suppressor genes, mainly p53.
7. Sanguinaria canadensis:
• The common bloodroot plant Sanguinaria canadensis has been used since 1982 and found to be effective against plaque build up and gingivitis.
• Sanguinaria-associated leukoplakia is a unique form of oral leukoplakia attributed to the chronic use of oral rinses and toothpastes containing the extract of the plant.
• It is usually located on the attached gingiva and the alveolar mucosa of the maxillary vestibule.
• Preparations containing Sanguinaria should be avoided until the risk for malignant transformation is determined.