1. What’s Neoplasm?
1.1. abnormal mass of tissue, the growth of which exceeds, is independent of and uncoordinated with that of the normal tissues and continues in the same manner after cessation of the stimuli, which have initiated it.
2. Classifications
2.1. Odontogenic
2.1.1. Epithelium
2.1.1.1. Benign
2.1.1.2. Malignant
2.1.2. Mesenchymal
2.1.2.1. Benign
2.1.2.2. Malignant
2.1.3. Mixed
2.1.3.1. Benign
2.1.3.2. Malignant
2.2. Non Odontogenic
2.2.1. Epithelium
2.2.1.1. Benign
2.2.1.1.1. Squamous papilloma
2.2.1.1.2. Verruca vulgaris
2.2.1.1.3. Focal epithelial hyperplasia
2.2.1.1.4. Keratoacanthoma
2.2.1.1.5. Pigmented cellular nevus
2.2.1.2. Malignant
2.2.1.2.1. Squamous cell carcinoma
2.2.1.2.2. Basal cell carcinoma
2.2.1.2.3. Verrucous carcinoma
2.2.1.2.4. Malignant melanoma
2.2.2. Mesenchymal
2.2.2.1. Benign
2.2.2.2. Malignant
3. POTENTIALLY MALIGNANT DISORDERS (PREMALIGNANT LESIONS AND CONDITIONS)
3.1. Definition
3.1.1. Precancerous Lesion: A morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart
3.1.1.1. Examples
3.1.2. Precancerous Condition: A generalized state associated with a significantly increased risk for cancer
3.1.2.1. Examples
3.2. LEUKOPLAKIA
3.2.1. Most common oral precancerous lesion
3.2.2. Leuko= white; Plakia= patch
3.2.3. Definition
3.2.3.1. white patch or plaque that cannot be characterized clinically or pathologically as any other lesion
3.2.3.2. Cannot be scraped off (NON-SCRAPABLE)
3.2.4. Etiology
3.2.4.1. Tobacco: smoking, smokeless
3.2.4.2. Alcohol
3.2.4.3. Sanguinaria
3.2.4.4. UV radiation
3.2.4.5. Microorganisms: Candida, Treponema pallidum, HPV
3.2.4.6. Trauma: frictional keratosis, cheek biting, ill fitting dentures etc
3.2.5. C/F
3.2.5.1. > 40yrs
3.2.5.2. Male predilection
3.2.5.3. Site
3.2.5.3.1. Lip vermilion, buccal mucosa, gingiva, floor of mouth
3.2.5.4. Types
3.2.5.4.1. Mild/ thin
3.2.5.4.2. Homogenous/ thick
3.2.5.4.3. Granular leukoplakia
3.2.5.4.4. Verrucous leukoplakia
3.2.5.4.5. Proliferative verrucous leukoplakia (PVL)
3.2.5.4.6. Speckled leukoplakia
3.2.6. H/P
3.2.6.1. Hyperkeratosis: para/ Ortho
3.2.6.2. Acanthosis
3.2.6.3. Atrophy/ Hyperplasia
3.2.6.4. Variable chronic inflammatory cells
3.2.6.5. Most leuloplakias not dysplastic
3.2.6.6. 5%-25% malignant transformation
3.2.6.7. PVL - variable appearance
3.2.6.7.1. Papillary exophytic - verrucous leukoplakia
3.2.6.7.2. Down growth of WD epith, blunt rete ridges
3.2.6.7.3. Invasion - less WDSCC
3.2.6.8. Section
3.2.7. Dysplasia?
3.2.8. DIFFERENTIAL DIAGNOSIS: -
3.2.8.1. Lichen planus
3.2.8.2. Candidiasis
3.2.8.3. OSMF
3.2.8.4. Tobacco pouch keratosis
3.2.8.5. Lupus erythematosus
3.2.8.6. Frictional keratosis
3.2.8.7. White sponge nevus
3.2.8.8. Leukoedema
3.2.8.9. OSCC
3.3. ERYTHROPLAKIA
3.3.1. Synonym - Erythroplasia, Erythroplasia of Queyrat
3.3.2. Precancerous lesion, greater malignant transformation than leukoplakia
3.3.3. Definition
3.3.3.1. Red patch that cannot be clinically or pathologically diagnosed as any other condition
3.3.3.2. Significant dysplasia, Ca in situ, invasive SCC
3.3.3.3. May occur in conjunction with leukoplakia or early invasive Ca
3.3.4. C/F
3.3.4.1. Age & sex incidence - Older males, 65-70 yrs
3.3.4.2. Site - Floor of mouth, tongue, soft palate
3.3.4.3. Signs & symptoms -
3.3.4.3.1. Multiple lesions
3.3.4.3.2. Well demarcated erythematous macule/ plaque, soft velvety texture
3.3.4.3.3. Asymptomatic, associated with adjacent leukoplakia
3.3.4.3.4. D/D: mucositis, candidiasis, psoriasis, vascular lesions
3.3.5. H/P
3.3.5.1. 90% lesions severe dysplasia/ Ca in situ/ invasive Ca
3.3.5.2. Epithelium: lack of keratin production, atrophic/ hyperplastic
3.3.5.3. CT: chronic inflammation
3.4. ORAL SUBMUCOUS FIBROSIS (OSMF)
3.4.1. Definition
3.4.1.1. Chronic mucosal condition affecting any part of the oral mucosa
3.4.1.2. characterized by mucosal rigidity of varying intensity
3.4.1.3. due to fibro-elastic transformation of the juxtaepithelial connective tissue layer
3.4.1.4. Chronic, progressive, scarring, high risk precancerous condition of oral mucosa. Indian subcontinent, South East Asia
3.4.2. Etiology
3.4.2.1. Assoc. with chewing betel (areca) nuts.
3.4.2.2. Areca nut + slaked lime + tobacco => Epithelial alterations + carcinogenesis.
3.4.2.3. Sub-mucosal change: areca nut (arecholine)
3.4.2.4. Nutritional deficiency - increase fibrosis
3.4.2.5. Genetic predisposition
3.4.3. C/F
3.4.3.1. Age&sex Young males with betel nut habit
3.4.3.2. Site
3.4.3.2.1. Buccal mucosa, retromolar area, soft palate.
3.4.3.3. Signs & symptoms:
3.4.3.3.1. Initial
3.4.3.3.2. Later
3.4.3.3.3. Advanced
3.4.3.3.4. Inter incisal distance < 20 mm - severe
3.4.3.3.5. Sub-mucosal fibrous bands palpable on buccal mucosa, soft palate, labial mucosa
3.4.3.3.6. Surface leukoplakia noted.
3.4.3.3.7. Tongue if involved -immobile, diminished in size, devoid of papillae.
3.4.3.3.8. Mutation of fibroblasts: production of abnormal collagen which cannot be degraded
3.4.4. H/P
3.4.4.1. Early
3.4.4.1.1. Sup epith vesicles
3.4.4.2. Advanced
3.4.4.2.1. Oral epi atrophic+ hyperkeratosis+ complete loss of rete ridges
3.4.4.3. Epithelial atypia may be present
3.4.4.4. Underlying CT - severe hyalinization with homogenization of collagen bundles
3.4.4.5. Decrease number of fibroblasts, blood vessels completely obliterated/ narrowed
3.4.4.6. Variable infiltration of inflammatory cells in CT
4. MALIGNANT EPITHELIAL NEOPLASMS
4.1. SQUAMOUS CELL CARCINOMA
4.1.1. Introduction
4.1.1.1. 50% cases usually die within 3 years of diagnosis
4.1.1.2. Older age group 55-65 yrs
4.1.1.2.1. More in males
4.1.1.3. Racial predilection: more in African American men & people of Indian subcontinent.
4.1.2. Etiology
4.1.2.1. Extrinsic factors
4.1.2.1.1. Tobacco
4.1.2.1.2. Alcohol
4.1.2.1.3. Sunlight (Ca of lip vermilion), X-irradiation
4.1.2.1.4. Microorganisms: Candida albicans, oncogenic viruses, Treponema pallidum
4.1.2.2. Intrinsic factors
4.1.2.2.1. Nutritional Deficiency: Iron, Vit A
4.1.2.2.2. Immunosuppression
4.1.2.2.3. Oncogenes and tumour suppressor genes
4.1.3. C/F
4.1.3.1. Age incidence: 5th – 6th decades
4.1.3.2. Sex incidence : more in males
4.1.3.3. Site
4.1.3.3.1. Floor of mouth Soft Palate Gingiva Buccal mucosa Labial mucosa Hard palate
4.1.3.4. Signs & symptoms -
4.1.3.4.1. Pain rare (delay in seeking professional care)
4.1.3.4.2. Varied clinical presentation:
4.1.4. RADIOLOGICAL FEATURES: -
4.1.4.1. If underlying bone is involved: moth eaten radiolucency
4.1.5. METASTASIS
4.1.5.1. Lymphatic spread to ipsilateral lymph nodes
4.1.5.2. Lymph node with metastatic deposit - firm, fixed, stony hard, non tender & enlarged
4.1.5.3. Occasional contralateral and bilateral metastatic deposits
4.1.5.4. Distant metastasis (below clavicles): breast, lungs, bones, prostate
4.1.6. STAGING: -
4.1.6.1. Prognosis depends on tumor site, extent of metastatic spread
4.1.6.2. Tumor-node-metastasis (TNM) System
4.1.6.2.1. T - size of primary tumor in cm
4.1.6.2.2. N - involvement of local lymph nodes
4.1.6.2.3. M - distant metastasis
4.1.7. H/P
4.1.7.1. Arises from dysplastic surface epithelium
4.1.7.2. Invasive islands and cords of malignant squamous cells
4.1.7.3. Strong inflammatory / immune response to invading tumor cells
4.1.7.4. Tumour cells =>
4.1.7.4.1. Abundant eosinophilic cytoplasm, large hyperchromatic nuclei
4.1.7.4.2. Increased N/C ratio
4.1.7.4.3. Varying degrees of cellular pleomorphism
4.1.7.4.4. Keratin pearls, individual cell keratinization
4.1.7.5. Low grade / Well differentiated SCC
4.1.7.5.1. Mature cells, resemble tissue of origin, slow growing, metastasize late
4.1.7.6. High grade / Poorly differentiated SCC
4.1.7.6.1. Much cellular and nuclear pleomorphism
4.1.7.6.2. Immature cells, do not resemble tissue of origin
4.1.7.6.3. Rapid growth, early metastasis
4.1.7.7. Moderate differentiated SCC:
4.1.7.7.1. Features intermediate betn well & poorly differentiated SCC.
4.1.7.7.2. Malignant cells may not resemble epith cells closely.
4.1.7.7.3. Keratin pearls may not always be present.
4.2. VERRUCOUS CARCINOMA
4.2.1. Introduction
4.2.1.1. Synonym – Ackerman’s tumor.
4.2.1.2. Slow growing, chiefly exophytic,
4.2.1.3. Superficially invasive, low metastatic potential
4.2.1.4. Usually treated by simple excision
4.2.2. C/F
4.2.2.1. Age incidence: 60 – 70 yrs.
4.2.2.2. Sex incidence: More in males
4.2.2.3. Site
4.2.2.3.1. - Buccal mucosa - Gingiva - Alveolar ridge - Palate and floor of mouth (occasionally)
4.2.2.4. Etiology
4.2.2.4.1. Tobaaco chewing + smoking, snuff dipping, ill fitting dentures
4.2.2.5. Exophytic, papillary, pebbly surface, sometimes covered with leukoplakic film
4.2.2.6. Rugae like folds, deep clefts.
4.2.2.7. Buccal mucosa: extensive, involve contiguous structures
4.2.3. H/P
4.2.3.1. Deceptive, wrongly diagnosed papilloma, epithelial hyperplasia
4.2.3.2. Marked epithelial proliferation, down growth of epithelium into CT
4.2.3.3. No true invasion
4.2.3.4. Epith - well differentiated, little mitotic activity, pleomorphism or hyperchromatism
4.2.3.5. Cleft like spaces lined by thick layer of parakeratin extending deep into the space: Parakeratin Plugging
4.3. BASAL CELL CARCINOMA
4.3.1. Introduction
4.3.1.1. Synonym - Basal cell epithelioma, rodent ulcer.
4.3.1.2. Practically no tendency for metastasis
4.3.1.3. Etiology - UV light, ionizing radiation, burn scars, chemicals
4.3.2. C/F
4.3.2.1. Age incidence: 4th decade or later
4.3.2.2. Sex incidence: More in males
4.3.2.3. Site: exposed surfaces of skin, face, scalp
4.3.2.4. Race: Blondes, fair complexioned
4.3.2.5. Initially - small slightly elevated papule, ulcerates, heals and breaks down again
4.3.2.6. Superficial crusting ulcer develops smooth rolled border representing tumor cells spreading laterally beneath the skin
4.3.2.7. Untreated lesions enlarge, infiltrate deeper tissues, may erode into bone and cartilage
4.3.3. H/P
4.3.3.1. Nests, islands/ sheets of cells showing indistinct cell membranes
4.3.3.2. Large hyperchromatic nuclei, variable no of mitotic figures
4.3.3.3. Periphery of cell nests: layer of well polarized cells suggestive of basal cells of skin
4.3.3.4. Basal cell pluripotent cell: hair, sebaceous and
4.3.3.4.1. and sweat glands, squamous epithelial cells, keratinization
4.4. MALIGNANT MELANOMA
4.4.1. Introduction
4.4.1.1. Third most common skin malignancy.
4.4.1.2. Malignant neoplasm of melanocytes.
4.4.1.3. Can arise from a benign melanocytic lesion or de novo from melanocytes.
4.4.2. Classifications
4.4.2.1. Superficial spreading melanoma
4.4.2.2. Nodular melanoma
4.4.2.3. Lentigo maligna melanoma
4.4.2.4. Acral lentiginous melanoma
4.4.3. RISK FACTORS: -
4.4.3.1. Acute sun damage.
4.4.3.2. Fair complexion and light hair.
4.4.3.3. Tendency to sunburn easily.
4.4.3.4. Indoor occupation with outdoor recreational habits.
4.4.3.5. History of melanoma in family or relatives.
4.4.4. PATHOGENESIS: -
4.4.4.1. 2 growth phases –
4.4.4.1.1. Radial
4.4.4.1.2. Vertical
4.4.5. C/F
4.4.5.1. Age incidence: Between 3rd to 8th decades.
4.4.5.2. Sex incidence: Slightly higher in males.
4.4.5.3. Site
4.4.5.3.1. Extremities (40%)
4.4.5.3.2. Head and neck (25%)
4.4.5.3.3. Trunk region
4.4.5.4. Signs & symptoms:
4.4.5.4.1. Can occur as a macule, papule, nodule or a malignant ulcer.
4.4.5.4.2. Usually begins as a macule or papule and later progresses to nodular stage and finally develops into an ulcer.
4.4.5.4.3. One of the most rapidly spreading and metastasizing cancers known.
4.4.6. - ABCD SYSTEM -
4.4.6.1. Initially - melanoma resembles benign melanocytic nevus very closely.
4.4.6.2. to differentiate melanoma clinically from the benign nevus ABCD system has been devised.
4.4.6.3. A – Asymmetry, due to uncontrolled growth. B – Border irregularity C – Color variation D – Diameter > 6 mm
4.4.7. H/P
4.4.7.1. Atypical melanocytes spreading first laterally along the basement membrane.
4.4.7.2. Later, these cells invade the basement membrane and enter the underlying CT
4.4.7.3. In CT, cells appear spindle shaped or epitheloid and proliferate in the form of loose cords or sheets.
4.4.7.4. Lesion may contain fine melanin granules or not at all.
4.4.7.5. Some lesions show granules but no melanin production =>??
4.4.7.5.1. production => AMELANOTIC MELANOMA
4.5. Carcinoma of maxillary sinus
4.6. Spindle cell carcinoma
5. BENIGN EPITHELIAL TUMORS & NEOPLASMS
5.1. SQUAMOUS PAPILLOMA
5.1.1. Definition
5.1.1.1. Benign proliferation of stratified squamous epithelium resulting in a papillary or verruciform mass
5.1.2. Etiology
5.1.2.1. Human Papilloma Virus (subtype 6 & 11)
5.1.3. C/F
5.1.3.1. Age incidence: 30-50 yrs
5.1.3.2. Site incidence: tongue, lips, soft palate
5.1.3.3. Features: Soft, painless, usually pedunculated exophytic nodule
5.1.3.4. Signs & symptoms -
5.1.3.4.1. Cauliflower / wart like appearance
5.1.3.4.2. Lesion: white/slightly red/ normal
5.1.3.4.3. D/D -
5.1.4. H/P
5.1.4.1. Proliferation of keratinized squamous epithelium in finger like projections
5.1.4.2. Thin, narrow fibro- vascular connective tissue cores
5.1.4.3. Whiter lesions have thickened keratin layer
5.1.4.4. Dysplasia – Usually absent
5.1.4.5. Koilocytes - (virus altered epithelial cells with dark pyknotic nuclei) in spinous layer
5.2. VERRUCA VULGARIS
5.2.1. Definition
5.2.1.1. Synonym – Common wart
5.2.1.2. Resembles squamous papilloma closely.
5.2.1.3. Rare in oral cavity – more commonly in skin.
5.2.1.4. Contagious
5.2.1.4.1. can spread to other parts of person's skin or mucous membranes by autoinoculation
5.2.2. Etiology
5.2.2.1. Human papilloma virus types 2, 4, 6 & 40.
5.2.3. C/F
5.2.3.1. Age incidence: Children & up to adults.
5.2.3.2. Site
5.2.3.2.1. Mostly skin of hands
5.2.3.2.2. Oral – vermilion border, labial mucosa & anterior tongue
5.2.3.3. Signs & symptoms:
5.2.3.3.1. Painless, pedunculated / sessile, papule / nodule which shows papillary projections.
5.2.3.3.2. Color – oral lesions usually white.
5.2.3.3.3. Size < 5mm.
5.2.3.3.4. Number - Multiple or clustered lesions common
5.2.3.3.5. D/D: -
5.2.4. H/P
5.2.4.1. Hyperkeratotic stratified squamous epithelium arranged into fingerlike projections with CT cores.
5.2.4.2. Chronic inflammatory cell infiltration into underlying CT
5.2.4.3. Abundant koilocytes seen in superficial spinous cell layer
5.3. FOCAL EPITHELIAL HYPERPLASIA
5.3.1. Definition
5.3.1.1. Synonyms - Heck's disease; Multifocal papilloma Virus epithelial hyperplasia.
5.3.1.2. Virus induced, localized proliferation of oral squamous epithelium.
5.3.2. Etiology
5.3.2.1. Produced by human papilloma virus type 13 and possibly 32 also.
5.3.3. C/F
5.3.3.1. Age incidence: Childhood.
5.3.3.2. Site: labial , buccal. and lingual mucosa, but gingival and tonsillar lesions also have been reported.
5.3.3.3. Signs & symptoms:
5.3.3.3.1. Multiple, soft, non-tender, flat / round papules of normal color.
5.3.3.3.2. Occasionally – superficial papillary change noted.
5.3.3.3.3. Size – 0.3 to 1 mm.
5.3.4. H/P
5.3.4.1. Considerable acanthosis of oral epithelium.
5.3.4.2. Widened rete ridges.
5.3.4.3. Koilocytes may be seen in some superficial cells.
5.4. KERATOACANTHOMA
5.4.1. Definition
5.4.1.1. Synonyms - Self healing carcinoma, Molluscum Sebaceum
5.4.1.2. Self limiting epithelial proliferation with a strong clinical and histopathologic similarity to well differentiated squamous cell carcinoma
5.4.1.3. Cutaneous lesions common, intraoral lesions rare
5.4.2. Etiology
5.4.2.1. HPV 26 or 37, sun damage, genetic predisposition, carcinogens
5.4.2.2. Hereditary predisposition for multiple lesions
5.4.3. C/F
5.4.3.1. Age incidence: 50-70 yrs
5.4.3.2. Sex incidence: More in males
5.4.3.3. Site
5.4.3.3.1. 90% tumors on sun exposed skin (cheeks, nose, dorsum of hands)
5.4.3.3.2. Intraoral lesions rare.
5.4.3.4. Signs & symptoms:
5.4.3.4.1. Elevated, umbilicated / crateriform with depressed central core / plug
5.4.3.4.2. Often painful
5.4.3.4.3. Regional lymphadenopathy may be present.
5.4.4. CLINICAL COURSE
5.4.4.1. First-Small firm nodule
5.4.4.2. Second-Full size (6-8 wks)
5.4.4.3. Third-Static lesion (4-8 wks)
5.4.4.4. Fourth-Regression, expulsion of keratin core
5.4.5. H/P
5.4.5.1. Hyperplastic squamous epithelium growing into underlying connective tissue
5.4.5.2. Surface: thick para/ ortho keratin with central plugging
5.4.5.3. Occasionally - dysplasia
5.4.5.4. Margins: normal adjacent epithelium elevated towards adjacent central portion of crater
5.4.5.5. Abrupt change to hyperplastic, acanthotic epithelium
5.5. PIGMENTED CELLULAR NEVUS
5.5.1. Definition
5.5.1.1. nevus is a congenital developmental tumor like malformation of skin or mucous membrane
5.5.1.2. Benign, localized proliferation of cells of neural crest origin.
5.5.1.3. Common skin lesion containing melanin: common mole
5.5.1.4. Controversy
5.5.1.4.1. whether these nevus cells are actually melanocytes or only closely related to them.
5.5.1.5. During development nevus cells migrate to epidermis and lesions may first appear shortly after birth.
5.5.1.6. Classifications
5.5.1.6.1. Congenital
5.5.1.6.2. Acquired (melanocytic nevus)
5.5.1.7. C/F
5.5.1.7.1. Age incidence: Appear during childhood.
5.5.1.7.2. Sex incidence: Slight female predilection.
5.5.1.7.3. Racial predilection: More in whites.
5.5.1.7.4. Site
5.5.1.7.5. Signs & symptoms
5.5.1.8. H/P
5.5.1.8.1. Small, ovoid cells with small nucleus, eosinophilic cytoplasm with indistinct cell boundaries.
5.5.1.8.2. 1) Junctional nevus –
5.5.1.8.3. 2) Compound nevus –
5.5.1.8.4. 3) Intradermal nevus –