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ALL Oral Epithelial Tumors I and II and III (Slide 7+8+9)
ALL Oral Epithelial Tumors I and II and III (Slide 7+8+9)
HPV-Associated Lesions Squamous Cell Carcinoma Premalignant Lesions and Conditions Basal Cell Carcinoma Melanocytic Nevi and Melanoma
mucosa.
pedunculated.
Presents as a warty or
Squamous Papilloma
layer, no dysplasia.
Fibrovascular core
keratin
sessile or pedunculated.
May be single or multiple. White due to hyperkeratosis. Common on fingers in children. Autoinoculation from fingers to lips.
around margins slope inwards towards center. Large vacuolated cells (koilocytes) with prominent keratohyalin granules.
Verruca Vulgaris
which grow and coalesce to form soft, pink, pedunculated or sessile papillary lesions.
manifestations of HIV infection.
Condyloma Acuminatum
Keratinization is not a
prominent feature.
HPV 13, 32
4th commonest cancer in men and 6th in women on a global basis, 6th for both combined.
8th in
Geographical variation in mortality rates: 30-40% in Western societies. Despite advances in treatment, mortality rates have not significantly changed. 5-year survival rates have increased significantly.
hydrocarbons.
Carcinogens in tobacco smoke may dissolve in saliva
and collect in areas where saliva tends to pool, increasing risk in FOM, dorsal and ventral tongue, and soft palate.
factors.
Evidence linking tobacco to
held Development of papilliferous and ulcerated mass Possible interactions between components of pans
Chewing Habits
In India: Betel nut and lime and tobacco in betel leaf:
Alkaloids are released from the nut
other chemicals in the beverage, congeners, may be responsible for increased cancer risk.
Increasing incidence of oral cancer, especially in younger
Mechanism of Alcohol
Possible carcinogenic effect of chemicals other than ethanol Alcohol may enhance transport of carcinogens across mucosal
atrophy.
esophageal, pharyngeal, and oral cancer in primary sideropenic anemia (Plummer-Vinson or Patterson-Kelly syndrome).
Iron defeciency lichen planus and
Epithelial atrophy:
tertiary syphilis
teeth, and ill-fitting dentures have been incriminated in etiology of oral cancer
Some oral cancer patients have poor dentitions but they also smoke and drink heavily. Mechanical irritation can act as a cancer promoter, but not initiator in experiments.
Some HPV proteins : inactivation of tumor-suppressor genes p53 and Rb. significant step in development of oral cancer. HPV is likely to be an important cofactor in at least some oral cancers.
deficiency may impair cellmediated immunity, but significance of this role is not established.
with some speckled leukoplakias, and chronic hyperplastic candidosis (candidal leukoplakia) have relatively high malignant transportation rates.
However, other chronic oral candidal
invasive carcinoma.
However, late stage syphilis is rare
now.
Tobacco smoking: pipes, cigars, cigarettes, bidis, reverse smoking. Smokeless tobacco: snuff dipping, tobacco sachets, tobacco chewing. Betel chewing, betel quid, areca nut. alcohol: spirits, wines and beers, alcohol and tobacco synergism. Diet and nutrition: iron deficiency, vitamins A & C, nutritional deficiencies & alcoholism. Dental factors. Ultraviolet light. Viruses: HSV, HPV, HIV. Immunosuppression. Chronic infections: candidosis, syphilis. Occupation.
cell.
During carcinogenesis: a. proto-oncogenes may undergo mutation and become activated oncogenes, or: b. tumor suppressor genes may be mutated and their products inactivated.
The result in both cases leads to deregulation of cell proliferation and tumor formation.
myc, ras, and erb B-1 has been reported in oral SCC.
influencing prognosis.
for which no cause can be found or which does not respond as expected when putative causes are eliminated.
asymptomatic.
Many forms of
presentation, most commonly: 1. White patch. 2. Small exophytic growth which in early stages shows no ulceration or erythema
6.
for early carcinoma: Persistent ulceration. Induration. Fixation to underlying structures. Destruction of underlying bone in alveolar ridge lesions. Enlarged reactive regional lymph nodes. Carcinoma of vermilion border of lip: slightly raised swelling, or crusty, lesion resembling delayed healing of herpes labialis.
present as:
1. Broad-based, exophytic mass with rough, nodular, warty, hemorrhagic, or necrotic surface.
of differentiation.
- Obvious squamous differentiation. - Masses of prickle cells with limiting layer of basal cells around them. - Recognizable intercellular bridges. - Central keratin pearl formation. - Nuclear and cellular pleomorphism is not prominnemt. - Relatively few mitotic figures.
tumors: - Less keratinization. - More pleomorphism of cells and nuclei. - Abundant and atypical mitotic figures. - Still readily identified as squamous type.
- Keratinization usually absent. - Marked atypical features. - Cells may be hardly recognizable as epithelial. - The need for immunohistochemistry - Subjectivity and overlap in grading.
In general:
- variable lymphocytic and plasma cell infiltration in supporting stroma, probably an immune reaction to tumor antigens, necrosis and ulceration.
invasion:
Better prognosis
Non- Cohesive:
Separate islands Individual malignant cells
infiltration and destruction: - lymphatic permeation - Vascular invasion - Sarcolemmal spread - perineural spread - bone invasion, edentulous/dentate.
- Through alveolar crest - Through PDL - Extent of bone invasion may
i.
ii.
describe severe epithelial dysplasia in which the whole, or almost the whole thickness of epithelium is involved, but basement membrane is intact and there is no invasion of lamina propria.
dysplasia or carcinoma-in-situ in epithelium surrounding an invasive carcinoma, which may suggest a field change in a wide area of mucosa
It is probable that some
carcinomas thought to be recurrent tumors, represent new primary lesions arising in such a field change.
which cancer is more likely to occur than in its normal counterpart, e.g. leukoplakia, i.e. the lesion itself undergoes malignant transformation.
Premalignant condition: a generalized disorder associated
with a significantly increased risk of cancer developing somewhere in the mouth, e.g. submucous fibrosis.
However, relatively few oral SCCs are preceded by a
1. Precancerous lesions: a) Leukoplakia- homogeneous, non-homogeneous, nodular, and speckled types, including chronic hyperplastic candidosis and proliferative verrucous leukoplakia. b) erythroplakia c) carcinoma in situ.
especially face.
chronic exposure to UV radiation. lips, particularly upper lip. spreading to involve vermilion border.
Occasionally presents on
oral mucosa of clinically pigmented and non-pigmented races, the difference being of activity and not number.
Their function is to produce melanin which they pass to
adjacent keratinocytes.
nevi present in adult life as slightly elevated, pigmented lesions on the hard palate or buccal mucosa.
Melanocytic nevi are considered hamartomatous lesions formed by proliferation of melanocytes or their precursors, with variable melanin pigment production.
They are separated histologically based on location of nevus cells relative to epithelium:
1. Junctional nevus.
2. Compound nevus. 3. Intramucosal (intradermal). Most oral nevi are of this type.
Nevus cells
Nevus cells
Nevus cells
most important factor, hence many arise in head and neck area.
pigmented plaques or nodular lesions and may be preceded by melanoma in situ characterized by horizontal spread within epithelium.
characterizes invasive melanoma and prognosis depends mainly on depth of invasion at time of diagnosis.
ABCD Clinical Features: 1. Asymmetry (uncontrolled growth pattern) 2. Border irregularity 3. Color variation 4. Diameter greater than 6 mm
using specific markers for malignant melanocytes (S-100 and HMB-45) are useful.
Ultrastructural examination to
maxillary alveolar ridge and hard palate. there is history of previous pigmentation in the area.
brown or bluish black slightly raised lesions with an uneven nodular or papillary surface.
reddish.
Prognosis is poor.