Oral Cancer & Precancer – Flashcards
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Oral Cancer
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The most common for of oral cancer is squamous cell carcinoma -Malignant neoplasm of the epithelial tissue
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Oral Cancer Statistics
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37,000 people in the US will be diagnosed with oral/pharyngeal cancer in 2012 -Over 8000 people will die of oral/pharyngeal cancer this year -About one death every hour -Survival rate is about 54% -Incidence in young adults is increasing
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Causes of Oral Cancer
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1. Tobacco (cigarettes, smokeless) 2. Betel quid -leaf used in Asia/Africa surrounding tobacco and other drugs to wrap inside of sulcus. 3. Alcohol 4. Iron deficiency 5. Immunosuppression 6. Poor nutrition
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Highest rate of smokeless tobacco users is found in:
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8-17 year old white males -Populations in the north-central/south-central states -Blue collar occupations -Indiana is 5th in the nation for smokeless tobacco use in teens
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Tobacco potent carcinogens:
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-Nitrosamines (nicotine) -Polycyclic aromatic hydrocarbons -Polonium (all form duct that suppresses DNA reparative gene, allows for errors to occur)
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Tobacco smoke contains:
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-Carbon monoxide -Thiocyanate -Hydrogen cyanide -Nicotine -Metabolites of all constituents
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Other Etiological Factors of Oral Cancer
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Human Papilloma Virus -Linked to cervical cancer -Women's chance of developing oral/cervical cancer are equal -HPV-16 is found in about 2 of 3 oral/pharyngeal cancers (tongue & tonsils)
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Molecular links between tobacco, alcohol, and carcinogenesis (cancer development)
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Tobacco and alcohol have an addictive effect: act together to increase chances of developing reactive oxygen species -ROS can increase chances for DNA damage and mutation -increases chances of oral cancer
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Reactive Oxygen Species
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-Superoxide anion (oxygen with unpaired electron) -Hydrogen peroxide -Hydroxyl radical -Organic hydroperoxides -Alkoxy/peroxy radicals -Hypochlorite anion -Peroxynitrite -Ozone
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Reactive Nitrogen Species
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-Nitric oxide -Peroxynitrite -Nitroaoperoxycarbonate -Nitrogen dioxide Dinitrogen trioxide Dinitrogem tetraoxide
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Mirco RNA and Oral Precancer
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MiRNA: highly conserved, small, regulatory RNA's that act by binding "target" mRNA through partial or complete base pair complementary at 3UTR leading to either a decrease rate of polypeptide synthesis or complete degradation of mRNA templates.
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miRNA Facts
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-More than 2500 miRNA molecules have been identified -many effect regulation of multiple cellular pathways in cancer development and susceptibility -Use Multi-dimensionality Reduction to understand relationship between miRNA and the risk of leukoplakia
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miRNA and Oral Cancer Cont...
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-miRNA can increase activity of tumor causing gene or decrease activity of tumor suppressing gene
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Microbiome-carcinogenesis
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Bacterial microbiome promotes carcinogenesis through several mechanisms. -Changes and host defenses may favor increased bacterial translocation leading to increased inflammation. -Effects may occur locally or through long-distance effects in other organs.
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Periodontal Disease/Oral Cancer Relationship
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-Those suffering from chronic inflammatory disorder harbor risk of cancer developing largely due to pro-growth environment generated by activated inflammatory cells. -Loss of epithelial integrity from microbial toxins result in activation of resident inflammatory cells and cytolytic activity may increase cancer risk and demote tumor development.
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Hypothesized that Periodontal Disease:
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Upregulates the serum pro inflammatory cytokine levels and bacteremia among immunocompromised patients supports the general hypothesis of chronic periodontal infection based oral carcinogenesis.
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Periodontal Pathogens
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1. Porphyromonas gingivalis 2. Fusobacterium nucleatum -Promote tumor progression in an oral specific chemical carcinogenesis model.
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Oral Cancer in Non-smokers
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Commonly: -females -young age Cancer of oral cavity (tongue and palate)
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Oral Cancer Signs & Symptoms
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-Middle aged individuals -sore that bleeds easily/does not heal -feeling as if something is caught in throat -lump or thickening -red or white patch that does not go away -unusual bleeding, pain, or numbness in mouth -difficulty or pain when chewing or swallowing -lump on lip or inside of mouth -swelling of jaw -pain in ear
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Verrucous Carcinoma
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"Finger like" -1-10% of oral squamous cell carcinomas -best prognosis of carcinomas
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Etiology of Verrucous Carcinoma
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-Use of chewing tobacco -Use of snuff -HPV infection
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Sites of Verrucous Carcinoma
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-Mandibular vestibule -Buccal mucosa -Hard palate -Gingiva -Site of common tobacco placement
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Clinical Features of Verrucous Carcinoma
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-White, may be slightly pink -diffuse, painless -thick mass with papillary cauliflower like projections -typically spreads laterally and involves more surface area than deep tissues
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Treatment of Verrucous Carcinoma
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-Surgical resection -Radiation therapy *less effective, lesions are often insensitive
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Squamous Cell Carcinoma Clinical Features
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-May be painless -Varied appearances/growth patterns -Exophytic: cauliflower like -Endophytic: burrowing -Intact or ulcerated surface -Granular or papillary -White, red, or mixed in color
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Hard, Indurated Nodules indicate:
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Malignant transformation in a homogeneous leukoplakia
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Carcinoma of the Lip
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-Usually starts at the vermilion border of lower lip -95% of lip cancer involves lower lip -Nodule that ulcerates and forms a small scab which fails to ever heal completely -Often misdiagnosed as a cold sore -Eventually margins of lesions become proliferative and extensive exophytic lesion with central ulceration develops
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Diagnosis of Oral Cancer
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Oral examinations -Sores found on lip, tongue, or around mouth -Ulcers or bleeding in the mouth Tests used to confirm findings -Cytology -Biopsy -Xrays, CT scans, MRI's, PET scans to check for metastasis TNM staging -Tumor size -Lymphnode involvement -Metastasis
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Treatment of Early Oral Cancer
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Surgery to remove tumor -Typically is not done if cancer has spread to neck -May need reconstructive surgery afterwards Radiation therapy
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Treatment of Advanced Oral Cancer
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Chemo and radiation therapy -Targeted therapy -Speech therapy (improves movement, chewing, swallowing, and speech)
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Oral Cancer Survival
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-Five year survival rates are roughly 50% -Survival rate number increases to 80-90% when discovered early
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Oral Precancer
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Most cases or oral caner are preceded by oral precancerous lesions.
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Precancerous Lesion
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(Precancer, premalignancy) -Benign, morphologically altered tissue which has greater than normal risk of containing microscopic focus of cancer at diagnosis or of transforming into a malignancy after diagnosis.
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Malignant Potential
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The risk of cancer being present in a precancerous lesion/condition, either at time of initial diagnosis or at a future date. The potential for mucosa without precancerous lesion/condition is termed normal.
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Importance of Precancer
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-Potentially curable early stages of diagnosis -Represent lesions that can be screened in populations in attempt to reduce/prevent cancer -May aid in identification of environmental factors that cause cancer and be steps in the way to prevention strategies -Provide evidence in support of multi-step carcinogenesis
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Leukoplakia Etiological Factors
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-Tobacco use -Virus (HPV, Human herpes simplex virus) -Fungal: infection with candida albicans -Alcohol
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Clinical Features of Leukoplakia
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Homogeneous -flat, uniform, predominantly white plaques -may show shallow cracks/fissures Non-homogeneous (worse prognosis) -irregular/nodular thickened surface, raised edges -often speckled with areas of erythroplakia -indurated lesions: very likely to become cancerous, edges become hard and attach to underlying tissue Verrucous leukoplakia -lesions may take on distinctly warty appearance, described as verrucous lesions
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Leukoplakia
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Predominantly white lesion of the oral mucosa that can not be characterized as any directly identifiable lesion. -any white patch without directly identifiable cause, does not have to be precancerous lesion -slightly raised white patch that can not be wiped off -heterogeneous/homogeneous
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Erythroplakia
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Red patch in the oral mucosa that can not be characterized by any other identifiable lesion -slightly raised red patch that can not be wiped off -smooth/velvety
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Leukoplakia Histopathology
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-Wide range of appearances which reflect varying degrees of keratosis, epithelial thickness, epithelial dysplasia, and chronic inflammatory cell infiltration in lamina propria -Dysplasia: very important disorder of growth since it is premalignant condition of real clinical significance -Leukoplakia with dysplasia exhibit greater potential for malignant transformation -Biopsy needed to prove significant change in cell formation (if word dysplasia is seen, precancerous change was found)
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Malignant Potential of Leukoplakia & Erythroplakia
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-Both are clinical terms with no histological implication -Many oral cancers begin clinically as leukoplakia -5-25% of leukoplakia and most erythroplakia are diagnosed as dysplasia -Some are coexistent with squamous cell carcinoma *not all -Both considered to be premalignant lesions
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Tissue Architecture Changes with Epithelial Dysplasia
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-Hyperkeratosis -Acanthosis -Irregular stratification -Loss of polarity -Basal cell hyperplasia -Bulbous rete-ridges -Chronic Inflammation
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Cellular Changes with Epithelial Dysplasia
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-Dyskeratosis -Abnormal mitosis -Increased nuclear cytoplasmic ratio -Increased normal mitosis -Hyperchomatism
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Carcinoma-in-situ
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Severe epithelial dysplasia in which the whole, or almost whole, thickness of the epithelium is involved but the basement membrane is intact and there is no invasion of the lamina propria.
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Field Cancerization
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Most common inital genetic changes: Loss of heterozygosity in long arm of chromosomes 3 and 9.
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Differential Diagnosis of Leukoplakia
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-Frictional keratosis -Leucoedema -Nicotina palatinus -Chemical burns
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Nicotina Palatinus
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-Common clinical lesion observed in smokers (pipe mostly) -Dark brown pigmentations of oral mucosa (smoker's melanosis) -White leathered lesions of the palate, usually referred to as nicotine stomatitis or smoker's palate -Highly prevalent with pipe smokers. -End arteries with lack of blood supply
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Leucoedema
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-Translucent, milky, whiteness of the surface of the mucosa with a slightly folded appearance -Often encountered bilaterally in buccal mucosa and at borders of the tongue -Etiologically best regarded as a variation of normal
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Frictional Keratosis
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-Chronic frictional irritation leads to epithelial thickening and hyperkeratinization -Irritants like a sharp tooth, cheek biting, prolonged wearing of ill-fitting dentures -Must resolve when source of irritation is removed
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Chemical Trauma
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Acute: aspirin burn Chronic: tobacco use smoking or chewed -Habits produce epithelial thickening and hyperkeratosis in similar manner as chronic friction -Relatively common
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Aspirin Burn
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Severe insult produced by the topical use of aspirin likely to produce epithelial necrosis, sloughing, and ulceration.
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Smokeless Tobacco Keratosis
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-Thin, gray-white plaque, velvety fissured, rippled -Older lesions: leathery or nodular -Gingival recession, dental caries, staining.
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Oral Precancerous Condition
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General state that makes the patient more cancer prone -disease or patient habit that is known to have a greater than normal risk of precancer or cancer development -Oral submucous fibrosis -Oral lichen planus -Iron deficiency anemia
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Oral Submucous Fibrosis
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Precancerous condition -chronic insidious disease characterized by chronic inflammation and progressive fibrosis of oral mucosa
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Features of Submucous Fibrosis
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-Burning sensation when eating spicy foods -Fibrous bands bilaterally in oral mucosa -Progressive lesion which the opening of mouth becomes progressively limited -Occurs most exclusively in India, associated with chewing on thyme leaves.
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Oral Submucous Fibrosis is a Precancerous Condition
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Malignant potential: 7.6% Co-existent with oral leukoplakia and squamous cell carcinoma
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Clinical Features of Submucous Fibrosis
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-Palatal vesicles -Reduced mobility of soft palate -White fibrous bands -Decreased interincisal opening -Atrophic tongue -Trismus
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Other Epithelial Neoplasms
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Benign: -Squamous papilloma -Adenoma Malignant neoplasms: -Carcinoma -Malignant melanoma
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Squamous Papilloma
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-Common benign tumor, usually solitary lesion and can occur anywhere on oral mucosa -Warty or cauliflower like growths with white or pink surface depending on the amount of keratin present -Associated with HPV infection -Pedunculated/sessile
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Pigmented Lesions
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Melanocytes are melanin producing cells contributing to pigmentation of skin/mucosa -Oral melanotic macule: focal increase in melanin deposition -Very uncommon in oral cavity: except for Japanese populations -Not usually malignant -Important to ask if lesion has changed in size and color
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Pigmented Lesion Terminologies
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Nevus: developmental lesion on skin or mucosa (biological term for mole) Macule: flat, distinct, colored area of skin that is less than 1cm in diameter and does not include change in skin texture or thickness (any lesion that is flat) Papule: small elevated lesion on skin or mucosa greater than 1cm in diameter
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Melanocytic Nevi
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Harmartomatous (developmental variation) lesion formed by proliferation of melanocytes or their precursors -Common in skin but rare in oral mucosa Macular: sharply demarcated brown/black lesion that is not raised Papule: elevated soft papule with smooth surface
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Malignant Melanoma
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-Rare -Most are advanced and extensively invasive lesions at presentation -Some history of previous pigmentation in area with resemblance to nevus clinically -Histological sections show proliferation malignant nevus cells in epithelium spreading to underlying connective tissue. -Positive staining for S-100 protein
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Differential Diagnosis for Oral Mucosa Melanoma
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-Nevi -Melanotic macules -Kaposi's sarcoma (HIV lesion) -Physiological pigmentation
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Treatment of Oral Mucosa Melamoma
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Complete surgical excision Chemotherapy and radiation
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Focal Epithelial Hyperplasia
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Heck's disease -In native North Americans and Inuit -characterized by multiple small elevated epithelial plaques or polypoid lesions frequently involving lower lips and buccal mucosa -HPV types 13 and 32 -Differential diagnosis for benign epithelial lesions -No clinical significance -No pain
