Oral Cancer I – Flashcards
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What types of cancer can be called oral cancer?
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Throat, mouth, larynx, sinuses, salivary glands, and skin.
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What is unique to oral cancer?
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Often difficult to treat and high rate of recurrence
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What are the treatment options for oral cancer?
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Surgery, Chemo, Radiation, and Novel approaches.
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What are the scary stats for oral cancer?
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Over 40k will be diagnosed each year and over 50% will die of the disease.
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How are oral cancers classified clinically?
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Through TNM Staging and differentiation of tumor histology or grading.
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What does TNM refer to?
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T is based on size and extent of Tumor, N is whether it has reached the lymph nodes and then M refers to whether it has metastasized or not.
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What are some diagnostic aids to diagnose cancer and pre cancer?
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Oral exam, Brush cytology, Toluidine Blue or TB staining, Visualization adjuncts (light based) and Scalpel Biopsy (gold standard).
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What are some oral carcinogens?
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Tobacco, Infectious agents (viruses), Alcohol, GERD, Diet, Radiation
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What does oral cancer epidemiology refer to?
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Factors affecting the non-random distribution of cancer in a population....like cancer rates, mobidity vs. mortality, Survival.
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What are the anatomical site for oral cancer?
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Oral cavity, Pharynx, Tongue, and Esophagus.
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What are some common tumors?
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Benign connective tissue growths of hard or soft tissues, Benign epithelial surface growths like papillomas or Nevi (moles), benign salivary gland tumors, malignant epithelial surface growths, Metastatic lesions, and salivary gland malignancies.
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What are some malignant epithelial surface growths?
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Squamous cell carcinoma, Basal cell carcinoma, and Melanocarcinoma.
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What are some uncommon tumors?
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Ones with hereditary association, Lymphomas, Malignant CT growths, melanocarcinomas, and odontogenic tumors.
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What is Myeloma?
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It is an uncommon tumor, a lymphoma that is a plasma cell tumor.
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What are 3 types of surgical intervention for oral cancer?
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Ablative surgery, Mohs microsurgery, Radical neck dissection.
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What is a Trojan peptide?
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It is a type of novel vaccine for oral cancer in testing to treat squamous cell carcinoma. It is made from HPV 16, MAGE-A3...it is very large and a chaperone cell aids it entry into the cells. It is thought that larger peptide might trigger a stronger response from the body.
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What is oncology?
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The study and treatment of cancer that usually includes a multidisciplinary approach.
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How does a regular cell become a renegade cell?
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A mutational event that begins a malignant transformation.
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What is carcinogenisis?
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A multi-step process where cells propagate to a threatening phenotype where aberrant proteins produce aberrant genes.
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What are the six hallmarks of Cancer?
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Growth signal autonomy, Evasion of growth inhibitory signals, Evasion of apoptosis, Unlimited replicative potential, Angiogenesis (new blood vessels), Invasion and Metastasis.
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How does Cancer Kill?
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Organ Failure, Obstruction of GI tract, ducts and hollow organs, Cachexia, and infection.
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What is cachexia?
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Extreme weight loss or wasting.
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Is there a cure for oral cancer?
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Yes by understanding biology, current treatments, new treatments, screening, and prevention.
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Lecture 2:
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How are staging and grading related?
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Staging is clinical and grading is histological.
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What is staging?
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It is a way to describe how much the cancer has spread and takes into account size, depth, invasion of adjacent organs, if lymph nodes have metastasized, and spread to distant organs.
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What is the most powerful predictor of survival?
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The stage diagnosis, Treatments are changed based on stage.
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What is the TNM system?
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It is a clinical staging system where T stands for tumor, N stands for nodes, and M stands for metasteses. Every tumor has a unique TNM classification. Once TNM classification is determined then you can divide tumors into stages I-IV
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How is T determined in the TNM system?
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Size of tumor. TX-can't be assessed, TO no evident primary tumor, T1-2cm or less, T2-from 2-4 cm, T3-tumor greater than 4 cm, T4 tumor invades adjacent structures.
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What are the general names for epithelial and CT tumors?
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Epithelial origin are carcinomas and CT tumors are called sarcomas.
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How is N denoted within the TNM staging system?
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It indicates size and number of involved nodes. N=regional lymph nodes, NX= no regional lymph node metastasis. N1= metastisis to a single ipsilateral lymph node, N2= from 3-6 cm or bilateral, N3=greater than 6 cm.
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How is the M noted in the TNM system?
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The M is M0 or M1....either it has metastasized or no
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What is the TNM staging system used for?
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Asses prognosis, determine treatment, and compare results from different protocols and centers worldwide.
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What is the weakness of the TNM classification system?
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It is empiric in nature until you can do a histologic evaluation....it might then be restaged.
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What are the treatments for Stage I and II oral cancer?
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Surgery alone or radiation alone for both
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What are the treatments for stage III and IV oral cancer?
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Surgery 1st and then radiation or radiation 1st and then surgery.
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What are the leading causes of Cancer?
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Most to least....Tobacco, diet and obesity, sedentary lifestyle, family history of cancer, occupational factors, viruses and other biological agents, alcohol, pollution, UV radiation. Alcohol and tobacco are synergistic.
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What is the difference between leukemia and lymphoma?
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Leukemia proceeds from the bone marrow and lymphoma starts in lymph nodes and goes from there.
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What do you do if you detect lymph node enlargement?
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Determine the mobility and consistency of the nodes. Neoplasias and chronic granulomatous conditions they will be endurated and immobile.
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What is recommended with respect to order of the extraoral/intraoral exam?
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Be systematic
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Can you draw the locations of the lymph nodes based on the roman numerals?
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Maybe...
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Which area is the crossroads/spaghetti bowl for the head and neck lymph nodes?
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Level II. This drains area from lateral tongue bilaterally and so if you have oral cancer here it is much more likely to spread bilaterally than a cancer on the lip.
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Where are the level two lymph nodes located?
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At the division of the internal and external carotid arteries.
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How do epithelial tumors (carcinomas) generally spread?
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Through the lymphatics
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How do CT tumors (sarcomas) generally spread?
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Through the blood vessels.
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What does a mass on the midline of the neck usually indicate?
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A problem with the thyroid. You can tell by having the patient swallow. If the mass moves while swallowing then it is thyroid associated.
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What should we look for in the lips in the I/E oral exam?
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A distinct border, nodules, soft tissue swellings,
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What objective findings can help rule out a malignancy with the tissues?
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Color, Symmetry, texture, size, and contour.
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What should we do if we find something abnormal?
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Assess invasiveness by palpating and when possible documentation w/photos is useful for follow-up comparisons.
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What is the most common abnormality in oral cavity?
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Fibroma
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What does the ending "oma" usually indicate?
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That a tumor is benign except with lymphoma and melanoma.
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How can you tell if the buccal mucosa is discolored due to leukedema?
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Stretch it to see if goes away.
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What does smooth, red gingival indicate in kids?
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Nothing, but in adults it is pathologic.
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Is bleeding on probing normal?
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No, it is common, but it is always pathologic.
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In what area are oral cancers most common?
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Where the saliva pools under the tonge and on the lingual side of dentition. These tissues are also more susceptible because they are unkeratinized.
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Etiology part I
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Adjunctive tests fall under what part of SOAP?
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Objective information
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What objective information is collected for soft tissue lesions?
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Color, Size, Location, and Surface
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What is the order of severity (least to greatest) by site for oral cancer?
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Oral cavity, Tongue, Tonsil, Pharynx and Esophagus
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What is the most common malignancy in the head and neck?
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Lip SCC. Lower lip >85%, 5 yr survival 90%, presents as persistent non-healing ulcer of exophtic tumor
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Where are 75% of all tongue cancers located?
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Anterior 2/3 of tongue, 55% 2 yr survival
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What % of pt with SCC at the base of the tongue have cervical lymph node involvement at diagnosis?
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50-75%, 1/3 of all tongue cancers, ulcerative infiltrative and aggressive
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Where is the most common intra-oral malignancy located?
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The tongue. Metastasizes to ipsilateral submandibular of jugulodigastric nodes
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What is the most aggressive SCC in the oral cavity?
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Floor of the mouth SCC, most aggressive and potentially fatal, more common in men
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In palatal SCC is the hard or soft palate affect more often?
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Soft palate 75% and hard palate 25%
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Is gingival SCC more common in the maxilla or mandible?
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70% arise in mandibular gingiva
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What is buccal mucosal SCC associated with?
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Smokeless tobacco and leukoplakia, has a high rate of recurrence
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Which virus is associated with tonsilar SCC?
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HPV. Those with HPV related tumors who are non-smokers have better survival rates
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what are the best diagnostic tools available?
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Your eyes, ears and fingers. Observe the lesion, palpate it and listen to the pt
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why is the health history important?
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Provides a pattern of pt health status and mode of life, it is a barometer of physical conditioning and resistance to disease
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what are early signs of oral cancer?
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Persistent red and/ or white patch, non-healing ulcer, progressive swelling, unusual surface changes, sudden tooth mobility w/out apparent cause, unusual bleeding or epistaxis, and prolonged harseness
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what are late signs of oral cancer?
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Paresthesia/ dysesthesia of tongue or lips, persistent pain or referred pain, chronic earache, altered vision, dysphagia, trismus, cervical lymphadenopathy indurated area
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what is the gold standard for determining oral cancer?
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Scalpel biopsy
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when screening oral cancer what does the sensitivity of a test refer to?
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The probability that someone who has a target disease will generate a positive result
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what does specificity refer to in screening tests?
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The probability that someone who does not have cancer will generate a negative finding
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what is positive predictive value?
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The probability that someone w/ positive test results actually has cancer
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what is negative predictive value?
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The probability that a person w/ negative test results does not have the disease
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when might brush cytology have a place in diagnosis?
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In diagnosing red lesions. Observe lesion for 2-3 wks if still present carry out brush cytology if report is suspicious or positive the biopsy must be done
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What does the research say about the effectiveness of adjunctive cancer screening techniques?
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There is a lack of data to support or refute their effectiveness so clinicians must rely on a thourough oral mucosa exam.
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What are Toluidine Blue tests based on?
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It selectively binds to DNA that is more acidic (neoplastic)
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How to Toluidine Blue tests fair with respect to sensitivity and specificity?
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It is over 90% in sensitivity and between 70 and 90% in specificity. Specificity in the 70's isn't that great. There is a risk of a false negative.
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How do tissue reflectance tests work?
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Irregular cells take on a different color, but these tests just help identify the need for further testing. Why waste time with this....You might have just wasted two weeks in observation when you could have known for sure with a biopsy.
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Which test helps ensure to not get a false positive for oral cancer?
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A biopsy gives a definitive Diagnosis
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What are the 4 common types of biopsy?
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Excisional (removed in its entirety), Incisional (a slice of tissue), Needle (cores a deep mass), and Punch (used to remove surface lesions like pigmented nevi)
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How does the prognosis of a white lesion compare to that of a red lesion?
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In a white lesion the cells are still producing keratin and it has a much better prognosis. About ¼ of oral white lesions will be cancerous.
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How should clinicians approach oral cancer?
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We need to learn to HATE the disease and hunt it down relentlessly. Always assume it is cancer unless proven otherwise. Keep a high index of suspicion.
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How can early diagnosis affect the outcome of oral cancer?
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As many as 80% can be saved vs. the 50% without early detection.
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Epidemiology
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What is the cornerstone of public health research?
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Epidemiology
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What is cancer epidemiology?
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Study of the factors affecting cancer, as a way to infer possible trends and causes
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What are the two phases of cancer progression?
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Compensated - tumor does not cause any damage or distress. De-compensated - when the pt suffers
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Where does cancer rank on the leading causes of death in the us?
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#2 behind heart disease
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What is the ancient historical perspective on cancer?
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Hippocrates used Carcinos and carcinoma to describe tumors. Ancient Egypt details documenting 8 cases of tumors occurring on the breast
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When was tobacco recognized as a carcinogen?
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Observational studies published as early as the 1700s. 1960s the surgeon general published the dangers of smoking
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When were Diet/ BMI/ and physical activity tied to chronic diseases and cancer?
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British sailors and limes. 70s and 80s linked specific dietary factors to risks for cancers,
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What are risk factors for oral cancer?
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Tobacco use #1, Alcohol consumption #1 for non-smokers, diet low in fruits and vegetables, surgeries/ medication, lifestyle, HPV, Sun exposure
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What is the 5 yr survival rate for oral cancer?
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57%
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Where do most cancers on the larynx begin?
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On the vocal cords
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What are symptoms of laryngeal cancer?
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Hoarseness or other changes in the voice, lump on the neck, sore throat, earache
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How high is the risk for pts, who overcome laryngeal cancer, to develop a second cancer?
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20X
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What are the 3 ways to speak after a laryngectomy?
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Esophageal speech, Artificial larynx, and tracheoesophageal Puncture (voice prosthesis)
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Where does oral cancer fit in the most common cancer list?
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Sixth most common cancer about 2.4% of all cancers in US
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What % of people with oropharyngeal cancer have no risk factors at all?
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25%
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Does Tongue or lip cancer have a better 5 year survival rate?
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Lip cancer by 10-20% across all 4 stages.
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Which area of oral cancer has the lowest 5 year survival rates?
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Oropharynx and tonsil followed by The Floor of the mouth.
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Molecular Biology of Cancer:
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What is allows you to metabolize alcohol?
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Alcohol dehydrogenase or ADH
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Which ADH variant increase RR of oral cancer by 5X over ADH1 and ADH2?
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ADH3
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How does alcohol affect the cell membrane?
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It increases the fluidity of the membrane which exacerbates the actions of smoking
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What is the RR of smoking and alcohol together?
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It is 195 in stead of the mere sum of the two on their own which would be 28.
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Who is at higher risk for oral cancer in Nevada?
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Males 50 and older.
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What group is the exception to incidence and mortality of Oral cancer?
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Black Females are an increased risk and the risk for all other groups has decreased.
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How does cigarette smoke affect growth factor receptor activation?
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It can cause ligand-independent phosphorylation of these receptors. 80-100% of oral cancers show EGFR activation and over-expression.
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How do EGF mutations compare between non-smokers and smokers?
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They occur in 51% of non-smokers vs. 4% of smokers....which implies a protective effect, but that is bologna.
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What happens when you have EGFR activation?
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You get TGF alpha transcription and activated matrix metalloproteases which instigates autocrine signaling.
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What does cyclin D1 do?
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It phosphorylates Rb, allowing G1/S progression in the cell cycle.
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Where is Cyclin D1 over expression seen?
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25-70% of all oral cancers
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Which two constituents of tobacco smoke enhance DNA methylation?
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Polycyclic aromatic hydrocarbons PAH and Nicotine-derived nitrosamines (NDN)
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Which two enzyme are directly affected by PAH and NDN?
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DNA methylase activation and DNA methyltransferase activation.
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What is a common site for DNA methylation?
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P53, at codons 248 and 273, CpG rich exons
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What doe DNA methylation affect?
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Transcriptional down regulation or mutations during replication.
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What type of DNA replication errors are common at the methylated CpG sites?
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G to T transversions
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How do rate of p53 mutations compare between smokers and non-smokers?
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300% more likely in smokers.
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What molecular transformations is one of the first detectible genetic events?
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9P21:p16 and 3p12: FHIT
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What is the most commonly deleted gene in Hean and Neck Squamous Cell Carcinoma?
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9p21, removal inactivates p16 the inhibitor of cyclin CDK that leads to progression through the cell cycle.
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How common is a 3p allelic imbalance?
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Occurs in 60% of HNSCC where Fragil Histidine Triad Gene FHIT is methylated. FHIT has tumor suppressor functions.
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What molecular transformation events occur at 8p?
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p14/p19 simultaneous deletion in many oral cases
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What is the last molecular transformation seen?
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17p and 14q: p53....p53 alters Rb phosphorylation removing the block from G1 to S progression.
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What signal is important in angiogenisis?
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VEFG Vascular Endothelial Growth Factor has a similar transduction pathway as EGFR it is just further down stream.
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How do Fruits and Veggies affect oral cancer?
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Consuption lowers oral cancer risk even among smokers and drinkers...more servings = lower risk.
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How does folate supplementation affect rates of oral cancer growth in vitro?
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It increased the rate.
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What is the most important oncovirus?
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HPV
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What do E6 and E7 of HPV do regarding oral cancer?
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They are the early genes that act to block p53 activity which leads to cell growth and proliferation.
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How do folate and HPV interact?
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Folate helps methylate HPV sequences because the HPV genome is CpG rich.
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Carcinogens:
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What are carcinogens?
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Any substance, radionuclide or radiation which is directly involved in the promotion of cancer or facilitation of its propagation.
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What are two common examples of carcinogens?
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Inhaled asbestos (mesothelioma) and tobacco smoke.
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What are two broad classifications of carcinogens?
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Genotoxic that cause genetic damage by mutation or DNA binding, and Nongenotoxins promote growth via hormones or other organic compounds.
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What might serve as a genotoxic carcinogen?
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Chemical agents like MNu, non chemical agents like UV light or viruses..
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How does the Internation Agency for Research on Cancer classify carcinogens?
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Group 1 (definitely carcinogenic) Group 2A (probable carcinogen), 2B (possible carcinogen), group 3 (not carcinogenic), and group 4 (probably not carcinogenic)
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What are 3 viruses that are associated with cancer as possible carcinogens?
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EBV, HPV, and Helio pylori
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What are other possible risk factor for oral cancer besides smoking?
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Poor hygiene, Diet, Environmental contaminants, Marijuana.
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When was a conclusive link presented between tobacco, lung cancer and premature death?
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1964 by the surgeon general.
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How many different carcinogens are in tobacco?
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60 in smoke and 16 in unburned tobacco.
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What are the strong carcinogens in tobacco?
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Cause tumors with low doses of PAH, Nitrosamins, and Aromatic amines
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What are weak carcinogens in tabacoo?
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Cause tumors after high dose exposure. Acetaldehyde
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What is the relationship of dose and response to tobacco?
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There is a positive linear relationship. As dose increases so does response. Duration of exposure is more important than intensity
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What are two main carcinogens of tobacco that exposure might result from occupational exposure?
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BaP and PAH, both derived from incomplete combustion of coal-derived sources.
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What are the tobacco-specific nitrosamines that are carcinogens?
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NNK and NNN...can induce local and systemic tumors. In combination they induce oral cavity tumors.
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How much NNK and NNN are found in tobacco?
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Enough to be similar to the amounts in total doses required to produce cancer in lab animals.
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Do tobacco specific nitrosamines cause cancer?
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Several lines of evidence strongly indicate that nitrosamines have a major role especially in the causation of snuff-dippers.
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What do epidemiologic studies demonstrated about snuff-dipping?
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It causes oral cancer. NNK and NNN are quantitatively the most prevalent known carcinogens in snuff
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Why does NNK play a role in the induction of lung cancer by tobacco smoke?
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Its organo-specificity for the lung
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What are used as ideal bio-markers for assessing human exposure to and metabolic activation of tobacco smoke carcinogens?
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Adducts of tobacco-specific nitrosamines
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What is a DNA adduct?
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An abnormal piece of DNA covalently bonded to a cancer causing chemical
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What six carcinogens form DNA adducts?
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BaP, NNK, NDMA, NNN, Ethylene Oxide, and 4-ABP
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What is the main active chemical in Marijuana?
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THC (delta-9-tetrahydrocannabinol)
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How does marijuana effect the brain?
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THC changes the way in which sensory information gets inot and is acted on by the hippocampus
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What similarities do marijuana smokers and tobacco smokers have?
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May have many of the same respiratory problems. Marijuana smoke causes abnormal functioning of lung tissue because of injury by smoke
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What is the effect of marijuana on the lungs?
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Regardless of THC content: amount of tar inhaled and level of CO absorbed is 3-5Xs greater than tobacco smoke. 4Xs higher TAR burden
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What are short term effects of mamrijuana?
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Dry mouth/ throat, increased heart rate, and anxiety also so lack of coordination and lower cognitive ability
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What are the long term effects of marijuana?
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1-3 joints per day produces the same lung damage and potential cancer risk as smoking 5-15 cigarettes per day
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What is the cancer risk factor for those who drink or smoke?
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3-9Xs for drinking or smoking. Together they produce a 100Xs risk factor
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What cancers are alcoholic beverages causally related to?
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Oral cavity, pharynx, larynx, and esophagus
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What are the 6 pathways through which drinking alcohol may cause cancer?
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1. Alcohol's contact-related local effects 2. The solvent effects on tobacco and other carcinogens 3. Induction of microsomal enzymes involved in carcinogen metabolism 4. Formation of oxygen radicals and lipid peroxidation products 5. Nutritional deficiency especially vit and mineral deficiencies 6. Suppressed immune function
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What is the major carcinogen in alcohol?
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Acetaldehyde which interacts w/ DNA to form DNA adducts
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What are 2 infectious agents of oral cancer?
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EBV and HPV
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Of the 100+ types of HPV which is most notable?
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Cervical cancer
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In the mouth which cancer is HPV often seen in?
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tonsillar squamous cell carcinoma
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What do HPV 1 and 2 cause?
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Warts on soles of feet or palms of the hands, respectively
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What do HPV 6 and 11 cause?
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Irregular warts known as condyloma accuminata on the genitals
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Are HPV 1,2,6,and 11 cancer causing?
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Not generally associated w/ an increased risk of cancer
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Which HPV strains are cancer causing?
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HPV types 16 and 18 may cause head/ neck and other cancers
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Where does papillomaviruse replicate?
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Exclusively in kerativocytes: skin and mucosal surfaces like the oral mucosa and vagina
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Where is the release of free radials etiologically significant to ulcers?
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Stomach ulcers
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Why do duodenal ulcers form?
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90% of pts have H. pylori infections in the stomach and acid is still important too (without acid in stomach pts never get duodenal ulcers)
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What disorder related to GERD gives an elevated risk for laryngeal and pharyngeal carcinoma?
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Barrett's esophagus
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What is barrett's esophagus?
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Normal squamous epithelial cells that line the esophagus turn to specialized columnar cells. 5-10% of pts develop cancer of distal esophagus
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What type of diet increases cancer risk?
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High in saturated animal fats and low in fruits and vegetables
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How does over cooking food cause a cancer risk?
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Charred residue on BBQ meats is identified as a carcinogen along w/ many other tars
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Dr. Woo
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What is the parotid papilla and where is it located?
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It is the opening to stensen's duct and it is located in the buccal mucosa opposite the 1st molar
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How might the labial mucosa feel on palpation?
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Slightly pebbly
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What is the posterior demarcation of the soft palate?
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Uvula, anterior tonsillar pillars
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What structures are located on either side of the lingual frenum?
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Sublingual caruncles and Wharton's ducts
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What are the histologic features of the buccal and labial mucosa, soft palate and floor of the mouth?
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Epithelium: stratified squamous, shallow rete pegs, nonkeratinized surface. Connective tissues: minor salivary gland lobules, striated muscle, blood vessels, nerves and losse fibroadipose connective tissue
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What demarcates the division between attached gingiva and alveolar mucosa?
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The mucogingival junction
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What are the histologic features of attached gingiva?
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Epithelium: paraderatinized surface, elongated pointed rete ridges, stratified squamous Connective tissue: NO salivary gland lobules, dense, fibrous connective tissue
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What does alveolar mucosa look like histologically?
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Similar to the buccal/ labial mucosa, FOM and soft palate. Nonkeratinized surface with shallow rete pegs
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What does hard palate look like histologically?
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Epithelium: thin orthokeratinized surface, elongated pointed rete pegs. Connective tissue: prominent blood vessels and nerves, minor salivary gland lobules
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What are the 4 types of papillae on the dorsum of the tongue?
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Filiform, fungiform, circumvallate, and foliate
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What does the ventral/ lateral tongue look like histologically?
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Similar to buccal/ labial mucosa, FOM and soft palate. Rare minor salivary gland lobules in the CT
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What histologic features does the dorsum of the tongue have?
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Epithelium: rough, parakeratinized surface, taste buds, prominent rounded rete pegs Connective Tissue: striated muscle, rare minor salivary gland lobules
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What 9 categories are used to describe oral lesions?
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Location, Color, Surface architecture, Size, Consistency, Surface texture, Base characteristics, Growth pattern, and Specific characteristics
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What is a macule?
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Focal color change, neither raised nor depressed
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What is a plaque: a slightly elevated patch (usually epithelial)
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...
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What is a papule?
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Solid, round, raised, usually <5mm in diameter (usually epithelial)
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What is a nodule?
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Solid, round, raised, >5mm (usually submucosal)
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What is amass?
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Solid, mostly raised, larger than nodule (epithelial or submucosal)
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If none of the above apply how might surface architecture be described?
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Growth or lesion
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What do pedunculated and sessile mean?
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Pedunculated - narrow base, sessile - Broad base
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What are the specific characteristics to note?
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Vesicle, bulla, pustule, erosion, and ulcer
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What is the difference between a vesicle and a bulla?
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Vesicles are <5mm and bulla are larger than 5mm
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When describing radiographic pathology what 8 categories are used?
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Location, Density, Borders, Size, Shape, Internal architecture, Effect on adjacent structures and symmetry
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When describing the location of a radiographic lesion?
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Site, relationship to other structures, and relationship to teeth
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What are the options for describing density?
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Radiolucent, radiopaque and mixed
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How are borders defined?
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Well-defined (corticated or non corticated) and ill-defined (irregular, ragged, and moth-eaten)
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What is acanthosis?
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Increase in epithelial thickness due to intercellular edema in spinous layer
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What is metaplasia?
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Reversible alteration from one mature cell line to another
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What is pseudoepitheliomatous hyperplasia?
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Benign, reactive overgrowth of squamous epithelium, can mimic squamous cell carcinoma
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Common and Uncommon Tumors I
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...
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What is the definition of leukoplakia?
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A white, plaque-like lesion which cannot be wiped off AND cannot be clinically diagnosed as any other disease entity. This is a clinical term that is not associated with a specific histologic diagnosis
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What is the short list of clinically distinct entities that must be exclude before diagnosing a leukoplakia?
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Frictional hyperkeratosis (morsicatio), Leukoedema, Linea alba, Nicotine stomatitis, Smokeless tobacco keratosis, Lichen planus, and others
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What are the results after microscopic examination of leukoplakias?
answer
5-25 % are epithelial dysplasia (pre-cancer), 4% SSC. True leukoplakias are considered to be potentially premalignant lesions
question
What is the #1 proposed etiologic cause of leukoplakia?
answer
Tobacco, > 80% of leukoplakias occur in smokers. Alcohol has not yet been associated on its own but has synergistic effects with tobacco
question
What is sanguinaria?
answer
AKA blood root, contained in Viadent products, causes leukoplakia in the mazillary vestibule, maxillary alveolar mucosa and may cause epithelial dysplasia
question
Who gets ultraviolet radiation associated leukoplakia?
answer
Immunocompromise pts especially transplant pts
question
What microorganisms are proposed etiologies of leukoplakia?
answer
Treponema pallidum on the dorsal tongue in tertiary syphilis and HPV types 16 and 18
question
What trauma events are proposed etiologies of leukoplakia?
answer
Heat eg nicotine stomatitis in response to heat of smoking, and mechanical eg frictional hyperkeratosis, response to low grade trauma. These have no malignant potential and are not true leukoplakias.
question
What is the most common oral premalignancy?
answer
Leukoplakia. M>>F, high risk sites for dysplasia and SSC include lip vermillion, lateral-ventral tongue, floor of mouth and soft palate
question
What does a leukoplakia look like clinically?
answer
Gray to white, plaques, well-defined borders, Early - soft thin, translucent. Late - firm, thickened, opaque
question
What is proliferative verrucous leukoplakia (PVL)?
answer
Multifocal leukoplakias. Female predilection, little assoc. with smoking, typically develops dysplastic changes, SCC
question
What is Erythroleukoplakia, speckled leukoplakia?
answer
Leukoplakia admixed with erythroplakia typically exhibits dysplastic changes
question
What does thick fissured leukoplakia suggest?
answer
Dysplasia (mild/moderate)
question
What does granular verruciform leukoplakia suggest?
answer
Moderate/ severe dysplasia
question
What does erythroleukoplakia (speckled leukoplakia) suggest?
answer
Severe dysplasia or carcinoma in situ
question
What changes are pr-malignant?
answer
Dysplasia and carcinoma in situ(CIS). SCC is malignant
question
What are typical features of epithelial dysplasia?
answer
Enlarged nuclei and cells, Increased nuclear to cytoplamic (N:C) ratio, Hyperchromatic nuclei, Pleomorphic nuclei and cells, Increased mitotic activity and Abnormal mitotic figures, Bulbous tear dropped rete ridges, and loss of polarity
question
What is mild/ moderate/ severe dysplasia?
answer
Mild Dysplasia involving the lower 1/3 of epithelium, Moderate involves lower 2/3, Severe estending to upper 1/3
question
What is carcinoma in situ?
answer
Dysplasia involving the entire thickness of the epithelium
question
What is important to remember when removing leukoplakias?
answer
Preserve specimen for histological exam
question
How do you treat leukoplakia?
answer
Surgical removal, careful long-term follow up and cessation of contributing factors
question
What is the risk for leukoplakia transforming to SCC?
answer
Moderate dysplasia 4-11% chance, Severe dysplasia 20-35% chance
question
Common tumors II
answer
...
question
What is squamous cell carcinoma?
answer
Malignant neoplasm of squamous cells
question
Who gets SCC?
answer
Caucasian males >65 yrs and middle aged AA males
question
What % of oral cancers are SCC?
answer
94% of oral cancers are SCC
question
What are the extrinsic and intrinsic factors that play a role in SCC?
answer
Extrinsic - tobacco, alcohol etc. Intrinsic factors - systemic diseases, immunocomprommise. Most SCC is preceded by a premalignat lesion such as leukoplakia
question
What are 11 etiologic agents of oral SCC?
answer
Tobacco smoking, Smokeless tobacco, Betel quid, Alcohol, Radiation, Iron deficiency, Vit-A deficiency, Syphilis, Oncogenic viruses, Immunosuppression, and Oncogenes and tumor suppressor genes
question
Which type of smokeless tobacco imposes the greatest risk for SCC?
answer
Dry snuff> moist snuff> chewing tobacco. Over all RR of smokeless tobacco is 2 to 26
question
What type of radiation causes oral SCC?
answer
Any type, UV, x-irradiation to head and neck. Risk is dose dependent. Common cause of lip SCC
question
What are the characteristic of Iron deficiency SCC?
answer
Develops at a younger age, SCC of esophagus, oropharynx, and posterior mouth. Syndromes such as plummer-Vinson syndrome cause sever iron deficiency
question
What do those with a vitamin-A deficiency present with?
answer
Low serum retinol and dietary betacarotene placing them at greater risk of SCC
question
Which syphilis causes increased risk for SCC?
answer
Tertiary syphilis, dorsal tongue SCC RR of 4
question
Which strains of HPV are high risk strains for oral SCC?
answer
HPV - 16, 18, 31, and 33
question
What increases the already high risk for immunosuppressed pts (AIDS/ transplant pts)?
answer
Use of tobacco and alcohol
question
How do oncogenes and tumor suppressor genes cause cancer?
answer
Activation of oncogenes (ras, myc, EGFR) and inactivation of tumor suppressor genes( p53,pRb, p16, E-cadherin)
question
What are the high risk sites for SCC?
answer
Tongue (lateral border, ventral), FOM, and Softpalate. FOM SCC - high risk of second primary malignancy
question
How does oropharyngeal SCC present?
answer
In tonsil, posterior soft palate, or base of tongue. Usually large tumor size, cervical and distant metastasis at presentation because of delays in diagnosis
question
Which lip in affected more?
answer
Lower lip 90%, preceded by actinic cheilitis
question
What does SCC look like radiographicly?
answer
May cause destruction of underlying bone, radiolucency ill-defined (moth eaten) borders and can mimic periodontal disease
question
What does SCC look like histologically?
answer
Invasive islands of dysplastic (atypical, anaplastic) squamous cells
question
When is SCC said to have regional metastasis?
answer
When metastasis is to ipsilateral cervical lymph nodes and nodes are non-tender, firm, hard +or- fixation. 21% pt have cervical mets at presentation
question
What is distant metastasis?
answer
Mets to distant organs: lungs, liver bones. 2% of pts at presentation
question
To which nodes do tumors of the oropharynx mets to?
answer
Jugulo-digastric and retropharyngeal
question
To which nodes do tumors of the posterior oral cavity mets to?
answer
High jugular digastrics nodes
question
To which nodes do tumors of the lip vermilion and FOM mets to?
answer
Submental nodes
question
What is the treatment for intraoral SCC?
answer
Surgical resection is #1 other additional treatments include radiation, chemo, and neck dissection
question
What can molecular markers be useful for?
answer
Predictors of malignant transformation and prognostic indicators
question
What is chemoprevention used for?
answer
Oral dysplasias and pts at risk for second primary recurrences
question
What is a fibroma?
answer
The most common benign soft tissue lesion of the mouth, likely caused by reactive hyperplasia to local irritation. Most often seen in buccal mucosa along occlusal line
question
What are the clinical features of fibroma?
answer
Normal mucosal colored or white, smooth surface, nodule or mass, Firm
question
What do fibroms look like histologically?
answer
Proliferation of dense fibrous CT, intact or ulcerated stratified squamous epithelium
question
How are fibromas treated?
answer
Conservative surgical excision then submit for histologic examination to rule out other entities. If gingival scale adjacent teeth to remove local irritants
question
What causes pyogenic granuloma formation?
answer
Likely reactive hyperplasia to a local irritations. It is neither pyogenic nor granulomatous in nature
question
Where do pyogenic granulomas usually form?
answer
On the gingiva
question
Who gets Pyogenic franulomas?
answer
F>M, children and young adults
question
What are the clinical features?
answer
Pink, red, purple, often lobulated, nodule or mass, may initially grow rapidly, may bleed on palpitation
question
What is a pregnancy tumor?
answer
PG during pregnancy that typically occurs in 1st trimester increase in frequency to 7th month, due to estrogen and progesterone levels
question
What is Epulis granulomatosum?
answer
PG that occurs in healing extraction socket, response to foreign bony, bone spicule in socket
question
What is granulation tissue?
answer
Inflamed and well-vascularized fibrous connective tissue
question
What happens to long standing PG?
answer
fibrous maturation PG turns into a fibroma
question
What is the treatment for PG?
answer
conservative surgical excision with histologic examination, if gingival scale adjacent teeth. Defer treatment with pregnancy tumor may resolve after pregnancy
question
What is a pleomorphic adenoma?
answer
Benign neoplasm of ductal epithelial and myoepithelial cells. The most common salivary gland tumor and the most common salivary gland tumor of childhood
question
Who gets pleomorphic adenoma?
answer
F slightly> M, 30-60 yr but really any age
question
Where are pleomorphic adenomas seen the most?
answer
Parotid gland: superficial lobe > deep lobe, Minor salivary glands: palate> upper lip > bu mucosa
question
What are the clinical features for a parotid PA?
answer
swelling over ramus anterior to ear, angle of mn if it's the superficial lobe for the deep lobe mass of lateral pharyngeal wall/ soft palate, slowly growing, mostly movable, can become very large, usually asymptomatic.
question
What are the clinical features of a minor salivary gland PA?
answer
slowly growing, mucosal colored, smooth surfaced dome shaped, mass, +/- secondary ulceration, movable if involving lips and bu mucosa
question
What histologic finding are seen with PA?
answer
well circumscribed, mostly encapsulated, containing - ductal 1. epithelial cells, 2. myoepithelial cells, and 3. chondromyxiod stroma
question
How are PAs treated?
answer
Superficial parotid PA - superficial parotidectomy w/ preservation of CN VII. Deep lobe Pas - total parotidectomy w/ preservation of CN VII. Submandibular - excision of tumor and gland. Minor glands - excision of tumor.
question
What % of PAs will under go malignant transformation if not removed?
answer
5% called carcinoma ex PA
question
What is the most common odontogenic tumor?
answer
Ameloblastoma
question
What is an ameloblastoma?
answer
Benign but locally aggressive neoplasm of odontogenic epithelium
question
What are the 3 subtypes of ameloblastomas?
answer
1. Solid or multicystic 86% 2. Unicystic 13% 3. Peripheral 1%
question
Where are ameloblastomas usually located?
answer
Mandible 85% usually in the posterior (molar, ascending ramus area)
question
What are the clinical features of ameloblastoma?
answer
Usually asymptomatic/ painless, swelling, bone expansion, buccal and lingual cortical expansion, can become very large
question
What are the radiographic features of ameloblastoma?
answer
Shape: multilocular, Density: radiolucent, Borders: well defined/ scalloped borders, Internal architecture: soap bubble/ honeycomb, Location: may be associated w/ unerupted tooth, Effect on adj. structures: +/- root resorption/ tooth displacement
question
What are ameloblasitc features?
answer
Palisaded peripheral cells, reversed polarity, and stellate reticulum cells
question
What is the histology of ameloblastoma?
answer
Islands of odontogenic epithelium with ameloblastic features
question
How is ameloblastoma treated?
answer
Treatment is controversial: enucleation vs. resection. Curettage has a 50-90% recurrence. Long term clinical and radiographic follow up is needed
question
HIV and Oral Path:
answer
...
question
What are the general characteristics of HIV?
answer
It is a lentivirus with a prolonged latency period. It infecs CD4+ Helper T lymphocytes and ultimately reduces the number of T cells and sets up an immunocompromised state.
question
What are the common modes of transmission of HIV?
answer
Sexual Contact and parenteral exposure, contaminated blood, and maternal transmission....other modes rare.
question
What are the most common exposure categories for HIV?
answer
MSM and IDU
question
What is the Course of HIV?
answer
Acute viral syndrome (symptoms like mono/IM), prolonged asymptomatic stage (persistant neck lymphadenopathy 70%), and Symptomatic stage (AIDS related complex and over AIDS)
question
What is AIDS related complex?
answer
ARC is part of the symptomatic stage of HIV where you might see chronic fever, weight loss, diarrhea, oral candidiasis, herpes zoster, or oral hairy leukoplakia (OHL).
question
What is considered to be over AIDS?
answer
Part of the symptomatic stage of HIV in which you get multisystem involvement (respiratory, musculoskeletal, GI, oral, and others), and CNS involvement with neurologic and psychiatric symptoms.
question
What are the EC-clearinghouse classifications for oral manifestations of HIV?
answer
Group 1: strongly associated with HIV—candidiasis, OHL, KS, NHL, and PD, Group 2: Less commonly associated—Bacterial infections, hyperpigmentation, necrotizing ulcerative stomatitis, Viral infections, oral ulcerations Group 3: Seen in HIV: Other bacterial infections, drug rxn, fungal infections, neurologic disturbances, apthous ulcers.
question
How many aids pts get candidiasis?
answer
33% of HIV and over 90% of AIDS patients
question
What are the 4 types of clinical presentations of Candidiasis?
answer
Pseudomembranous, Erythematous, Chronic hyperplastic, and mucocutaneous. (the first 3 are common with HIV)
question
What are the 5 types of Erythematous Candidiasis?
answer
Acute atrophic, Central papillary atrophy, chronic multifocal, Angular cheilitis, and Denture stomatitis
question
At what CD4 counts is it common to see pseudomembranous and erythematous type candidiasis?
answer
Pseudomembranous <200, and Erythematous < 400.
question
What are the characteristics of pseudomembranous Candidiasis?
answer
Adherent white plaques on buccal mucosa, palate and dorsal tongue that can be wiped off. Mucosal erythema. Commonly seen in those taking broad spectrum antibiotics like immunocompromised. Usually CD4+ less than 200.
question
What are is characteristic of Erythematous candidiasis?
answer
Mucosal erythema (bald appearance) 3 most common types with HIV...are central papillary atrophy, angular cheilitis, and chronic multifocal variants. Usually seen with CD4+ less than 400.
question
What is central papillary atrophy?
answer
A type of erythematous candidiasis. Aka median rhomboid glossitis. Seen at the mid dorsal tongue with a well-defined bald area/loss of filiform papillae. RX: antifungals
question
What is angular Cheilitis?
answer
A type of erythematous candidiasis. Aka perleche. Common in immunocompromised and with loss of vertical dimension. Erythemal, fissuring, and scaling of the coners of the mouth. Common coinfection with candida and Staph Aureus.
question
What does the histology of candidiasis look like?
answer
You will see candidal hyphae in the parakeratin layer, also PMN in epithelium and elongated rete pegs seen under the staining of a Periodic Acid Schiff (PAS), GMS, or KOH stain.
question
How do you diagnose Candida?
answer
Clinical features and a fungal culture (Sabourad's agar), cytology smear, and tissue biopsy.
question
What is the treatment for Candidiasis?
answer
We always do a med consult before prescribing anything to an HIV/AIDS patient, but usually it is treated with antifungal therapy.
question
When do you do systemic antifungal treatment for candidiasis?
answer
If CD4's are under 50 or pt is not on antiretrovirals tx then Fluconazole is the drug of choice as azoles are synergistic with antiretrovirals
question
What are the 3 type of antifungal medications?
answer
Polyenes (amphotericin B), Imidazoles (clotrimazole), or Triazoles (fliconazole) dentists might prescribe the imidazoles or triazoles but usually not polyenes.
question
What is LGE?
answer
Common in HIV. A red band of free gingival margin. Responds to fluconazole.
question
What are the characteristics of NUG?
answer
Ulceration and necrosis or 1 or more interdental papilla with no loss of attachment. Features ulceration, necrosis of papilla, bleeding, pain, and halitosis.
question
What is NUP?
answer
Gingival ulceration and necrosis with rapid loss of attachment and alveolar bone, tooth mobility, and in multiple isolated sites, bleeding, pain, edema, and halitosis.
question
What is the treatment for NUP and NUG?
answer
Debridement—frequent and often until stable, Antimocrobials—CHK rinses or systemic metronidazole, Long term maintenance by quitting contributing habits.
question
What is Herpes Simplex Virus?
answer
DNA virus part of HHV family, two types HSV-1 (affects above the waiste) and HSV-2 (affects the skin below the waist. There is some cross reactivity between HSV1 and HSV2. If you have had one type you have reduced chance of getting the other.
question
What is the normal course of HSV infections?
answer
You get a primary infection that is taken up by sensory nerves, into the ganglia and remains latent until reactivated to give a secondary infection. The trigeminal ganglion is the most common site for latency of HSV-1.
question
What can trigger a reactivation of a primary infection?
answer
UV light exposure.
question
Are secondary herpes infections symptomatic?
answer
Most are, but not all and the virus can be shed without any active lesions.
question
What are the two main presentations of primary HSV infections?
answer
Acute herpetic gingivostomitis or pharyngotonsillitis.
question
What are the two most common presentations of secondary/recurrent HSV infections?
answer
Herpes labialis and Intraoral recurrent herpes.
question
What are the characteristics of herpes labialis?
answer
A cold sore, UV light trigger, occurs in young adults and throughout life at the vermillion border and adjacent skin. Usually preceded by a prodrome and then presents as a cluster of vesicles then crusts then ulcers.
question
When is herpes labialis most contagious?
answer
During the vesicular stage (1st 48 hrs) as there is active viral replication occurring.
question
How does secondary intraoral recurrent herpes present?
answer
Young adults with recurrences throughout life, on the keratinized mucosa, seen as vesicles, then red macules, then ulcerations that coalesce and then heal in 7-10 days.
question
What are HSV infections like for the immunocompromised?
answer
Frequent recurrence due to loss of host immune response, can be life threatening with continued spreading until treated with antivirals, it has atypical characteristics: seen in Keratinized and NK mucosa, you see necrosis, large ulcers with raised, yellow border. Maybe coninfection with CMV....send persistant ulcer tissue to biopsy for HIV patients.
question
What does the histology of HSV look like?
answer
Free floating cells in vesicles (Tzanck cells) and then the 3 m's of herpes infected cells: Multinucleation, Chromatin Margination, and Nuclear Molding with ballooning degeneration....(these features also common in VZV infections)
question
How do you Dx HSV?
answer
Clinical presentation and viral culture, cytologic smear/tissue biopsy, or serologic tests.
question
What is the Tx for HSV in HIV patients?
answer
Oral antivirals for prevention, IV antivirals if active HIV infection (acyclovir). Gancyclovir if coinfection with HSV and CMV.
question
What is OHL?
answer
Oral Hairy Leukoplakia?; Caused by EBV (HHV-4), reduced with HAART, on the lateral border of tongue. Seen as a white plaque with vertical corrugations that can become shaggy and doesn't wipe off.
question
What is the histology of OHL?
answer
Hyperparakeratinosis with epithelial hyperplasia, surface corrugations, and balloon cells (perinuclear halo with chromatin beading) in the upper epithelial layer. EBV can be isolated with in situ hybridization and PCR...
question
What is the DX for OHL?
answer
Clinical and EBV identification in tissue biopsy
question
What is the TX for OHL?
answer
Not tx necessary will resolve with antivirals with common recurrences.
question
What is HPV associated with in the immunocompetent?
answer
Oral lesions like squamous papilloma, verruca vulgaris, and condyloma acuminatum.
question
What are the features of HPV in the immunocompromised?
answer
On most surfaces of oral cavity, cauliflower like surface, multifocal blunt or sharp projections.
question
What does the histology of HPV look like?
answer
Papillary stratified epithelium with hyperpara or hyperorthokeratosis, epithelial hyperplasia with Koilocytes in upper epithelial layer. HPV can be located in situ via PCR.
question
What are koilocytes?
answer
Vacuolated cells with shrunken nuclei that are HPV + and found in the upper epithelial layer.
question
How do you dx HPV?
answer
Clinically and HPV identification on tissue biopsy
question
What are the tx's for HPV?
answer
Surgical excision but recurrence is common, long term observation especially if dysplastic.
question
What is KS?
answer
Malignant neoplasm of vascular endothelial cells. Associated with KSHV. Most common malignancy in HIV pts, Seen in skin of upper body or on the oral mucosa, hard palate, gingival, and tongue.
question
What does KS look like?
answer
Flat, brown-red areas (macules, pathches) that don't blanch with diascopy and later they are raised plaques or nodules, with bleeding, pain, and necrosis. Can invade bone.
question
What does the histology of KS look like?
answer
Vascular proliferation, Small, slit-like blood vessels with spindled endothelial cells, with RBC's within and outside the vessels.
question
What are lymphomas?
answer
Malignant neoplasms of the lymphoreticular cells. Most are NHL's, many associated with EBV. 2nd most common neoplasm in HIV. More common in extranodal sites.
question
What are the clinical features of lymphoma?
answer
Red to purple, boggy swellings in soft tissues, swelling and bone expansion with possible tooth mobility and nerve parasthesia and an ill-defined radiolucency.
question
What does the histology of lymphoma look like?
answer
A sheet of atypical lymphocytes
question
What is the treatment for lymphoma?
answer
Chemo and radiation with a poor prognosis.
question
How do you dx HIV?
answer
Viral culture with enzyme immunoassay (EIA) good for screening but possible false positives occur. Usually done with a western blot.
question
What is the TX for HIV?
answer
HAART. Combo of nucleoside reverse transcriptase inhibitors and non nucleoside reverse transcriptase inhibitor and a protease inhibitor.
question
At what level is it AIDS?
answer
Less than 200 cells or less than 14% of total lymphocites.
question
What are some common diseases which are used as indicator diseases for dx of AIDS?
answer
Candidiasis, Cervical cancer, KS, Lymphoma, HSV with chronic ulcers and soar throat, and Pneumocystis carini pneumonia.
question
What are the clinical features of AIDS?
answer
Opportunistic infections, Multisystem involvement, and Neurologic dysfunction.
question
What is in store for the future of HIV and AIDS?
answer
Public Health interventions, New therapeutic agents, and HIV vaccine.
