Presentation on theme: "DESEASES OF HEAD, NECK, EAR, NOSE and TRHOAT"— Presentation transcript:
1DESEASES OF HEAD, NECK, EAR, NOSE and TRHOAT Associate ProfessorDr. Alexey PodchekoSpring 2015The “realm” of “ENT”, or otolaryngology, includes diseases of the nose, nasal cavity, nasopharynx, oral cavity, oropharynx, larynx, laryngopharynx, “upper” airway, defined as airspaces leading ultimately into the lung, and all the structures in these spaces, such as the for pairs of nasal sinuses, auditory tubes, ears, nasolacrimal duct, tonsils, and salivary glands.ENT docs do thyroid surgery too.
2Topics:1. oral cavity 2. upper airways, including the nose, pharynx, larynx, and nasal sinuses; 3. ears 4. neck 5. salivary glands
3EVERYTHING that touches AIR (columnar) or FOOD (squamous) in the HEAD/NECK region ORAL CAVITY“UPPER” RESPIRATORY TRACTEARSNOSESALIVARY GLANDSBecause a tougher stratified squamous mucosa is needed when these spaces come into contact with particulate matter, or material other than air or water, this type of mucosa, no matter where it is in the ENT domain, behaves similarly to degenerative, inflammatory, and neoplastic influences. Similarly, upper “airway” mucosa, classically subject only to air contact, is pseudostratified ciliated columnar in histology, and behaves similarly to these three influences as well. Upper airway mucosa, however, often transforms into stratified squamous by a process called “squamous metaplasia” as a non specific response to a wide variety of injurious stimuli.
4INTENDED LEARNING OUTCOMES Understand the common disorders of the upper airway and upper digestive tract (i.e., head and neck) in the usual context of:DEGENERATIVE,INFLAMMATORY,andNEOPLASTIC…deviations of normal anatomy and histologyOnce again, amid the numerous brilliant adjectives one can place before the word “diseases”, from a solid anatomical point of view, the classifications of DEGENERATIVE, INFLAMMATORY, and NEOPLASTIC cover almost all basis, and is a good way to think of disease classifications of any organ or system.
5ORAL CAVITY Common pathologic conditions of the oral cavity TEETH/GINGIVA/ALVEOLAR BONEINFLAMMATORY/”REACTIVE” LESIONSINFECTIONS: HSV, VIRAL, FUNGILEUKOPLAKIA/”HAIRY” LEUKOPLAKIASQUAMOUS TUMORS: BEN/MALIGODONTOGENIC CYSTS/TUMORSCommon pathologic conditions of the oral cavity
7Time frame of teething Incisors 10-15mo Bicuspids 15-18mo Molars 18-24mo
8Tooth Decay (Cavities, “Caries”) Dental caries one of the most common diseases, is the most common cause of tooth loss before age 35Result of mineral dissolution of tooth structure“Processed” carbohydrates, i.e., sugarsBacterial (Strep. Viridans: Strep. Mutans + Strep. Sanguis; Lactobacilli, Actinomycetes) acidic erosion of enamel due to ability to produce insoluble dextransRole of pH, spacing, brushing, FlTartarplaquecalculus = bacteria, proteins, cells
9Gram Positive cocci isolated from the blood of patient with bacteremia synthesize dextrans from glucose. The bacteria most likely contribute to which of the following pathological states?A GlomerulonephritisB. SarcoidosisC. Erythema nodosumD. Migratory polyarthritisE. Anterior uvetisF. Dental Caries
10Vindans streptococci, notably S. mutants and S Vindans streptococci, notably S. mutants and S. sanguis, are normally present in the human mouth and are major contributors of tooth decay and the initiation of dental caries. The organisms also cause bacterial endocarditis. Viridans streptococci are adhere to the surface of tooth enamel and heart valves and multiply in those locations due to their ability to produce insoluble dextrans.
11Find the “cavity”, i.e., caries, i.e., enamel erosion
12GINGIVITISGingiva - squamous mucosa in between the teeth and around themGingivitis is inflammation of the mucosa and the associated soft tissues.Causes:Bacteria: Actinobacilli, Porphyromona, PrevotellaViruses: HSV1 and 2Symptoms: erythema, edema, bleeding, changes in contour, and loss of soft-tissue adaptation and sores12
13PeriodontitisDefinition: inflammatory process that affects the supporting structures of the teeth: periodontal ligaments, alveolar bone, and cementumCauses: Bacteria, adult periodontitis is associated primarily with:Actinobacillus actinomycetemcomitans,Porphyromonas gingivalisPrevotella intermediaAffected structures: Gingiva, periodontal ligaments, bone, cementum
14Periodontitis Component of several different systemic diseases: 1. AIDS2. Leukemia3. Crohn's disease4. Diabetes mellitus5. Down syndrome6. Sarcoidosis,7. Syndromes associated with polymorphonuclear defects (Chédiak-Higashi syndrome, agranulocytosis, and cyclic neutropenia)Etiologic factor in several important systemic diseases:1. infective endocarditis,2. pulmonary and brain abscesses,3. averse pregnancy outcomes (preeclampsia)
15A 67-year-old male is hospitalized with low-grade fevers fatigue and a diastolic murmur at the left sternal border. Blood cultures reveal Gram positive cocci that are catalase-negative and able to grow in the presence of optocin. This patient’s medical history is most likely to reveal which of the following procedures in the past month?A. Dental extractionB. Skin biopsyC. Sinus drainageD. Nasal polypectomyE. Cystoscopy
16(Choice A) Dental extraction is associated with endocarditis caused by S. viridans, a Gram positive coccus. In most cases, S. viridans causes subacute bacterial endocarditis in already abnormal heart valves (e.g. congenital valvular abnormalities valves damaged by rheumatic fever.)
18Inflammatory/Reactive Tumor-like Lesions MC fibrous proliferative lesions of the oral cavity:fibroma (61%)reactive nodules of the oral cavity peripheral ossifying fibromapyogenic granulomaperipheral giant-cell granulomagingival hyperplasia
19Irritation fibromaprimarily occurs in the buccal mucosa along the bite line or at the gingivodental margin.Morphology: nodular mass of fibrous tissue, with few inflammatory cells, covered by squamous mucosa.Rx: Surgical excisionSmooth pink exophytic nodule on the buccal mucosa.
20“Irritation” FibromaOften the terms “inflammatory” or “reactive” refers to this type of “fibroma”.
21Peripheral ossifying fibroma Growth of the gingiva that is considered to be reactive in nature rather than neoplastic.Result of the maturation of a long-standing pyogenic granulomaRx: Surgical excision down to the periosteum (recurrence rate of 15% to 20%)
22Pyogenic granulomaHighly vascular pedunculated lesion on the gingiva (children, young adults, pregnant women (pregnancy tumor).Growth can be rapid, raising the fear of a malignant neoplasm.Histology: vascular proliferation that is similar to granulation tissue (capillary hemangioma?)Regress with formation of peripheral ossifying fibroma.Rx: surgical excision
23PYOGENICGRANULOMAGranuloma or neoplasm or granulation tissue? Who cares?A pyogenic granuloma pops out like a “tumor” and is 100% indistinguishable from normal granulation tissue, and looks nice and pink and healthy like granulation tissue, i.e., organizing inflammation, too. The least thing it can be called is a granuloma, because it rarely has clusters of macrophages or giant cells. Would you expect a pyogenic granuloma to “blanch” and a fibroma NOT to “blanch”? Answer: YES
24A 6-year-old boy presents with a painful sore in his mouth A 6-year-old boy presents with a painful sore in his mouth. Physical examination reveals a small, elevated, and locally ulcerated red-purple gingival lesion. A soft red mass measuring 1 cm in diameter is surgically removed. Histologic examination discloses highly vascular granulation tissue, with marked acute and chronic inflammation. What is the most likely diagnosis?(A) Acute necrotizing gingivitis(B) Aphthous stomatitis(C) Herpes labialis(D) Pyogenic granuloma(E) Tuberculosis
25Peripheral giant cell granuloma bluish purple tumor-like lesionHistology: aggregation of multinucleate, foreign body–like giant cells separated by a fibroangiomatous stroma, not encapsulatedcan cause resorption of alveolar boneRx: Surgical excisionDif. diagnosis: central giant-cell granulomas of bones and “brown tumors” seen in hyperparathyroidism
26Histology of peripheral giant cell granuloma reveals a dense infiltrate of histiocytes and multi-nucleated giant cells within the subepithelial fibrous stroma.
27APHTHOUS ULCERS (CANKER SORES) superficial ulcerations of the oral mucosa affect up to 40% of the population in the United StatesEtiology: stress, fatigue, illness, injury from accidental biting, hormonal changes, menstruation, sudden weight loss, food allergies, and deficiencies in vitamin B12, iron, and folic acid , recurrent apthous ulcers may be associated with celiac disease and inflammatory bowel disease.Clinic: extremely painful and often recurrent sores, tendency to be prevalent within certain families.Morphology: Single or multiple, shallow, hyperemic ulcerations covered by a thin exudate and rimmed by a narrow zone of erythemaHistology: Mononuclear infiltratePrognosis: Spontaneously resolve in 7 to 10 days or be stubbornly persistent for weeksRx: local anesthetics
28“Canker” sore = Aphthous ulcer Obscure etiology, 40% of us have had them, painful, and you can bet there are inflammatory cells at the base. You know what they are. You’ve had them.Things related to them include: stress, fatigue, illness, injury from accidental biting, hormonal changes, menstruation, sudden weight loss, food allergies, and deficiencies in vitamin B12, iron, and folic acid (wikipedia). Whenever a condition is associated with LOTS of things, like this, we call this an “obscure” etiology ;)
29GLOSSITIS Inflammation of the tongue atrophy of the papillae of the tongue and thinning of the mucosa, exposing the underlying vasculatureAtrophic Glossitis Causes: Deficiencies of vitamin B12 (pernicious anemia), riboflavin, niacin, or pyridoxine, sprue and iron-deficiency anemia.Ulcerative Glossitis Causes: : jagged carious teeth, ill-fitting dentures, and, rarely, with syphilis, inhalation burns, or ingestion of corrosive chemicalsClinic: Plummer-Vinson syndrome - combination of iron-deficiency anemia, glossitis, and esophageal dysphagia mostly in postmenopausal women
30Glossitis: Bacterial or viral infections (including oral herpes simplex). Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other traumaExposure to irritants such as tobacco, alcohol, hot foods, or spices.Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in candy, plastic in dentures or retainers, or certain blood-pressure medications (ACE inhibitors).Disorders such as iron deficiency anemia, pernicious anemia and other B-vitamin deficiencies, oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris, syphilis, and others.Occasionally, glossitis can be inherited. (Wikipedia)If a “geographic” tongue mans only a part of the tongue is inflamed, i.e., “red”, then the tongue on the right has the geography of Maine or Illinois? Or India?
31HERPES SIMPLEX VIRUS INFECTIONS Mostly herpes simplex virus type 1 (HSV-1)Enveloped double-stranded DNA virusPrimary HSV infection typically occurs in children age 2 to 4 years,Forms:acute herpetic gingivostomatitis – MOST Common form of primary infectioncold sores (Herpes labialis)recurrent herpetic stomatitis
32HERPES SIMPLEX VIRUS INFECTIONS Herpetology is the study of creepy critters, reptiles and amphibians. Herpetic vesicles “creep” over mucosal surfaces.Like CMV and V-Z viruses, the various herpes viruses (mainly type 1 and 2) are, amazingly, in the “herpes” family of viruses.Early lesions crop up as vesicles, after a few days, these vesicles can be irritated, ulcerated, inflamed, and secondarily pustulated.Classically type 1 was predominantly oral mucosa, and the slightly nastier type 2 was more genital, but nowadays, crossover is so common, who cares any more?The virus recurs often for many years, triggered off by god-knows-what, and the newer antiviral agents have shown amazing efficacy in preventing recurrences.Just about everybody had been exposed to herpes of some type.HERPES SIMPLEX VIRUS INFECTIONS32
33HERPES SIMPLEX VIRUS INFECTIONS Morphology:Intracellular and intercellular edema (acantholysis) yielding clefts that may become transformed into macroscopic vesicles.Cells have eosinophilic intranuclear viral inclusions,multinucleate polykaryonsTzanck test: microscopic examination of the vesicle fluid to find multinucleated polykarions
34TZANCK SMEARThe neat thing about a Tzanck smear is that you can do it easily in your office, just gently scrape a vesicle, smear it, stain it with just about anything, and look for much larger than usual squamous nuclei with inclusions. Most vesicles cause by herpes family viruses can have a POSITIVE Tzanck (pronounced “zank”) smear, or test.Would you rule out herpes if the test was negative? Would you tend to be more likely to rule it in, if the smear was positive?The neat thing about a Tzanck smear is that you can do it easily in your office, just gently scrape a vesicle, smear it, stain it with just about anything, and look for much larger than usual squamous nuclei with inclusions. Most vesicles caused by herpes family viruses can have a POSITIVE Tzanck (pronounced “zank”) smear, or test.34
35A 2-year-old male is brought to clinic with fever irritability, and decreased oral intake. Physical examination reveals swollen gums with ulcerative lesions and enlarged, tender cervical lymph nodes. Oral lesion scrapings demonstrate cells with intranuclear inclusions. Which of the following is most likely responsible for this patient’s disease?A. Enveloped double-stranded DNA virusB. Non-enveloped double-stranded DNA viruC. Non-enveloped single-stranded DNA virusD. Non-enveloped positive-sense RNA virusE. Enveloped positive-sense RNA virusF. Enveloped negative-sense RNA virus
36A 5-year-old male is brought to the clinic with a several day history of fever, irritability and refusal to eat. Physical examination demonstrates painful gingival ulcers, swollen gums, and cervical lymphadenopathy. Microscopic examination of the oral ulcer base scrapings is shown on the slide below. This patient current situation is most likely represent:A Primary infectionB. Virus reactivationC. Latent infectionD. Abortive infectE. Slow virus infection
37ORAL CANDIDIASIS (THRUSH) Candidiasis is by far the most common fungal infection in the oral cavity.Factors:(1) immune status of the individual;(2) the strain of C. albicans present(3) the composition of an individual's oral flora(4) Abt therapy(5) Underlying diseases (AIDS, Diabetes)Major clinical forms of oral candidiasis:Pseudo-membranous (thrush)ErythematousHyperplastic,Monilia, thrush-mouth, candida: they all mean the same thing. Look for a whitish oral film without much underlying inflammation (i.e., redness).Common in babies, diabetics, immunocompromised people. Candida (almost always ablicans) always affects moist, usually non-keratinized, stratified squamous mucosa, i.e., mouth, vagina, moist genital skin areas. Everybody has it lying around waiting for an immunocompromised condition to occur.
38White filmy patches NOT firmly attached to the underlying moist non-keratinized stratified squamous mucosa. Minimal redness. Candida is on all of us. It LOVES to proliferate on moist NON-keratinized stratifies squamous mucosae, especially in immune deficiency situations.
39Finding the NON-septate hyphae (i. e Finding the NON-septate hyphae (i.e., “pseudo”-hyphae) along with yeasts and budding yeasts in your simple office lab, is diagnostic. Almost any simple stain will show this. The “PAS” stain is best, because it imparts a bright red color to yeasts and pseuduhyphae
42HAIRY LEUKOPLAKIAHairy leukoplakia - white patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically as any other disease, caused mostly by EBV infection80% of patients with hairy leukoplakia are infected with the human immunodeficiency virus (HIV)!!!Dif. diagnosis with Candidiasis - lesion cannot be scraped off.Histology: Hyperparakeratosis and acanthosis with “balloon cells” in the upper spinous layer, koilocytosis of the superficial, nucleated epidermal cells,Prognosis: In HIV-positive individuals, with hairy leukoplarkia, symptoms of AIDS follow in 2 to 3 years!
43“Hairy” leukoplakiaLEUKOPLAKIA. This is defined as a dry flat “plaque” of, usually, the oral mucosa, due to ANY reason, many (most?) of which are NON-malignant, NON-dysplastic, and 100% reversible, but some of which are premalignant. Please understand “leukoplakia” is a clinical description, and NOT a specific clinical or pathological entity, and can range anywhere between hyperkeratosis/inflammation to carcinoma.
44“Hairy” leukoplakia“Hairy” leukoplakia however, is usually a sign of HIV.
45Premalignant lesions in the oral cavity Leukoplakia - a white patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically as any other diseaseuntil it is proved otherwise via histologic evaluation, all leukoplakias must be considered precancerous!Erythroplakia -red, velvety, possibly eroded area within the oral cavity that usually remains level with or may be slightly depressed in relation to the surrounding mucosaSpeckled leukoerythroplakia :Erythro+Leukoplakia
46Histologic progression of Leukoplakia into squamous cell carcinoma EXTREMELY IMPORTANT concept in the insidious development of squamous cell carcinoma of ANY location, no matter what the genetics, molecular biology, or etiology is! UNDERSTAND THIS FOR THE REST OF YOUR LIFE!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!NORMAL DYSPLASIA CARCINOMA-IN-SITUINFILTRATING MALIGNANCY
47Head and Neck are Squamous Cell Carcinomas (HNSCCs) 95% of cancers of the head and neckoverall long-term survival has remained at less than 50%individual who is fortunate to live 5 years after the initial primary tumor has up to a 35% chance of developing at least one new primary tumor within that period of timeEtiology: Tabacco, Alcohol, actinic radiation (sunlight), pipe smoking, chewing of betel quid, mouthwash (25% alcohol)
48Morphology of squamous cell carcinoma of the oral cavity Favored locations:1. ventral surface of the tongue2. Floor of the mouth3. Lower lip, soft palate, and gingiva
49Does this look like more than a simple “plaque” Does this look like more than a simple “plaque”? Like, perhaps, ulceration and induration under the ulcer bed.This is a classic appearance of INFILTRATING or INFILTRATIVE SQUAMOUS CELL CARCINOMA of the mouth. Can there be any other type?Where would you take the biopsy?Morphology of squamous cell carcinoma of the oral cavity Raised, firm, pearly plaques or as irregular, roughened, or verrucous areas of mucosal thickening
50Morphology of squamous cell carcinoma of the oral cavity Well, moderate, poor.These are the 3 types of differentiation of squamous cell cancer, no matter what the current trendy buzz words or grading letters/numbers are!!!In “well” you can see “pearls”. This is a pearl above.In “moderate”, you can usually see “intercellular bridges”, but not pearls.In “poor” you usually have no real idea that it even looks squamous at all, and you have to rely on squamous or immunochemical markers, such as cytokeratin markers, or a whole host of others.There are the 3 types of differentiation of squamous cell cancer: Well, moderate, poor.In “well” you can see “pearls”. (pearl above).In “moderate”, you can usually see “intercellular bridges”, but not pearls.In “poor” you usually have no real idea that it even looks squamous at all, and you have to rely on squamous or immunochemical markers, such as cytokeratin markers, or a whole host of others.
52ODONTOGENIC CYSTSDefinition: cyst like structures derived from epithelial linings or epithelial remnants in the jaw boneClassification:INFLAMMATORY CYSTS (e.g., Periapical “Radicular” - most common)DEVELOPMENTAL CYSTS (DENTIGEROUS - most common)As a rule of thumb, all cysts submitted by oral surgeons are benign. Many types often recur however. It is only a question of whether the cyst is “developmental”, i.e., an abnormal development, ultimately from embryology, or “inflammatory” in etiology.
54Periapical cyst extremely common lesions found at the apex of teeth. Result of long-standing pulpitis or periapical abscess.Periapical inflammatory lesions persist as a result of the continued presence of bacteria or other offensive agents in the area
55Dentigerous cystDef: Cyst that originates around the crown of an unerupted tooth and is thought to be the result of a degeneration of the dental follicle.Xray: unilocular lesions and are most often associated with impacted third molar (wisdom) teeth.Histology: they are lined by a thin layer of stratified squamous epithelium with chronic inflammatory cell infiltrate in the connective tissue stroma.Rx: ExcisionComplications: recurrence or, very rarely, neoplastic transformation into an ameloblastoma or a squamous cell carcinoma.
56DENTIGEROUSCYSTClassical histologic image of a dentigerous cyst.lined by a thin layer of stratified squamous epithelium with chronic inflammatory cell infiltrate in the connective tissue stroma
57Odontogenic keratocyst (OKC) locally aggressive and has a high rate of recurrenceMost often diagnosed in patients between ages 10 and 40.Males within the posterior mandible.Xray: well-defined unilocular or multilocular radiolucenciesHisto: layer of parakeratinized or orthokeratinized stratified squamous epithelium with a prominent basal cell layer and a corrugated appearance of the epithelial surface.Rx: Complete removal of the lesion
58Odontogenic tumorsOdontoma- the most common type of odontogenic tumors (app. 70%), arises from epithelium but shows extensive depositions of enamel and dentin. Odontomas are probably hamartomas rather than true neoplasms and are cured by local excision.Ameloblastoma (app. 30%) - from odontogenic epithelium. It is commonly cystic, slow growing, and locally invasive but has an indolent course in most cases
59Circular sunburst opacity surrounded by a thin radiolucent border Odontoma on x-ray?Ameloblastoma on x-ray?Circular sunburst opacity surrounded by a thin radiolucent borderLarge expansile multilocular or soap-bubble radiolucency; favored location is posterior mandible
60Histologic view of odontoma and ameloblastoma Ameloblastoma: notice the stellate reticlulum and the row of ameloblasts with vacuoles (40x).Odontoma consists of a mixture of hard substances, epithelial structures, and empty spaces formerly occupied by enamel matrix, 20x