DESEASES OF HEAD, NECK, EAR, NOSE and

TRHOAT

Associate Professor Dr. Alexey Podcheko

Spring 2015

1. oral cavity2. upper airways, including the nose, pharynx, larynx, and nasal sinuses; 3. ears 4. neck5. salivary glands

Topics:

EVERYTHING that touches AIR (columnar) or FOOD (squamous) in the HEAD/NECK region

ORAL CAVITYORAL CAVITY

““UPPER” RESPIRATORY TRACTUPPER” RESPIRATORY TRACT

EARSEARS

NOSENOSE

SALIVARY GLANDSSALIVARY GLANDS

INTENDED 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,

and

NEOPLASTIC

…deviations of normal anatomy and histology

ORAL CAVITY• TEETH/GINGIVA/ALVEOLAR BONE• INFLAMMATORY/”REACTIVE”

LESIONS• INFECTIONS: HSV, VIRAL, FUNGI• LEUKOPLAKIA/”HAIRY”

LEUKOPLAKIA• SQUAMOUS TUMORS: BEN/MALIG• ODONTOGENIC CYSTS/TUMORS

Time frame of teething

• Incisors 10-15mo

• Bicuspids 15-18mo

• Molars 18-24mo

Tooth Decay (Cavities, “Caries”)

• Dental caries one of the most common diseases, is the most common cause of tooth loss before age 35

• Result of mineral dissolution of tooth structure • “Processed” carbohydrates, i.e., sugars• Bacterial (Strep. Viridans: Strep. Mutans + Strep.

Sanguis; Lactobacilli, Actinomycetes) acidic erosion of enamel due to ability to produce insoluble dextrans

• Role of pH, spacing, brushing, Fl• Tartarplaquecalculus = bacteria, proteins,

cells

• Gram 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 Glomerulonephritis• B. Sarcoidosis• C. Erythema nodosum• D. Migratory polyarthritis• E. Anterior uvetis • F. Dental Caries

• 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.

Find the “cavity”, i.e., caries, i.e., enamel erosion

Gingiva - squamous mucosa in between the teeth and around them Gingivitis is inflammation of the mucosa and the associated soft tissues. Causes: Bacteria: Actinobacilli, Porphyromona, PrevotellaViruses: HSV1 and 2

Symptoms: erythema, edema, bleeding, changes in contour, and loss of soft-tissue adaptation and sores

GINGIVITIS

Periodontitis• Definition: inflammatory

process that affects the supporting structures of the teeth: periodontal ligaments, alveolar bone, and cementum

• Causes: Bacteria, adult periodontitis is associated primarily with: – Actinobacillus

actinomycetemcomitans,

– Porphyromonas gingivalis

– Prevotella intermedia

• Affected structures: Gingiva, periodontal ligaments, bone, cementum

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)

Periodontitis

• A 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 extraction B. Skin biopsy C. Sinus drainage D. Nasal polypectomy E. Cystoscopy

• (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.)

Inflammatory/Reactive Tumor-like Lesions

MC fibrous proliferative lesions of the oral cavity:

• fibroma (61%)

• reactive nodules of the oral cavity peripheral ossifying fibroma

• pyogenic granuloma

• peripheral giant-cell granuloma

• gingival hyperplasia

Irritation fibroma

• primarily 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 excision Smooth pink exophytic nodule on the buccal mucosa.

“Irritation” Fibroma

Peripheral 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 granuloma

• Rx: Surgical excision down to the periosteum (recurrence rate of 15% to 20%)

Pyogenic granuloma• Highly 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

PYOGENIC

GRANULOMA

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

Peripheral giant cell granuloma• bluish purple tumor-like lesion• Histology: aggregation of

multinucleate, foreign body–like giant cells separated by a fibroangiomatous stroma, not encapsulated

• can cause resorption of alveolar bone

• Rx: Surgical excision• Dif. diagnosis: central giant-

cell granulomas of bones and “brown tumors” seen in hyperparathyroidism

Histology of peripheral giant cell granuloma reveals a dense infiltrate of histiocytes and multi-nucleated giant cells within the subepithelial fibrous stroma.

APHTHOUS ULCERS (CANKER SORES)

• superficial ulcerations of the oral mucosa affect up to 40% of the population in the United States

• Etiology: 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 erythema

• Histology: Mononuclear infiltrate • Prognosis: Spontaneously resolve in 7 to 10 days or be

stubbornly persistent for weeks• Rx: local anesthetics

“Canker” sore = Aphthous ulcer

GLOSSITIS • Inflammation of the tongue• atrophy of the papillae of the

tongue and thinning of the mucosa, exposing the underlying vasculature

• Atrophic 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 chemicals

• Clinic: Plummer-Vinson syndrome - combination of iron-deficiency anemia, glossitis, and esophageal dysphagia mostly in postmenopausal women

HERPES SIMPLEX VIRUS INFECTIONS

• Mostly herpes simplex virus type 1 (HSV-1)• Enveloped double-stranded DNA virus• Primary HSV infection typically occurs in children

age 2 to 4 years,• Forms: • acute herpetic gingivostomatitis – MOST Common

form of primary infection• cold sores (Herpes labialis)• recurrent herpetic stomatitis

HERPES SIMPLEX VIRUS INFECTIONS

HERPES 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 polykaryons• Tzanck test: microscopic examination of the

vesicle fluid to find multinucleated polykarions

TZANCK SMEAR

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.

• A 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 virus B. Non-enveloped double-stranded DNA viruC. Non-enveloped single-stranded DNA virusD. Non-enveloped positive-sense RNA virus E. Enveloped positive-sense RNA virus F. Enveloped negative-sense RNA virus

• A 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 reactivation C. Latent infection D. Abortive infect E. Slow virus infection

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:1. Pseudo-membranous (thrush)2. Erythematous3. Hyperplastic,

ORAL CANDIDIASIS (THRUSH)

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

Oral Manifestations of Systemic Disease

Oral Manifestations of Systemic Disease

HAIRY LEUKOPLAKIA

• Hairy 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 infection

• 80% 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!

“Hairy” leukoplakia

“Hairy” leukoplakia

Premalignant 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 disease

• until 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 mucosa

• Speckled leukoerythroplakia :Erythro+Leukoplakia

NORMAL DYSPLASIA CARCINOMA-IN-SITUINFILTRATING MALIGNANCY

Histologic progression of Leukoplakia into squamous cell carcinoma

Head and Neck are Squamous Cell Carcinomas (HNSCCs)

• 95% of cancers of the head and neck • overall 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 time

• Etiology: Tabacco, Alcohol, actinic radiation (sunlight), pipe smoking, chewing of betel quid, mouthwash (25% alcohol)

Morphology of squamous cell carcinoma of the oral cavity

• Favored locations:• 1. ventral surface

of the tongue• 2. Floor of the

mouth• 3. Lower lip, soft

palate, and gingiva

Morphology of squamous cell carcinoma of the oral cavity

Raised, firm, pearly plaques or as irregular, roughened, or verrucous areas of mucosal

thickening

•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.

Morphology of squamous cell carcinoma of the oral cavity

WELL

MODERATE

POOR

ODONTOGENICCYSTS

• Definition: cyst like structures derived from epithelial linings or epithelial remnants in the jaw bone

• Classification: • INFLAMMATORY CYSTS (e.g., Periapical

“Radicular” - most common)• DEVELOPMENTAL CYSTS

(DENTIGEROUS - most common)

Periapical cyst

Periapical 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

Dentigerous cyst• Def: 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: Excision• Complications: recurrence or,

very rarely, neoplastic transformation into an ameloblastoma or a squamous cell carcinoma.

DENTIGEROUS

CYST

lined by a thin layer of stratified squamous epithelium with chronic inflammatory cell infiltrate in the connective tissue stroma

Odontogenic keratocyst (OKC)

• locally aggressive and has a high rate of recurrence

• Most often diagnosed in patients between ages 10 and 40.

• Males within the posterior mandible.

• Xray: well-defined unilocular or multilocular radiolucencies

• Histo: 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

Odontogenic tumors

1. Odontoma- 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.

2. Ameloblastoma (app. 30%) - from odontogenic epithelium. It is commonly cystic, slow growing, and locally invasive but has an indolent course in most cases

Odontoma on x-ray?

Circular sunburst opacity surrounded by a thin radiolucent border

Ameloblastoma on x-ray?

Large expansile multilocular or soap-bubble radiolucency; favored location is posterior mandible

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

Histologic view of odontoma and ameloblastoma

Ameloblastomas

Odontomas