Oral Cavity and Esophagus PDF

Diseases of ORAL CAVITY & ESOPHAGUS Ahmed Almobarak ORAL CAVITY Infections Herpes simplex infections Most orofacial herpes caused by HSV-1 Common but mild cold sores Acute herpetic gingivostomatitis vesicles and ulceration of oral cavity Recurrent herpetic stomatitis...

Diseases of ORAL CAVITY & ESOPHAGUS Ahmed Almobarak ORAL CAVITY Infections Herpes simplex infections Most orofacial herpes caused by HSV-1 Common but mild cold sores Acute herpetic gingivostomatitis vesicles and ulceration of oral cavity Recurrent herpetic stomatitis ORAL CAVITY Apthous Ulcers Common superficial ulcerations of oral mucosa Single or multiple, shallow ulcerations Heal spontaneously, often recurrent More painful than serious Glossitis Beefy-red tongue seen in deficiency states Atrophy of papillae and thin mucosa Deficiencies of vitamin B12, iron deficiency Apthous ulcer ORAL CAVITY Oral candidiasis (Thrush) Superficial white patches or fluffy membrane Matted organisms within fibrinosuppurative exudate Easily detached, reddened underlying surface Candida normal flora of oral cavity Occurs in individuals that are diabetic, neutropenic and immuno- compromised (HIV) Commonest fungal infection in oral cavity ORAL CAVITY Oral manifestations of Systemic Disease Hairy Leukoplakia Seen in immunocompromised patients (esp HIV) White fluffy thickenings on lateral parts tongue Epstein-Barr virus present in most cases – cause Infections Measles (Koplik spots), infectious mononucleosis, diptheria Dermatologic conditions Lichen planus, pemphigus, erythema multiforme (include Steven-Johnson syn.) Oral manifestations of systemic disease Haematologic disorders Pancytopenia, monocytic leukaemia Miscellaneous Phenytoin ingestion, pregnancy, melanotic pigmentation Oral Manifestations of Some Systemic Diseases Acute pharyngitis and tonsillitis that may cause coating with a gray-white exudative membrane; enlargement of lymph nodes in the neck Diphtheria characteristic dirty white fibrinosuppurative, tough, inflammatory membrane over the tonsils and retropharynx  Oral Manifestations of Some Systemic Diseases Human immunodeficiency virus infection; (AIDS) predisposition to opportunistic oral infections, particularly with herpesvirus, Candida, and other fungi; sometimes oral lesions of Kaposi sarcoma and hairy leukoplakia.  Oral Manifestations of Some Systemic Diseases Scarlet fever Fiery red tongue with prominent papillae (raspberry tongue); white coated tongue through which hyperemic papillae project (strawberry tongue) Measles A spotty enanthema in the oral cavity often precedes the rash; ulcerations on the buccal mucosa about Stensen duct produce Koplik spots Infectious mononucleosis  Oral Manifestations of Some Systemic Diseases Dermatologic Conditions Lichen planus Reticulate, lacelike, white keratotic lesions that rarely become bullous and ulcerate; seen in more than 50% of patients with cutaneous lichen planus; rarely, is the sole manifestation  Oral Manifestations of Some Systemic Diseases Pemphigus : usually vulgaris; vesicles and bullae prone to rupture, leaving hyperemic erosions covered with exudate Bullous pemphigoid : oral lesions resemble macroscopically those of pemphigus but can be differentiated histologically  Erythema multiforme : a maculopapular, vesiculobullous eruption that sometimes follows an infection elsewhere, ingestion of drugs, development of cancer, or a collagen vascular disease; when it involves the lips and oral mucosa, it is referred to as Stevens- Johnson syndrome  Miscellaneous Melanotic pigmentation : may appear in Addison disease, hemochromatosis, fibrous dysplasia of bone (Albright syndrome), and Peutz-Jegher syndrome (gastrointestinal polyposis)  Miscellaneous Phenytoin (Dilantin) ingestion striking fibrous enlargement of the gingivae Pregnancy a friable, red, pyogenic granuloma protruding from the gingiva ("pregnancy tumor")  Miscellaneous Rendu-Osler-Weber syndrome : autosomal dominant disorder with multiple aneurysmal telangiectasias from birth beneath the skin or mucosal surfaces of the oral cavity, lips, gastrointestinal tract, respiratory tract, and urinary tract as well as in internal viscera  Hematologic Disorders Pancytopenia (agranulocytosis, aplastic anemia) : severe oral infections in the form of gingivitis, pharyngitis, tonsillitis; may extend to cellulitis of the neck (Ludwig angina)  Hematologic Disorders Leukemia : With depletion of functioning neutrophils, oral lesions may appear like those in pancytopenia Monocytic leukemia Leukemic infiltration and enlargement of the gingivae, often with accompanying periodontitis ORAL CAVITY Precancerous lesions Leukoplakia and erythroplakia Leukoplakia a clinical term – white plaque Cannot be removed by scraping Until proven otherwise to be regarded as precancerous Erythroplakia – red velvety erosions, less common but more ominous Multiple causes – use of tobacco (cigarettes, pipes, cigars and chewing tobacco) most common antecedent. ORAL CAVITY Leukoplakia and erythroplakia Morphology: Leukoplakia – solitary or multiple white patches. Histology of epithelium range from hyperkeratosis to severe dysplasia Erythroplakia show dysplasia to early cancer in 90% of cases  Tumors and Precancerous Lesions Many of these tumors (e.g., papillomas, hemangiomas, lymphomas) also occur elsewhere in the body and are Only oral squamous cell carcinoma and its associated precancerous lesions.  leukoplakia The term leukoplakia is defined by the World Health Organization as "a white patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically as any other disease.“ As such, white patches caused by entities such as lichen planus and candidiasis are not leukoplakias.  Approximately 3% of the world's population have leukoplakic lesions, and somewhere between 5% and 25% of these lesions are premalignant. Thus, until it is proved otherwise via histologic evaluation, all leukoplakias must be considered precancerous.  Erythroplakia. Related to leukoplakia, but much less common and much more ominous It represents a 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. The epithelium in such Leukoplakia of the hard palate ORAL CAVITY Squamous Cell Carcinoma Associations : Smoked tobacco, alcohol Regional – betel quid chewing, sirih, paan Sunlight, pipe smoking – cancer of lower lip Sites – floor of mouth, tongue, hard palate, base of tongue Ulcerating lesions with raised rolled borders Histology – usually well diff squamous Spread – cervical, mediastinal nodes, lungs, liver Sites of SCC of the oral cavity Carcinoma of the tongue Clinical, histologic and molecular progression of Oral cancer  Odontogenic tumors are a complex group of lesions with diverse histology and clinical behavior some are true neoplasms (both benign and malignant), while others are more likely hamartomas. Odontogenic tumors are derived from odontogenic epithelium, ectomesenchyme, or both. The two most common and clinically significant tumors are: 1- Ameloblastoma, which arises from odontogenic epithelium and shows no ectomesenchymal differentiation. It is commonly cystic, slow growing, and locally invasive but has a benign course in most cases. 2- Odontoma, the most common type of odontogenic tumor, 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.  1. Tumors of Odontogenic Epithelium Benign a. Ameloblastoma b. Calcifying epithelial odontogenic tumor (Pindborg tumor) c. Squamous odontogenic tumor Malignant a. Ameloblastic carcinoma b. Malignant ameloblastoma c. Clear cell odontogenic carcinoma  2. Tumors of Odontogenic Ectomesenchyme a. Odontogenic fibroma b. Odontogenic myxoma c. Cementoblastoma  3. Tumors of Odontogenic Epithelium and Ectomesenchyme Benign a. Ameloblastic fibroma b. Ameloblastic fibro-odontoma c. Ameloblastic fibrosarcoma d. Adenomatoid odontogenic tumor e. Odontoameloblastoma f. Complex odontoma g. Compound odontoma Malignant a. Ameloblastic fibrosarcoma DISEASES OF SALIVARY GLANDS SALIVARY GLANDS 3 major salivary glands parotid, submandibular, sublingual Minor salivary glands Inflammations (Sialadenitis) Mucocoele - most common inflammatory lesion of salivary gland Fluctuant swelling of lower lip Blockage or rupture of salivary gland duct SALIVARY GLANDS Sialolithiasis/sialadenitis Viral sialadenitis – Mumps affect esp. parotid Autoimmune – assoc with Sjogren syndrome Bacterial – secondary to ductal obstruction by stones (sialolithiasis) Staphylococcus and Streptococcus SALIVARY GLAND Tumours Majority occur in the parotid 65-80% Likelihood of malignancy greatest in sublingual > submandibular > parotid BENIGN Pleomorphic adenoma Commonest parotid tumour 60% Encapsuated with tongue-like protrusions Mixed tumour – epithelial and mesenchymal elements (myxoid, hyaline, chondroid) SALIVARY GLAND Pleomorphic adenoma Painless, slow-growing mobile mass Recurrence rate up to 25% with enucleation Malignant transformation can occur years later as malignant mixed tumour (aggressive) Warthin tumour (Adenolymphoma) Second commonest salivary tumour Rounded mass with cleft-like spaces 2 layered epithelium with lymphoid stroma Pleomorphic adenoma of parotid Pleomorphic adenoma Warthin tumour – epithelial and lymphoid elements SALIVARY GLAND MALIGNANT Mucoepidermoid Tumour Commonest malignant tumour in salivary glands Can be radiation-induced Mixture of squamous and mucus cells Adenoid cystic carcinoma Common in submandibular, sublingual Small dark cells in solid or cribriform pattern Tendency for perineural invasion Often recurrent with distant metastasis Mucoepidermoid carcinoma – squamous cells and mucus cells DISEASES OF ESOPHAGUS ESOPHAGUS Pathology Many diseases of esophagus produce similar symptoms: 1. Dysphagia – difficulty in swallowing deranged motor function narrowing/obstruction of lumen 2. Heartburn – retrosternal chest pain regurgitation of gastric contents 3. Pain 4. Haematemasis ESOPHAGUS Congenital anomalies Atresia/Fistula Incompatible with life – early feeding problems Esophageal atresia usually associated with TOF Stenosis, Webs, Rings Stenosis – result of inflammatory scarring by reflux, radiation, caustic injury Dysphagia the major problem, women affected Mucosal webs and rings protrude into lumen Associated anemia Plummer-Vinson syndrome Esophageal atresia and tracheaesophageal fistula ESOPHAGUS Major Lesions with motor dysfunction Achalasia Hiatal hernia Diverticulum Mallory-Weiss tear Achalasia (“Failure to relax”) Mostly as primary disorder of uncertain etio. Progressive dilatation of esophagus Secondary cause – Chagas disease (T. cruzi) Progressive dysphagia classical symptom Risk of developing esophageal carcinoma Esophagus – motor dysfunctions ESOPHAGUS Motor dysfunctions Hiatal hernia Sac-like protrusion of stomach above diaphragm Cause unknown Complications include ulceration, bleeding Regurgitation and heartburn Diverticulum Outpouching of all layers of esophagus Mallory-Weiss tear Result of severe retching: alcoholics Upper GI bleeding - hematemesis ESOPHAGUS Reflux esophagitis (Gastroesophageal reflux disease) Reflux of gastric contents into lower esophagus Many causative factors involved Acid-pepsin action cause mucosal injury Clinically – dysphagia, heartburn Mucosa reddened with increased inflammatory cells, basal zone hyperplasia Complication – bleeding, ulceration, stricture, Barrett esophagus and its risks.  Reflux Oesophagitis superficial portion of the mucosa. Numerous eosinophils within the squamous epithelium, elongation of the lamina propria papillae, and basal zone hyperplasia are present Reflux esophagitis of superficial mucosa ESOPHAGUS Barrett Esophagus Complication of long-standing gastro- esophageal reflux in 10% of GERD Endoscopy – red, velvety mucosa Distal squamous mucosa replaced by metaplastic columnar epithelium containing gastric or intestinal/goblet cell types Important to search for dysplasia and grade it Clinically – bleeding, stricture Most important risk factor for esophageal adenocarcinoma 40x Barrett esophagus Barrett esophagus – red, granular zone Barrett esophagus – squamous mucosa and intestinal goblet cells in glandular mucosa ESOPHAGUS Esophagitis: Infections/Chemicals Mucosal irritants – alcohol,corrosive acids and alkalis Cytotoxic anticancer therapy Herpes simplex, CMV Fungals – Candida Uraemia Radiation injury Graft vs Host disease ESOPHAGUS Varices Portal hypertension induce formation of collateral channels at lower esophagus Varices – dilated esophageal submucosal plexus 90% of cirrhotics No symptom until rupture – upper GI bleeding hematemesis Fatal 40% Esophageal varices of submucosal veins ESOPHAGUS Squamous cell carcinoma Differences in incidence and epidemiology worldwide Dietary and environmental factors modified by genetic factors Alcohol, tobacco (Europe and USA) Fungal contamination and nitrosamine containing foodstuffs (China) Distribution: middle third 50% lower third 30% upper third 20% ESOPHAGUS Squamous cell carcinoma Grossly: polypoid, diffuse infiltrating, ulcerated Histology: moderate to well differentiated Spread: Local extension to adjacent mediastinal structures occurs early – rich lymphatics Upper third: cervical nodes Middle third: mediastinal, tracheal nodes Lower third: gastric, coeliac nodes Clinical: Insidious dysphagia, weight loss haemorrhage, sepsis from ulceration, fistula Treatment: surgery  ESOPHAGUS Squamous cell carcinoma of esophagus  ESOPHAGUS SCC of esophagus with invasion into submucosa ESOPHAGUS Adenocarcinoma Complication of Barrett esophagus Multistep process with development of dysplasia Lower third esophagus and GE junction About 50% of all esophageal cancers in US Nodular masses with ulceration Adenocarcinoma mucin secreting, intestinal type Males>females, whites>blacks (c.f. squamous) Clinical features similar to SCC Adenocarcinoma of gastro-eso. junction arising from Barrett mucosa Figure 17-12 Anatomy and histology of the stomach. A, Gross anatomy. B, Microscopic view of antral mucosa. C, Microscopic view of fundic mucosa. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 March 2006 09:23 AM) © 2005 Elsevier