patoloji-ders-notlari

Title

Serdar Balcı

Pathology of Oral Cavity and Esophagus

Serdar BALCI, MD

ORAL INFLAMMATORY LESIONS

Aphthous Ulcers (Canker Sores)

Aphthous ulcer

Single ulceration with an erythematous halo surrounding a yellowish fibrinopurulent membrane

Robbins Basic Pathology

Aphthous Ulcers

• Superficial mucosal ulcerations
• Affects 40% of the population
• Common in the first two decades of life
• Painful, resolve spontaneously, recurrent
• Tend to be prevalent within some families
• May be associated with
  • Celiac disease, inflammatory bowel disease (IBD), and Behçet disease
• Solitary or multiple
• Shallow, hyperemic ulcerations
• Thin exudate, rimmed by a narrow zone of erythema

Herpes Simplex Virus

• Most orofacial herpetic infections caused by HSV-1
• Oral HSV-2 (genital herpes) is increasing
• Primary infections
  • Children, 2-4 yrs
  • Often asymptomatic
  • Acute herpetic gingivostomatitis
    • 10-20%
    • Abrupt onset of vesicles and ulcerations
• Adults harbor latent HSV-1
  • Virus can be reactivated
  • Cold sore (uçuk), recurrent herpetic stomatitis

HSV Reactivation

Trauma

Allergies

Exposure to ultraviolet light

Upper respiratory tract infections

Pregnancy

Menstruation

Immunosuppression

Exposure to extremes of temperature

At the site of primary inoculation

Adjacent mucosa innervated by the same ganglion

Groups of small (1 to 3 mm) vesicles

Lips (herpes labialis), nasal orifices, buccal mucosa, gingiva, and hard palate are the most common locations

Infected cells become ballooned

Have large eosinophilic intranuclear inclusions

Adjacent cells commonly fuse to form large multinucleated polykaryons

Oral Candidiasis

• Most common fungal infection of the oral cavity
• Candida albicans
  • Normal component of the oral flora
• Modifying factors
  • Immunosuppression
  • The strain of C. albicans
  • The composition of the oral microbial flora (microbiota)

Clinical forms of oral candidiasis

Pseudomembranous

Erythematous

Hyperplastic

Pseudomembranous Oral Candidiasis

Most common, thrush

Superficial, gray to white inflammatory membrane

Matted organisms enmeshed in a fibrinosuppurative exudate

Readily scraped off to reveal an underlying erythematous base

Superficial or invade depending on immune status

FIBROUS PROLIFERATIVE LESIONS

Fibroma

Submucosal nodular fibrous tissue

Chronic irritation

Reactive connective tissue hyperplasia

Buccal mucosa, along the bite line

Robbins Basic Pathology

Pyogenic granuloma

Pedunculated masses

Gingiva of children, young adults, and pregnant women

Richly vascular, ulcerated

Growth can be rapid, raise fear of a malignant neoplasm

Leukoplakia

• White patch or plaque that cannot be scraped off
• Cannot be characterized clinically or pathologically as any other disease
• Lesions with known etiology are not leukoplakia
  • Lichen planus, candidiasis
• 3% of the world’s population has leukoplakia
  • 5-25% premalignant, may progress to squamous cell carcinoma

Erythroplakia

Red, velvety, eroded area

Flat, slightly depressed relative to the surrounding mucosa

Much greater risk of malignant transformation than leukoplakia

Leukoplakia and Erythroplakia

• Adults at any age
• 40-70 years
• M:F=2:1
• Multifactorial
  • Tobacco use
  • Cigarettes, pipes, cigars, and chewing tobacco

Morphology

• Leukoplakia
  • Hyperkeratosis
  • Overlying thickened, acanthotic, orderly mucosal lesions
  • Marked dysplasia
  • Carcinoma in situ
• **Erythroplakia **
  • Most severe dysplastic changes
  • 50% of these cases undergo malignant transformation

DISEASES OF SALIVARY GLANDS

Diseases of Salivary Glands

• Parotid
• Submandibular
• Sublingual
• Minor salivary glands
  • Wide distribution

Xerostomia (Dry mouth)

• Decrease in the production of saliva
• >20% of individuals above the age of 70 years
• Reasons:
  • Sjögren syndrome
    • accompanied by dry eyes
  • Complication of radiation therapy
  • Side effect of drugs
• Results in:
  • Dry mucosa
  • Atrophy of the papillae of the tongue
  • Increased rates of dental caries
  • Candidiasis
  • Difficulty in swallowing and speaking

Sialadenitis(inflammation of the salivary glands)

• Caused by:
• Trauma
• Viral or bacterial infection
  • Mumps
  • Staphylococcus aureus and Streptococcus viridans
    • occur after sialolithiasis
• Autoimmune disease
  • Sjögren syndrome

Mucocele

• Most common inflammatory lesion of the salivary glands
• Blockage or rupture of a salivary gland duct
• Leakage of saliva into the surrounding connective tissue stroma
• Cystlike space
  • lined by inflammatory granulation tissue or fibrous connective tissue
  • filled with mucin and inflammatory cells, macrophages

ESOPHAGUS

Mechanical Obstruction

• Atresia
• Fistulas
• Duplications
• They are discovered shortly after birth
  • Regurgitation during feeding
  • Require surgery

#

• Absence (agenesis)
  • extremely rare
• Atresia
  • more common
  • thin, noncanalized cord
  • occurs at or near the tracheal bifurcation
  • Associated with a fistula connecting the upper or lower esophageal pouches to a bronchus or the trachea
  • Result in aspiration, suffocation, pneumonia, or severe fluid and electrolyte imbalances

**Fistula (without atresia) **

Esophageal stenosis

• Narrowing of mucosa
  • fibrous thickening of the submucosa
  • atrophy of the muscularis propria
  • secondary epithelial damage
• Caused by
  • gastroesophageal reflux
  • Irradiation
  • Caustic injury

Zenker’s Diverticulum

A 67-year-old man presented to the gastroenterology clinic with an 8-month history of progressive dysphagia, weight loss, regurgitation, and halitosis. A physical examination revealed no palpable cervical mass. Laboratory studies showed a moderately low serum albumin level. A barium swallow examination showed stasis of barium in the upper esophagus with an outpouching lesion anterior to the C5 and C6 vertebrae (arrow). Upper gastrointestinal endoscopy revealed a pharyngoesophageal diverticulum, or Zenker’s diverticulum. Zenker’s diverticula are herniations of the hypopharynx through a defect in Killian’s triangle, an area bound by the inferior pharyngeal constrictor muscles and cricopharyngeus muscles. These diverticula are thought to result, in part, from abnormalities of the upper esophageal sphincter. Small diverticula can be asymptomatic and left untreated, whereas large diverticula can result in dysphagia, regurgitation, chronic aspiration, or cough, and surgery may be warranted. In this patient, an endoscopic Zenker’s diverticulectomy was performed. Within 3 days after the surgery, the dysphagia, regurgitation, and halitosis had resolved, and the patient remained asymptomatic at a follow-up visit 8 months later.

N Engl J Med 2017; 377:e31 November 30, 2017 DOI: 10.1056/NEJMicm1701620

Functional Obstruction

Dyscoordination in peristaltic contractions

Esophageal dysmotility

May result in diverticulum

Achalasia

Caused by:

incomplete LES relaxation

increased LES tone

esophageal aperistalsis

Primary achalasia

• Failure of distal esophageal inhibitory neurons
• Idiopathic
• Degenerative changes in neurons
  • intrinsic to the esophagus
  • within the extraesophageal vagus nerve
  • dorsal motor nucleus of the vagus

Secondary achalasia

Chagas disease

Trypanosoma cruzi infection

destruction of the myenteric plexus

failure of LES relaxation

esophageal dilatation

Duodenal, colonic, and ureteric myenteric plexuses also affected

Achalasia-like disease

• diabetic autonomic neuropathy
• malignancy
• amyloidosis
• sarcoidosis
• lesions of dorsal motor nuclei
  • polio or surgical ablation

Ectopia

• Developmental rests
• A normal tissue in an abnormal position
• Inlet patch:
  • Ectopic gastric mucosa in the upper third of the esophagus
  • acid release result in dysphagia, esophagitis, Barrett esophagus, rarely adenocarcinoma

Esophageal Varices

• Enlarged veins in the esophagus
  • subepithelial and submucosal venous plexus
• One of the “portal shunt” areas, collaterals
• Portal hypertension
• Severe bleeding
• 90% of cirrhotic patients
• Hepatic schistosomiasis

Lacerations

• Mallory-Weiss tears
  • severe retching or vomiting
  • acute alcohol intoxication
  • Normal relaxation of sphincters are lost in prolonged vomiting
  • Longitudinal linear lacerations crossing GE junction
• Boerhaave syndrome
  • transmural esophageal tears
  • mediastinitis

Autopsy Pathology: A Manual and Atlas

Chemical Esophagitis

• Alcohol
• Corrosive acids or alkalis
• Excessively hot fluids
• Heavy smoking
• pill-induced esophagitis
• Self-limited pain
  • odynophagia (pain with swallowing)
• Iatrogenic esophageal injury
  • cytotoxic chemotherapy, radiation therapy, graft-versus-host disease
• Ulceration and accumulation of neutrophils

Infectious esophagitis

Debilitated, immunosuppressed

HSV

CMV

Candida

Mucormycosis and aspergillosis

punched-out ulcers

Other diseases

Bullous pemphigoid

Epidermolysis bullosa

Crohn disease

Prevention against reflux esophagitis

• Stratified squamous epithelium
  • Resistant to food
  • Sensitive to acid
• Submucosal glands secrete mucin
• Constant LES tone
  • Prevent gastric content to go back

Netter’s Illustrated Human Pathology, Second Edition

Reflux Esophagitis

Most frequent cause of esophagitis

Most common outpatient gastrointestinal diagnosis

Gastroesophageal reflux disease (GERD)

Reflux of gastric juices

Duodenal bile reflux occurs in severe disease

• Decreased LES tone or increased abdominal pressure
  • alcohol and tobacco use
  • obesity
  • central nervous system depressants
  • pregnancy
  • hiatal hernia
  • delayed gastric emptying
  • increased gastric volume
• Morphologic changes
  • Hyperemia
  • Eosinophils are recruited into the squamous mucosa
  • Neutrophils, associated with more severe injury
  • Basal zone hyperplasia
  • Elongation of lamina propria papillae

Eosinophilic Esophagitis

• Food impaction and dysphagia in adults
• Feeding intolerance or GERD-like symptoms in children
• Epithelial infiltration by large numbers of eosinophils
  • far from the gastroesophageal junction
• Majority of patients are atopic

Hiatal hernia

separation of the diaphragmatic crura

protrusion of the stomach into the thorax

Congenital hiatal hernia

in infants and children

Netter’s Illustrated Human Pathology, Second Edition

Netter’s Illustrated Human Pathology, Second Edition

Barrett Esophagus

• Complication of chronic GERD
• Intestinal metaplasia within the esophageal squamous mucosa
• Incidence of Barrett esophagus is rising
  • White males, 40-60 years of age
  • Increased risk of esophageal adenocarcinoma
• Barrett esophagus is a premalignant condition
  • After metaplasia, dysplasia develops and it leads to neoplasm
  • Most persons with Barrett esophagus do not develop esophageal cancer
    • but they should be followed up
• Endoscopically
  • Tongues or patches of red, velvety mucosa extending upward from the gastroesophageal junction
• Microscopically
  • Intestinal metaplasia
  • Low grade dysplasia
  • High grade dysplasia
  • Intramucosal carcinoma

Netter’s Illustrated Human Pathology, Second Edition