This document summarizes various topics related to the oral cavity and esophagus. It describes the normal flora of the oral cavity and defines terms used to describe localized inflammation in specific oral sites. It also discusses premalignant lesions of the oral cavity such as leukoplakia. The document further summarizes cancers of the tongue and esophagus, including risk factors, clinical features, pathogenesis and histology of various esophageal conditions like reflux esophagitis, Barrett's esophagus and tumors.

1. ORAL CAVITY

2.  Bacteria, spirochetes, viruses, fungi, and
parasites are normal in the oral cavity and are
usually harmless.
 The following terms are used to describe
localized inflammation of the oral cavity:
 Cheilitis (lips)
 Gingivitis (gum)
 Glossitis (tongue)
 Stomatitis (oral mucosa)

4.  Premalignant lesions include
 leukoplakia,
 Erythroplakia,
 speckled leukoplakia.
 The terms reflecting the presence of a white, red,
or mixed white/red lesion, respectively.
 Leukoplakia is an asymptomatic white lesion
on the surface of a mucous membrane.

5.  Some of these lesions undergo transformation
to squamous cell carcinoma.
 As a preneoplastic lesion, the causes of
leukoplakia are diverse and include use of
tobacco products,
 alcoholism,
 and local irritation.

6.  Clinically defined white patch or plaque that
that cannot be scraped off has been excluded
from other disease entities
 Presence of dysplasia, carcinoma in situ, and
invasive carcinoma from all sites 17-25%
 Etiology- associated with tobacco (smoking,
smokeless tobacco), areca nut/betel
preparations

7. Site of Leukoplakia
 Risk of dysplasia/carcinoma higher
 with floor of mouth,
 Ventro lateral tongue,
 retro molar trig one,
 soft palate than with other oral sites

8.  Erythroplakia is the red equivalent of
leukoplakia but is less common.
 Red areas associated with leukoplakic lesions
are referred to as speckled leukoplakia
 In contrast to leukoplakia, Erythroplakia may
represent moderate to severe dysplasia or
carcinoma.
 Not all of these lesions herald dysplasia or
carcinoma, as many red oral mucosal lesions
may be inflammatory in nature.

9. Infections of the Oral Cavity
• Bacteria, spirochetes, viruses, fungi, and parasites
are normal in the oral cavity and are usually
harmless.
• The following terms are used to describe
localized inflammation of the oral cavity:
• Cheilitis (lips)
• Gingivitis (gum)
• Glossitis (tongue)
• Stomatitis (oral mucosa)

10. Cancer of the tongue common in male around the
age of 50 years (50-70 years)
predisposing causes:
 Chronic irritation by smoking, sepsis, spices and
spirits (alcohol).
 Pre-cancerous lesions which include syphilis, ch.
superficial glossitis, dental ulcers and papilloma.
 Poor oral hygiene and mal-nutrition.
 Betel chewing.

11.  Two-thirds of the tongue cancer arise in the
ant. 2/3rd and 1/3rd in the posterior part.
 The commonest sites are the sides of the ant.
2/3rd of the tongue.
 Posterior tumors are much more to be in the
midline.

12.  The tumor usually occurs as malignant ulcer.
 Less often it take, the form of hard sub mucous
nodule or deep fissure.
 Rarely it occurs as diffuse hard infiltration of
whole tongue. (wooden tongue)

15. The tumor is usually Squamous cell
carcinoma.
.

16.  Local (direct to the floor of the mouth, gums
and pharynx).
 Lymphatic spread.
 Blood spread (very rare)

17.  For patient with LN negative with tumors in
the ant. 2/3rd there is 50%, 5 years survival.
 For patient with posterior 1/3rd of the tongue
with negative LN 20-25%, 5 years survival.

23. PLEOMORPHIC ADENOMA (BENIGN MIXED
TUMOR)
• Composed of cells exhibiting ability to differentiate
into; epithelial cells and mesenchymal components
• Gross: Round to ovoid, encapsulated or partly
encapsulated mass Cut surface; homogeneous tan to
white

25. PLEOMORPHIC ADENOMA MICROSCOPY
• Epithelial cells - Trabeculae/ ducts - Cysts lined by
squamous epithelium Mesenchymal components -
Fibrous - Myxochondroid - Osseous

27. PLEOMORPHIC ADENOMA CLINICAL COURSE
• Most common, any age , common in females
• Slow growing, asymptomatic, presents as single
nodular, firm, mobile mass rarely exceed 6cm in
diameter
• Malignant transformation increases with duration
(2% less than 5 yrs and10% less than 15 yrs duration)

28. PLEOMORPHIC ADENOMA CLINICAL COURSE
• Carcinoma ex pleomorphic adenoma; adenocarcinoma or
undifferentiated carcinoma-a very aggressive tumor S/S of
malignancy; sudden increase in size in short period, fixity to
surrounding tissue or facial nerve palsy Diagnosis; clinical
assessment, FNA, excision biopsy

29. WARTHIN’S TUMOR
• May be unilateral or bilateral,
• Common in males (26:1) and in smokers

30. WARTHIN’S TUMOR
• Gross Round, encapsulated mass, 2-4cm in size Cut
surface multiple cysts exude a clear fluid
• Microscopy Cystic spaces, papillary projections lined
by tall columnar cells Lymphoid tissue with/without
germinal center

32. ESOPHAGUS
• Normal gross Normal histology

33. ESOPHAGITIS
• Inflammation of the esophageal mucosa
• Etiological factors physical; e.G intubation, radiations
chemical; e.G uremia, ingestions of corrosive biologic agents;
e.G tuberculosis, candidiasis, herpes simplex, CMV others;
crohn disease, graft verses host disease (GVHD)

34. REFLUX ESOPHAGITIS (GERD)
• Reflux of gastroduodenal contents into esophagus due to
dysfunction of LES
• Contributory factors
 Presence of sliding hiatal hernia
 Vagal dysfunction
 Increased gastric volume and slowed esophageal clearance of
refluxed material
 Impaired reparative capacity of mucosa by prolong exposure
to gastric juices
 Others ; CNS depressants, tobacco and alcoholism

35. REFLUX ESOPHAGITIS (GERD)
• Pathogenesis Reflux of gastric juices, mucosal injury,
in severe cases duodenal bile reflux increases the
mucosal damage
• Gross Mucosa, hyperemic and red

36. REFLUX ESOPHAGITIS (GERD)
• Microscopy Epithelial hyperplasia due to basal cell
proliferation
• Intraepithelial eosinophils Lamina propria; neutrophils,
eosinophils and lymphocytes
• Tips of elongated lamina propria papillae shows congested
venules

38. REFLUX ESOPHAGITIS CLINICAL
MANIFESTATIONS
• Heartburn, chest pain ,dysphagia
• Outcome: reflux esophagitis may progress to:
• Superficial ulceration
• Bleeding, hematemesis and melena
• Spread of inflammation to the wall Circumferential fibrosis
with stricture formation
• Tendency to develop Barrett esophagus

39. BARRETT ESOPHAGUS
• A segment of distal esophagus above the level
of LES shows metaplastic columnar epithelial
lining with goblet cells

40. PATHOGENESIS BARRETT ESOPHAGUS
• Ulceration and subsequent re-epithelization by
columnar cells to cope with existing conditions
• Ulceration, induced by reflux and occurs in 10% of
these patients
• Columnar cells could arise from migration of gastric
mucosa or from stem cells of mucosa

41. BARRETT ESOPHAGUS
• Endoscopy
 Mucosa red and velvety, involvement might be
circumferential or in the form of finger like projections or
islands
• Microscopy
 Intestinal metaplasia with a villiform surface and crypts
lined by columnar and goblet cells most significant for
diagnosis

43. BARRETT ESOPHAGUS
• Diagnosis Endoscopic examination and biopsy
• Main complications 1. Peptic ulcer 2. Stricture 3.
Bleeding 4. Dysplasia and adenocarcinoma (Persons
with Barrett esophagus have 30 to 100 fold greater
risk of developing adenocarcinoma)

44. TUMORS OF ESOPHAGUS
• Non-neoplastic
• Mucosal polyp
• Squamous papilloma
• Benign neoplasms: Leiomyoma, Fibroma,Neurofibroma
• Malignant neoplasms: Squamous cell carcinoma,
Adenocarcinoma Carcinoid

45. SQUAMOUS CELL CARCINOMA
• Epidemiology
• Most frequent in men over 50yrs of age
• Male to female ratio; 4:1
• Smoking and alcoholism; two well known risk
factors

46. RISK FACTORS FOR SCC OF THE ESOPHAGUS
• Dietary
 Betel chewing
 Deficiency of vitamins (A, C,
riboflavin, thiamine,
pyridoxine)
 Deficiency of trace elements
(zinc, molybdenum)
 Fungal contamination of
foodstuffs
 High content of nitrites or
nitrosamines
 Lifestyle Burning-hot
beverages or food Alcohol
consumption Tobacco use
• Esophageal Disorders
 Long-standing esophagitis
• Genetic Predisposition
 Others HPV found in SCC
 P53 and p16INK4 mutations
 Ampilfication of CyclinD1, C-
MYC, and EGFR

47. SCC ESOPHAGUS
• Location
 Any part of esophagus; middle thirds 50%, lower
thirds 30%, upper thirds 20%
• Gross
• Three morphologic pattern; Exophytic 60%,
Ulcerated 25%, Flat 15%
• Early lesion small grey white plaque like thickenings
• Late circumferential tumor mass, thickened wall,
often ulcerated with sharply demarcated margins

49. SCC ESOPHAGUS
• Microscopy
• Intraepithelial neoplasia/dysplasia/ carcinoma-in-situ
Intramucosal carcinomas; that do not invade beyond
lamina propria
• Superficial carcinomas; do not invade beyond
submucosa
• Superficially spreading carcinomas; shows a lateral
intramucosal spread of at least 2cm beyond the
invasive tumor
• Grade; Well to Poorly-differentiated

50. SCC ESOPHAGUS CLINICAL FEATURES
• Slow on set of dysphagia, Weight loss, hemorrhage
and anemia
• Diagnosis: Exfoliative cytology and Endoscopic
biopsy
• Prognosis: Overall prognosis is poor; the median
survival after diagnosis being one year
• Metastasis: To distant organs particularly liver, lung
and adrenal gland common
• Stage: In situ and intramucosal carcinomas are almost
always curable

51. ADENOCARCINOMA OF ESOPHAGUS
• Typically arises in a background of Barrett's
esophagus
• Accounts for 5-10% of all esophageal cancers
• Most patients, white males, average age 57 years
• Tumor may be multicentric and is usually advanced at
the time of diagnosis with extension through the wall
and nodal metastasis

52. ADENOCARCINOMA ESOPHAGUS
MORPHOLOGY
• Initial flat or raised patches intact mucosa
• Late; nodular polypoid mass up to 5cm
• Diffusely infiltrative or deeply ulcerated
Mucin producing glandular tumor of intestinal
type
• Diagnosis: Multisite biopsy Prognosis: Poor,
stage by stage same as to SCC

54. THANK YOU