This document discusses the structure and pathology of the oral cavity and esophagus. It begins by describing the general four-layer structure of the esophagus which includes the mucosa, submucosa, muscularis and serosa layers. It then provides more details on the histology and functions of each layer. The document goes on to describe common oral pathologies like aphthous ulcers, oral candidiasis, leukoplakia and erythroplakia. It also discusses salivary gland structures, diseases like Sjogren's syndrome, mucoceles, ranulas, sialolithiasis and various benign and malignant salivary gland tumors.

1. Oral Pathology
& Esophagus
Dr. Evith Pereira

2. General Structure
Four Layers
1. Mucosa
2. Submucosa
3. Muscularis
4. Serosa/
Adventitia

3. General Structure
Mucosa (mucous membrane)
1. epithelium
2. lamina propria
3. muscularis mucosa
4. functions
a. barrier / protection
b. absorption
c. secretion

4. Submucosa
1. dense CT
2. blood & lymph vessels
3. submucosal (Meissner’s) plexus
4. glands
General Structure

5. General Structure
Muscularis
1. two smooth muscle layers
a. inner circular
b. outer longitudinal
2. myenteric (Auerbach’s) plexus
3. function
a. mix
b. propel

6. General Structure
Serosa
1. mesothelium
2. loose CT

7. Oral Cavity (e.g., cheek, lips)
A. Mucosa
1. Stratified squamous nonkeratinized epith.
2. lamina propria
B. Submucosa
1. Microscopic salivary (seromucous) glands
C. Muscularis
1. facial skeletal muscles

8. Aphthous ulcers ( Canker sores )
• Common
• Superficial ulcerations of the oral mucosa
• Affects 40% of population in the united states
• 1st two decades of life.
• Painful/recurrent/tend to prevalent within
certain families
• Lesions: single or multiple, shallow, hyperemic
ulcerations. Covered by a thin exudate & rimmed
a narrow zone of erythema.

9. Aphthous ulcers ( Canker sores)
• Inflammatory infiltrate of mononuclear cells,
if secondary bacterial infection, numerous
neutrophils.
• Lesions clear within a wk.
• Cause –obscure
• Treatment- symptomatic

10. Oral candidiasis( oral thrush )
• Candida- fungus is a normal inhabitant of the
oral cavity & cause mischief in individuals who
are diabetic, neutropenic, or
immunoincompetent ( AIDS) e.t.c
• Oral lesions: superficial, curdy, gray to white
inflammatory membrane composed of matted
organisms enmeshed in a fibrinosuppurative
exudate that can be readily scraped off to reveal
an underlying erythematous inflammatory base.

11. White plaques and ulcerations in the esophagus indicate
infection with
Candida

12. Candida encrusting the surface and invading the esophageal wall.

13. GMS stain shows characteristic
pseudohyphae and buds of Candida

14. Tumors & precancerous lesions
• Leukoplakia: means simply white plaque.
• Def: a white plaque on the oral mucous membrane
that cannot be removed by scraping & cannot be
classified clinically or microscopically as another
disease entity.
• D/D lichen planus, candidiasis
• Leukoplakic plaques range from benign epithelial
thickening to highly atypical lesions with dysplastic
changes that merge with carcinoma in situ.Thus,
leukoplakia is a clinical term; until it is proved
otherwise, it must be considered precancerous.
• 5-15% undergo transformation to cancer

15. LEUKOPLAKIA

16. Erythroplakia ( dysplastic leukoplakia)
• Lesions: red, velvety, eroded area within oral
cavity that usually remains level with or may
be slightly depressed in elation to the
surrounding mucosa.
• Epithelial changes are markedly atypical, with
higher risk of malignant transformation than
that with leukoplakia.

17. Speckled leukoerythroplakia
• Intermediate forms that have the
characteristics of both leukoplakia &
erythroplakia.

18. Leukoplakia & Erythroplakia
• Age: adults at any age; 40 -70yrs.
• M:F = 2 :1
• Multifactorial origins
Antecedent:
use of tobacco ( cigarettes, pipes, cigars &
particularly chewing tobacco & buccal
pouches )

19. Leukoplakia & Erythroplakia
• Potentiating influences
Alcohol
ill-fitting dentures
Chronic exposure to persistent irritants.
HPV ( Human papilloma virus) ,serotype 16
have been identified in tobacco –related
lesions.

20. Morphology
• Leukoplakia occur any where in oral cavity
( buccal mucosa, floor of mouth, ventral
surface of tongue, hard palate).
• Solitary or multiple, white patches or plaques
with indistinct or sharply demarcated borders.
• Slightly thickened & smooth or wrinkled &
indurated.
• May be raised, corrugated, verrucous plaques.

21. Histology: Leukoplakia
• Hyperkeratosis overlying thickened acanthotic
but orderly mucosal epithelium to lesions with
dysplastic changes.
• The more dysplastic or anaplastic the lesion,
the more likely a subjacent inflammatory
infiltrate of lymphocytes & macrophages.

22. Leukoplakia. Note enlarged, atypical squamous cell nuclei.

23. Histology: : erythroplakia
• Epithelial atypia is more marked
• Intense subepithelium inflammatory reaction
with vascular dilation accounts for the red
appearance of the lesion.

24. Squamous cell carcinoma
• 95% of cancers of oral cavity
• Others: adenocarcinoma ( of mucous gland
origin),melanomas, various cacarcinomas.
• Age: 50 to 70yrs
Pathogenesis:
• Use of tobacco & alcohol
• Nondrinking smokers = 2-fold to 4-fold
greater risk

25. Squamous cell carcinoma
• Drinking & smoking : 6-fold to 15-fold
• Chewing tobacco & buccal pouches.
• Use of marijuana
• Chewing of betel nuts & pan in India.
• HPV serotype 6,16 & 18 – identified in half of oral
carcinomas arising in waldeyer tonsillar ring & in
10%- 15% in tongue & other parts of oral cavity.
• Deletions of chromosome regions 18q, 10p, 8p,& 3p;
mutations in p53; &amplification of the INT2 &
BCL1 oncogenes.
• protracted irritation

26. Morphology
• Site: floor of the mouth, tongue, hard palate & base
of tongue.
• Clinically, a well-defined, white plaque caused by
hyper- and parakeratosis
• Raised,firm,pearly plaques or as irregular,
roughened or verrucous areas of mucosal
thickening.
• As enlarges, create protruding masses or undergo
central necrosis, forming, au irregular, shaggy ulcer
rimmed by elevated ,firm, rolled borders.

27. TONGUE, SQUAMOUS CELL CARCINOMA

28. Microscopy: SCC
• Begin as in situ lesions.
• Slowly to rapidly growing lesions.
• Infiltrate locally before they metastasize.
• Metastasis: mediastinal lymph nodes, lungs,
liver,& bones.
• 50% of tongue and 60% of floor of mouth SCC
are in nodes at diagnosis
• 30% five year survival for SCC of tongue and
floor of mouth

29. Microscopy: SCC
• Well- differentiated keratinizing neoplasms to
anaplastic.
• Gross - Types:
 Ulcerative type :most frequent
 Papillary or verrucous: soft & wart like growth
 Nodular: firm, low growing submucosal nodule.
 Scirrhous: infiltration into deeper structures.

30. Squamous cell carcinoma

31. Salivary gland
Dr Manisha Y Tambekar

33. Introduction
• Three major salivary glands- Parotid, submandibular,&
sublingual & innumerable minor salivary glands
distributed throughout mucosa of the oral cavity.
• Xerostomia: dry mouth
• Major feature of autoimmune disorder sjogren
syndrome( accompanied by dry eyes, enlargement of
salivary glands)
• A lack of salivary secretions may be a complication of
radiation therapy.
• Oral cavity:Dry mucosa or atrophy of paillae of tounge,
with fissuring & ulcerations

34. Sjogren’s Syndrome
• Immune-mediated destruction of the lacrimal
and salivary glands. (Primary form or sicca
syndrome)
• often occurring in association with rheumatoid
arthritis or another autoimmune disorder
( secondary form )
• Xerostomia( dry mouth) and keratoconjunctivitis
sicca ( dry eyes)
• Biopsy shows dense lymphoplasmacytic
inflammatory infiltrate with destruction of
glandular tissue

35. Lymphocytic infiltrate destroying salivary gland in Sjogren’s syndrome.

36. Gross appearance of Mikulicz’s disease of parotid gland. There is a combination of
solid areas resulting from infiltration by lymphocytes and small cystic formations
representing dilated ductal lumina.

37. Prominent proliferation of duct epithelium in a patient with Mikulicz’s disease.

38. Inflammation( Sialadenitis ):
Causes
• Infectious
– Mumps
– Bacterial (usually
associated with
ductal obstruction)
• Autoimmune
(Sjogren’s)
• Traumatic

39. Mucocele
• Common lesion
• Results from blockage or rupture of a salivary gland duct,
with consequent leakage of saliva into surrounding CT
stroma.
• Lower lip: result of trauma
• Toddlers, young adults, geriatric population ( as a result of
falling )
• Fluctuant swellings of the lower lip, have blue translucent
hue to them
• Complete excision of cyst with minor salivary gland lobule
of origin.
• Incomplete excision- recurrence.

40. Mucocele

41. Mucocele

42. Mucocele

43. Cystlike space tht is lined by inflammatory granulation tissue or by fibrous CT.
Cystic spaces are filled with mucin & inflammatory cells ( macrophages)

44. Mucocele

45. Ranula
• Ranula: Histologically identical to a mucocele
• Mucoceles that arise when the duct of
sublingual gland is damaged.
• Plunging ranula: extremely large ,when it
dissects its way through the CT stroma
connecting the two bellies of mylohyoid
muscle.

47. Sialolithiasis with secondary chronic sialadenitis. A large stone is blocking a major
salivary duct. Common offenders: staph aureus & strep. Viridans )

48. Sialolithiasis

49. Sialolithiasis

50. Sialadenitis

51. Gross appearance of suppurative
Sialadenitis.

52. Chronic Sclerosing Sialadenitis

53. Salivary Gland
• < 2% of tumours in humans
• Parotid gland : 65-80% ( 15-30% malignant)
• Submandibular gland -10%
• Minor SG ( sublingual)- Remainder
• Salivary gland tumor being malignant is more or
less inversely proportional to the size of the gland
• Usually occur in adults
• Female predominance(warthin’s tumor in M>F)
• 5% occur in children ( younger than age 16yrs)
• Benign – 5th -7th decade
• Malignant – later

54. Pleomorphic Adenoma (mixed tumor of
salivary gland)
• Most common salivary gland tumor
• Most often arises in superficial parotid
• Circumscribed,glistening, myxoid lesion
• Histologically shows heterogeneous mix of ducts,
acini, and sheets of cells in a myxoid or chondroid
stroma
• Complete resection is necessary to prevent
recurrence (10% recurrence rate)
• Low percentage show malignant areas

55. Pleomorphic Adenoma (mixed tumor
of salivary gland)
• Most common salivary gland tumor
• Most often arises in superficial parotid
• Parotid gland : 60%
• Submandibular gland –less common
• Minor SG ( sublingual)- rare
• Derived from a mixture of ductal ( epithelial) & myoepithelial cells
& therefore show both epithelial & mesenchymal differentiation
• Reveal epithelial elements dispersed throughout a matrix along
with varying degrees of myxoid ,hyaline, chondroid & osseous
tissue.
• Radiation exposure increases the risk.

56. Pleomorphic Adenoma (mixed tumor
of salivary gland)
• Gross: rounded ,well –demarcated masses ( 6cm in greatest
dimension)
• Encapsulated
• In palate- capsule is not fully developed, expansile growth
produces tongue like protrusions into the surrounding gland.
• C/s gray-white with myxoid & blue translucent areas of
chondroid.
• Micriscopy:

57. Large Pleomorphic adenoma

58. sharply outlined character and predominantly solid & glistening surface indicative of
cartilaginous differentiation.

59. sharply outlined and predominantly solid cut surface. A glistening surface indicative of
cartilaginous differentiation.

61. Benign mixed tumor. The myoepithelial cells are undergoing cartilaginous metaplasia.

62. Benign mixed tumor with a markedly hypercellular appearance.

63. Microscopic of pleomorphic adenoma; note cartilage admixed with
benign glandular epithelial elements.

64. Benign mixed tumor (left) with area of malignant transformation in the form of poorly
differentiated carcinoma (right).

65. Warthin’s Tumor/ adenolymphoma /
Papillary cystadenoma lymphomatosum
• Benign tumor of the parotid gland
• 2nd most common SG neoplasm.
• M>F
• 5th -7th decade
• 1o% -multifocal, 10% B/L
• Smokers : 8 times the risk than nonsmokers.
• Well-encapsulated green-brown mass with cleft-like
spaces on the cut surface
• Admixture of oncocytic epithelium and subjacent
lymphoid tissue
• 10% recurrence rate

66. Warthin’s Tumor
• Morphology:
• Gross: rounded to oval
• Encapsulated masses
• 2-5cm in dia
• c/s Pale gray surface punctuated by narrow
cystic or cleft like spaces filled with a
mucinous or serous secretions.

67. gross appearance of Warthin’s tumor of parotid gland. The presence of multiple large
cystic spaces is characteristic of this lesion.

68. Warthin’s Tumor

69. Low-power appearance of Warthin’s tumor.
Spaces are lined by double layer of epi cells resting on a dense lymphoid
stroma, sometimes bearing germinal centers
Spaces narrowed by polypoid projections of the lymphoepithelial elements.

70. Papillary oncocytic epithelium and prominent
lymphoid component in Warthin’s Tumor.

71. Oncocytic
epithelium
Prominent
Lymphoid
component

72. High-power view of the lining of one of the cysts of Warthin’s tumor.
The epithelium is tall and oxyphilic ( palisade of columnar cells having abundant finely
granular, eosinophilic cytoplasm) ,
with a discontinuous layer of small cells at the base(cuboidal to polygonal cells ).
The stroma beneath contains a monotonous lymphocytic infiltrate.

73. Mucoepidermoid carcinoma
• Composed of variable mixtures of Mucous,
squamous, and intermediate cells
• 15%- all SG neoplasms
• 60- 70% - parotid gland
• Common malignant tumor primary in SG
• Most common radiation induced neoplasm

74. Gross appearance of mucoepidermoid carcinoma.
solid, without cystic formations commonly seen in low-grade
lesions.
• Range: 8cm in dia
• Circumscribed
• Lack well- defined capsule
• Infiltrative at margins
• C/S pale-gray white, small
mucin containing cyst.

75. Mucoepidermoid carcinoma.
Cords, sheet, or cystic configuration of Mucous, squamous, and intermediate cells can
be seen.

76. Mucoepidermoid carcinoma
• Subclassification:
• Low: mucus secreting cells-forming glandular
spaces, invade locally, recur-15% & rarely
metastasize.
• Intermediate
• High grade; largely squamous cells with
scattering of mucus –secreting cells.
recur- 25-30%, disseminate to distant site.

77. Adenoid cystic carcinoma
• Common- minor SG ( poor prognosis)
• Uncommon : parotid gland
• Other sites: nose, sinuses, upper airways
• Slow growing
• Recurrence rate is high
• Disseminate- bone, liver, brain.
• Gross: small, poorly encapsulated, infiltrative,
gray pink

78. Adenoid cystic carcinoma. Typical low-power appearance.
Small cells- dark, compact nuclei & scanty cytoplasm
Pattern: tubular, solid, cribriform
spaces b/w tumor cells are filled with hyaline material ( excess basement
membrane)

79. Adenoid cystic carcinoma. Numerous “cylinders” containing a
homogeneous acidophilic material can be seen.

80. Adenoid cystic carcinoma
prominent perineural invasion( most painful salivary gland tumor)

81. Adenoid cystic carcinoma combining tubular
and solid features

82. Acinic cell tumor
• Composed cells resembling serous cells of
salivary gland.
• Uncommon ( 2-3% of SG )
• Common- parotid than submandibular
• Minor SG ( rarely)
• Gross: Small, discrete lesions
• Recurrence : level of pleomorphism
• 10-15% - metastasize to lymphnodes.

83. Acinic cell carcinoma.
cells have an abundant cytoplasm filled with basophilic zymogen
granules.
Sheets, Microcystic, glandular, follicular or papillary
Few mitosis, little anaplasia