ORAL CAVITY &

SALIVARY GLANDS
Dr. Geener .K .John
Recommended reading –
Pages 583- 589 from
Robbins – Basic Pathology 10th edition
Session Learning Objectives (SLOs)
 SLO# 1: Describe the clinical and pathological features of
inflammatory lesions affecting oral mucosa (Aphthous Ulcer,
Herpes virus infection, Candidiasis).
 SLO# 2: Discuss the pathological features and clinical
importance of leukoplakia and erythroplakia.
 SLO# 3: Discuss the risk factors, gross and microscopic
features, routes of spread and prognosis of carcinoma of the
oral cavity and tongue.
 SLO# 4: List the inflammatory lesions of the salivary gland.
 SLO# 5: Classify the tumors of the salivary gland.
 SLO# 6: Discuss the clinical presentation, gross and
microscopic features, and behavior of pleomorphic adenoma
and Warthin tumor.
 mouth

Oral Cavity 1. Stomatitis

Aphthous Ulcer
Herpes virus infection
Candidiasis
2. Leukoplakia
white patch

3. Oral cancer

Salivary Gland 1. Sialadenitis inflammation of salivary gland

2. Tumors
Aphthous Ulcer (Canker)
Most common oral ulcers

Common in first 2 decades

Single / multiple

Small, shallow, painful

A condition that resolves on its own and has no long-term harmful effect on a person's health

Appear in crops, self limiting but recurs

Triggered by stress, fever & activation of IBD

Herpes virus infection
Organism – HSV Type I
Spread – person to person
Primary Infection - acute herpitic gingivostomatitis
↓
Dormancy in ganglion
↓
Reactivation- recurrent
herpetic stomatitis
Factors producing reactivation - trauma, allergy,
pregnancy, menstruation, resp. tract infection etc.
Microscopy:-
Intra epithelial vesicles
Intra nuclear inclusions & giant cells
Tzank test herpes skin test
Oral candidiasis a condition in which the fungus Candida
albicans accumulates on the lining of your mouth

fungus

Candida albicans normal grow in mouth

Moniliasis, Oral thrush

Factors
1. Species of Candida
2. Impaired defense mechanism
Diabetic
medications that can make yeast flourish and
cause infection :

Steroid therapy
1- conticosteroid
2- antibiotic
3- birth cotrol pills
AIDS patients
3. Alteration of normal oral flora
Antibiotic therapy
Morphology
vreamy white slightly raised lesions in your mouth

patch

Curdy white plaque

Pseudomembrane
or
Pseudo hyphae
& budding yeast
forms
Leukoplakia
WHO definition -"a white patch or plaque that
cannot be scraped off and cannot be characterized
clinically or pathologically as any other disease."
These patches can't be
scraped off.

Gross:- Leathery white discrete areas

of mucosal thickening
Microscopy:-

Hyperkeratosis with or without dysplasia

5-25 % Malignant transformation
Erythroplasia
Red velvety areas
Dysplastic features present
>50% turn malignant

Tobacco use (cigarettes and chewing tobacco) is the

most common risk factor for leukoplakia and
erythroplakia.
Cancer of Oral cavity & Tongue
Mostly (95%) Squamous cell type important point

Others are salivary gland carcinoma

Age group : 50-70 years important point

Multiple primary tumors may be present

simultaneously - “field cancerization ”
, after repeated carcinogenic Field cancerization or
exposures, the entire field effect is a biological
superficialepitheliium of the process in which large
areas of cells at a tissue
upper aerodigestive tract has
surface or within an organ
an increased risk for are affected by
developing (pre)malignant carcinogenic alterations.
lesions because of multiple The process arises from
exposure to an injurious
genetic abnormalities. environment, often over a
lengthy period.
Risk Factors:-

1. Precancerous lesions Erythroplasia Leukoplakia

2. Carcinogens - Tobacco use

Alcohol abuse
3. Chronic friction sharp teath —> weakly assosiated
human papiloma virus

4. HPV Infection type 16 & 18

Prognosis for patients with HPV-positive
tumors is better than for those with HPV-
negative tumors because lesser number of mutation
Morphology
Gross:-
Favored sites
under

ventral surface of the tongue,

floor of the mouth,
lower lip, soft palate and gingiva
only on mucous

deeper
Microscopy
Epithelial Dysplasia
↓
Carcinoma insitu
b.m in intanct

↓
Invasive carcinoma
Spread:-

Local infiltration
LN metastasis cervical nodes
Prognosis:-
Early stage 90% survival
Better for carcinoma lip
Floor of mouth & tongue
LN. negative 40% survival
LN. positive 20% survival

a swollen salivary gland.
Sialadenitis
It's caused by infections, 1- Bacterial or viral infection.
autoimmune diseases and 2- Dehydration.
salivary gland stones 3- Sialolithiasis
4- Sjogren’s syndrome
Sialadenitis usually goes
away in about a week

1. Viral – Mumps – Paramyxovirus

Children – Self limited
Adult – pancreatitis, orchitis sterlic

2. Bacterial – Sialolithiasis stones in salivary gland

Dehydration
3. Autoimmune – Sjogren’s syndrome
Xerostomia salivary gland

Kerato conjunctivitis sicca lacrimal gland

Neoplasms of Salivary gland
Common in 6th or 7th decade, M:F ratio almost equal
Incidence more size, less malignancy

Tumors Malignancy
Parotid 80%
larger , more chnce of tumor
15-30%
Submandibular 10% 40%
Minor Glands 10% >50%

The likelihood that a salivary gland tumor is malignant

is inversely proportional to the size of the gland.
Classification

Benign Malignant

Pleomorphic adenoma Mucoepidermoid carcinoma

Warthin tumor Adenoid cystic carcinoma

Malignant mixed tumor

 within the
parotid or
submandi

Pleomorphic Adenoma bular

areas

Most common (45%) of all salivary tumors

90% of all benign salivary tumors
Presentation looks
like

Painless slow growing swelling, apparently

encapsulated
Microscopy:-
1.Epithelial areas-ducts, acini, tubules, or sheets

2.Mesenchymal areas-myxoid or chondroid material

Both of myoepithelial origin
“ Mixed Tumor”

2.Epithelium and myepithelium cells proliferation

3.Capsule
Prognosis:-

Recurrence removing only the cell without the canpsule

25% following enucleation

4% following parotidectomy
carcinoma coming from pre existing tumor

Malignant transformation- carcinoma ex pleomorphic

adenoma or malignant mixed tumor
Incidence increases with the duration of the tumor
Warthin Tumor

Almost always in parotid

5 times more common in male

5th to 7th decade

Gross:-

Round or oval encapsulated cystic mass

Cut section cystic or cleft like spaces

Microscopy:-
1.Spaces lined by double layered epithelium showing
oncocytic change glandular shape

2.Lymphoid tissue forming germinal centers

Prognosis:- Recurrence only 10%

Malignant transformation rare