classification,theories

1. GOOD MORNING
SURAJ NAIR
SENIOR LECTURER
Dept. of Pedodontics
Malabar dental college, Manoor

2. CYSTS AND TUMORS OF
SALIVARY GLANDS

3. INTRODUCTION
 Salivary glands are important exocrine glands
 Their prime function being secretion of saliva
 Tumors of salivary glands represent 2 to 4 %
of head and neck neoplasms
 They are broadly classified into benign and
malignant tumors

4.  70% of salivary gland tumors originate in
the parotid gland
 8 % in the submandibular glands
 22 % in the minor salivary glands and
sublingual

5.  75% of parotid tumors are benign
 50% of tumors of submandibular and 60-80%
of minor salivary gland tumors are malignant
 Pleomorphic adenomas are the most
common benign tumors comprising 85 % of
all salivary gland neoplasms

6. CLASSIFICATION
 Salivary gland diseases vary in their incidence
and they are usually classified into
Neoplastic
Non-neoplastic

7. CLASSIFICATION OF NON-NEOPLASTIC
SALIVARY GLAND DISEASES
 DEVELOPMENTAL
 Aplasia
 Hypoplasia
 Atresia
 Accessory salivary duct
 Diverticuli
 Polycystic disease of parotid gland

8.  INFECTIOUSAND INFLAMMATORY
 Bacterial
1 Acute sialadenitis
2 Chronic sialadenitis
 Viral
1 Mumps
2 HIV associated salivary gland diseases
3 EBV infection
4 Coxsackie A infection
5 Cytomegalic sialadenitis

9.  OBSTRUCTIVE AND TRAUMATIC LESIONS
1 Sialolithiasis
2 Extravasation cysts
3 Retention cysts
4 Fistula
5 Necrotizing sialometaplasia
6 Radiation induced sialadenitis
7 Pneumoparotitis

10.  FUNCTIONAL DISORDERS
1 Xerostomia
2 Sialorrhea
3 Cystic fibrosis
 ALLERGIC AND IMMUNOLOGICAL DISORDER
1 Allergic sialadenitis
2 Sjogrens syndrome
3 Mikulicz’s disease
4 sarcoidosis

11.  METABOLIC AND HORMONAL DISORDER
1 Sialosis
2 Acromegaly
 AGEING - Oncocytosis
 IDIOPATHIC
1 Necrotizing sialometaplasia
2 Benign cysts of parotid glands
3 Cheilitis glandularis

12. CLASSIFICATION OF SALIVARY
GLAND NEOPLASMS
 They are remarkable for their histologic
diversity
 They include :
 Benign
Malignant
 They may be of epithelial, mesenchymal and
lymphoid origin

13. Classification by Foote and
Frazell1954)
Benign Malignant
 Pleomorphic adenoma
 Oxyphil adenoma
 Sebaceous cell adenoma
 Benign lymphoepithelial
lesion
 Papillary cystadenoma
lymphomatosm
 Malignant mixed tumor
 Mucoepidermoid tumor
 Squamous cell carcinoma
 adenocarcinoma

14. Classification by Thackeray and
Sobin 1972
 Epithelial tumors :
 Pleomorphic adenoma
 Monomorphic adenoma
 Mucoepidermoid tumor
 Acinic cell tumor
 Carcinomas
 Adenoid cystic carcinoma
 Adenocarcinoma
 Epidermoid carcinoma
 Undifferentiated carcinoma

15.  Nonepithelial tumors
 Unclassified tumors
 Allied conditions
 Benign lymphoepithelial lesion
 Sialosis
 Oncocytosis

16. Revised classification by
WHO 2005
 Malignant
 Benign
 Soft tissue tumors
 Hematolymphoid tumors
 Secondary tumors

17.  Malignant epithelial tumors
Acinic cell carcinoma
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Epithelial myoepithelial carcinoma
Clear cell carcinoma
Basal cell adenocarcinoma
Sebaceous carcinoma
Cystadenocarcinoma
Oncocytic carcinoma
Salivary duct carcinoma
Myoepithelial carcinoma
adenocarcinoma

18.  Benign epithelial tumors
o Pleomorphic adenoma
o Myoepithelioma
o Basal cell adenoma
o Warthins tumor
o Oncocytoma
o Canalicular adenoma
o Sebaceous adenoma
o Lymphadenoma
o Ductal papillomas
o cystadenoma

19.  Soft tissue tumors
• Hemangioma
 Hematolymphoid tumors
• Hodgkin’s lymphoma
• Diffuse large B-cell lymphoma
 Secondary tumors

20. ETIOLOGY
1. VIRUSES : EBV – lymphoepithelial
carcinoma
2. RADIATION : high frequency of
mucoepidermoid carcinoma and warthins
tumor
3. OCCUPATION :
{Rubber, arsenic, plumbing, automobile and
cosmetics}

21. 4 LIFESTYLE AND NUTRITION
Smoking –Warthin’s tumor
Tobacco use and alcohol – no association
5 HORMONES

22. HISTOGENESIS
 Histogenic concepts that were evolved were
 Unicellular theory
 Bicellular theory
 Reverse cell hypothesis
 Multicellular histogenetic concept

23.  UNICELLULAR THEORY
 Proposed that the neoplasm arise from their
adult differentiated counterparts of salivary
gland units
 Theory was later rejected
* induction of neoplasm requires
dedifferentiation of already specialized cells

24.  BICELLULAR THEORY :
 Eversole in 1971
 Semipleuripotential theory
 Based on the embryonic development of
palatal minor salivary glands
 Eversole observed existence of reverse cell
during embryogenesis of palatal salivary
glands

26.  Palatal minor salivary glands develop as
downgrowth of bilayered ducts
 Inner layer develop from outer basal layer
 These basal layer was considered as reverse
cells
 Stem cells
 They are confined to basal region and
thought to cause tumors
 Rejected – lack of specificity

27.  REVERSE CELL HYPOTHESIS :
 Regezi and Batsakis i 1977
 Proposed that differentiated cell types in
mature salivary glands are incapable of
undergoing neoplastic alteration
 Stem (reverse )cells are solely at risk for
neoplastic transformation

28.  MULTICELLULAR HISTOGENETIC CONCEPT
 Dardick in 1991
 Proposed that any of the cells found in the
normal salivary system could probably serve as
the precursor for neoplasm
 Both in vitro and in vivo studies have shown
that mitotic figures are frequently seen in inner
cell layer

31. TUMOR PROGRESSION IN SALIVARY
GLAND TUMORS
 Multistep process
 Involves sequential accumulation of genetic
changes
 It may progress in many ways

32.  They are :
Malignant transformation of benign salivary
gland tumors
Progression from low grade to high grade
carcinoma
Dedifferentiation of a carcinoma to high
grade carcinoma with loss of original line of
differentiation
Stromal invasion

33. DEDIFFERENTIATION OF SALIVARY GLAND
TUMORS
 Transformation of salivary gland carcinoma
to a high grade carcinoma in which the
original line of differentiation is no longer
evident
 Acinic cell carcinoma – first to be reported

34.  Dedifferentiated component could be a form of
o High grade carcinoma
o Poorly differentiated carcinoma
o Undifferentiated carcinoma
Other tumors reported were –
• Mucoepidermoid carcinoma
• Adenoid cystic carcinoma
• Myoepithelial carcinoma
• Salivary duct carcinoma
• Hyalinizing clear cell carcinoma

35. GENETIC COMPONENTS
 Genetic changes that could mediate
dedifferentiation are p53 mutation, increased
cyclin D1 expression , loss of expression of Rb
protein and gene amplification

36. Thank
you