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GOOD MORNING
SURAJ NAIR
SENIOR LECTURER
Dept. of Pedodontics
Malabar dental college, Manoor
CYSTS AND TUMORS OF
SALIVARY GLANDS
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
 70% of salivary gland tumors originate in
the parotid gland
 8 % in the submandibular glands
 22 % in the minor salivary glands and
sublingual
 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
CLASSIFICATION
 Salivary gland diseases vary in their incidence
and they are usually classified into
Neoplastic
Non-neoplastic
CLASSIFICATION OF NON-NEOPLASTIC
SALIVARY GLAND DISEASES
 DEVELOPMENTAL
 Aplasia
 Hypoplasia
 Atresia
 Accessory salivary duct
 Diverticuli
 Polycystic disease of parotid gland
 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
 OBSTRUCTIVE AND TRAUMATIC LESIONS
1 Sialolithiasis
2 Extravasation cysts
3 Retention cysts
4 Fistula
5 Necrotizing sialometaplasia
6 Radiation induced sialadenitis
7 Pneumoparotitis
 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
 METABOLIC AND HORMONAL DISORDER
1 Sialosis
2 Acromegaly
 AGEING - Oncocytosis
 IDIOPATHIC
1 Necrotizing sialometaplasia
2 Benign cysts of parotid glands
3 Cheilitis glandularis
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
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
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
 Nonepithelial tumors
 Unclassified tumors
 Allied conditions
 Benign lymphoepithelial lesion
 Sialosis
 Oncocytosis
Revised classification by
WHO 2005
 Malignant
 Benign
 Soft tissue tumors
 Hematolymphoid tumors
 Secondary tumors
 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
 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
 Soft tissue tumors
• Hemangioma
 Hematolymphoid tumors
• Hodgkin’s lymphoma
• Diffuse large B-cell lymphoma
 Secondary tumors
ETIOLOGY
1. VIRUSES : EBV – lymphoepithelial
carcinoma
2. RADIATION : high frequency of
mucoepidermoid carcinoma and warthins
tumor
3. OCCUPATION :
{Rubber, arsenic, plumbing, automobile and
cosmetics}
4 LIFESTYLE AND NUTRITION
Smoking –Warthin’s tumor
Tobacco use and alcohol – no association
5 HORMONES
HISTOGENESIS
 Histogenic concepts that were evolved were
 Unicellular theory
 Bicellular theory
 Reverse cell hypothesis
 Multicellular histogenetic concept
 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
 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
 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
 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
 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
TUMOR PROGRESSION IN SALIVARY
GLAND TUMORS
 Multistep process
 Involves sequential accumulation of genetic
changes
 It may progress in many ways
 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
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
 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
GENETIC COMPONENTS
 Genetic changes that could mediate
dedifferentiation are p53 mutation, increased
cyclin D1 expression , loss of expression of Rb
protein and gene amplification
Thank
you

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salivary gland

  • 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
  • 25.
  • 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
  • 29.
  • 30.
  • 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