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Non neoplastic lesions of the
salivary gland
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com
OBJECTIVES
At the end of the lecture student should be able to :
•Describe the etiology, clinical features, histopathological
features of necrotizing sialometaplasia
•Describe the etiology, clinical features, histopathological
features of adenomatoid hyperplasia of salivary glands
•Describe the etiology, clinical features, histopathological
features of sialadenitis
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• An uncommon, locally destructive inflammatory
condition of the salivary glands
• Result of ischemia that leads to local infarction
• Predisposing factors: Traumatic injuries
Dental injections
Ill-fitting dentures
Upper respiratory infections
Adjacent tumors
Previous surgery
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• 75% on posterior palate
• 2/3rds are unilateral
• Most common in adults – mean 46 yrs
• M > F
• Initially seen as non-ulcerated swelling, often
associated with pain or paraesthesia
• Later, crater-like ulcer develops
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Necrotizing
sialometaplasia
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• Squamous cell carcinoma
• Mucoepidermoid carcinoma
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• Acinar necrosis
• Squamous metaplasia of associated ducts
• Overall architecture is maintained
• Liberated mucin may be associated with
inflammatory response
Squamous metaplasia
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• Biopsy to rule out malignancy
• No specific T/t
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• It is an uncommon benign non-neoplastic
enlargement
• 1st
described by Giansati & Waldron in 1971
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• Painless, tumor-like swelling of the palate
• Age range : 39-50 yrs
• M>F
• Hard palate > soft palate
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• Largely unknown
• May be a reaction to chronic trauma
• Some authors have seen predominance in
smokers, denture-wearers or both
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• Glandular tissue is hyperplastic
• Morphology is normal, but some isolated
lobules may appear hypertrophic
• Ductal dilatation seen
• Inflammation when present is focal
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• Complete excision
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• Slow-growing non-neoploastic lesion
• Age range: 12-63 yrs
• M=F
• Almost always in parotid glands
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• Circumscribed, but lack encapsulation
• Consist of sclerotic, hyalinized connective tissue
• Hyperplastic ductal and acinar elements are seen in
the fibrous tissue.
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• Ductal lining fequently shows apocrine-like
metaplasia and hyperplasia, sometimes with
formation of transluminal bridges giving
cribriform appearance.
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• Sometimes ducts are seen surrounded by
eosinophilic globules.
• Foci of acinar components may contain large,
strongly eosinophilic, PAS-positive cytoplasmic
granules.
• Lymphocytic infiltration of variable intensity seen .
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Cystic spaces
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• Wide excision
• D/D: Mucoepidermoid or other Ca
• Pleomorphic adenoma
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Developmental conditions
• Atresia – exceedingly rare, congenital occlusion
or absence of one/more major salivary gland
ducts
• Aberrancy – occasional cases seen within body
of mandible
• Stafne cyst
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Infectious Conditions
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• Represents inflammation mainly involving the
acinoparenchyma of the gland
• Acute infection more often affects the major
glands than the minor glands
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• Retrograde contamination of the salivary ducts
and parenchymal tissues by bacteria inhabiting
the oral cavity
• Stasis of salivary flow through the ducts and
parenchyma promotes acute suppurative
infection
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• Systemic dehydration (salivary stasis)
• Chronic disease and/or immunocompromise
– Liver failure
– Renal failure
– DM, hypothyroid
– Malnutrition
– HIV
– Sjögren’s syndrome
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• Neoplasms (pressure occlusion of duct)
• Sialectasis (salivary duct dilation) increases the risk
for retrograde contamination. Is associated with
cystic fibrosis and pneumoparotitis
• Extremes of age
• Poor oral hygiene
• Calculi, duct stricture
• NPO status (stimulatory effect of mastication on
salivary production is lost)
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• More common in parotid gland
• Suppurative parotitis, surgical parotitis, post-
operative parotitis, surgical mumps, and
pyogenic parotitis.
• The etiologic factor most associated with this
entity is the retrograde infection from the
mouth.
• 20% cases are bilateral
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Suppurative
parotitis
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SUMMARY
– etiology, clinical features, histopathological
features of necrotizing sialometaplasia
– etiology, clinical features, histopathological
features of adenomatoid hyperplasia of salivary
glands
– etiology, clinical features, histopathological
features of sialadenitis
www.indiandentalacademy.com
BIBLIOGRAPHY
• Text book of oral pathology Shafer's, 5 & 6th
edition
• Surgical Pathology of Salivary Glands Ellis 1st
Edition
• Color Atlas of Oral Diseases Cawson, R. 2nd
edition
• Oral and Maxillofacial Pathology Neville, Brad W.
2nd
• Lucas’s Pathology Of Tumor’s of the Oral Tissues
• Cawson, R. A., Bennie, W. H 5th
edition
www.indiandentalacademy.com
• THANK YOU
www.indiandentalacademy.com

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Non neoplastic diseases 3/ dental implant courses

  • 1. Non neoplastic lesions of the salivary gland INDIAN DENTAL ACADEMY Leader in continuing Dental Education www.indiandentalacademy.com
  • 2. OBJECTIVES At the end of the lecture student should be able to : •Describe the etiology, clinical features, histopathological features of necrotizing sialometaplasia •Describe the etiology, clinical features, histopathological features of adenomatoid hyperplasia of salivary glands •Describe the etiology, clinical features, histopathological features of sialadenitis www.indiandentalacademy.com
  • 3. • An uncommon, locally destructive inflammatory condition of the salivary glands • Result of ischemia that leads to local infarction • Predisposing factors: Traumatic injuries Dental injections Ill-fitting dentures Upper respiratory infections Adjacent tumors Previous surgery www.indiandentalacademy.com
  • 4. • 75% on posterior palate • 2/3rds are unilateral • Most common in adults – mean 46 yrs • M > F • Initially seen as non-ulcerated swelling, often associated with pain or paraesthesia • Later, crater-like ulcer develops www.indiandentalacademy.com
  • 6. • Squamous cell carcinoma • Mucoepidermoid carcinoma www.indiandentalacademy.com
  • 7. • Acinar necrosis • Squamous metaplasia of associated ducts • Overall architecture is maintained • Liberated mucin may be associated with inflammatory response Squamous metaplasia www.indiandentalacademy.com
  • 8. • Biopsy to rule out malignancy • No specific T/t www.indiandentalacademy.com
  • 9. • It is an uncommon benign non-neoplastic enlargement • 1st described by Giansati & Waldron in 1971 www.indiandentalacademy.com
  • 10. • Painless, tumor-like swelling of the palate • Age range : 39-50 yrs • M>F • Hard palate > soft palate www.indiandentalacademy.com
  • 11. • Largely unknown • May be a reaction to chronic trauma • Some authors have seen predominance in smokers, denture-wearers or both www.indiandentalacademy.com
  • 12. • Glandular tissue is hyperplastic • Morphology is normal, but some isolated lobules may appear hypertrophic • Ductal dilatation seen • Inflammation when present is focal www.indiandentalacademy.com
  • 14. • Slow-growing non-neoploastic lesion • Age range: 12-63 yrs • M=F • Almost always in parotid glands www.indiandentalacademy.com
  • 15. • Circumscribed, but lack encapsulation • Consist of sclerotic, hyalinized connective tissue • Hyperplastic ductal and acinar elements are seen in the fibrous tissue. www.indiandentalacademy.com
  • 16. • Ductal lining fequently shows apocrine-like metaplasia and hyperplasia, sometimes with formation of transluminal bridges giving cribriform appearance. www.indiandentalacademy.com
  • 17. • Sometimes ducts are seen surrounded by eosinophilic globules. • Foci of acinar components may contain large, strongly eosinophilic, PAS-positive cytoplasmic granules. • Lymphocytic infiltration of variable intensity seen . www.indiandentalacademy.com
  • 19. • Wide excision • D/D: Mucoepidermoid or other Ca • Pleomorphic adenoma www.indiandentalacademy.com
  • 20. Developmental conditions • Atresia – exceedingly rare, congenital occlusion or absence of one/more major salivary gland ducts • Aberrancy – occasional cases seen within body of mandible • Stafne cyst www.indiandentalacademy.com
  • 22. • Represents inflammation mainly involving the acinoparenchyma of the gland • Acute infection more often affects the major glands than the minor glands www.indiandentalacademy.com
  • 23. • Retrograde contamination of the salivary ducts and parenchymal tissues by bacteria inhabiting the oral cavity • Stasis of salivary flow through the ducts and parenchyma promotes acute suppurative infection www.indiandentalacademy.com
  • 24. • Systemic dehydration (salivary stasis) • Chronic disease and/or immunocompromise – Liver failure – Renal failure – DM, hypothyroid – Malnutrition – HIV – Sjögren’s syndrome www.indiandentalacademy.com
  • 25. • Neoplasms (pressure occlusion of duct) • Sialectasis (salivary duct dilation) increases the risk for retrograde contamination. Is associated with cystic fibrosis and pneumoparotitis • Extremes of age • Poor oral hygiene • Calculi, duct stricture • NPO status (stimulatory effect of mastication on salivary production is lost) www.indiandentalacademy.com
  • 26. • More common in parotid gland • Suppurative parotitis, surgical parotitis, post- operative parotitis, surgical mumps, and pyogenic parotitis. • The etiologic factor most associated with this entity is the retrograde infection from the mouth. • 20% cases are bilateral www.indiandentalacademy.com
  • 28. SUMMARY – etiology, clinical features, histopathological features of necrotizing sialometaplasia – etiology, clinical features, histopathological features of adenomatoid hyperplasia of salivary glands – etiology, clinical features, histopathological features of sialadenitis www.indiandentalacademy.com
  • 29. BIBLIOGRAPHY • Text book of oral pathology Shafer's, 5 & 6th edition • Surgical Pathology of Salivary Glands Ellis 1st Edition • Color Atlas of Oral Diseases Cawson, R. 2nd edition • Oral and Maxillofacial Pathology Neville, Brad W. 2nd • Lucas’s Pathology Of Tumor’s of the Oral Tissues • Cawson, R. A., Bennie, W. H 5th edition www.indiandentalacademy.com