pathology of salivary gland tumours Flashcards
4 causes in change in gland size
Secretion retention (commonest)
* Mucocele
* Duct obstruction e.g. sialolith
Chronic sialadenitis (viral – mumps; bacterial; other causes)
Gland hyperplasia
* Sialosis
* Sjögren’s Syndrome
Salivary neoplasms
silosis
gland hyperplasia
enlargement of the glands that is non neoplastic, non-inflammatory, non tender (no pain) (particularly in parotid)
can be in alcohol dependence, some eating disorders, diabetes
salivary neoplasms/tumours
characteristics
Major gland: localised swelling
* Neurological change - facial nerve in parotid (paraesthesia, facial palsy)
Usually
* Painless
* Slow growing
* Well defined
epidemiology of salivary gland tumours
uncommon, most in adults
* 10 per 100,000 of general population (varies,)
3% of head and neck neoplasms
75% of them are benign (overall)
* malignant salivary gland tumours seem to be increasing
aetiology of salivary gland tumours
unclear
possible links to - radiation, viruses (EBV), racial susceptiblity
order of glands affected by salivary neoplasms
10:1:1 rule (parotid 10x more than sublingual and minor)
larger the gland the less incidence of malignancy smaller the gland less overall incidence of tumours – but more likely to be malignant
Histological typing of salivary gland neoplasms
WHO classification 2017
Epithelial neoplasms
* Benign (adenoma) 11 types with subtypes
* Malignant (adenocarcinoma) 20 types with subtypes
Non-epithelial neoplasms – Sjogrens, immunocompromised
* Lymphoma
* Sarcoma
Complex due to salivary glands arising from different stem cell lines so pathology may be complex
clincal features of major salivary gland neoplasms
Lump in affected gland
* Asymmetry
* Obstruction
* Pain, facial palsy (late signs)
clinical features of minor salivary gland neoplasms
Sites
* Junction of hard/soft palate (commonest area)
* Upper lip/cheek
* Tongue
Ulcerate late (malignant)
3 dx techniques for salivary gland neoplasms
fine needle aspirate (FNA)
* harder to access lesions (directly underneath the skin)
* small amount of tissue – not enough to gain full understanding of pathology and dx
* can differentiate between benign or malignant
* relatively non invasive
core biopsy
* more invasive than FNA – LA, incision, core into little tray
* more tissue than FNA
**incisional biopsy **
* used for easy intraoral access enlargements
3 dx techniques for salivary gland neoplasms
fine needle aspirate (FNA)
* harder to access lesions (directly underneath the skin)
* small amount of tissue – not enough to gain full understanding of pathology and dx
* can differentiate between benign or malignant
* relatively non invasive
core biopsy
* more invasive than FNA – LA, incision, core into little tray
* more tissue than FNA
**incisional biopsy **
* used for easy intraoral access enlargements
problems in dx of salivary neoplasms
Number of tumour type
Variation within a tumour because tissues originate from different stem cell lines so pathology may be complex.
Common features between types
Not all tumours fit the classification e.g. Adenocarcinoma NOS (not otherwise specified)
Immunohistochemistry may be needed to differentiate many of these tumours.
Molecular markers used in some cases (key genomic alterations)
* Next generation sequencing
pleomorphic adenoma occurence
75% of all salivary neoplasms (commonest)
characteristics of pleomorphic adenoma
Parotid most common
Slow growth
Varied histology - “mixed tumour” variety of tissue appearances between different PSAs
* Duct epithelium
* Myoepithelial cells
* Myxoid areas – loose, gelatinous hard to remove surgically
* “chondroid” areas
Connective tissue Capsule variable
tx for pleomorphic salivary adenoma
wide local excision
problems in tx of pleomorphic salivary adenoma
Recurrence (can be multifocal – 1 found and removed, 2 or 3 come back)
* Due to connective tissue capsule being incomplete and myxomatous tissue making it hard to remove all of tumour
* Need to remove a healthy border around the PSA
Progression to carcinoma (5%)
* The longer it is left without removal, more likely to be come malignancy
* Carcinoma ex pleomorphic adenoma
warthin’s tumour (adenolymphoma)
occurence
15% of all salivary tumors
warthin’s tumour characteristics
Most in the parotid (almost exclusive)
Occasionally multiple/bilateral (10%) unusual feature
women more than men
Histology
* Cystic
* Distinctive epithelium
* Lymphoid tissue
distinct histology
tx of warthin’s tumour
Treated by excision
* Completely encapsulated so easier
Rare – recurrence and malignant potential
Adenoid cystic carcinoma
characteristics
5%, more in minor glands
Varied patterns
* cribriform (“swiss cheese”)
* others: tubular, solid
Local spread - nerves, bone
Difficult to treat = recurrence
* very infiltrative – hard to eradicate - grows along nerve fibres (perineural fibres) and grows along trabecular bone
* Late spread – metastasis, by blood to lung (different from other carcinomas; complicates tx)
long term prognosis is poor (at 20 yrs)
clinically
* Slow growing, painless nodule
* Ulcerate and painful later
Adenoid cystic carcinoma
characteristics
5%, more in minor glands
Varied patterns
* cribriform (“swiss cheese”)
* others: tubular, solid
Local spread - nerves, bone
Difficult to treat = recurrence, proximity to vital structures and anatomcal obstacles (sinus, nasal cavity, pharynx)
* very infiltrative – hard to eradicate - grows along nerve fibres (perineural fibres) and grows along trabecular bone
* Late spread – metastasis, by blood to lung (different from other carcinomas; complicates tx)
long term prognosis is poor (at 20 yrs)
clinically
* Slow growing, painless nodule
* Ulcerate and painful later
histology of adenoid cystic carcinoma
Look cyst like on histology – but filled with ground substance (cribriform has better prognosis than other types)
Malignant grow around the nerve and spread within myelin sheath
difficulty in tx adenoid cystic carcinoma
recurrence,
proximity to vital structures and anatomcal obstacles (sinus, nasal cavity, pharynx)
very infiltrative – hard to eradicate - grows along nerve fibres (perineural fibres) and grows along trabecular bone
* Late spread – metastasis, by blood to lung (different from other carcinomas; complicates tx)
long term prognosis is poor (at 20 yrs)
mucoepidermoid carcinoma
characteristics
3-5%, esp. USA
Histology – 2 cell types
* Squamous (epidermoid)
* Glandular (mucous)
Grading/differentiation – cystic or solid diff from SCC
* Higher the sum = higher the grade of malignancy = worse prognosis
Unpredictable behaviour growth speed
Lymphatic spread (rare)
Intraosseous may sometimes occur – source
Cystic lesions lined with odontogenic epithelium (multi-potential - can form mucous cells)
* Odontogenic cysts act as source = rare
* Ectopic salivary gland tissue in the mandible
alcian blue – stains mucous secreting cells and mucous blue
