Saliva Flashcards
Parotid
Preauricular
Serous
Cont. 20-40% saliva
Submandibular
Submandibular location
Mucous and serious
60-70% saliva
Sublingual
FOM, under tongue
Mucous secretion
10% saliva
Minor salivary glands
Everywhere but mainly lips, palate, cheeks, tongue
800+ total
Mucus except one exception
Exception - serous glands of von Ebner
5-10% saliva
Stafnes bone cavity
Non-neoplastic developmental anomaly
Unilocular, corticated well-defined radiolucency at angle of mandible under ID canal
Thought to be pathological cystic lesion
Now know is normal salivary tissue pushing on mandible making dent - appearing as lucency on rad
Sialedenitis
Acute - bacterial (acute, recurrent - adults/kid), viral
Chronic - bacterial, post-irradiation, Sjogren’s
Acute parotitis
Ascending infection
oral bacteria - S. aureus
Acute swelling, pain
Pus exudes from ducts
Usually 2^ to dry mouth - radiotherapy, Sjogrens, drug-induced
Recurrent parotitis - adults
40-60
F > M
Unilateral
Recurrent ascending infections
Secondary to xerostomia
Xerostomia due to: irradiation, drug-induced, Sjogren’s
Recurrent parotisis of childhood
4m - 15 years
M = F
No obvious cause
Bilateral parotid swellings
Sudden onset
Periods of quiescence
Days - weeks duration
NOT suppuration but may be other signs of infection - pain, fever, redness
Sialography shows punctate sialectasis - ‘snowstorm’ appearance
Gradual destruction of acinar elements - reduced salivary flow
Non specific histology but shows dilation of salivary ducts with fibrosis replacing salivary tissue
Lots of lymphocytes extending into epithelium and around ducts
Acute viral sialedenitis: mumps
Complications
Epidemic parotitis
Mumps virus - paramyxovirus
Rare - <1000 cases/year
Mainly in children
Very painful, malaise, fever
Acute bilateral parotid swelling
Incubation period - 2-3 weeks. Droplet or direct spread
Self limiting - 10-14 days
May spread to other glands/organs
Complications:
Orchitis - 30%
Meningitis - 10%
Oophoritis - 5%
Pancreatitis - 5%
Cranial nerve palsies
VIII nerve deafness
Chronic sailodenitis is usually….
…..secondary to duct obstruction due to calculi
Salivary caliculi
Accumulation of calcium and phosphate salts which deposit in salivary ducts or gland
Usually unilateral
M>F
Submandibular - 80% due to: saliva being pushed upwards against gravity in mouth and tortious course of gland
Parotid 20%, minor glands 1-15%
Calculus - concentric circles of calcium salts deposited around cellular debris and mucous
When obs by calculus occurs, get saliva retention and inflammation of gland = swelling and fibrosis, then continued fibrosis and loss of function
Radiation sialodenitis
Doses >20Gy
High risk of permanent damage >30Gy
Severe damage >50Gy
Serous acini most sensitive
Inflammation and fibrosis of glands
Loss of function
Important consideration in cancer pt’s
Eg’s of obstruction and trauma
Salivary caliculi Mucous cysts (mucoceles) Necrotising sialometaplasia
Mucous extravasation cyst
85% mucoceles
Younger age - 20-30
Lower lip commonest site - 50%
Rupture of ducts, saliva spills out into surrounding CT - forming cyst like area lined by granulation and fibrous tissue
Histology:
Lumen filled with mucous
Macrophages filled with mucous
Lining of inflamed, compressed granulation tissue
Mucous retention cyst
15% mucoceles
Older age range - 40-60
Buccal mucosa, FoM
Due to blocked duct but with NO rupture
Blockage of duct leads to dilation and expansion of duct epithelium
Histology:
Mucous in lumen
Lining of ductal epithelium
Cyst wall of fibrous tissue with glands
Ranula
Floor of mouth
Usually extravasation cysts
Mainly sublingual
Usually children
Painless swellings
Rupture and recur
2-3cm
Necrotising sialometaplasia
Presents as indurated, ulcerated swelling
Usually on palate
Often biopsied as malignant
But is acc benign inflammatory disease
Heals spontaneously after 4-8 weeks
Histology:
Squamous metaplasia of salivary ducts - islands of squamous epithelium deep in CT’s BUT
Also see necrosis of acini with ‘ghosts’ of normal structures
Classification of salivary gland tumours WHO 2017
Benign
- Pleomorphic adenoma
- Warthin tumour
- Cystadenoma
- Basal cell adenoma
- Canalicular adenoma
Malignant
- Mucoepidermoid carcinoma
- Acinic cell carcinoma
- Polymorphous adenocarcinoma
- Adenoid cystic carcinoma
- Carcinoma ex pleomorphic adenoma
Pleomorphic adenoma
Most common salivary gland tumour
Parotid most common, then palate
Age 30-60
M=F
Benign
May recur
Pleomorphic adenoma histology
Mixed (pleomorphic) pattern
Islands and strands of epithelium
Encapsulated
Usually lobulated
Myxoid, mucoid or chondroid stroma
Duct like structures
Typical appearance: duct like structured w/inner and outer layer. Pink secretions inside
Occasionally, tumours are solid - made up of lots of cells with no stroma
Myoepithelial cells surrounding duct-like structures - fried egg appearance
Warthin tumour + histology
10% of benign salivary gland tumours
Always in parotid gland
Male:female 60:40
Associated with smokers
Sometimes bilateral or multifocal
Completely benign
Histology: irregular cysts, lined by oncocytic duct epithelium, stroma composed of lymphoid tissue
Mucoepidermoid carcinoma + histology
Most common malignant salivary tumour
Parotid most common site
Also palate, cheek, retromolar
Seen occasionally in children
15% metastasise
Histology:
Mixture of mucous and epidermoid cells (squamous cells)
Lesions usually multicystic
High grade lesions may be solid with few mucous cells
Occasional lesions have many clear cells
Adenoid cyStic carcinoma + histology
Second most common salivary malignancy
Infiltrative tumour - no capsule
Parotid most common
Cheeks, palate, Sinuses
Highly malignant
75% pt’s die within 20 years
Metastasis via blood stream and nerve invasion
Histology:
Non-encapsulated
Characteristic multicystic/cribriform pattern - ‘Swiss-cheese’
Infiltrates widely - through bone, blood vessels, along nerves
Polymorphous adenocarcinoma
Only intra-orally
Palate 70%, lips, cheek 30%
3rd most common I/o malignancy
>50 years
Variable histological pattern - lobules, ductal structures, cribriform areas, papillary cystic pattern, single cell filing
Perineural infiltration typically
Infiltrative growth
Bland, monotonous cytology
Often misdiagnosed on incisional biopsies as pleomorphic adenoma or adenoid cystic carcinoma - need great care with small palatal biopsies
Survival >90% at 5 years
Metastases 10-15%
Similar to mucoepidermoid
Unpreditable - lesions with papillary cystic pattern and cytological atypia may have worse prognosis
Acinic cell carcinoma
5% salivary malignancies
mostly parotid
10% recurrence, 15% metastasise
Variable histological appearance - solid, microcystic, papillary cystic, follicular
Lymphoid tissue and germinal centres common
Carcinoma ex pleomorphic adenoma
10% pleomorphic adenomas may become malignant
Usually long standing or recurring lesions
Elderly - 60+
History of long term slow growing lesions with recent increase in size
Sjogren’s and clinical features
Sjogren’s - autoimmune disorder characterised by lymphocyte mediated destruction of the exocrine glands resulting in dry eyes and dry mouth
Primary - dry eyes and mouth
Secondary - dry eyes and mouth +/- CT disease e.g. RA, SLE
Clinical features:
90% female
Middle age
Oral symptoms - dry mucosa, lobulated tongue, candidosis, caries
Dry eyes - keratoconjunctivitis
Parotid swelling in 20%
Pathology of Sjogren’s + histology
Lymphatic infiltrates in salivary glands
In minor glands - lymphocytic sialedenitis
In major glands - lymphoepithelial lesion
in 3-5% cases, these lesions may progress to lymphoma
HISTOLOGY:
Gland replaced by lymphocytes
Acini disappear, but ducts proliferate to form epithelial islands
Epithelial island infiltrated by lymphocytes - ‘lymphoepithelial lesion’
Imaging - dry mouth
Ultrasound if suspect Sjogrens. Can be followed by sialography if necessary
Sjogren’s is the only cause of dry mouth that can be identified on imaging - disease process destroys the gland parenchyma, producing a typical pattern of changes on imaging
Blobs and dots of xray contrast within gland
US - normal parotid tissue replaced with black spaces = inflammation
Imaging - obstructive sialedenitis
Calculi most common in submandibular, strictures more common in parotid. Obstruction of sublingual rare
Imaging - plain film rads then sialography.
For submandibular obstruction - lower true occlusal (90degrees) and posterior oblique film + possibly sectional OP
For parotid obstruction, AP extra oral film plus small dental film inside cheek useful
Sialography - injecting iodinated contrast along submandibular or parotid ducts. The iodine in the contrast makes it densely radiopaque, stones less dense to appear radiolucent
Txt of submandibular caliculi
If visible in anterior ⅓rd of duct - surgical excision under LA - intra-orally
If small, mobile and anterior to mylohyoid bend - basket removal
If beyond mylohyoid bend, or too large for basket, surgical excision - extra orally
Basket removal + complications
Intra-ductal technique done under LA
Helical wire basket placed (closed) into duct opening. Advanced past calculus then opened. Calculus snared into helical basket and advanced to duct opening
Small incision - papillotomy to release calculus. No sutures as would cause stenosis
Complications:
Pain and swelling expected post-procedure
Failure to retrieve stone
Basket stuck in duct - stone may be adhered to duct wall, needs to be mobile on sialogram
Persisting symptoms even after removal
Treatment of parotid obstruction
Strictures: balloon dilation if in the extra-glandular duct (most common).
Articaine and iodinated dye passed down parotid to identify stricture site and give topical anaesthesia. Submucosal buccal lidocaine also injected along course of duct
Dilation of parotid papilla using lacrimal probe. Angioplasty 2-3mm balloon inserted (uninflated) and advanced to stricture site with x-ray guidance.
Balloon inflated - 15psi 90 secs, may need 2-3x inflations
In some cases, stricture may be too tight to pass balloon, even when fine wire guide used.
Despite LA, inflating balloon is uncomfortable. Some will not dilate, even after several inflations
⅓rd dilated parotid strictures will restenose within 2 years and need repeating
Stones: if visible at duct opening - simple surgical excision
If in the extra-glandular duct, anterior to posterior border of ramus and small and mobile - basket retrieval as per submand
If in gland parenchyma or too large, lithotripsy (sound waves to break up) or superficial parotidectomy
