Salivary Gland Problems Flashcards
Function of salivary glands
Avid buffering
Mucosal lubrication
Taste facilitation
Antibacterial
Cause of dry mouth
Salivary gland disease
Drugs ( reduce salivary flow by having an anti-muscarinic anticholinergic action which reduces stimulation to the glands)
Medical conditions and dehydration
Radiotherapy and cancer treatment
Anxiety and somatisation disorders
Salivary changes from 17 years of age onwards
Acinar tissue loss
- submandibular (37%)
- parotid (32%)
- minor glands (45%)
This is normal physiological occurrence
Indirect salivary problems
Anti-muscarinic cholinergic drugs
- tricyclic antidepressants
- antipsychotics
- amitriptyline 26% reduction
Antihistamine
Atropine
Diuretics- benzodiazapine 10%reduction
Even though number is not so high, but when combined with age and decreased flow due to the age, can be significant
Cytotoxics as part of chemotherapy
Lithium (for bipolar disorder)- 70% reduction and increased caries risk
Chronic medical problems inducing dehydration:
Diabetes
Stroke
Addison disease
Persistent vomiting
Acute medical problems:
Acute oral mucosal disease
Burns
Vesiculobullous diseases
Haemorrhage
Cause is external to the gland
Direct salivary gland problems
Aplasia (ectodermal dysplasia-hair, nails, teeth, salivary and sweat glands)
Sarcoidosis (granulomatous condition which will cause an infiltrate whitin the gland and prevent it from functioning properly)
HIV disease ( causes increase in size but decrease in function, can be first sign of HIV so offer a test if seen)
Gland infiltration
Cystic fibrosis (affects all gland secretions throughout the body)
Investigation for salivary disease
Blood tests: FBC, liver function, CRP
Glucose
Anti ro and anti la antibody
Antinuclear antibody
Complement C3 and C 4
Functional assay- salivary flow
Tissue assay-labial gland biopsy
Imaging- plain radiographs, sialography, MR sialography
Ultrasound
Frequent somatoform diseases
Oral dysaesthesia
TMD pain
Headache
Neck/back pain
Dyspepsia
IBS
Normal and reduced flows
Resting flow:
Normal: 0.3-0.4 ml/min
Reduced: less than 0.1 ml/min
Stimulated flow
Normal: 1-2 ml/min
Reduced: less than 0.5 ml/min
Treatable causes of dry mouth
Dehydration
Medicines with anti muscarinic side effects
Medicines causing dehydration
Poor diabetes control
Somatoform disorders
Removal/solution of all above should remove dry cause
Dry mouth with only symptomatic treatment
Sjogren syndrome
Dry mouth from cancer treatment or salivary gland disease
They cannot be brought back to normal salivary flow so only symptomatic relief offered/reduction in disability
Management:
Intensive dental prevention!
Salivary substitutes
Salivary stimulants
Other investigation for dry mouth
Dry eye test
Schitmer test- tear flow less than 5mm wetting of test paper in 15 min
Tear film
Tissue examination- labial gland biopsy (lower lip-looking for lymphocytic infiltrate and focal acinar disease)- not often as can lead to nerve damage and lip numbness
Dentists management of dry mouth
Prevent oral disease is the key
- caries risk assessment
-candida/ staphylococci awareness and reduction- low sugar diet and OHI
(Angular cheilitis, sore tongue)
Maximal preventative strategy
- diet
-fluoride
-treatment planning for caries risk mouth
Saliva substitute
Sprays: (usually discouraged due to low pH
Glandosane
Saliva orthana
Lozenges:
Saliva orthana
SST (saliva stimulating tablet)
Salivary stimulants
Pilocarpine ( helps to increase residual gland function, but side effects: sweating, tachycardia)
Oral care systems
Oral balance
Frequent sips of water
Causes of hypersalivation
True(rare) - actual increase in salivary flow
-drug uses, dementia, CJD, stroke (neurodegenerative - increase in salivary stimulation from lack of normal regulation)
Perceived (common)- NO increase in salivary flow
-swallowing failure (anxiety, stroke, motor neurone disease, MS)
-postural drooling (being a baby, cerebral palsy)
Drugs causes of hypersalivation
Parasymphatomimetics
Buprenorphine
Anticholinesterase
Haloperidol
Clonazepam
….
Dealing with excess saliva
Treat the cause (anxiety disorders)
Drugs to reduce salivation (anti-muscarinic agents, Botox to prevent gland stimulation)
Biofeedback training (swallowing control)
Surgery to salivary system (gland removal, duct repositioning)
Reasons for salivary gland changes in size
- Viral inflammation - mumps, HIV
- Secretion retention- mucocele, duct obstruction
- Gland hyperplasia - sialosis (unknown cause of gland hyperplasia), Sjogrens syndrome
Mumps
MMR vaccine protects
Signs and symptoms: headache, joint pain, nausea, dry mouth, mild abdominal pain, tired, loss of appetite, pyrexia…
* Can lead to sterility if testicles are involved severely
It is paramyxovirus
Droplet spreading
Incubation period 2-3 weeks
Third of people have no symptoms
Management: symptomatic treatment only
HIV salivary disease
HIV can be cause of salivary swelling
Pt may have no HIV symptoms when presenting/ this can be one of the first signs!
Generally does not improve with treatment
It is lympho-proloferative enlargement of the glands
Mucocele
Caused by secretion retention with in the duct or if extravasated into the tissues
It leads to recurrent swelling that bursts in days
Causing salty taste
Common sites are junction of hard and soft palate
Lower lip
Subacute obstruction
Swelling associated with meals
Swelling will increase as salivary flow starts and reduces when salivary flow stops
Usually happens in submandibular, occasionally on parotid
Can be slowly progressive- over weeks
Eventually becomes fixed and painful
Causes:
Duct obstruction
If in submandibular - usually due to duct blockage
If in parotid-isually due to duct stricture
Can be due to sialolith(stones), mucous plugging, ductal damage from chronic infection (scarring)
Investigation:
Low dose plain radiography ( if normal dose, it may not be seen and calcium in stones is not as high as in teeth)
Lower true occlusal
Sialography- when infection free
Isotope scan if gland function uncertain
Ultrasound assessment of duct system
Duct dilatation
Defect preventing normal emptying
Micro-organisms grow and lead to persisting and recurrent soalodenits
Gland function gradually lost and persisting infection leads to gland removal
May follow recurrent parotitis of childhood at age 20-30
Subacute obstruction, management and outcomes
Management:
Surgical sialolith removal if practical
Sialography for “no stone” causes- washing effect
Consider gland removal if fixed swelling
Outcome:
Reformation of stone/obstruction
Deformity of duct-stasis and infection
Gland damage-slow salivary flow, ascending infection
Other changes in gland size
Increase in gland tissue- hyperplasia
-sialosis, Sjogrens
Sialosis: major gland enlargement
No identified cause
-can be due to alcohol abuse, cirrhosis, DM, drugs
Investigation for sialosis
Blood tests
Glucose
FBC, LFTs, bilirubin
BBV-HIV, hep B,C
Autoantibody screen- ANA, anti Ro, anti La
Other:
MRI of major salivary glands
USS for Sjogrens
Labial gland biopsy
Tear film
Sialography -occasionally
Photography
Sjogren syndrome
Partial- sicca syndrome
Primary- no connective tissue disease
Secondary - connective tissue disease
- SLE ( hair loss, joint pain, joint swelling, photosensitivity, oral ulcers), Rheumatoid arthritis (joint pain and swelling, fatigue, malaise, SOB, neuropathy), scleroderma (Raynaud’s, GI)
It is autoimmune disease ( part of infection, toxic chemicals, dietary components, genetics)
Sjogren - prevalence
0.2-1.2% in US
Mostly women (10:1)
Diagnostic delay due to late presentations
Lifespan not effected
Risk of neonatal lupus in baby if pregnant
Systemic involvement: lungs, kidney, liver, pancreas, blood vessels, nervous system or general fatigue and chronic pain
Sjogrens aetiology
Speculative genetic- genetic predisposition but no specific inheritance (associated with anti-Ro and anti-La is genetic)
Low oestrogen risk gives a risk of getting connective disease
Incomplete apoptosis leads to antigens being improperly exposed
Dysregulation of inflammatory process with dendritic AP cells recruiting T cells response and pro-inflammatory cytokines
Speculative environment - EBV association-weak evidence
Sjogrens- consequences of syndrome
Gradual loss of salivary /lacrimal gland tissue through inflammatory destruction
Enlargement of major salivary glands- usually symmetrical and usually painless
Increased risk of any lymphoma (by 5%), salivary marginal B-cell lymphoma (MALT)
Ocular and oral effects of loss of tears and saliva
Diagnosis of Sjogrens
Complex- no single test gives the answer
Balance of probabilities from multiple criteria
Different scoring systems in use:
American-European consensus group ( dry eyes/mouth, antibody findings z imaging findings, radio nucleotide assessment, histopathology findings -4 or more positive criteria for diagnosis)
ACR- EULAR joint criteria (histopathology findings, autoantibody findings-anti-Ro, dry mouth/eyes- objective salivary flow, schirmer test, ultrasound)
Sjogrens syndrome AECG- oral and eye symptoms
Oral:
Daily feeling of dry mouth for more than 3 months
Recurrent swelling of salivary glands in adults
Frequently drink liquid to aid swallowing dry foods
Abnormal UNSTIMULATED whole salivary flow (less than 1.5 ml in 15 min)
Ocular:
Persistent troublesome dry eyes for more than 3 months
Recurrent sensation of sand/gravel in eyes
Tear substitute used more than 3x a day
Abnormal schirmer test (less than 5 mm wetting in 5 min)
Autoantibodies in Sjogrens syndrome
What do positive autoantibodies mean?
-not causative in disease process
- associated with the clinical pattern
- antibodies possible without disease-need clinical and lab findings
Anti-Ro and anti-La antibodies
- collection of proteins found in the cell
- different ones found in different patients
Other autoantibodies?
- other extractable nuclear antigens (ENA) not associated
ANA and RF not associated with sjogrens
What possitive labial gland biopsy means in Sjogrens?
Collection of more than 50 lymphocytes around a duct- lymphocytic focus
Generalised lymphocytic infiltrate is non specific sialadenitis
More than one focus score (FS) consistent with sjogrens syndrome
Labial biopsy is the MOST diagnostic feature on ACR- EULAR criteria
What tests to do for Sjogrens
Look at PT mouth:
Early sjogrens may not have dry mouth or complain of one
Do the least harmful tests first:
UWS in 15 min (less than 1.5 ml)
Anti-Ro antibody
Salivary USS
Baseline MRI of major salivary glands (for comparison for future lymphoma screen)
If still equivocal, do labial gland biopsy (risk of numbness following the procedure, informed consent needed)
LGB and anti-Ro may be the only positive results in early Sjogrens
Management of Sjogren syndrome
If pt presenting with a dry mouth and salivary deficit:
Gland function is already very low
Oral health needs paramount - OHI, diet, 5000 ppm toothpaste
Symptomatic treatment of oral dryness
Salivary stimulants- pilocarpine
If pt is presenting early-NO dry mouth yet but active gland disease
Liaise with rheumatologist -multisystem disease
Consider immune modulating treatment - hydrocychloroquine, methotrexate
Complications of sjogrens
Effect of oral dryness: caries risk denture retention, infection, functional issues like speech, swallowing
Salivary enlargement -sialosis
Can occur at any time-usually permanent
Reduction surgery possible but not advised
Lymphoma risk
Salivary lymphoma may present with unilateral gland swelling at any stage
Increased general lymphoma risk too
GDP should be doing screening/review
Features on the histological examination of labial gland biopsy that is compatible with Sjogrens syndrome
Focal lymphocytic infiltrate typically collecting around intralobular ducts -1 focus ( more than 50 lymphocyte in 4mm3)
Adjacent normal/intact acini (key differentiating feature of Sjogrens from chronic sialadenitis)
Characteristics of Warthin’s tumour
May be incidental finding
May be bilateral
May be multifocal
