Salivary Gland Disorders Flashcards
salivary gland disorders
- mucocele/ranula
- sialolithiasis
- acute/chronic sialadenitis
- sialadenosis
- xerostomia
- benign lymphoepithelial lesion (BLEL)
- Sjogren syndrome
- necrotizing sialometaplasia
- sialorrhea
T/F: salivary gland neoplasia is benign
false, it is benign and malignant
mucocele
oral mucosal swelling caused by rupture of salivary gland DUCT
what does the rupture of a salivary gland duct lead to?
spillage of mucin
T/F: mucocele is common
true
who is affected by mucocele?
all ages but especially children, young adults
what is the most common site for a mucocele?
lower lip (82%)
what sites are affected by mucocele?
- lower lip
- buccal mucosa
- ventral tongue
- floor of mouth
clinical features of mucocele
- non-tender, soft swelling
- may be fluctuant or firm
- color: translucent to bluish
T/F: reoccurance does not happen with mucocele
false, may have history of repeated swelling and resolution
ranula
type of mucocele seen on the floor of the mouth
what does ranula arise from?
sublingual gland
T/F: ranula develops on the floor of the mouth to the right of midline
false, can be right or left of midline
clinical features of ranula
similar as mucocele
histopathologic features of mucocele/ranula
- extravasated mucin
2. granulation tissue with variable numbers of inflammatory cells
treatment of mucocele/ranula
- microscopic exam to rule out neoplasm
2. excision of mucous deposit including involved gland
T/F: some mucocele/ranula resolve without treatment especially superficial ones
true
T/F: treatment for ranula may include marsupialization (“unroofing”)
true
marsupialization
making incision into the lesion and suturing the edges so inner and external surfaces are continuous
prognosis of mucocele/ranula
excellent
mucocele/ranula will occasionally recur if what?
if the involved gland is not excised
sialolithiasis
deposition of calcium salts around nidus of debris in lumen
what causes sialolithiasis?
unclear but can possibly due to
- chronic sialadenitis
- partial ductal obstruction
where does sialolithiasis occur?
submandibular gland, parotid or minor glands
what percent of sialolithiasis occur in the submandibular gland?
80%
clinical features of sialolithiasis
- hard submucosal mass in soft tissue
- ± symptoms
- may have swelling prior to or during meals
radiographic features of sialolithiasis
soft tissue film shows opaque, lamellated structure
histopathologic features of sialolithiasis
- concentric laminatiosn that may surround a nidus of amorphous debris
- periductal inflammation
- acute or chronic sialadenitis of the feeding gland
if the duct associated with sialolithiasis is removed, then it often demonstrates what histopathologically?
squamous metaplasia
treatment for sialolithiasis
- gentle massage to “milk” saliva toward orifice
- sialogogues (medications which stimulate saliva)
- sour sugarless candies
- increase fluid intake to “flush”
- moist heat
- surgical removal, may include gland if significant inflammatory damage
- lithotripsy, sialendoscopy with basket retrieval (major gland)
prognosis of sialolithiasis in minor glands
good
prognosis of sialolithiasis in major glands
good, but morbidity if gland requires removal
acute/chronic sialadenitis
inflammation of the salivary gland
causes of acute/chronic sialadenitis
- bacterial
- viral
- ductal obstruction, retrograde infection
bacteria that causes acute/chronic sialadenitis
often penicillinase-producing staph
virus that causes acute/chronic sialadenitis
most often mumps
acute/chronic sialadenitis caused by ductal obstruction, retrograde infection is associated with what?
xerostomia, may follow general anesthesia
T/F: chronic may follow acute sialadenitis due to ductal damage
true
clinical features of acute/chronic sialadenitis
- diffuse
- unilateral swelling
- painful/tender, especially around meal times
- may feel warm
- overlying skin may be erythematous
- may have low-grade fever
- may have trismus
acute sialadenitis usually affects which gland?
parotid
what may be expressed in acute sialadenitis?
purulent exudate expressed from the parotid papilla
chronic sialadenitis usually affects which gland?
submandibular gland
radiographic feature of chronic sialadenitis
sialography: “sausage-link” appearance of ductal system due to ductal dilatation
histopathologic features of acute/chronic sialadenitis
- chronic inflammatory cell infiltrate
- dilated ducts
- acinar atrophy
- fibrosis
treatment of acute/chronic sialadenitis
- screening radiograph to rule-out sialolith
- antibiotic therapy - broad spectrum (i.e. tetracycline)
- culture and sensitivity if purulence
- massage (with caution)
- warm compress
- sialogogues with hydration (or sugarless lemon drops)
- ductal stenting
- sialoendoscopy with saline irrigation
- surgical drainage
- surgical removal of affected gland may be needed
T/F: antibiotics prescribed for acute/chronic sialadenitis may adjusted depending on culture and sensitivity result
true
prognosis of acute/chronic sialadenitis
can range from excellent to poor if gland must be removed
why does acute sialadenitis reported to have 20-50% mortality rate in debilitated patients?
because of the spread of the infection and sepsis
treatment for chronic sialadenitis
conservative therapy to surgical intervention
T/F: the etiology of sialadenosis is infectious
false, non-infectious etiology
what is sialadenosis associated with?
associated with underlying systemic condition
- diabetes
- malnutrition
- alcoholism
- bulimia
treatment for sialadenosis
- often unsatisfactory - control of underlying disease
- partial parotidectomy cosmetic reasons
- pilocarpine reported to be beneficial
prognosis of sialadenosis
fair-poor, depending on disease
xerostomia
subjective symptom of dryness
xerostomia predisposes people to what?
- mucosa susceptible to injury due to lack of lubrication
- oral candidiasis
- increased caries, especially cervical
causes of xerostomia
- medications especially polypharmacy
- glandular aplasia or hypofunction
- radiation therapy
- graft vs host disease
- Sjogren syndrome
polypharmacy medications
- antihistamines
- antidepressants
- sedatives and anxiolytic agents
- antihypertensive agents
clinical features of xerostomia
- meticulous oral hygiene and early disease
- absence of pool of saliva at FoM
- lipstick on teeth
- glove, gauze or mirror sticks to mucosa
- saliva frothy, stringy or sticky
- oral malodor
treatment for xerostomia
- good hydration/frequent sips of water
- artificial saliva/lubricants
- sialogogues, SUGAR-FREE lemon drops
- 1% neutral sodium fluoride gel or toothpaste nightly
- antifungal therapy as needed
- more frequent dental recall
prognosis of xerostomia
variable
T/F: people with xerostomia are at a high risk for caries
true, think prevention
benign lymphoepithelial lesion (BLEL)
an autoimmune condition that causes proliferation of epithelial cells and lymphocytes (mainly parotid and lacrimal glands)
what might BLEL be associated with?
Sjogren syndrome
recent data suggests that a portion of the infiltrate in BLEL is monoclonal, perhaps representing what?
a low-grade lymphoma in situ
who is affected by BLEL?
female predilection, middle-aged or older
clinical feature of BLEL
unilateral or bilateral, firm, non-tender swelling of the parotid area
radiographic feature of BLEL
sialography: “blossoms on a tree” pattern of punctate sialectasis often observed
histopathologic features of BLEL
- destruction of the normal parotid parencyma with replacement by a diffuse lymphocytic infiltrate
- occasionally see germinal centers
- remnants of ductal epithelium “epimyoepithelial islands”
what does epimyoepithelial islands represent when seen histopathologically in BLEL?
residual ductal structures
epimyoepithelial islands are also seen histopathologically in what other disease besides BLEL?
lymphoma
why does treatment for BLEL vary?
varies depending on how much appearance bothers patient
treatment for BLEL
- do nothing
- low-dose radiation
- corticosteroid therapy
prognosis for BLEL
good
can BLEL transform?
yes, malignant transformation of lymphoid or epithelial components have been reported
what are the 2 forms of Sjorgen syndrome?
- primary
2. secondary
T/F: Sjogren sydrome is an acquired condition
false, autoimmune condition
Sjogren syndrome is thought to be a continuation of what condition?
BLEL
primary Sjogren syndrome
aka sicca syndrome
- xerostomia and keratoconjunctivitis sicca (dry eyes)
secondary Sjogren syndrome
sicca syndrome plus any other autoimmune disease (e.g. rheumatoid arthritis, systemic lupus erythematosus, Hashimoto’s thyroiditis, mixed CT disease, etc.)
Sjogren syndrome
autoimmune process attacks lacrimal and salivary glands
who is affected by Sjogren syndrome?
usually middle-age to older adults, but has been seen in children
T/F: Sjogren syndrome has a 9:1 male predilection
false, 9:1 FEMALE predilection
clinical features of Sjogren syndrome
- partoid swelling (BLEL) may or may not be dramatic
- patients often complain of dry, gritty feeling in eyes and a dry mouth
- cervical caries, often rampant
- increased prevalence of oral candidiasis
- burning feeling on tongue
- angular cheilitis
- atrophy of dorsal tongue papillae
diagnosis of Sjogren syndrome
- serology
- laboratory
- international classification criteria for Sjogren syndrome
- labial salivary gland biopsy
How do people with Sjogren syndrome measure their salivary flow on the Schirmer tear test?
normal salivary flow wets the entire strip; Sjogren less than 5 mm
T/F: most of the time, serology tests are relatively specific
false, relatively NON-SPECIFIC
how do patients with Sjogren syndrome score on serology test?
patients tend to have an elevated erythrocyte sedimentation rate (ESR) and polyhypergammaglobulinemia, especially IgG
T/F: laboratory tests used to diagnose Sjogren syndrome tests a variety of autoantibiodies, which are characteristic but specific
false, characteristic but NOT specific
how do patients with Sjogren syndrome score on laboratory tests?
- positive rheumatoid factor (RF) in ~60%
2. anti-nuclear autoantibodies (ANAs) in ~80%: anti-Rho and anti-La
labial salivary gland biopsy technique
- lower labial mucosa, lateral to midline, uninflammed
- 1 cm incision, parallel to vermilion zone
- remove at least 5 minor glands through the incision and place them in routine 10% buffered formalin
histopathologic features of Sjogren syndrome
- aggregates (foci) of >50 lymphocytes ± plasma cells scattered throughout glandular parenchyma
- 1 or more foci of 50 or more cells per 4-mm^2 of glandular tissue supports Dx of
Sjögren syndrome
why are lobules of gland exhibiting acinar atrophy and interstitial fibrosis excluded from diagnosing Sjogren syndrome?
these are non-specific features related to aging
treatment for Sjogren syndrome
- hydration
- artificial tears and artificial saliva/lubricants
- sialogogues
- daily topical fluorides for natural teeth
- anti-fungal agents for candidiasis, as needed
- more frequent dental prophylaxis; plaque control
- for secondary Sjogren syndrome, appropriate therapy for other autoimmune processes
prognosis of Sjogren syndrome
fair
patients with Sjogren syndrome have a what increase in lymphoma compared to age- and sex-matched population?
44x increase
what causes nectrotizing sialometaplasia?
thought to be due to ischemic necrosis
- traumatic injury
- dental injections
- ill-fitting dentures
- upper respiratory infection
- eating disorders (binge-purge)
- adjacenet tumor
- previous surgery
who is affected by nectrotizing sialometaplasia
adults, rare in children
T/F: nectrotizing sialometaplasia has a female predilection
false, male
where is the most common location for nectrotizing sialometaplasia?
possterior hard palate/anterior soft palate
clinical features of nectrotizing sialometaplasia
- swelling ± pain, paresthesia
- sharply demarcated ulcer, non-elevated margins
- minimal peripheral erythema
what do patients with nectrotizing sialometaplasia usually report ~2 weeks after diagnosis?
“a piece of my palate fell out”
how long does it take for nectrotizing sialometaplasia heal?
4-6 weeks
what is nectrotizing sialometaplasia easily mistaken for?
SCC or mucoepidermoid carcinoma (a cancer of salivary gland) by an inexperienced pathologist
early stages of nectrotizing sialometaplasia show what?
only lobular ischemic necrosis
histopathologic features of nectrotizing sialometaplasia
- pseudoepitheliomatous hyperplasia (PEH) of surface epithelium
- acinar necrosis, but overall architecture of involved gland is preserved
- squamous metaplasia of the ductal epithelium - confined to normal boundaries of the gland
pseudoepitheliomatous hyperplasia (PEH)
nonspecific reactive hyperplasia (no separation) stratified mucocutaneous epithelia, which simulates squamous cell carcinoma (diagnostic pitfall)
sialorrhea
constant hypersalivation (“pool and drool”)
primary sialorrhea causes what?
increased salivary flow
secondary sialorrhea causes what?
impaired swallowing
what is the most common cause of sialorrhea?
neuromuscular dysfunction
causes of sialorrhea
- neuromuscular dysfunction
- hypersecretion
- motor or sensory dysfunction
- drug-induced (antipsychotics esp. chozapine, meds for Alzheimer’s dementia and myasthenia gravis, exposure to heavy metal toxins, insecticides, nerve agents)
why may sialorrhea be problematic?
- social implications
- skin irritation
- requirement for numerous clothing changes
sialorrhea in more severe cases may cause what?
dehydration and aspiration pneumonia
treatment for sialorrhea
- surgical
- botulinum toxin A (Botox)
- anticholinergics
surgical treatment for sialorrhea
- submandibular duct relocation
- ductal ligation
- removal of gland
T/F: management of sialorrhea is a challenge for it depends on underlying condition and individual’s response to therapies
true
