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General OTOHNS > Benign Salivary/Oral cavity > Flashcards

Benign Salivary/Oral cavity Flashcards

1
Q

What are 7 functions of saliva?

A
  1. Lubrication/moisturization
  2. Digestion (Amylase)
  3. Taste modulation
  4. Antibacterial properties (Secretory IgA, Lactoferrin, Lysozyme, Salivary peroxidase)
  5. Deglutition
  6. Dental protection (via inorganic ions - Calcium, Fluoride, phophate, Mg)
  7. Buffering (keep pH 6-7, HCO3, PO4)
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2
Q

Describe the physiology of salivation and types of saliva

A
  • 24h salivary flow volume = 1-1.5L
  • Submandibular glands responsible for majority of non-stimulated salivary flow (70% in 24h period)
  • Parotid supplies 66% of total stimulated salivary flow, overall 25% of total 24h flow

Types of saliva:
1. Parotid - serous
2. Sublingual - mucinous
3. SMG - mixed serous/mucinous

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3
Q

What are 3 muscles originating off the styloid and their innervations?

A
  1. Stylohyoid (CNVII)
  2. Stylopharyngeus (IX)
  3. Styloglossus (XII)
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4
Q

Describe the parasympathetic pathway/autonomic innervation of the parotid gland

A
  • Parasympathetic system mediates secretion of saliva

PRE-GANGLIONIC
1. Inferior salivatory nucleus
2. CNIX (makes U-turn in jugular foramen) via Jacobsen’s nerve in tympanic plexus (enters middle ear via inferior tympanic canaliculus; exits via superior tympanic canaliculus
3. Emerges out of skull base via foramen ovale via Lesser superficial petrosal nerve

SYNAPSES: Otic ganglion (located below foramen ovale)

POST-GANGLIONIC:
1. Auriculotemporal nerve (V3) - enters the infratemporal fossa via foramen ovale
2. Innervates parotid gland

Go through Dr. Henry’s lecture to confirm these

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5
Q

Describe the parasympathetic pathway/autonomic innervation of the submandibular gland

A
  • Parasympathetic system mediates secretion of saliva

PRE-GANGLIONIC FIBERS
1. Superior salivatory nucleus
2. Nervus intermedius
3. Facial nerve
4. Chorda tympani (then exits skull through petrotympanic fissure, which then exits via infratemporal fossa)
5. Lingual nerve (branch of V3), travels between medial pterygoid muscle and ramus of mandible

SYNAPSES: Submandibular ganglion

POST-GANGLIONIC
1. Emerges from submandibular ganglion to submandibular/sublingual gland

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6
Q

Describe the parasympathetic pathway/autonomic innervation of the minor salivary glands

A

PREGANGLIONIC:
1. Superior salivary nucleus
2. Nervus intermedius
3. Facial nerve
4. Enters greater (superficial) petrosal nerve from the geniculate ganglion
5. Merges with deep petrosal nerve
6. 4+5 forms the Vidian nerve

SYNAPSES:
1. Pterygopalatine ganglion

POST-GANGLIONIC:
1. Emerges from pterygopalatine ganglion via palatine nerves and innervates minor salivary acini

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7
Q

Describe the sympathetic pathway/autonomic innervation of the major and minor salivary glands

A
  • Sympathetic system modulates the composition of saliva (more mucinous, less flow overall)

PATHWAY:
1. Nucleus = Sympathetic chain T1-5 (originates from Thoracolumbar spine) - nuclei of lateral horn
2. Preganglionic = Travels along Sympathetic chain
3. Ganglion = Superior cervical ganglion synapses
4. Postganglionic = Run with blood vessels supplying the glands
- Parotid = External carotid artery (posterior auricular and superficial temporal artery) and IMAX to middle meningeal
- Submandibular = Facial artery (submental/sublingual artery)
- Sublingual = Lingual artery (submental/sublingual artery)
- Minor salivary glands = ECA + IMAX and palatal branches

Go through Dr. Henry’s lecture to confirm these

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8
Q

What are five indications for sialography?

A
  1. Autoimmune disease (e.g. Sjogren’s, BLL)
  2. Suspicion of sialadenitis - chronic, recurrent or non-specific (not acute)
  3. Sialolithiasis
  4. Post-op or post-traumatic fistula/stricture/cyst
  5. Juvenile recurrent parotitis
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9
Q

What are two contraindications for sialography?

A
  1. Acute sialadenitis
  2. Iodine allergy
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10
Q

What are 3 findings for chronic inflammation on sialography?

A
  1. Saccular dilatation of terminal ducts/acini
  2. Segmental strictures and dilatation (sialadenosis)
  3. Pseudocyst formation
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11
Q

What are findings of autoimmune disease on sialography?

A
  1. Punctate sialectasis < 1mm or globular 1-2mm
  2. Cavitary lesion or collections
  3. Complete destruction of gland
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12
Q

Regarding Sialolithiasis, describe:
1. What is their composition?
2. Pathophysiology
3. Location and common epidemiology?
4. Associated diseases
5. Diagnostic findings

A

COMPOSITION:
1. Glycoproteins
2. Mucopolysaccharides
3. Cellular debris

PATHOPHYSIOLOGY:
- Formation around an inorganic nidue

LOCATION:
1. 80% submandibular - usually within the duct (more susceptible because saliva more alkaline and higher concentration of calcium phophate with high mucous content)
2. 20% parotid - usually within the hilum or parenchyma
3. < 1% sublingual
4. Minor gland calculi can be seen in upper lip and buccal mucosa
5. 75% single calculi found
6. Multi-gland in 3% with male preponderance and middle age

ASSOCIATIONS:
1. Gout is the only disease known to cause sialoliths (not caused by uric acid however)

DIAGNOSTIC FINDINGS:
1. 90% parotid calculi are radiolucent on x-ray (< 2mm will be missed on imaging)
3. Ultrasound is best for imaging

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13
Q

What are El Deeb’s predisposing factors for submandibular gland calculi formation?

A

SUBMANIDBULAR SALIVA (6): “mocaps”
1. M: High mucin content
2. O: Higher percentage of organic matter
3. C: Low carbon dioxide level
4. A: Alkaline pH
5. P: High phosphatase enzyme content
6. S: High concentration of calcium and phosphate salts

ANATOMY (4): “sold”
1. S: Size of orifice smaller than duct lumen
2. O: Position of ductal orifice
3. L: Length and irregular course of Wharton’s duct
4. D: Dependent position of gland and duct system
5. Larger duct caliber

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14
Q

When is sialendoscopy used?
What are the sizes of scopes?

A

SIALENDOSCOPY:
- Treatment of sialolithiasis, ductal pathology, and inflammatory salivary gland disease
- Scope sizes: 0.8-1.6mm
- Removal of stones - Submandibular < 4mm, Parotid < 3mm
- 5-6mm stones - may need lithotripsy
- >1cm - possibly need open procedure

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15
Q

Why is the parotid gland more susceptible to infection?

A
  1. Serous secretions are less bacteriostatic than mucinous secretions
  2. Mucinous secretions contain lysozymes, secretory IgA, sialic acid, and glycoprotein which have antimicrobial properties
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16
Q

Regarding the diagnosis of Mumps, discuss:
1. What is the cause?
2. Clinical presentation? Transmission
3. Complications?
4. Investigations?
5. Treatment?

A

CAUSE:
1. Paramyxovirus, single stranded RNA virus (most common viral disorder of the salivary gland, most common cause of parotid enlargement)

CLINICAL PRESENTATION:
1. Fever, malaise
2. Myalgia
3. Headache
4. Either unilateral or bilateral parotid swelling
5. Peak incidence 4-6 years old, generally self-limiting

TRANSMISSION:
1. Transmitted by respiratory droplets
2. Incubation 14-25 days after which time prodromal symptoms occur and last ~3-5 days
3. Patient is infectious 6 days before and 9 days after facial swelling is apparent

COMPLICATIONS:
1. Sudden SNHL
2. Facial paralysis
3. Vocal cord paralysis
4. Meningitis
5. Encephalitis
6. Pancreatitis
7. Orchitis
8. Nephritis
9. Arthritis

INVESTIGATIONS:
1. RT-PCR performed on serum or buccal/oral swab
2. Viral culture (blood/swab)
3. Mumps IgM in serum

TREATMENT:
1. Supportive
2. Vaccine for prevention; 3rd dose of MMR for exposed individuals at high risk
3. Isolation/prevention: Droplet precautions until parotid swelling resolves
4. This is a reportable disease

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17
Q

List 6 viral causes of sialadenitis

A
  1. Mumps (Paramyxovirus)
  2. Coxsackie A
  3. Influenza
  4. HIV
  5. CMV
  6. Echovirus
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18
Q

What is the bacteriology of acute sialadenitis? List 8

A
  1. Staph aureus (90%)
  2. Strep viridans
  3. Strep pneumoniae
  4. Hemophilus influenzae
  5. Escherichia coli
  6. Bacteroides melaninogenicus
  7. Peptostreptococcus
  8. Strep micros
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19
Q

Regarding Sialadenitis, discuss:
1. Pathophysiology
2. Causes
3. Clinical presentation
4. Treatment

A

PATHOPHYSIOLOGY:
- Normal salivary flow is protective against retrograde colonization and overgrowth of bacteria
- Stasis of saliva reduces flow and obstruction –> increased incidence of infection

CAUSES:
1. 30-40% occur in post-op patients (GI procedures common POD3-7)
2. Stasis of secretions, reduced flow and obstruction (6-7th decade of life)

CLINICAL PRESENTATION:
1. Parotid most commonly affected
2. Sudden onset diffuse enlargement of gland
3. Tender gland

TREATMENT:
1. CT if abscess suspected
2. MASH protocol: massage gland, antibiotics, sialogogues, heat compress and hydration

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20
Q

Regarding necrotizing sialometaplasia, discuss:
1. What is it?
2. Pathophysiology
3. Clinical presentation
4. Diagnosis
5. Differential of this lesion?
6. Histologic features (6)
7. Treatment

A

NECROTIZING SIALOMETAPLASIA:
- Non-neoplastic, self-healing (inflammatory) process of unknown etiology

PATHOPHYSIOLOGY/SUSPECTED CAUSES:
- Possibly secondary to ischemia
- Necrosis of minor salivary glands due to trauma (e.g. palatal infiltrations of local anesthetic or trauma during intubation)
- Idiopathic

CLINICAL PRESENTATION:
- Asymptomatic painless mucosal ulceration or nodular lesion of the minor salivary glands
- Hard palate (most common)
- Junction of hard and soft palate

DIAGNOSIS:
1. Excisional biopsy

DIFFERENTIAL:
1. Kaposi Sarcoma
2. Gumma from Tertiary Syphillis (granulomatous lesions)
3. SCC

HISTOLOGIC FEATURES:
1. Preserved lobular architecture
2. Lobular infarction with or without mucous extravasation
3. Inflammation secondary to extravasated mucous
4. Pseudoepitheliomatous hyperplasia at periphery of lesion
5. Squamous metaplasia of ducts and acini
6. “Drop-out” of acini (collection of clear spaces)

TREATMENT:
1. Self-limiting, should resolve in 6-10 weeks

Vancouver pg 39
Kevan notes Pediatrics

https://www.pathologyoutlines.com/topic/salivaryglandsnecrotizingsialo.html

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21
Q

What is the differential diagnosis for recurrent parotid swelling?

A

AUTOIMMUNE (“pseudosialectasis” - sialectasis = duct dilation):
1. IgG4 - localized to parotid gland, adult and pediatric
2. Sjogren’s - primary, secondary

NON-AUTOIMMUNE
1. Recurrent sialadenitis
2. Sialosis/Sialoadenosis
3. Sialolithiasis
4. Multinodular gland
5. Sarcoid
6. Juvenile Recurrent Parotitid

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22
Q

Regarding Sialosis/Sialadenosis, discuss:
1. Definition and presentation and causes
2. Location
3. Associations
4. Histologic findings (3)
5. Complications

A

DEFINITION/PRESENTATION/CAUSE:
- Nonspecific term
- Recurrent bilateral non-tender, non-inflammatory, non-neoplastic enlargement of a salivary gland
- Most cases are idiopathic, but many associations
- Some sources still call this “Mikulicz disease”

LOCATION:
- Usually parotid

ASSOCIATIONS:
1. Obesity - secondary to fatty hypertrophy
2. Cirrhosis/recurrent pancreatitis
3. Diabetes mellitus (most common)
4. Malnutrition (kwashiorkor, beriberi, bulimia)
5. Alcoholic cirrhosis (30-80%)
6. Malabsorption of nutrients (e.g. celiac disease, etc.)
7. Ovarian, thyroid, or pancreatic insufficiency
8. Drugs - antihypertensives, iodinated compounds, catecholamines (also phenothiazine, ethambutol)
9. Pregnancy/lactation

HISTOLOGY:
1. Acinar hypertrophy
2. Fatty infiltration
3. Combination

COMPLICATIONS:
1. 80% will have long term Xerostomia

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23
Q

What is the differential diagnosis of multinodular parotid gland?

A
  1. Granulomatous disease (e.g. TB, sarcoid)
  2. Lymphoproliferative disorders (e.g. lymphoma)
  3. Warthin’s tumor
  4. Other tumors (see parotid tumor differentials)
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24
Q

What is the differential diagnosis of salivary gland cysts? What is the incidence and which gland is typically involved?

A
  • 2-5%
  • Usually parotid

CONGENITAL:
1. Branchial cleft cyst
2. Epidermoid cyst
3. Dermoid cyst

ACQUIRED:
1. Benign lymphoepithelial lesion (HIV)
2. Mucous retension cyst or mucocele
3. Neoplasms (e.g. Warthin’s, Acinic cell, Oncocytoma)
4. Sialocele (pseudocyst, associated with trauma)

Vancouver notes pg 40 HIV benign lymphoepithelial lesions multicystic lesion

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25
Q

List the differential diagnosis for unilateral parotid cyst

A
  1. Warthin’s tumor
  2. Sialocele
  3. First branchial cleft cyst
  4. Parotid lymphangioma
  5. Benign lymphoepithelial cyst
  6. Necrotic lymph nodes (esp. SCC)
  7. Infected lymph node(s)
    - Parotid typically has ~7 superficial nodes, ~2 deep nodes
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26
Q

Differentiate the following:
1. Mucous retention cyst
2. Mucocele
3. Ranula
4. Plunging ranula

A

MUCOUS RETENTION CYST:
- True cyst of the minor salivary gland (lined with epithelial layer)
- Differentiate from a mucocele by “air” around the cyst (seeing the epithelial layer)

MUCOCELE:
- Not a true cyst
- Extravasation of mucous into soft tissue

RANULA:
- Mucocele of the floor of mouth, usually from the sublingual gland, extravasation of mucous superior to the mylohyoid
- Arise from partial obstruction of the sublingual duct, leading to extravasation
- ?Vancouver notes suggests there is formation of an epithelial lined cyst
- Cummings: “mucous retention cyst and/or pseudocyst” - General consensus is that Ranula = pseudocyst

PLUNGING RANULA:
- Ranulas that extend into the cervical tissue
- Extension below the mylohyoid muscle - either through a dehiscence in the mylohyoid, or around the posterior border of mylohyoid
- May present as a neck mass

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27
Q

Discuss the management of Ranulas and Plunging Ranulas, including investigations and treatment

A

WORKUP:
- US of neck
- Needle aspiration (mucous with prominent histiocytes/macrophages; high amylase and protein content)

MEDICAL TREATMENT:
- Sclerotherapy (See card on sclerotherapy)

SURGICAL TREATMENT (Ranula):
1. Excision of sublingual gland and ranula = gold standard (recurrence 1.2%)
2. Marsupialization (unacceptably high failure)
3. Placement of a suture or seton (left for 7 days for the tract to marsupialize)
4. CO2 laser ablation to ablate the tract and scar the gland
5. Radiation therapy (for patients that cannot tolerate surgery)

Plunging Ranula:
1. Similar as treatment above
2. Trans-oral excision of sublingual gland + needle draining cervical mucous is sufficient
3. Trans-cervical approach - indicated if trans-oral approach failed for the non-lingual component

Note
- Ranula likely can do transoral excision
- Plunging ranula may need transcervical approach

See peds card on ranula

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28
Q

List the components of tears and where they are produced from?

A
  1. Lipid layer: from Meibomian glands
  2. Aqueous portion: from Lacrimal gland
  3. Mucin: from Goblet cells
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29
Q

What are the epithelium types in the upper aerodigestive tract?

A
  1. PSEUDOSTRATIFIED COLUMNAR EPITHELIUM WITH GOBLET CELL (RESPIRATORY EPITHELIUM)
    - Sinonasal beyond liimen vestibuli
    - Eustachian tube
    - Anterior nasopharynx
    - Larynx except for true VC and false VC edges
  2. NON-KERATINIZING SQUAMOUS CELL EPITHELIIUM
    - Oral cavity
    - Oropharynx
    - Hypopharynx
    - Nasopharynx - majority (posterior nasopharynx, to vomer superiorly, to ET orifice laterally, to palate inferiorly
  3. OLFACTORY EPITHELIUM
  4. CILIATED COLUMNAR CELLS WITH AREAS OF SIMPLE CUBOIDAL EPITHELIUM
    - Middle ear cleft
30
Q

Name the four types of tongue papillae and their innervation

A
  1. Filliform: Non-sensory, exist all over, general sensory
  2. Fungiform: CNVII (anterior 2/3 taste)
  3. Foliate: CNIX
  4. Circumvallate: CNIX

Vancouver notes Page 41/42

31
Q

What are four sensory nerves that supply the tongue?

A
  1. Lingual nerve (V3) - general sensory anterior 2/3
  2. Chorda Tympani (Facial nerve) - special sensory anterior 2/3
  3. Glossopharyngeal nerve (IX) - general and special sense posterior 1/3
  4. Vagus nerve (X) - SLN (laryngeal epiglottis), Palatoglossus
32
Q

Describe the pathway of afferent taste fibers from the oral tongue

A
  1. Lingual nerve (also IX & X)
  2. Chorda tympani (through Huguier canal)
  3. CNVII
  4. Geniculate ganglion (cell bodies present anteriorly)
  5. Nervus intermedius
  6. Nucleus tractus solitarius (pons)
  7. Ventroposteromedial nucleis of the thalamus (VPMT)
  8. Cortex (Operculum & anterodorsal insula)
    - Behaviour response - aversion, gastric response, feeding behaviour
33
Q

Describe how Taste Transduction work? Describe the different components.

A
  1. Stimuli entering mouth first interact with sites on the microvilli within the taste pore
  2. Salt & sour interact with ion channels, sweet and bitter react with protein compounds
  3. Taste receptors trigger transduction cascades –> activate synapses –> excitation of nerve fibers –> signal to brain gustatory stimulus
  4. Taste receptor proteins are located on apical surface of cells and enter the cell via ion channel (salt, sour), or via cyclic AMP (bitter/sweet)
  5. Stimulant enters the cell causes change in internal electrical state of cell –> leads to secretion of a neurotransmitter and activation of a nerve fiber

Each taste serves a specific purpose in health maintenance:

  1. Salt: Guides NaCl intake & salt-water homeostasis
  2. Sweet: Receptor is a proteinaceous molecule analogous to an olfactory receptor
    - Involves GPCRs
    - Responds to soluble carbohydrates
    - Regulates caloric intake, nutrition, energy balance
    - Hedonic (pleasant) effect, well developed in infants
  3. Bitter: Receptor part of G-protein, sets off GPCR, warns body to protect against ingestion of harmful compounds
    - Bearable in low concentrations, repulsive when strong
  4. Sour: recognition of complex foods, acid-base regulation (sensitive to extracellular pH changes)
    - Pleasant in low concentration
    - Unpleasant taste in high concentrations leading to avoidance
  5. Umami: Derived from L-glutamate
    - MSG taste, chicken broth, meat extracts, aging cheese, helps guide the intake of peptides and proteins
    - Similar to bitter and sweet receptors (involve GPCRs) - function not entirely clear
    - Theory: Amino acid L-glutamate binds to a type of GPCR mGluR4

GPCR:
1. Umami
2. Sweet
3. Sour
4. Bitter

Bailey’s Page 730

34
Q

What is venous taste? How does it work?

A

Venous taste = phenomenon that you can taste your IV fluids, thought to occur at a receptor level below the microvilli in the taste cell.

Example:
1. Sense of sweet taste with IV saccharine
2. Bitter with acidic medication such as chemotherapy

  • Salt/sour = ion channel mediated
  • Sweet/bitter/umami = membrane receptors
  • Palatal taste = mediated by lesser superficial petrosal nerve (V2)
35
Q

What is the difference between taste and flavour?

A
  • Taste = mediated by papilla only
  • Flavour = taste + smell (more likely to decrease with age due to decrease in olfaction)
36
Q

Discuss the conditions that can alter taste (hypoguesia and dysgeusia)

A

AGING
- Decrease in all tastes, sweet being the most robust and longest lasting
- Males affected more (thresholds and intensities)
- NaCl threshold related to fungiform papillae (more = more sensitivity, lower threshold)
- Degenerative changes leads to decrease in gustatory papillae
- Olfaction is more affected than taste in aging and leads to decrease in flavour overall
- Sucrose lasts longest lead to health-related side effects
- No changes to sensation of taste
- Decrease saliva also decrease taste
- Thresholds improve with better hygeiene

SYSTEMIC DISEASES
1. Diabetes (neuropathies)
2. Gastric disease
3. Hypothyroidism
4. Liver disease
5. Chronic renal failure (Uremia = toxins that lead to taste alterations)
6. Depression
7. Alzheimer’s, Parkinson’s
8. Perimenopausal women (burning mouth syndrome – lower bitter taste threshold and release of oral pain inhibition)
9. Medications: Antihypertensives, Chemotherapy - lower bitter threshold, change cell turnover
10. Smoking (bitter) - recovery is 6 months
11. Xerostomia (Medications or Sjogren’s)
12. Reflux

NERVE DAMAGE
1. Surgery (e.g. tonsillectomy, middle ear surgery, cancer resection) - temporary as overlapping fibers, contralateral activation; lasts < 2 years
2. Phantom taste (e.g. Chorda/IX/Nervus intermedius injury; Bell’s palsy; vestibular schwannom) - generally last 6 months and resolve
3. Injury to trigeminal nerve - intensification of sensations like oral burning and oral touch (fatty foods less palatable)
- Taste fibers overlap and inhibit each other across midline; so if there is nerve damange on one side, this leads to a “release” (undoing) of inhibition of the contralateral nerves, increasing their taste, so everyday taste is generally not inhibited

RADIATION & CHEMOTHERAPY
- May have partial (hypogeusia), complete (aguesia), or abnormal taste (dysgeusia)
- Metallic taste with chemotherapy for H/N cancer, may also have oral sores and inflammation
- Sour taste most affected, decreased buds after chemo
- 6 month recovery in taste but not bud numbers

37
Q

Discuss the symptomatic management of hypogeusia and ageusia

A
  1. Awareness is optimal so that people can maintain a balanced diet
  2. Adding extra flavours to food
  3. Zinc supplementation to enhance taste along with vitamins A, B12, and folic acid for taste bud integrity
  4. Burning mouth syndrome - capsaicin for desensitization, clonazepam as a gamma-aminobutyric acid agonist
38
Q

How do you test the 4 main tastes?

A
  1. NaCl - salty
  2. Sucrose - sweet
  3. Acetic or citric acid - sour
  4. Quinine sulfate of caffeine - bitter

Each taste is presented to each tongue region 4 times (96 trials)
- Anterior right
- Anterior left
- Posterior right
- Posterior left

Other methods:
1. Electrogustometry (weak electric stimulus to produce a sour taste when applied to taste receptors; measures taste in a specific loci of anterior tongue, but cannot measure specific tastes)
2. Videomicroscopy (quantifies taste receptors) - 3-4 taste pores per papilla

39
Q

What is phantom taste? How is it diagnosed?

A

Phantom taste = a lingering, often unpleasant taste even though there is nothing in your mouth. People will often experience hypogeusia as well

Diagnosis:
- Anesthetizing the tongue, phantom taste will persist or increase, while genuine taste will disappear
- Central taste loss = unilateral pontine hemorrhage or rostral insular cortex (operculum)

40
Q

List a differential diagnosis for tongue twitching

A
  1. Myoclonus
  2. Giant cell arteritis
  3. ALS
41
Q

List the differential diagnosis of leukoplakia (white) on the oral mucosa.
What % risk of malignancy?
What is the management?

A

10-20% of malignancy

  1. Hyperkeratosis
  2. Lichen planus
  3. Leukoedema
  4. Hairy leukoplakia
  5. White sponge nevus (autosomal dominant defect in keratinization of the oral mucosa - the entire mouth is covered with gray, diffuse, painless, spongy and folded plaques. Presents in childhood)
  6. Candidiasis
  7. SLE
  8. Psoriasis
  9. Secondary syphillis
  10. Geographic tongue
  11. Koplik spots (measles)
  12. Fordyce granules

All require biopsy/follow-up
Other options: laser resurfacing, or cis-retinoic acid

“ALL WHITE”
A: Autoimmune (SLE, psoriasis)
L: Leukoplakia/leukoedema
L: Lichen planus
W: White spongy nevus
H: Hairy leukoplakia
I: Infection (e.g. candida, syphillis, Koplik spots)
T: Tongue geographic, & granules fordyce
E: Excess keratin (hyperkeratosis)

42
Q

What is the differential diagnosis of a red lesion in the oral cavity (erythroplakia)?
What is the risk of malignancy?

A

90% risk of malignancy

  1. Erythroplakia
  2. Pyogenic granuloma
  3. Papilloma
  4. Inflammatory papillary hyperplasia
  5. Pigmented nevi
  6. Kaposi’s sarcoma
  7. Leukemia
  8. Hemangiosarcoma
  9. Mycosis Fungoides
  10. Polycythemia Rubra Vera

“HELP My PINK”
H: Hemangiosarcoma
E: Erythroplakia
L: Leukemia
P: Polycythemia rubra vera
My: Mycosis Fungoides
P: Pyogenic granuloma, Papilloma
I: Inflammatory papillary hyperplasia
N: Nevi (pigmented)
K: Kaposi sarcoma

43
Q

List the differential diagnosis of pigmented lesions of the oral cavity

A

FOCAL LESION:
1. Hemangioma/hematoma/thrombus/varix
2. Amalgam tattoo (silver filling particles in tissue)
3. Other FB tattoo
4. Blue nevus
5. Melanotic macule
6. Pigmented nevus
7. Melanoma

DIFFUSE LESION:
1. Addison’s disease
2. Acromegally
3. Heavy-metal toxicity
4. Kaposi’s sarcoma
5. Drug-induced
6. Post-inflammatory
7. Smoking

44
Q

List the differential diagnosis of glossitis (8)

A
  1. Iron deficiency
  2. Plummer vison syndrome
  3. Pernicious anemia
  4. Pellagra (B3 deficiency)
  5. Celiac/Crohns
  6. Behcet’s
  7. Thrush
  8. Lead poisoning
45
Q

Regarding Geographic Tongue, discuss:
1. What is it?
2. Associated conditions
3. Clinical presentation
4. Physical exam and histology
5. Treatment
6. Risk of malignancy

A

GEOGRAPHIC TONGUE:
- aka. Benign migratory glossitis
- Inflammatory condition that results from loss of papillae, making the tongue appear smooth, with red patches of different shapes and sizes
- Unknown cause, but many conditions associated
- Affects ~3% of population

ASSOCIATED CONDITIONS:
1. Psoriasis
2. Type 1 diabetes
3. Allergy/asthma
4. Celiac disease
5. Local inflammation
6. Atrophic glossitis

CLINICAL PRESENTATION:
1. Usually non-painful, asymptomatic
2. Lesions come and go, usually resolve spontaneously
3. May be associated with burning mouth syndrome
4. Fissured tongue

PHYSICAL EXAM/HISTOLOGY:
1. Erythematous central region
2. Peripheral white, serpiginous (looks like snake) border
3. Atrophy of filiform papillae
4. Usually affects lateral/dorsal tongue, but can affect any oral mucosa

TREATMENT:
1. None
2. Topical lidocaine and steroids if there is associated burning mouth syndrome
3. No malignant potential

Vancouver Page 44

46
Q

What is burning mouth syndrome? List different causes. (14)
What are some treatment options?

A

BURNING MOUTH SYNDROME:
- Painful condition described as burning, scalding, or tingling feeling in the mouth that occurs every day for months or longer. May be primary or secondary (due to other reasons)

CAUSES:
1. Nutritional deficiencies (Iron, Zinc, folate B9, Thiamine B1, Riboflavin B2, Pyridoxine B6, Cobalamin B12)
2. Allergies or Atopy (reactions to foods, flavourings, additives, fragrances, dyes or other substances)
3. GERD
4. Medications: ACE inhibitors, TCAs, diuretics, antiHTN
5. Neuropathy
6. Endocrine disorders (hyperglycemia in diabetes, hypothyroidism)
7. Hormone imbalances (post-menopausal women, but many others - changes in hormones may affect composition of saliva)
8. Crohn’s disease
9. Xerostomia - can be related to certain medications (TCAs, CNS depressants, lithium, diuretics, antiHTNs), aging, Sjogren’s syndrome, radiation
10. Thrush
11. Denture use/irritating dentures (muscle stress and mucosal irritation)
12. Geographic tongue
13. Excessive irritation (e.g. excessive brushing of tongue, tongue biting, overuse of mouthwashes, consuming too many acidic drinks)
14. Oral habits (e.g. unconscious activities such as tongue thrusting and bruxism)
15. Psychological - Anxiety, depression, extreme fear of cancer
16. Poor oral hygiene
17. HSV infection
18. Aging

“BURNING”
B12 deficiency
Unclean
Reflux
Nutritional deficiency
Imbalanced hormones/irritation
Neuropathy
Geographic tongue

TREATMENT:
1. Treat underlying causes
2. Topical lidocaine
3. Topical steroids
4. Topical clonazepam
5. CBT or antidepressants
6. Alpha-lipoic acid (caprylic acid-derived antioxidant)

47
Q

What is lichen planus?
Name the 6 common subtypes of LP.

A

LICHEN PLANUS:
- Rare, chronic, inflammatory autoimmune skin and mucous membrane disease
- Rare malignant transformation (1-2%)

6 COMMON SUBTYPES:
1. Reticular (most common, fine lacy appearance on buccal mucosa - “wickham’s striae”, asymptomatic)
2. Atrophic
3. Plaque (leukoplakia)
4. Papular
5. Erosive (1-5% malignancy rate, very painful)
6. Bullous - painful

Vancouver Page 45

48
Q

Describe the pathophysiology and histopathology of lichen planus

A

PATHOPHYSIOLOGY:
- T-cell mediated destruction of the basal cell layer

HISTOPATHOLOGY (3):
- Saw-tooth configuration of Rete Pegs (epithelial extensions that project into the underlying connective tissue in both skin and mucous membranes)
- Dense lymphocytic submucosal infiltrate
- Civatte bodies = Degenerative (dead) eosinophilic basal keratinocytes

Vancouver Page 45

https://www.pathologyoutlines.com/topic/skinnontumorlichenplanus.html

Civatte bodies: https://upload.wikimedia.org/wikipedia/commons/c/c4/Civatte_body.jpg

49
Q

Discuss common triggers of lichen planus

A
  1. Genetic predisposition
  2. Emotional stress
  3. Drug, food, or dental material hypersensitivity
50
Q

Where are the common lesions that lichen planus occur in the oral cavity?

A

The lesions most often occur on the buccal mucosa, gingiva, and tongue but can also be found on the lips and palate.

51
Q

What are 9 treatment options for lichen planus?

A
  1. Avoidance of triggers (e.g. NSAIDs, antimalarials, ACEis, BB, cinnamon, mints, teeth-whitening products, red wine)
  2. Improve oral hygiene
  3. Steroids - oral or topical (e.g. orabase, kenalog, oracort)
  4. Cyclosporin 500mg once daily x 4-8 weeks (immunosuppressant)
  5. Cryotherapy
  6. UV light
  7. Laser surgery
  8. Dapsone (type of antibiotic)
  9. Topical retinoids
52
Q

What is the Koebner Isomorphic Phenomenon?

A

Lichen planus lesions provoked by physical trauma (e.g. scratching)

53
Q

What is black hairy tongue?
What is it associated with?
What is the treatment?
Complications?

A

BLACK HAIRY TONGUE:
- Hypertrophy and elongation of filliform papillae on the surface of the tongue with brownish-black discoloration

ASSOCIATIONS:
1. Poor oral hygiene
2. Use of tobacco
3. Use of irritating mouthwashes
4. Antibiotic use (tetracyclines)

TREATMENT:
1. Withdrawal of precipitating agents and good oral hygiene

COMPLICATIONS: None

Vancouver Page 45

54
Q

What are Fordyce granules?

A

Yellow spots on the buccal mucosa lateral to the edges of the lips, usually bilateral, representing remnants of atrophied sebaceous cysts

Vancouver Page 46

55
Q

List the differential diagnosis of oral cavity Vesiculobullous lesions (9)

A
  1. HSV stomatitis (primary, secondary on hard palate/attached gingival or vermillion border) - primary is first episode; secondary is repeat episode in patient with previous immunity
  2. VZV stomatitis (primary, secondary)
  3. Coxsackie (herpangina) - hand foot and mouth
  4. Lupus (Discoid Lupus Erythematosus > Subacute Cutaneous Lupus Erythematosus > Systemic Lupus Erythematosus)
  5. Erythema multiforme (allergic reaction)
  6. Cicatrical pemphigoid (mucosal involvement > cutaneous involvement overall)
  7. Bullous pemphigoid (cutaneous involvement > mucosal involvement overall)
  8. Pemphigus vulgaris
  9. Lichen planus (erosive or bullous form)
56
Q

List 6 syndromes with congenital neurofibromas or fibromas of tongue and jaw

A

Neurofibroma = type of peripheral nerve tumor that forms soft bumps on/under skin, develops within a major or minor nerve anywhere

Fibroma = benign growth consisting of fibrous, connective tissue

Syndromes:
1. NF1
2. NF2
3. MENIIb
4. Tuberous sclerosis
5. Cowden’s disease
6. Gardner syndrome

57
Q

Regarding Gardner Syndrome, discuss:
1. Genetics and inheritance
2. Features

A

GENETICS:
1. APC (adenomatous polyposis coli gene) on chromosome 5q21
2. Autosomal dominant

FEATURES:
1. Fibromas
2. Osteomas (mandible and skull, maxilla and long bones) - often first sign
3. Lipomas
4. Leiomyomas (stomach and ileum)
5. Epidermal cysts
6. Thyroid carcinoma - well differentiated
7. Polyposis of colon and rectum - 40% malignant degeneration potential
8. Pilomatrixoma

58
Q

List diseases that cause oral ulcerations

A

A. TRAUMA

B. AUTOIMMUNE
1. Behcet’s disease
2. Reiter’s syndrome (conjunctivitis, urethritis, oral ulcers, arthritis)
3. Inflammatory bowel disease
4. Celiac disease
5. Erythema multiforme
6. Pemphigus vulgaris
7. Lichen planus (erosive)
8. Selective IgA deficiency

C. NUTRITIONAL
1. Vitamin B12 deficiency
2. Vitamin C deficiency (Scurvy)

D. INFECTIOUS/IDIOPATHIC
1. Recurrent aphthous ulcers
2. HSV stomatitis
3. VZV stomatitis
4. Herpangina (coxsackie)
5. EBV
6. HIV
7. Bacterial (primary or secondary)
8. Syphillis
9. Borrelia Vincentii (trench mouth - Necrotizing Ulcerative Gingivitis; Vincent’s Angina)
10. Candida

E. NEOPLASIA
1. Epidermoid cancers
2. Minor salivary gland cancers

F. OTHER
1. Necrotizing sialometaplasia

59
Q

What is the most common cause of oral ulcerative lesion?

A
  1. Recurrent aphthous stomatitis
    - Only occurs on non-keratinizing mucosa
    (HSV occurs on keratinizing)
60
Q

Regarding oral candidiasis, discuss:
1. Definition
2. Etiology
3. Risk factors
4. Clinical types
5. Diagnosis
6. Treatment

A

DEFINITION: Opportunistic infection of the oral cavity

ETIOLOGY:
1. Candida albicans (most common; latter ones more common in immunocompromised or neutropenic patients)
2. Candida tropicalis
3. Candida Krusei
4. Candida glabrata

RISK FACTORS:
1. Local factors (mucosal barrier function)
- Topical and inhalational corticosteroids
- Xerostomia
- Heavy smoking
- Denture appliances
- Radiated-induced mucositis
- Mucosal tumors

  1. Systemic factors
    - Immunosuppression, age, virus, retrovirus, chemotherapy, and corticosteroid use
    - Diabetes mellitus
    - Intrinsic immunodeficiency
    - Myelodysplasia/leukemia
    - Antibiotic use

CLINICAL TYPES:
A. ACUTE
1. Pseudomembranous (classic presentation of thrush) - cheesy white patches that can be scraped off to reveal erythematous/bleeding base
2. Acute Erythematous/Atrophic: stomatitis, midline rhomboid glossitis

B. CHRONIC
1. Hyperplastic(candidal leukoplacia): increased epithelial atypia and malignant transformation likely, buccal adherent, asymptomatic, white plaques that do not rub off
2. Chronic erythematous/atrophic: denture related, common in older adults, cracked oral commissures
3. Median rhomboid glossitis
4. Chronic Mucocutaneous: most serious, immuncompromised, 20% familial

C. ANGULAR CHEILITIS (most common)

DIAGNOSIS:
1. Smear: Potassium hydroxide over smear preparation; or use tissue stain such as PAS or methenamine silver preparation
2. Culture: Sabouraud dextrose agar medium
3. 50% of adults are normal carriers (aka will have positive culture tests)

TREATMENT:
1. Nystatin mouth rinse
2. Ketoconazole
3. Fluconazole
4. Itraconazole
5. IV Amphoteracin B

61
Q

List a differential diagnosis of gingival hypertrophy

A
  1. Poor oral hygiene
  2. Autoimmune - diabetes, crohn’s
  3. Drug effects - phenytoin most common, also cyclosporine A, calcium channel blockers
  4. Inherited - Cowden’s disease
  5. Pregnancy
62
Q

Describe the different types of recurrent aphthous stomatitis. What is the treatment?

A
  1. Minor aphthae: < 1cm, heal in 7-10 days, without scarring
  2. Major aphthae: 1-3cm in size, or >1 ulcer, can leave scarring - biopsy to r/o SCC
  3. Herpetiform aphthae: 1-3mm, begin as multiple - up to 150, unrelated to herpes virus

TREATMENT:
1. Chlorohexidine rinse
2. Topical steroids

https://www.msdmanuals.com/-/media/manual/home/images/m/2/8/m2800216-minor-aphthous-ulcer-lip-science-photo-library-high-resized.jpg?mw=350&thn=0&sc_lang=en

63
Q

Regarding HSV stomatitis, discuss:
1. What are the features of primary HSV?
2. What triggers reactivation?
3. Histology?
4. Treatment?

A

PRIMARY FEATURES:
1. Seronegative
2. Ulcers
3. Malaise
4. Fever

REACTIVATION TRIGGERS:
1. UV light
2. Stress
3. Immunodeficiency
4. Trauma
5. Stress

HISTOLOGY:
1. Intradermal vesicles
2. Multinucleated giant cells

TREATMENT:
1. Acyclovir

https://www.pathologyoutlines.com/topic/skinnontumorherpeszoster.html

64
Q

Regarding Erythema Multiforme/Steven-Johnson syndrome/Toxic epidermal necrolysis, discuss:
1. What is it and what type of reaction is it?
2. Cause?
3. Types/continuum classification?
4. Treatment?

A

DEFINITION:
- Target lesions “targetoid” caused by deposition of antigen-antibody complexes in small vessels of dermis and submucosa
- Type IV hypersensitivity reaction
- Severe form is Steven-Johnson syndrome, with systemic involvement of GI, genitals, and eyes
- Even more severe = toxic epidermal necrolysis

CAUSE:
1. Reaction to infections (e.g. HSV, EBV, histoplasmosis
2. Reaction to certain medications (e.g. Sulfonamides, allopurinol, barbituates, dilantin)

CONTINUUM:
1. EM Minor: Acral involvement only (hands/feet)
2. EM Major: Acral + mucous membranes (epidermal detachment < 10% total body surface area)
3. Steven-Johnson Syndrome: blisters of trunk and face, erosions of mucous membranes, >10% TBSA
4. Toxic Epidermal Necrolysis: similar to SJS but >30% TBSA

TREATMENT:
1. IVIg
2. Supportive medications
3. Steroids
4. Treat the underlying cause

Vancouver Page 47

65
Q

What are four most common drugs associated with toxic epidermal necrolysis?

A
  1. Sulfonamides (TMP-SMX, sulfasalazine)
  2. Allopurinol
  3. Barbiturates
  4. Dilantin (phenytoin)

“Skin Always Breaks Down”

66
Q

What are the 3 different types of pemphigoid diseases?

A
  1. Cicatrical Pemphigoid (aka. mucous membrane pemphigoid)
  2. Bulbous pemphigoid
  3. Epidermolysis Bullosa Acquisita
67
Q

Regarding Cicatricial Pemphigoid, discuss:
1. What is it, and what is another name?
2. Epidemiology?
3. Clinical presentation?
4. Diagnosis? Biopsy findings?

A

CICATRICIAL PEMPHIGOID:
- Pemphigoid = autoimmune disorder against the basement membrane/subepithelial layer
- Aka. Mucous membrane pemphigoid
- Mucousa involvement, with subepithelial bullae and blistering
- Cicatrical = severe adhesions (aka. scarring) that form with healing

EPIDEMIOLOGY:
- Diagnosed 5-6th decade
- F:M 1.5 > 1
- No racial or geographic predilection

CLINICAL PRESENTATION:
- Affects both cutaneous and mucosal surfaces, most common oral and ocular mucosa
- Buccal, palate, alveolar ridge, tongue, lower lip –> present with desquamative gingivitis
- 40% scarring of conjunctiva and scleral fusion, entropion, potential loss of vision
- Webs and stenosis of aerodigestive tract
- Also: nasopharynx, laryhnx, urogenital tract
- Nikolsky’s sign can be positive

DIAGNOSIS:
1. Biopsy (perilesional)
- Subepithelial separation with inflammatory infiltrate (detachment of dermis and epidermis seen)
- Direct immunofluorescence: linear deposits of IgA, IgG, ± C3 along epithelial basement membrane zone
- Autoantibodies to basement membrane components (basement membrane lights up): Bullous Pemphigoid antigen, laminin 5 and 6, type VII collagen
- Indirect immunofluroescence: autoantibodies binding to epidermal or dermal side of salt-split skin (membrane liights up between the two areas)

TREATMENT:
1. Corticosteroids
2. Immunosuppressants (azathioprine, cyclophosphamide, cyclosporine)
3. Immunoglobulins, plasmapheresis
4. Biologics (rituximab, etanercept, infliximab)
5. Ophthalmology consult (potential for symblepharon formation aka. abnormal healing)

Kevan Gen #114
Vancouver Page 48

68
Q

Regarding Bulbous Pemphigoid, discuss:
1. What is it? Epidemiology?
2. Clinical presentation
3. Diagnosis
4. Treatment and prognosis

A

BULBOUS PEMPHIGOID:
- Cutaneous subepidermal autoimmune disorder

EPIDEMIOLOGY:
1. European
2. Age > 60

CLINICAL PRESENTATION:
- 10-40% oral manifestations
- Ocular involvement atypical
- Widespread blistering of skin
- Onset can be associated with exposure to UV light, radiotherapy, medications (e.g. nSAIDs, antibiotics)

DIAGNOSIS: Same as Cicatrical pemphigoid above

TREATMENT:
1. SImilar to cicatrical pemphigoid above, plus can consider topical treatment (may prevent systemic side effects in advanced patient age)

PROGNOSIS:
- Remission in 2-5 years typically
- Can be life threatening in debilitated patients

69
Q

Regarding Epidermolysis Bullosa Acquisita, discuss:
1. What is it?
2. Pathophysiology?
3. Diagnosis?
4. Treatment?

A

EPIDERMOLYSIS BULLOSA ACQUISITA:
- Rare, autoimmune (autoantibodies) to type VII collagen of the basement membrane (Type VII collagen = major component of the anchoring fibrils which provide stability to the dermal-epidermal adhesion on the dermal site)
- Seen commonly on skin and upper aerodigestive tract
- Inherited form = epidermolysis bullosa

PATHOPHYSIOLOGY:
- Mechanical trauma –> blistering and resultant scarring –> severe atrophy –> microstomia
- Epidermolysis bullosa is worse for scarring compared to EB acquisita
- Presents in early adulthood

DIAGNOSIS: Biopsy, rule out other bullous diseases

TREATMENT:
1. High dose steroids
2. Immunosuppressants (azathioprine, cyclophosphamide, cyclosporine)

70
Q

Regarding Pemphigus Vulgaris, discuss:
1. What is it? Epidemiology and risk factors?
2. Pathophysiology?
3. Variants?
4. What are the features?
5. Examination signs?
6. Investigations and Pathology?
7. Treatment and Prognosis?

A

PEMPHIGUS VULGARIS:
- More severe, B-cell mediated autoimmune disease with IgG auto-antibodies against intercellular bridges (desmosomes)

EPIDEMIOLOGY:
- Up to 5 per 100000 cases
- Mean age = 50-60 years old
- Slight female predilection

RISK FACTORS:
1. Other autoimmune disorders (RA, MG, SLE, pernicious anemia)
2. Ashkenazi jews
3. Mediterranean and southern asia

PATHOPHYSIOLOGY:
- IgG antibodies binds to desmoglein 3 (oral) and desmoglein 1 (cutaneous)
- Variants:
1. Mucosal-dominant PV: Target antigen is desmoglein 3 –> oral lesions
2. Mucocutaneous PV: Target antigen is Desmoglein 3 and 1 –> Oral and cutaneous

FEATURES:
- Oral (90%) - cheek, palate, tongue, lips common (oral epithelium expresses cadherin-type cell adhesion molecule –> desmoglein 3 autoantibodies form): Painful fluid-filled blisters that break and expose erythematous irregular ulcerated lesions, Intraepithelial bullae, acantholysis; typically have > 1 year of oral disease prior to other cutaneous manifestations
- Nose (10%): Ulceration, crusting, septal perforation
- Larynx (rare): Supraglottic bullae, slough with swallowing
- Involves detachment between keratinocytes and basal membrane (suprabasal split)

EXAM:
1. Positive Nikolsky sign - development of new lesion (blister), or sloughiing of epithelium (secondary to loss of cell-to-cell adhesion) with pressure applied on an asymptomatic area
2. Asboe-Hansen sign (direct pressure over bulla causes extension)

LABS:
1. Serum antibodies assessed by indirect immunofluorescence or enzyme-linked immunosorbent assays

HISTOPATHOLOGY:
1. Tzanck cells are pathognomonic - large round keratinocytes having hyperchromatic nucleus with perinuclear halo and deep basophilic cytoplasm.
2. Perilesional biopsy - assess for intercellular deposits of IgG and C3 (by direct immunofluorescence)

TREATMENT:
1. Steroids (long-term, or pulse)
2. Immunosuppressants (azathioprine, cyclophosphamide, cyclosporine)

Prognosis: POOR
“PemphigUS will kill US” - deadlier than pemphigoid

Acantholysis - Vancouver Pg 48
Tzanck cells: https://ijdvl.com/content/126/2005/71/4/Images/ijdvl_2005_71_4_295_16632_2.jpg

71
Q

What is Van Der Woude’s disease? What is pathognomonic for this disease?

A

Lower lip pits = Pathognomonic

High incidence of cleft palate and lip (genetic form of cleft lip and palate)

72
Q

Regarding Vincent’s Angina, discuss:
1. What is it?
2. Etiology?
3. Associations?
4. Diagnosis?
5. Treatment?

A

VINCENT’S ANGINA:
- aka. Trench mouth
- aka. Necrotizing Ulcerative Gingivitis

ETIOLOGY:
- Gram negative bacilli - Fusiformis fusiformis
- Spirochete - Borrelia vincentii

ASSOCIATIONS:
1. Poor dental hygiene
2. Malnutrition
3. Immunosuppression –> HIV

DIAGNOSIS: Clinical

TREATMENT:
1. Oral hygiene (chlorhexidine or proviodine-iodine rinses)
2. Debride necrotic areas
3. Address underlying causes (nutrition, immunosuppression, poor social supports, etc.)

Kevan Gen #129

General OTOHNS (9 decks)

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