Oral Pathology Flashcards Preview

DOD > Oral Pathology > Flashcards

Flashcards in Oral Pathology Deck (194):

Premalignant and Malignant
Skin Findings

• Solar/Actinic Keratosis: precancerous

• Keratoacanthoma

• Basal Cell Carcinoma

• Squamous Cell Carcinoma

• Melanoma


Solar/Actinic Keratosis: precancerous

precancerous and caused by sun damage

"Actinic" = related to the sun
"Keratosis" = white appearance (lots of keratin) precancerous

Description: white, scaly, crusty area



rapid growth (unlike basal cell carcinoma), low-grade malignancy, spontaneous

o A number of these cases will resolve on their own

Description: round nodules with a central depression; the term is "UMBILICATED" (meaning round space in the middle) that is filled
with a keratin plug


Basal Cell Carcinoma

- slow-growing, low-grade malignancy; rarely

- Most common human cancer

- Tends to occur a lot on the face (upper lip, nose, etc.)

- Description: Nodular with surface red blood vessels; can stick out or have ulcerations


Squamous Cell Carcinoma

-variety of clinical presentations, keratotic

- The most common cancer of the mouth

- Can be ulcerated, or sticking out

- Can be red or white or both



-About 5% of all skin cancers but is the worst case skin cancer

-Related to chronic sun exposure, but you can get
melanoma that arises de novo or from an existing mole

You can also have oral mucosal melanoma (not related to sun
exposure) – these are VERY rare (0.5% of all melanomas) but
basically a death sentence

- Immunotherapy is the new standard of treatment

Description: Pigmented, asymmetrical lesions

use ABCDE criteria to diagnosis


ABCDE Criteria

A: Asymmetric
B: irregular Borders
C: variable Color
D: Diameter (larger than the head of a pencil eraser)
E: Evolving


Seborrheric Keratosis (SK)

• Common after age 40

• Not caused by sun exposure

• No risk for skin cancer

• Raised growths on the skin with a waxy, “stuck-on” appearance

• May be multiple

• Commonly seen in African American patients
(think Morgan Freeman)


Examination of the Neck

• Must look at the midline and the lateral neck
• Feel for lymph nodes, examine for any thyroid enlargement (midline)
• Any neck mass in a patient over the age of 40 should be considered
malignant until proven otherwise!
• Most common congenital lateral neck mass: branchial cleft cyst
• Most common congenital midline neck mass: thyroglossal duct cyst
• Goiters are common as well


Branchial Cleft Cyst

Branchial fistulas (external) occur when the 2nd pharyngeal arch fails to
grow caudally over the 3rd and 4th arches
• Fistula (pipe) keeps 2nd, 3rd, and 4th clefts in contact with the surface
• Internal Branchial fistulas (rare) result from rupture of the membrane between 2nd cleft and 2nd pouch
• Branchial fistulas provide drainage for a lateral cervical cyst that failed to
• Branchial fistulas and Lateral cervical cysts are found directly anterior to
the sternocleidomastoid muscle


Thyroglossal Cyst

During migration of the thyroid gland from the foramen cecum, a canal
forms connecting the two (thyroglossal duct)
• Thyroglossal duct normally disappears. If not, you get a thyroglossal cyst
• found at midline

• If the patient sticks out their tongue or swallow, you can see the duct still and the lump will move

This should be treated because it can enlarge, impede function of other structures, or form a fistula which would lead to septsis and a whole bunch of bad stuff

OMF would remove it surgically; if sizable…. If its really small then you
Might not need to take it



• thyroid mass that is often quite extensive and firm/glandular
• Can be caused by autoimmune diseases, iodine deficiency, or hyper/hypothyroidism


Head and Neck Lymph
Node Distribution

Two most
important groups
for us:
and submental
lymph nodes
• Cancer of the
front of the
mouth or lip will drain into the submental area
• Rest of oral cavity or tongue will drain into submandibular area
• Lymphoma: Hodgkins & Non-Hodgkins/Metastatic Carcinoma (bump on the side of the neck that feels fixed and very hard)


Actinic cheilitis

• Mottled grey color of vermilion
• Blurred interface between the lip and skin
• Increased risk of squamous cell carcinoma
• Caused by too much sun exposure
• Eventually starts to ulcerate when progressing – should be
biopsied and removed before it turns into lip cancer
• Might feel firm when palpating sore


Angular Cheilitis

Location: commissures, often bilateral but can be unilateral
o Clinical Features
§ Erythema (redness)
§ Fissuring
§ Superficial erosion
§ May be red/ulcerated
o Etiology: candidiasis which is a fungal infection (may also be bacterial co-infection)
o Denture wearing is a risk factor
o Immunocompromised HIV patients or diabetic patients often have this; sometimes even vit/min deficient patients
o Treated with anti-fungal ointment and it will go away – doesn’t tend to be chronic, but can be recurring if you have not controlled
the underlying problem


Herpes Labialis

cold sores
o Tends to be recurrent
o Some patients may have it monthly, weekly, or
a couple times a year
o Tingling feeling, then become crops/groups of fluid filled vesicles,
then blister (this is the most infectious stage)
o Vesicles rupture then ulcerate and then crust


Squamous Cell Carcinoma (SCC) of lip

usually related to sun

Mass that feels firm/hard

Likely to also have enlarged lymph nodes



• A lesion formed when a salivary gland duct is severed and the mucous spills into the adjacent connective tissue

• Result of some event that leads to a break in the duct and the connective tissue moves aside and "bubbles up" forming a cyst like structure

• Is a "pseudocyst" (not lined by epithelium)

• Filled with mucous so it will feel soft and compressable
(fluctuant) upon palpation

• Might have blueish hue

• Need to be completely removed because the broken duct may still be there

• Might be history of them (recurrent)

• Other clinical clue: these might change in size depending on amount of salivation

• Most common location is the lower labial mucosa but can be found on any MOVABLE mucosa



Pink, firm, feel fibrous, and don’t change size
• These are very common and are due to chronic irritation or biting
• Sessile: lesion has a broad base
• Pedunculated: lesion has a smaller stalk than the top
• whole thing needs to be removed and you need to find the cause to remove the source


Tobacco pouch keratosis

• Usually in the
lower vestibule (where patients put their
tobacco pouch)

• These are considered precancerous and need a biopsy


Linear ulcer

can be a symptom of Crohn’s disease


Buccal Mucosa Variants of Normal

Linea Alba


Fordyce Granules

Melanin Pigmentation


Linea Alba

a raised “white line” that extends anteroposteriorly on the buccal mucosa along
the occlusal plane

Histological appearance: epithelial hyperplasia (thickening of mucosa) and hyperkeratosis (release of keratin in thickened epithelium)



Generalized, white (opalescent) appearance of the buccal mucosa

Disappears or lessens when tissue is stretched

Microscopic appearance: epithelial cells are larger and with clear


Fordyce Granules

ectopic sebaceous glands
which are most commonly observed on the buccal mucosa and lips


Melanin Pigmentation (physiologic melanosis)

common on darker skinned patients



aka traumatic fibroma, irritation fibroma
§ Occurs as a result of chronic trauma
§ Histological appearance: dense, scar-like fibrous connective tissue surfaced by epithelium
§ Needs to be removed and treat the underlying cause (might be due to a sharp restoration)


Lichen Planus

autoimmune disease where you get white lines (striae) in your mouth


Dorsal Tongue Variants of normal

Pigmented fungiform papillae

Fissured tongue: the dorsal surface of the tongue has deep fissures or grooves; cause unknown


Hairy Tongue

• Benign conditions
• Elongated filiform papillae
• Cause unknown
• Black/brown/green hairy tongue – color due to chromogenic bacteria
• Papillae are easily stained by food or tobacco
• You can move papillae from side to side like a rug to help diagnose and differentiate from coated tongue


Geographic tongue (benign migratory glossitis)

• Erythematous patches on the dorsal and lateral tongue surrounded by a white or yellowish-
white perimeter

• The location of the patches changes
and there are times of remission (if a spot doesn’t move then it might need to be biopsied)

• Patients occasionally complain of a burning sensation

• Cause unknown – condition has been associated with

• Ectopic geographic tongue: can be on the floor or roof of the mouth or the cheek


Median rhomboid glossitis

• Flat or raised discrete erythematous area (red patch) in the midline of the
posterior dorsal tongue

• May be associated with candidiasis

• Etiology not clear
• Lesions never go away


Lateral Tongue Abnormal Findings

• Traumatic Ulcer: area with a yellow/white membrane that is missing epithelium (cancers can look like this too so be careful in diagnosing something as a traumatic ulcer – look for a
source of trauma and follow up)
• Benign Condition of Unclear Etiology
o Geographic tongue
• High risk area for squamous cell carcinoma


Ventral Tongue

Normal structures
o Lingual varicosities
> Prominent, enlarged lingual veins


Floor of the Mouth

Normal findings:
> lingual frenum
> caruncle/orifices of Wharton's ducts

Variant of Normal
> mandibular tori


Mandibular tori

aspect of the mandible composed of dense, compact bone

Autosomal dominant inheritance pattern


Floor of the Mouth Lesions

- Ranula
- Sialolithiasis
- Leukoplakia



• Essentially a mucocele specifically located on the floor of the mouth unilaterally

• Associated with the ducts of the sublingual and submandibular gland

• Treatment: complete surgical excision, portion of major gland may need to be removed in extensive cases

• May break through mylohyoid and become a “plunging” ranula

• Tend to be larger than a mucocele, so they are more difficult to remove



• Salivary gland stones

• Most common location to find this is the floor of the
mouth – due to the curvature of the submandibular gland duct

• Hard-feeling stones – use bimanual palpation from outside and inside the mouth

•Clinical Features
> Minor glands: hard yellowish structure in soft tissue
> May be visible on a radiograph as radiopaque mass
> Patient may report recurrent swelling and pain at mealtimes (because you area creating more saliva which will be blocked by the stone)

• Occlusal radiograph is good to diagnose these (but these are not common)

• These need to be removed because they
block a salivary gland and lead to infection/swelling



• Clinical, descriptive term
• A white, plaque-like lesion of the oral mucosa that cannot be rubbed off and cannot be diagnosed as a specific entity or disease
• Pre-malignant potential so need to be biopsied



• Cancers are often indurated (hard and fixed)
• Might be friable (fall apart) and bleed easily
• Red is worse than white (good to know when choosing biopsy sites)


Maxillary Torus

(Palatal Torus): exophytic mass of
normal compact bone in the midline of the palate
- Autosomal dominant inheritance pattern


Abnormal Findings on Hard Palate

Nicotinic stomatitis

Denture stomatitis

Thermal/ pizza burn

Salivary gland tumor


Nicotinic stomatitis

- Result from the heat produced from smoking; can also occur in people who drink a lot of hot beverages (but mostly by heavy smoking (pipe, cigar, cigarette)
- Histology: hyperkeratosis with inflamed minor salivary glands (red dots with white borders)
- This is not a premalignant condition
- Can cover the whole palate or just in certain areas



Denture Stomatitis

patient can get irritation/fungal infection if they don’t remove and clean their denture every night


Thermal/pizza burn

ask patient if they remember getting burnt


Salivary Gland Tumor

there are a lot of minor
salivary glands on the palate which can get
tumors that can be benign or malignant


Bifid Uvula

this is the mildest form of cleft palate



HPV-related wart (these can occur in other parts of the mouth as well, but this is a common location) - need to be surgically removed


The 3 Ps

• Pyogenic granuloma: red, spongy, bleed easily (occur
more in pregnant women)

• Peripheral ossifying fibroma: forms bone and feels

• Peripheral giant cell granuloma: may have a
blue/purple color and is harder than the pyogenic
granuloma but softer than the peripheral ossifying

• These are very common lesions and need to be removed and biopsied
• These are usually hygiene related because the patient has food/plaque stuck between the teeth

• Need to removed AND scale and root plane (and give oral hygiene instruction) otherwise they tend to come back


Mucosal Smear

• Purpose: to examine the cells that can be collected by scraping the surface of a lesion (only for something in the keratin or the top of the epithelium)

• This technique is used for the diagnosis of:
- Oral candidiasis – a superficial proliferation of a fungal organism that is a component of the oral microflora
- Herpetic lesions – ulcers usually located on keratinized mucosa,
caused by the herpes simplex virus

• The mucosal smear involves taking a sample from the surface of the


Smear technique

- The kit contains a wooden scraper and glass slides with fixative (you can also just use the wooden end of a cotton tip applicator)
- Light to medium scraping (shouldn’t hurt patient – no anesthesia needed)
- Spread cell sample evenly on the glass slide (not in a clump)
- Then fix sample with a few drops of alcohol fixative (just enough to
cover the cells) – let it air dry
-Note: don’t take the alcohol-soaked gauze out and wipe the slide,
instead just squeeze out a few drops of alcohol
o Submit sample on slide once alcohol has dried


Oral Candidiasis

• Mucosal lesions of oral candidiasis can be either red (erythematous) or white or both
• Lesions are a response to a proliferation of a fungal organism that is a component of the oral microflora
• The mucosal smear takes a sample from the superficial layers of the epithelium (where candida resides)
• The fungal organisms that cause oral candidiasis are located in the superficial aspect of the epithelium – the mucosal smear collects the appropriate sample to make the diagnosis
• The laboratory uses a special stain (PAS) to show the fungal organisms in the keratin/epithelium when doing a surgical biopsy


Positive Mucosal Smear

Hyphae have to be invading epithelial
cells in order to have a positive diagnosis


Oral Herpetic Lesions

• There is herpes labialis on the lips that has visible vesicles that crust over
– usually in the mouth you will not see this, instead you will see ulcers
• You don’t really need a surgical biopsy for herpes
• Herpes virus takes cells and combines the nuclei to create large TZANCK
CELLS (these are multinucleated)

• Mucosal smears positive for herpes: you can see the Tzanck cells with
many nuclei


The Brush Biopsy

• Purpose: to examine a complete transepithelial sample of cells (goal is to
get all layers of epithelium; collect superficial, intermediate, and basal

• This is technique sensitive and the patient will report a little bleeding and

• This technique collects cells from all the layers of the epithelium – from
the basal cells to the surface keratin layer

• The brush biopsy technique will collect cells from all the layers of the

• A special brush is used to collect the sample from the epithelium and put
sample on a slide and fix with alcohol

• The brush is twisted through the epithelium to collect cells from all the


Brush Biopsy Technique

o Place sample on slide
o Fix with alcohol fixative
o Allow slide to air dry
o Send slide and laboratory request form to OralCDx

• Biopsy Result Options:
(1) Negative
(2) Atypical cells warranting further investigation (a real biopsy)
(3) Positive (net step: surgical biopsy)
(4) Insufficient for diagnosis (you didn’t submit a good sample)

• When to use this?
o Epithelial lesions: flat
white leukoplakias
o Lesions that have a very low index of suspicion: traumatic cheek /
lip chewing
o Lesions that clinician strongly suspects to be frictional hyperkeratosis due to chronic trauma / irritation

• Uses for brush biopsy: chronic lip biting, chronic cheek biting – can be
used as a starter step if the patient is worried about getting a biopsy

• Contraindications for brush biopsy:
o Non-epithelial nodular lesions such as soft tissue / salivary gland
o Ulcerated areas (because there is no epithelium there)
o Red lesions in high risk areas (these should have a real scalpel
o Pigmented or vascular lesions (these have a soft tissue component
so you won’t get a good diagnosis from this)


Incisional Biopsy

a representative sample of the lesion is taken and
submitted for microscopic examination


Excisional Biopsy

the entire lesion is removed and submitted for microscopic examination


Basic criteria for Biopsy

used to determine whether to perform incisional or
excisional biopsy:

1) Size of lesion: 1 cm guideline (under 1cm = excisional; over 1cm = incisional)

2) Location of lesion: access, proximity to vital structures
3) Degree of suspicion: very suspicious lesions should have incisional
biopsy and vice versa (if it is very suspicious leave the margins for the surgeon to observe so incisional is better)
4) Use clinical judgment for fibromas and pedunculated lesions
(should take the whole fibroma because there is no reason to leave it there, even if it is over 1cm)


Indications for Biopsy

• Lesions that have been present for more than 2 weeks with no healing or
decrease in size

• Lesions in high risk areas

• Suspicious lesions


Characteristics of
Suspicious Lesions

• Erythroplasia: lesion is totally RED or has a speckled red appearance

• Ulceration: lesion is ulcerated or presents as an ulcer

• Long duration: lesion has persisted for more than two weeks

• Fast growth rate: lesion exhibits rapid growth

• Bleeding: lesion bleeds on gentle manipulation (tumors are very vascular)

• Induration: lesion and surrounding tissue is firm to the touch

• Fixation: lesion feels attached to adjacent structures


General Biopsy Techniques

• Avoid ulcerated necrotic areas (unless entirely ulcer)

• Take a wedge of tissue: narrow deep specimen better than broad shallow

• Select the “worst-looking” area to biopsy: red areas better to biopsy than white areas, rough-surfaced areas better than smooth areas

• Multiple areas may be biopsied when the lesion is large or shows
significant variation

• Always be aware of regional anatomy


Biopsy Site Selection

• Red area (choose red area over white)
• Rough area (choose rough area over smooth)
• Peri-ulcer
• Velscope and T Blue (Velscope emits green light and wherever you see
black through that light is an area you should biopsy; Toludine blue stained areas should be biopsied)
• Striated areas for Lichenoid lesions (white striae) – in this case you biopsy the white striae, not the red areas
o Red areas will show
o When you think
something is Lichenoid
because it has striae,
biopsy the white
o When you don’t have
striae and have a mixed
red and white lesion,
biopsy the red because
you suspect cancer
• Perilesional for Pemphigus/Pemphigoid (go near peeling area)


Biopsy Supplies

• Blade handle with a No. 15 blade
o Disposable ones are not as good
• Small soft tissue forceps with minimal teeth
• Local anesthetic solution and syringe
• Retractor appropriate for the site
• Suction source and surgical suction tip (can’t use big suction tip)
• Gauze
• Sutures for traction or closure, if indicated
• Labeled specimen bottle containing formalin and biopsy request form –
also be sure to label the site if you are taking multiple biopsies


Anesthesia for Oral

• Local infiltration with minimal lidocaine with epi
• Never inject directly into lesion (it will distort it)
• Inject slowly so as not to distort tissue
• Inject at multiple points surrounding lesion
• Test area before proceeding to biopsy


Punch Biopsy

• Available in different diameters: 2.0 – 5.0 mm
• 4.0 mm punch good for most oral biopsies
• May be incisional or excisional biopsy depending on size of lesion and size
of punch
• Advantages:
o Ease of technique
o Sutures generally not required
o Usually faster, better healing
o More useful for lesions located on fixed, non-moveable tissue
• Disadvantages:
o May not be adequate for deep lesions
o Difficult to use for lesions on freely movable tissues


How to tell mental foramen
is not a periapical

trabeculae are superimposed, lamina
dura is still intact, or take a
different angle and use the SLOB rule


Periapical Granuloma

Mass of chronically inflamed granulation tissue that forms at the apex of the root of a non-vital tooth


Periapical Cyst

Caused by pulpal necrosis secondary to dental caries or trauma; Cyst and granuloma radiographically
Look the same so you would need to biopsy for definitive diagnosis


Residual Cysts

• The term RESIDUAL CYST is used most often for retained radicular cysts from teeth that have been removed
• A RADICULAR CYST is a cyst which has developed from embryonic tissue
remains, usually due to a dentogenous inflammational stimulus


Root Resorption

Root resorption is known to occur after trauma and in response to inflammation


Internal Root Resorption

Internal resorption is a condition where the slow or fast resorption of the dentin of the pulp, and the internal walls of the root canals occur


Periapical Cemento-
Osseous Dysplasia (PCOD)

is a benign condition of the
jaws that may arise from the fibroblasts of the periodontal ligaments

• It is most common in African-American females

• The three types are periapical cemento-osseous dysplasia, focal cemento-osseous dysplasia, and florid cemento-osseous dysplasia

• PCOD occurs most commonly in the mandibular anterior region, while FOCAL appears predominantly in the mandibular posterior region, and
FLORID in both maxilla and mandible in multiple quadrants



is an idiopathic, non-
neoplastic condition characterized by the excessive buildup of normal cementum (calcified tissue) on the roots of one or more teeth
• A thicker layer of cementum can give the tooth an enlarged appearance, which mainly occurs at the apex or apices of the tooth

• Down Syndrome and
Paget’s Disease patients
have a predisposition for


Dens Invaginatus

also known as dens in dente
("tooth within a tooth") is a condition found in teeth
where the outer surface folds inward
• Dens invaginatus is a malformation of teeth most
likely resulting from an infolding of the dental papilla
during tooth development or invagination of the
enamel organ in dental papillae


Fissural Cysts: Nasopalatine,
Globulomaxillary, and
Median Palatine Cysts

A cyst derived from epithelial remnants entrapped along the fusion line of embryonal processes


Dentigerous Cysts

• Forms around an impacted or unerupted tooth
• A dentigerous cyst, also known as follicular cyst is a type of odontogenic
• This cyst develops from the accumulation of fluid between the reduced
enamel epithelium and the crown of an unerupted tooth
• It attaches to the tooth neck at the cemetoenamel junction


Dentigerous Cysts

Forms around an impacted or unerupted tooth
• A dentigerous cyst, also known as follicular cyst is a type of odontogenic
cyst because the follicle never goes away and becomes cystic (goes from CEJ -> to CEJ on both sides)

• This cyst develops from the accumulation of fluid between the reduced
enamel epithelium and the crown of an unerupted tooth
• It attaches to the tooth neck at the cemetoenamel junction

• Once it gets past 2-3 mm and broadens it can be considered a dentigerous cyst


Malignant Lesions

• This is INVASIVE

• Bone is destroyed in an irregular pattern

• A malignant lesion will
invade the bone & a benign lesion will just move it

• Multilocular lesion: Local malignancy but can destroy the whole mandible



Tumor of odontogenic
epithelium (ameloblasts, or
outside portion, of the
teeth during development)
appearing in the lower jaw; From premolar to mandibular molars (angle of mandible)


Well-defined RO tumor in
the left maxillary sinus

If you see a lesion like this in the maxillary sinus – REFER this patient to
an ENT



• An odontoma is a benign tumor of odontogenic
origin (i.e. linked to tooth development)

• Specifically, it is a dental hamartoma, meaning
that it is composed of normal dental tissue that
has grown in an irregular way
• Compound odontoma - literally look like little
• Complex odontoma - mixture of RO and RL that are indistinguishable as


Paget’s Disease

• Disease of bone – this can be an incidental finding; characterized by s cotton ball appear of bone and is often seen with hypercementosis


Trabecular Pattern of

• Very large medullary spaces


Subjective Findings for Salivary Disorders

> follow up questions to swelling?
- how long?
- recurrent (come and go)
- persistent (always there; growing
> Continuously getting worse or worsen?
> Suddenly stopped growing
> throbbing, stabbing, burning

Dry Mouth (Xerostomia)?
> How dry does your mouth feel?


Objective Findings for Salivary Disorders

Extra-oral Examination
> Major gland enlargement
> Facial Asymmetry
> Visible swellings or masses

Intra-oral Examination
> Stenson's duct (opening on buccal mucosa by second max molar)
> Wharton's duct (floor of the mouth)
> Swellings/masses (visually or by palpation)

Evidence of hypo salivation
> Incisal/cervical caries (signaling lack of a buffer)
> dry mucosa
> fungal infections (signalling changes in oral flora due to a change in environment)
> glove/instrument sticking to mucosa
> sticky consistency of mucosa
- foamy, ropey appearance/feel


Bimanual Palpation

palpate from inside and outside the mouth at the same time; used for evaluating the SUBLINGUAL GLAND


Intra-oral exam landmarks for the sublingual gland

Sublingual caruncle: an eminence on either side of the frenulum of the tongue (frenulum linguae), on which the major duct of the sublingual gland and the duct of the submandibular gland open.

Ducts of Rivinus: multiple, ribbon-like ducts that open into the oral cavity separate from the sub mandibular duct

Bratholin's duct: the ducts of the sublingual gland usually consisting of multiple ducts of Rivinus


Where are minor salivary glands NOT found?

Anterior part of the hard palate (behind the rugae there are though)



Salivary Gland Diseases/Conditions

• Sialadenitis – acute (mainly neutrophils) and chronic (plasma cells and lymphocytes)

• Mucocele (recurrent)

• Ranula (floor of the mouth unilateral mucocele)

• Sialoliths

• Necrotizing Sialometaplasia (Occurs on the palate where the minor glands become necrotic due to an inciting event/trauma)


Acute and Chronic Sialadentitis

• Definition: Acute or chronic inflammation in major or minor salivary glands

Acute = you will see drainage emerging from the Stenson's duct (puss)

Chronic = repeated episodes of acute version –
you should do a biopsy to rule out a salivary gland
tumor, and a biopsy of this will show chronic inflammatory cells

• Causes:
> Obstruction of a salivary gland duct
> Infection
> Decreased salivary flow

• Parotid gland = parotitis
> Swelling, redness, heat, loss of function, pain =
signs of inflammatory response

Acute Chronic
• Treatment:
> Antibiotics (especially if there is exudate coming from it)
> Rehydration
> Surgical drainage
> Surgical removal of the affected gland (in chronic cases)


Chronic Sialadenitis - Histopathology

• Atrophy of acini
• Dilatation of duct
• Chronic inflammatory cells

Connective tissue starts to change as well - increased
# of plasma/lymphocytes


Plunging Ranula

Mucin has dissected through the floor of the mouth and is now visible extraorally


Necrotizing Sialometaplasia

• Locally destructive inflammatory condition of palate

• Salivary gland ischemia (tissue death)

• Predisposing factors (but sometimes you don’t have any of these)
> Local trauma
> Palatal injection of local anesthesia
> Previous surgery

Late stage looks really scary– like cancer – but it is not a malignancy and usually self-resolves

• Clinical Presentation:
> Initially appears as a non-ulcerated soft swelling of palate
> Usually unilateral, but can be bilateral
> Often associated with pain or paresthesia (numbness/tingling)
> Within 2-3 weeks, necrotic tissue sloughs off and becomes a crater-like ulcer (“a chunk of the roof of my mouth came off”)
> No treatment, spontaneously resolves within 6 to 10 weeks

• Early Stage Late Stage Bilateral Case
> Microscopic features:
- Necrosis of the salivary glands
- Metaplasia: Salivary gland duct epithelium is replaced by squamous epithelium – appear as islands of squamous epithelium deep in the connective tissue


Bilateral Salivary Gland Enlargement: Causes

• Sjögren’s Syndrome
• Alcoholism
• Diabetes mellitus
• Malnutrition
• HIV infection
• Drugs (Enaliprilat IV - ACE inhibitor rxn)
• Mumps
• Sarcoidosis
• Idiopathic


Sjögren’s Syndrome

• Autoimmune disease affecting the salivary and lacrimal glands

• Results in dry eyes and dry mouth (Sicca Syndrome)
> Dry eyes: Xerophthalmia
> Dry mouth: Xerostomia

• Diffuse firm enlargement of the major salivary glands in 1/3 to 1/2 patients with SS

• These patients will have many dental
problems because without enough saliva they will be very prone to decay

• Take measures to help prevent them from losing all their teeth

• Unfortunately there isn’t really much you can do to treat these patients

• Only 1/3 of patients will have bilateral salivary gland
enlargement MUCH more common in older women


Laboratory Values in Sjögren’s Syndrome

• Erythrocyte sedimentation rate (ESR) is high

• Serum immunoglobulin levels are elevated

• Positive Rheumatoid factor – 75%

• Antinuclear antibodies present in most cases

• Two particular anti-nuclear antibodies
> SS-A
> SS-B


Alcoholic Sialadenosis

The gland's granules become filled; occurs in people who are alcoholics; can also get fatty infiltration of parotid glands


Sialodenosis Associated with Diabetes

Has to do with autonomic nervous system; as a result, accumulation of granules in parotid cells; visible on an axial CT scan


HIV-Associated Salivary Gland Disease

• Clinical Findings: bilateral parotid gland enlargements

• Laboratory Findings
- HIV seropositive
- RF, SS-A, SS-B not present (rheumatoid factor or Sjogren's anti nuclear antibodies

• Histopathologic findings
- Lymphocytic infiltrate (Sjögren’s like)
- Cystic spaces within the parotid gland

• Radiographic findings: multiple radiolucencies (cysts in gland); Formation of cysts in the parotid gland; usually bilateral


Mumps (Paramyxovirus) Viral Infection

Infection effects the parotid glands and they swell; look for systemic signs - fever, fatigue, pain, etc.

No treatment; usually runs its course and people will just use pain relievers/cold/warm packs to the face



Autoimmune condition where you are forming granulomas in the parotid glands; swelling


Salivary Gland Tumors

• Location: major and minor salivary glands

• The most common site for salivary gland tumors is the parotid gland

• Most common intra-oral location: junction of the hard and soft palate

• Minor glands
- Palate > Labial mucosa > Buccal mucosa
- Upper lip > lower lip

• May form anywhere in the oral cavity where there are salivary glands

• Clinically most are painless and slow-growing***

• Require incisional biopsy, diagnosis and complete
surgical removal

• The larger the gland, the more likely there will be a tumor, and the more likely it will be benign

• The smaller the gland, the less likely it will be to get a tumor, but the more likely that they will be malignant


Benign Salivary Gland Tumors

• Pleomorphic Adenoma (Benign Mixed Tumor): the
most common salivary gland tumor, often on palate or parotid

• Monomorphic Adenoma: upper lip is common location, then buccal mucosa

• Warthin Tumor: only in parotid gland, more common in older men, only salivary gland tumor that MAY be bilateral


Pleomorphic Adenoma diagnosis

• Distinguish from early stage Necrotizing Sialometaplasia because it will be firm and not hurt, while NSM will hurt and not be firm

• These are SLOW growing and painless so they can get REALLY big if left untreated for long periods of time

• Any time you have something like this, one of the first things to do after you palpate it and suspect a tumor is to take an incisional biopsy


Malignant Salivary Gland Tumors

• Mucoepidermoid Carcinoma: most common SG malignancy, can occur in children or in jawbones (variable colors)

• Adenoid Cystic Carcinoma (cylindroma): bad long-term
prognosis due to perineural infiltration

• Carcinoma developing from Pleomorphic Adenoma: rare, develops from long-standing PA

• Others such as acinic cell carcinoma, polymorphous low grade adenocarcinoma (recognize these names but don’t need to know anything about them)


Adenoid Cystic Carcinoma

Swelling extends to hard palate and
Into buccal vestibule

(painful because they are around nerves)


Carcinoma ex Pleomorphic Adenoma

One side of the palate; ulcerated because it is growing
So fast that the skin can't compensate


Mucoepidermoid Carcinoma

Looks like a benign tumor so you can't give a definite diagnosis until you biopsy


Measurement of Salivary Flow

Should see some pooling of saliva in the floor of the
mouth in patients with normal salivary flow

• Unstimulated (at rest): drool into collection container for 5 minutes
> Hyposalivation, severe: <0.1 ml/min
> Hyposalivation, moderate: <0.2 ml/min
> Normal: 0.3-0.4 ml/min

• Stimulated: spit into collection container while chewing gum or paraffin for 5 minutes
> Low: < 0.7 ml/min
> Normal: 1.0 ml/min


Most Common Causes of Dry Mouth

• Medication side effects, polypharmacy
• Systemic diseases
• Head and neck cancer radiation treatment


Medications that are linked to dry mouth

• Anticholinergics: bronchodilators
• Antihistamines: used for allergies
• Antidepressants, antipsychotics
• Sedative and hypnotic agents: used for anxiety and sleep
• Antihypertensives: used for high blood pressure
• Antiparkinson drugs


Systemic Disease Associated with Dry Mouth

• Autoimmune diseases
• Cystic fibrosis
• Diabetes
• Dehydration


Head and Neck Radiotherapy


• Salivary glands sensitive to radiation
• Parotid gland is most radiosensitive
• Dysfunction is dose- and field-dependent
• Threshold of permanent destruction: 24-26 Gy


Orofacial Pain & Dysfunction

• Functional and pathologic disorders of sensory, motor, and structural systems pertaining to intraoral structures, the upper and lower face, and anatomically and physiologically related structures in the head and neck


Pain Management Treatment Model

1) First obtain chief complaint
2) History
3) TMJ exam
4) Myofascial pain (MFP) exam
5) Cranial nerve exam
6) Imaging
7) Diff. diagnosis
8) Treatment plan
9) Referral (if necessary)


Temporomandibular Disorders (TMD)

• Do we need to treat “clicks and pops”? NO
• TMJ arthralgia (a pain of joint origin.such as capsulitis and synovovitis)
• Internal derangement
• Disc displacement
• Multiple surgical/implant cases
• Age and sex distribution: more common in females ages ~20-40
• Open lock is when the condyle gets stuck in front of the articular eminence
• Closed lock is when the disc gets stuck in front of the condyle
• Clicking on its own, is not an indication of treatment.

• Internal Derangements of the TMJ: dysfunction based on localized anatomic faults:
> includes: clicking, locking, limited opening.

DC classified ID of the TMJ as: DD w R, wR and intermittent locking, DD w/o R w lim opening,

TMDs are the 2nd most common musculo-skeletal condition (after low back pain) resulting in pain and disability


Simple Classification of TMJ Disorders

• Muscle Disorders
• Joint Clicking
• Joint Locking
• Arthritides


Common TMDs

• Arthralgia
• Myalgia
• Myofascial Pain
• Disc Displacement Disorders
• Degenerative Joint Disease
• Subluxation
• Headache attributable to TMD


Stomatognathic Exam

Measure protrusive moment, sounds, range of motion with ruler


Classification of Joint Mechanics Problems

• Disc-Condyle Inco-ordination
- Anterior Disc Displacement with Reduction – Clicking
- Anterior Disc Displacement w/o Reduction – Close Lock (patients will still be able to open mouth, but with smaller range of opening)

• Open Dislocation
• Open Lock/ subluxation
• Posterior Disc Displacement
• Ankylosis
• Anchored disc phenomenon


Open Dislocation:

condyle is displaced anteriorly beyond the articular eminence, and the pt is unable to self reduce the condyle



the condyle is also anteriorly displaced but can be self reduced by the pt


Anchored disc phenomenon:

similar to closed lock but is severe, persistent and occurs suddenly opening of 10-30mm due to disc clinging to the articular eminence


“Normal” Joint Mechanics

• Posterior band of disc at 12 o’clock position
• Disc rotates posteriorly as condyle rotates
• As condyle passes over eminence, disc is at its most posterior position relative to condyle


Temporomandibular Joint Mechanics

Note that during the opening movement of the jaw, the disc rotates over the condyle from the starting
position at 12 o’clock to the back of the condyle, returning to the starting position in the closing
movement. The normal range of opening is between 40 mm and 60 mm.


Internal Derangement Clicking

• In anterior disc displacement with reduction or clicking, in the closed mouth position, the disc is in front
• There will be a pop/click when the disc pops back into position (3rd image) – then a 2nd pop (5th image)
• This is not treated unless it is really bad and bothering the patient – can use hyaluronic acid


Non-Painful Clicking (TMD)

• Does not require treatment if it is not painful
- (30% of the population have joint noises)
• May require treatment if “jamming” is occurring with increasing frequency


Intermittent Locking and/or Painful Clicking

• May require intervention with anterior advancement splint until joint inflammation subsides and joint adapts to the mechanical dysfunction


Are Clicking Noises Always Due to Disc Displacement?

• Altered shape of the condyle and/or the fibrocartilage lining of the joint
may cause deviation of form and bumps or flat spots on the condyle
• Tears or injury to the disk may create a noise without any displacement
• Noises can be due to stick-slip phenomena where there is inadequate
lubrication of the articular surfaces


Tests for Internal Derangements (ID)

Only need an MRI if you
don’t know where the disc
is – for example if they have
closed lock as well (anterior
disc displacement
WITHOUT reduction)

• Auscultation/Palpation
• Observation of opening deviations or deflections
• MRI not needed in most cases of ID
o Most clicks don’t progress into locking and MRI’s would not
substantially alter the treatment approach used at present
• For simple non-painful non-locking clicking, auscultation and charting is
the preferred method of diagnosis
• Note, that the prevalence of clicking stays relatively steady across
adulthood, which suggests a low level of progression to more serious



• Panoramic Radiograph (first thing to order)
• TMJ Tomograms (not done as much)
• MRI (when you want to see the joint or suspect a tumor)
• 3D TMJ Imaging (to see more bone detail)


Progression from Clicking to Locking

• Most patients with clicking do not progress into locking
• Studies estimate that only 5% to at most 10% of those with clicking are at
real risk for progression to more serious dysfunction of locking


Painful Internal Derangement with Episodic Locking (without reduction)

Episodic locking or “catching” may occur with anterior disc displacement. At the time of the lock, there is
a limited opening from 18 to 28 mm with or without pain. The intermittent locking can usually be
manipulated by the patient in order to achieve a normal range of opening. This condition does not
necessarily imply that the disc will become persistently locked and is not usually treated, although
treatment may be done if the intermittent locking events are accompanied by pain or are becoming
more numerous or protracted. The patient’s jaw is repositioned anteriorly by an orthosis to the point
where the reciprocal closing click is eliminated. Once this position is achieved, the jaw will not lock.
One theory suggests that the disc is deforming with the repeating locking and anteriorly repositioning
the jaw helps to reestablish a normal form for the disc and discourage the locking events.


Treating the Painful Episodic Locking Joint

• Home Care Protocol (don’t chew gum or chewy foods, etc.)
• Tomograms
• NSAID’s for inflammation (if they have really bad pain)
• Repositioning Splint Therapy (occlusal night guards)
• If the locking and clicking events are painful, treatment of the condition
may be done by fabricating an anterior repositioning appliance that
moves the condyle forward closer but not necessarily into the middle of
the disc – this helps reduce the irritation of the locking and clicking, lessening the pain
Don’t want to do repositioning (like splints) for more than 6 weeks because you don’t want to change their bite


Clinical Features of Anterior Disc Displacement
Without Reduction

• (1) Movement restriction – began suddenly
• (2) No remission
• (3) Passive opening ~ 28 mm (depending on the individual)
• (4) No noises now (because disc is in front and not going back)
• (5) Deflection (jaw deviates to one side when patient tries to open)
• (6) Stretch localize to TMJ
• (7) MRI shows immobile or displaced disc
• The appropriate historical evidence for a disk condyle restriction is 1)
patient reported TM joint movement restriction, which began suddenly
and has continued since that time without remission and 2) the affected
joint will have a history of joint noises, which stopped at the time of the
movement restriction. The appropriate clinical evidence for this disorder
is maximum passive stretch mouth opening (interincisal distance including
overbite) of less than 28 mm. (This amount of motion includes the
overbite as well). This opening is also usually accompanied by a deflection
to the side that is locked. The patient will usually have only a small
limitation of lateral motion if any loss is evident. Finally, if MRI's are taken,
the disk should show as being displaced, although there will be a few
cases where the disk is not displaced, but just stuck in place and not


Mechanism of ADD-NR

• (1) Adhesion of disc
• (2) Folding of disc
• (3) Rule out trismus

• The nature of the joint dysfunction can be verified by Magnetic Resonance Imaging of the TMJ (without contrast bilateral TMJ MRI)
• Routine radiographs of the TMJ are usually not diagnostic of any substantial changes in disk position or disk morphology since this structure cannot be seen on an X-ray
• Alternative terms are disk displacement with no reduction (DDNR) and closed locking


Treating the Anterior Displacement Without Reduction (Closed Lock)

• Manipulation
• Physical Therapy
• Arthrocentesis (pumping fluid in and out of the joint)
• Arthroscopic Surgery (to reposition the disc surgically)
• Treatment for the ADD-NR (Closed lock) jaw utilizes intracapsular injections of 2% lidocaine, saline solution and kenalog 40mg/mL (first block auriculotemporal nerve before blocking the TMJ)



Open lock: pull condyles
down and back to pop back
into place

• TMJ “locking” cases
o Intermittent locking
o Open lock (acute vs. chronic)
o Closed lock (acute vs. chronic)
• Non-invasive TMD treatments
o Home care
o Pharmacological
o Occlusal splint therapy
§ Stabilization, Repositioning

• Invasive TMD treatments
o TMJ injections
o “Pumping” procedures
o Arthrocentesis
o Arthroscopy


Myalgia/Myofascial Pain

Referral: the problem is in one location and the pain is
in another location

• Myalgia
o Muscle pain
o Without referral

• Myofascial Pain
o Muscle pain
o With referral
o Trigger points
o Headache

• Myofascial Pain Exam – palpate all head and neck muscles – palpate with 2-4 lbs of pressure for 10-15 seconds because you want to replicate the pain that is their chief complaint

• Treatment
o Home Care
o Myofascial Pain Protocol (heat, jaw stretching, jaw massages)
o Splint Therapy (only really if they are a grinder)
o Medications
- Cyclobenzaprine, Skelaxin (muscle relaxers)
- Amitriptyline, Nortriptyline (muscle relaxers and to prevent tension headaches)
- Trigger point injections (break apart knot with needle)



Neuropathic pain is the most common reason for
unnecessary dental treatment

• Neuralgia – brainstem related
o Trigeminal Neuralgia
o Post-herpetic neuralgia
o Glossopharyngeal neuralgia
o Occipital neuralgia

• Neuropathic pain – can develop secondary to nerve injury
o Peripheral (C-fiber sensitization)
o Central

• Cranial Nerve Exam – important when you suspect a nerve disorder


Trigeminal Neuralgia

• Sub-classified into idiopathic and symptomatic
• Idiopathic trigeminal neuralgia: due to an interaction between trigeminal
nerve and vasculature
• Symptomatic trigeminal neuralgia: caused by demonstrable structural
• Description
o A painful unilateral affliction of the face, characterized by brief
electric shock-like (lancinating) pains limited to one or more
divisions of the trigeminal nerve
o Pain evoked by washing, shaving, smoking, talking, brushing, air
blowing, or spontaneously occurring
o Pain is abrupt in onset and may remit for varying periods


Microvascular Decompression

Artery causes loss of myelin which causes pain – they
place a piece of Teflon between the nerve and
artery to stop the pain


Hyperalgesia and Allodynia

• Hyperalgesia and allodynia are hallmarks of neuropathic pain

• Allodynia: painful response to non-painful stimulus
• Hyperalgesia: increased pain response to painful stimulus



• Irritant ingredient in hot chili peppers

• Activates a distinct sub-population of primary sensory neurons with soma
in dorsal root or trigeminal ganglion
• Unmyleinated c-fibers

• 3 characteristic effects of capsaicin:
o (1) Excitation
o (2) Desensitization
o (3) Neurotoxicity


Peripheral vs. Centralized Pain

• How do you determine if something is peripheral or centralized?
Diagnostic blocking
• If patient has phantom tooth pain: put topical anesthetic over the gingiva
and wait 5 minutes
o If pain is 100% gone, diagnosis is peripheral trigeminal neuropathic
o If pain hasn’t gone away, then do an infiltration of the area
§ Now if the pain is 100% gone, diagnosis is still peripheral
trigeminal neuropathic pain
§ Now if pain is still not getting better, then we start thinking that it is maybe centralized pain (now you need anti-epileptics and TCA drugs to treat the pain)



• IHS classification
• Diagnosis required
• Treatment needed for success
• Proper training
• Headaches are the number 1 underdiagnosed and undertreated
neurological disorder


Herpes Simplex Virus Infection (HSV)

• 2 types
> HSV I: Oral infections
> HSV II: Genital infections but can also cause oral infections

• Oral HSV infection has 2 clinical manifestations:
> Primary herpetic gingivostomatitis
- Most patients are children, young adults (most
common age range is 5-10)
- Acute onset, fever, lymphadenopathy

> Secondary (recurrent) herpetic eruptions - HERPES LABIALIS
- Occurs in 20-40% of population
- Lesions localized to keratinized mucosa

• Usually clinical diagnosis – but in a biopsy or mucosal smear you see Tzank cells (large multinucleated cells found in ulcerated areas )


Primary herpetic gingivostomatitis

stomatitis = inflammation of the mouth

Primary outbreaks do not follow the rules but recurrent does meaning you can find it anywhere! not just on keratinized mucosa (buccal, labial mucosa etc. )

First, reassure patient that condition is self-limiting and will completely heal on its own – does not mean you will definitely have recurrent/secondary herpes
1 - Maintain fluid intake
2 - Antipyretics if fever present
3 - Viscous xylocaine/ OTC medication for pain
4 - Maintain oral hygiene/ rinses
5 - Advise patient about not spreading disease – no kissing, inoculating other areas of body
6 - Systemic valacyclovir generally for immuno-compromised patients; may be effectively used very early onset also; acyclovir suspension for kids


Treatment for Primary herpetic gingivostomatitis

Antipyretics for fever

Viscous xylocaine/ OTC pain management

Maintain oral hygiene

Prevent spread

Systemic Valacyclovir for immune compromised patients


Treatment of Herpes Labialis

Zovirax ointment 5% (acyclovir)

Disp: 15 gm. tube

Apply continuously during prodromal stage and then 6 times daily for three days

Abreva OTC (docosanol)

"VALTREX" is an antiviral but it is only for immunocompromised patients or, as shown by some studies, usage very early on for kids says it might work


Secondary Herpetic Eruptions

Herpes labialis is the most common and first presents as vesicles or blisters that will pop, ulcerate and crust;
blisters can also coalesce together

when on the gingiva/ intraorally, it usually presents as a very shallow "CROP" of herpetic ulcers with white borders

Can be reactivated at any time; usually triggered by something (stress, weather, dental work, etc.)

If they have a known trigger you can give valtrex as a preemptive measure


Treatment of Recurrent herpes infections (herpes labialis & intraoral secondary herpes)

• Valtrex 500 mg (valacyclovir)
> Disp: 8 tabs
> Sig: Take 4 tabs (2 g) as soon as prodromal signs appear and then 4 tabs 12 hours later

• Prophylaxis to prevent recurrent herpes:
> Valtrex 500 mg tabs (prescribe if expecting outbreak or be on it every day if they have very recurrent outbreaks)
- 1 tab twice a day
- Re-evaluate regularly
> Lysine 1000 mg/day – every day
- Etiology: alteration of lysine/arginine ratio that interferes with viral replication


Herpes Zoster (Shingles)

> Infectious disease caused by varicella-zoster virus

> Manifests as pain for 3-5 days over area supplied by cranial nerve ganglion (and follows a dermatomal sensory distribution)

> Virus lives in the sensory nerve ganglion and manifests on the face
– vesicles have active virus in them

> Vesicles usually distributed unilaterally

> Lesions will heal spontaneously in about 2 weeks


Recurrent Aphthous Stomatitis (RAS) aka canker sores

• Round or oval ulcer (no epithelium), fibrin/neutrophil coating, red halo around it, found on movable non keratinized mucosa

• Minor type (canker sores)
> Most common type, less than 1 cm
> Tend to occur more in the front of the mouth

• Major type (Sutton’s disease)
> Greater than 1 cm, heal with scarring
> Tend to occur more in the back of the mouth

• Herpetiform ulcerations
> Differs from herpes by lack of vesicle stage

• Treatment: Topical Steroids (only if absolutely necessary)

• 20% of population affected; more common in women and in families

• Can be indicative of an immune dysregulation


Recurrent Aphthous Stomatitis Treatment

Generally you don't treat these especially f it's just a couple however, if there is A LOT and/or the patient is super persistent, then prescribe topical steroid

• Minor aphthous ulcerations (treatment 1)
> Temovate ointment 0.05% (Clobetasol, Halobetasol)

• Minor aphthous ulcerations (treatment 2)
> Dexamethasone rinse 0.5 mg/5 ml
- Option 1 if localized: Soak 2 x 2 gauze and hold over
affected area as long as possible four times daily (QID)
- Option 2 if generalized: Rinse with 5 ml for at least 2 min and spit out four times daily

• Major aphthous ulceration if localized):
1 – Temovate ointment (Clobetasol)
2 – Dexamethasone rinse

• If long standing or diffuse disease:
1 – Prednisone 40 mg/day in AM for one week
2 – Re-evaluate and maintain on topical meds if
possible because it has LOTS OF NEGATIVE SIDE EFFECTS

• Herpetiform ulcerations
1 – Temovate ointment (clobetasol)
2 – Dexamethasone rinse

• Various other products for aphthous ulcer pain relief:
> Products which coat and/or numb ulcer: Orabase, Zilactin, Canker Cover
> Products which cauterize: Debacterol (this burns the ulcer and kills the nerve ending)



Systemic conditions associated with recurrent
aphthous stomatitis

• Behçet's syndrome
• Celiac disease/ gluten sensitivity
• Cyclic neutropenia
• IgA deficiency
• Immunocompromised conditions, including human immunodeficiency
virus (HIV) disease
• Inflammatory bowel disease: Crohn’s and ulcerative colitis
• Nutritional deficiencies (iron, folate, zinc, B-vitamins)


Types of Acute Candidiasis

1 – Pseudomembranous candidiasis (Thrush): wipeable white patches described to be "curd like;" when you wipe it, there may be nothing OR it might be red underneath; often accompanied with metallic taste or burning sensation

2 – Acute atrophic candidiasis (antibiotics): linked to antibiotic use (change to bacterial flora in your mouth which allows for fungal invasion)


Types of Chronic Candidiasis

1 – Chronic atrophic candidiasis (dentures): red, erythematous presentation where denture sits

2 – Hyperplastic candidiasis (leukoplakia) – need a biopsy because this resembles leukoplakia

3 – Angular cheilitis (corners of mouth)


Treatment for acute pseudomembranous candidiasis, acute atrophic candidiasis, and hyperplastic candidiasis

Anti-fungal medication:

• Mycelex troches 10 mg (clotrimazole) (they're like cough drops)
> max 70 troches - difficult to get patient compliance

• Newer treatment: Miconazole (Oravig)
> 50 mg discs (more expensive)


Treatment for Chronic atrophic candidiasis (dentures)

1 – Keep dentures out at night
2 – Soak in anti-fungal solution
3 – Nystatin ointment (100,000 units/gm)
> Apply to denture base and wear tid (3x daily)


Treatment for Angular cheilitis

1 - Mycolog Cream
> Dry and apply to corners of mouth qid (4x daily)

2 - Nystatin ointment


Treatment for Geographic Tongue (benign migratory glossitis)

• Generally no treatment/biopsy indicated
• Reassure patient condition is benign
• If tenderness or burning sensation, topical steroids may be used (Dexamethasone rinse)
• Recently suggested that zinc supplement may be effective


Desquamative Gingivitis

• Red, peeling, sloughing off gingiva(friable gingiva); usually misdiagnosed as severe gingivitis and do all thing treatment for that (cleaning, perio, etc.) with no success

Categorized by these four diseases:
1 - Erosive lichen planus (most common)
2 - Benign mucous membrane pemphigoid (second most common)
3 - Pemphigus vulgaris (second least common)
4 - Erythema multiforme (least common)

• If untreated these can go to affect other mucosa and the skin


Treatment for Erosive lichen planus

Patients will complain of ulcers

• Dexamethasone elixir 0.5 mg/5 ml
> rinse and spit out OR Soak 2 x 2 gauze and hold over affected area as long as possible q.i.d.

• Increase chance of fungal infection when giving them topical steroids

• Key features in biopsy: band of T-lymphocytes on top of the connective tissue, destruction of the basal cell layer that can cause separation of the epithelium


Lichenoid Mucositis

• Clinically indistinguishable from lichen planus
• Can be ulcerated and symptomatic
• Usually caused by systemic medications
• Topical causes can be from cinnamon-containing products or contact sensitivity to dental amalgam

Secondary to the intake of:
2 – COX-2 inhibitors
3 – Anti-hypertensive medications*****
4 – Anti-hyperglycemic medications****
5 – Cholesterol lowering agents*****
6 – Anti-gout medications
7 – Cardiac medications
8 - AMALGAM (isolated to areas with amalgam restoration)


Treatment: Lichenoid Drug Reactions

Dexamethasone elixir 0.5 mg/5ml

Rinse with 5 ml and spit out qid

For amalgam, remove and replace with composite


Histopathologic Difference between Lichen Planus and Lichenoid Mucositis

Lichen Planus = band of T-lymphocytes on top of the connective tissue and destruction of the basal cell layer that can cause separation of the epithelium

Lichenoid Mucositis: there is not a band of lymphocytes but is characterized by mixed chronic inflammatory cells (plasma and lymphocytes) seen around blood vessels as well and in clusters throughout


Benign Mucous Membrane Pemphigoid (Cicatrical

"Cicatrical" = scar making

• Autoimmune disease characterized by full-thickness, sub-epithelial cleavage

• Most commonly affects oral mucosa and conjunctiva, possible positive Nikolsky sign
> (+) Nikolsky sign: if you touch the tissue is sloughs off
• Twice as common in females, peak age of incidence is 40-50 years old

• Symblepharon: scar tissue connecting the eyelid
mucosa to the eye conjunctiva and part of Pemphigoid

• Pathogenesis thought to be due to deposition of Ig in basement membrane zone, leading to complement activation

• Diagnosed via Immunofluorescence in which a linear deposition of IgG and C3 in the basement
membrane zone presents as a glowing band visible between epithelium and CT

• Need a biopsy to diagnose and REMEMBER you need to do A PERILESIONAL BIOPSY (around the lesion)


Treatment for Benign Mucous Membrane Pemphigoid

• Topical steroids such as Clobetasol and Dexamethasone

• Severe cases may require initial systemic steroid course, then topical steroids

• Other medication used by specialists is DAPONE (anti-
inflammatory antibiotic)

• Regular eye exams by ophthalmologist

• Referral to dermatologist if skin lesions present


Pemphigus Vulgaris

• A life-threatening skin and mucous membrane disease which is autoimmune in nature on skin and oral mucosa

• Patients usually 50 years of age or older

• 50-60% of cases present with oral lesions before skin lesions – must diagnose and treat oral lesions because if left untreated, skin lesions WILL form

• Pathogenesis: Patients with PV produce IgG autoantibodies to desmoglein 3 (oral) and/or desmoglein 1 (skin), a transmembrane glycoprotein that mediates cell adhesion
> Body making antibodies against protein in desmosomes

• Positive Nikolsky sign


Treatment for Pemphigus Vulgaris

• Biopsy: cells falling apart (also called Tzank cells) – still have basal cells attached because they don’t have the same desmoglein proteins

• Immunofluorescence: intercellular deposition of IgG (chicken-wire effect)

1 – Combination of high dose steroid therapy and
immunosuppressive drugs
2 – IVIg (blockade of Fas ligand, which induces epithelial cell
3 – Immunotherapy such as Rituximab is promising
4 – Regular monitoring of Desmoglein 1 and 3 antibody titers and CBC/labs



Erythema Multiforme

• Type of acute, self-limiting, possibly recurring type 4 hypersensitivity reaction

• No key histopathologic features; it is a clinical diagnosis

• Minor vs. major types
> based on the number of sites involved

• MINOR: usually secondary to HSV infection

• MAJOR: (Stevens-Johnson Syndrome) – usually secondary to a severe drug reaction, often antibiotics and sulfa drugs


Erythema Multiforme Minor Description and Treatment

• Slightly more common in females
• Usually seen in young adults
• Relatively rapid onset
• Involvement of lips usually severe and appears as hemorrhagic crusted lesions ("Bloody Crusty Lip")
• Palmar or plantar surfaces may show “target” lesions (this is diagnostic, but only seen in 25% of cases)

• Prednisone 10 mg tabs; take 4 tabs in AM for 7 days

• IF chronic and recurrent:
1 – Lysine 1000 mg/day – every day
2 – Valtrex 500mg tabs – 1 tab twice a day


Erythema Multiforme Major Description and Treatment
(Stevens-Johnson Syndrome)

• Severe form of EM where patients demonstrate extensive hemorrhagic skin lesions with severe ocular involvement after drug exposure

• Oral and genital lesions also common

• Possible etiology: foreign antigens derived from offending drug localize at mucocutaneous sites leading to cell-mediated immune reaction

• Discontinue offending drug immediately

Treatment controversial:
• No definitive accepted treatment
• Some use systemic steroid therapy
•Others just supportive therapy: IV rehydration, topical
anesthetic and pain meds


Cancer Facts and Figures 2018

Estimated 51,540 new oral cavity and pharynx cancer cases will be diagnosed and >10,000 will die in the US in 2018


What percent does Oral/Pharyngeal cancer make up out of all cancers?



Are women or men more likely to get oral cancer?


3:1 MALE:FEMALE ratio



What is the median age at diagnosis for oral cancer?

63 years old

(not really seen under age 44 but about 7% are 44 and under)


Which type of oral cancer encompasses 90% of diagnoses?

Squamous Cell Carcinoma (SCC)


What cancer staging system is used for oral cancer?

T.N.M Staging

T = tumor
N = nodes
M = distant metastases

T1/T2 have no node involvement and no metastases meaning STAGE 1/2 are LOCALIZED cancers!! (but only 30% are in this stage at the time of their diagnosis)


SEER 5 year relative survival rate for localized cancers?



What is the overall 5 year relative survival rate for oral cancer?



In terms of detection/diagnosis what is the challenge with oral cancer?

It is detection or evaluation of “early stage” disease. (Secondary Prevention)


What does OPMD stand for and what is it?

ORAL POTENTIALLY MALIGNANT DISORDERS: Clinical diagnoses based on how the patient presents


What does OPMD stand for and what is it?


Any epithelial lesion for which a clinician can determine no clear cause should raise suspicion and must be evaluated to rule out malignancy or the potential for malignancy.


Oral Potentially Malignant Disorders Clinical Lesions Diagnostic Spectrum

Leukoplakia (1-5% prevalence) = non wipeable white patch you can't explain or give another diagnosis to that REQUIRES a biopsy to determine if its precancerous/cancer
- Homogeneous ( sharply demarcated, shallow fissuring, uniformly white)
- Non-homogeneous
○ Speckled leukoplakia (white patch with different textures/areas of severity)
○ Leukoerythroplakia (white with red areas)
○ Erythroleukoplakia (red with white areas)
○ Speckled erythroplakia (red and white with different textures/degrees of severity)
- Erythroplakia (<0.5% prevalence - just red and no white and usually are cancer)
○ +/- Ulceration, +/- Exophytic


Possible Precancerous Diagnoses

- Actinic cheilitis: outside a lot and vermillion border is shallow and not demarcated

- Oral Submucous fibrosis: rxn from Areca nut use aka betel nut

- Proliferative Verrucous Leukoplakia: a disease in women in their 60s and 70s that develop multiple focal leukoplakias; 70% of the time they will become malignant; show other risk factors and do not know why this happens


Histopathologic Diagnoses

1. Epithelial hyperkeratosis/hyperplasia - benign but means that they have a thickening of the epithelium which may be harboring early malignant changes; if unexplained, could still be precancerous

2. Mild dysplasia - when there are abnormal changes confined to the bottom basal level

3. Verrucous hyperplasia

4. Moderate dysplasia (2/3 of epithelial abnormal changes)

5. Severe dysplasia (more than 2/3 of epithelial abnormal changes)

6. Carcinoma - in - situ (full thickness of epithelium)

Carcinoma (squamous cell/verrucous infiltrating into CT)


Transformation to Malignancy

Progression to malignancy is not linear, not inevitable, and not predictable

Overall <5% transform to cancer


Factors Predicting Malignant Transformation

1. Increasing age
2. Lesion persistence
3. Site: Lateral tongue/floor of mouth
4. Large size/multiple sites
5. Clinical features (non-homo or red/white)
6. Unequivocal toluidine blue staining
7. High grade dysplasia
8. Loss of heterozygosity
9. Abnormal DNA content (ploidy)
10. Other emerging markers


Clinical Guidelines for Early Detection

STEP 1: Symptom and Risk Assessment

STEP 2: Extra-oral Examination

STEP 3: Intra-oral Examination +/- screening adjuncts

Then biopsy and/or refer to Oral Medicine specialist if abnormal findings are detected


What is the difference between a precancer and a cancer?

A cancer is defined as those cells that develop in the skin lining (mucosal lining) and invade through the basal lining into the underlining connective tissue

A precancer are abnormal cells that are only in the epithelium (epithelial dysplasia) and do not always become a cancer or appear before a cancer does