STC Flashcards
Irritation Fibromas
Composed of
Etiology
Clinical features ;Color
Location
Treatment
- AKA – Fibroma, Traumatic Fibroma
- Composed of dense, scar-like, fibrous connective tissue
- Occurs as a result of chronic trauma
- Clinical Features: Exophytic lesion
- Usually less than a centimeter in diameter
- Color: lighter pink than surrounding mucosa,the surface can be white sometimes bc it’s rubbing and bumping into other oral structures (like teeth), so they get surface keratinization
- Locations: buccal mucosa, tongue, lips, gingiva
- Very common; totally benign soft lesion
- Treatment: You don’t have to remove them, but the surgical Tx = to excise them bc pts will stop biting them and they’ll heal and stop the irritation
What is this clinical finding?

Irritation Fibromas
What is this clinical finding?

Irritation Fibromas
What is this clinical finding?

Chronic Hyperplastic Pulpitis (pulp polyp)

Giant Cell Fibroma
Chronic Hyperplastic Pulpitis
What is it?
Location?
Age?
Clinical Appearance?
Treatment?
• AKA: pulp polyp
• An e_xcessive proliferation of chronically inflamed dental pulp tissue_ – granulation tissue/ fibrous tissue with inflammatory cells (like a little fibroma that
occurs from pulp tissue) ( benign soft tissue leasion)
• Location:
• Teeth with large, open carious lesions
• Primary or permanent molars
• Age: Children & young adults
• Clinical Appearance: A red or pink nodule of soft tissue protruding from the
pulp chamber and fills the entire cavity of the tooth
• Treatment: RCT or extraction of tooth
Giant Cell Fibroma
- Very small form of fibrous tumour that show giant cells
- Age: relatively rare in paediatric patients.
- Clinically it is presented as a painless, sessile, or pedunculated growth which is usually confused with other fibrous lesions like irritation fibromas or Retrocuspid papilla
- Location: Largely occur on lower gingivae and on palate\
What are these clinical findings (what is the name of the syndrome or complex?)

Tuberous sclerosis complex
we see A lot of gingival enlargement – is this overgrowth from disease or from seizure medication? Multi organ system involvement
What is this clinical finding?

Epulis Fissuratum
Cowden Syndrome
- (multiple hamartoma and neoplasia syndrome)
- • Autosomal dominant disorder affecting multiple organ systems
- • Caused by mutations in the phosphatase and tensin homolog gene (PTEN, a tumor suppressor gene)
- • Oral and perioral findings include
- *multiple papules on the lips and gingivae,**
- papillomatosis (benign fibromatosis) of the buccal, palatal, faucial, and oropharyngeal
- mucosae often producing a “cobblestone” effect, and the tongue may also present as pebbly or fissured.
- • Multiple papillomatous nodules (histologically inverted follicular keratoses or
- trichilemmomas) are often present on the perioral, periorbital, and perinasal skin, the pinnae of the ears, and neck.
- • These nodules are often accompanied by lipomas, hemangiomas, neuromas, vitiligo, café au lait spots, and acromelanosis .
- • A variety of neoplastic changes occur in the organs exhibiting hamartomatous lesions,with an increased rate of breast and thyroid carcinoma and gastrointestinal malignancy.
- Squamous cell carcinoma of the tongue and basal cell tumors of the perioral skin have also been reported.
- Incredibly rare ( board loves it)
What is this clinical finding?

Inflammatory Papillary Hyperplasia of the Palate
What is these clinical findings? (what is the name of the syndrome or complex?)
Cowden Syndrome
Very rare!
Tuberous sclerosis complex
• is an inherited disorder caused by mutations in the tuberous sclerosis complex (TSC1 or TSC2) genes
• Characterized by seizures and mental retardation associated with hamartomatous glial proliferations and neuronal deformity in the central nervous system.
• Fine wart-like lesions (adenoma sebaceum) occur in a butterfly distribution over the cheeks and forehead, and histologically similar lesions (vascular fibromas) have been described intraorally.
• Characteristic hypoplastic enamel defects (pitted enamel hypoplasia)
occur in 40 to 100% of those affected.
• Rhabdomyoma of the heart and other hamartomas of the kidney,
Epulis Fissuratum
AKA
Cause
Location
Clinical presentation
Composed of
Treatment
• AKA: denture-induced fibrous hyperplasia, fibrous inflammatory hyperplasia
• Cause: ill-fitting denture
• Location: vestibule (maxilla or mandible), along the
denture border
•Clinical presentation: Arranged in elongated folds of tissue into which the
denture flange fits; • Surface ulceration within the folds is common
• Composed of dense fibrous connective tissue
• Treatment: surgical excision (scalpel vs CO2 laser -laser is better)
and reline then remake of denture
What is the clinical finding?

Pyogenic Granuloma
We can see the corresponding radiograph;
-although the radiograph suggests generalized bone loss, there is a lot of calculus on
the distal of #16 > it makes sense that this is a pyogenic granuloma

What is this clinical finding?

Pyogenic Granuloma:
Pyogenic Granuloma
Histology
They are filled with blood vessels so they’re very very rich
in vascularization > they tend to bleed easily

What is this clinical finding?

A parulis
It is not a pyogenic granuloma
A parulis is a proliferation of granulation tissue at the opening of a sinus tract
When the infection breaks through the alveolar bone and presents itself,
it will sometimes cause this proliferation of granulation tissue
Inflammatory Papillary Hyperplasia of the Palate
Majority occur with what disease?
Associated with what?
Clinical appearance
Treatment
- Majority occur with denture stomatitis
- Associated with a removable full or partial denture or orthodontic
- appliance (Something you see in patients who wear denture all the time, don’t take it out, chronic denture wear)
-
Clinical Appearance: Palatal vault is covered by multiple erythematous papillary projections (fibrous connective tissue surfaced by epithelium) –(papillary but no papilla, instead it’s bumpy and bosselated)
- Granular or cobblestone appearance
- Erythema is usually due to superinfection with candida
- Treatment:Treat underlying candidiasis, fix denture. These bumps can be removed, take electrosurgery loop, and scrape off the bumps – heals well
What is this clinical finding?

Peripheral Ossifying or Cementifying Fibroma
Lesion in the image is pedunculated – put a periodontal probe on normal gingiva and glide along underneath it, there’s a stalk
Peripheral Ossifying Fibroma
Histology
- When sessile, when removing it, take scalpel blade and just cut into it
- If has a little bone or cementum formation inside it, you can feel the bone with the scalpel

What is this clinical finding?

Peripheral Giant Cell Granuloma
Peripheral Giant Cell Granuloma
Histology
Giant cells inside the lesion

What are the 3P
or 4P?
• Pyogenic granuloma/pregnancy tumor
• Peripheral ossifying**_or_**cementifying fibroma
• Peripheral giant cell granuloma
• Peripheral fibroma (4P)
Memorize these well!
All benign soft tissue lesions
Pyogenic Granuloma
What a differential diagonsis to consider if we see it
- if it’s on the gingival tissues, take a radiograph
- always consider SCC as a differential diagnosis
What is this clinical finding?

Inflammatory Gingival Enlargement
Example of someone with true hyperplastic gingivitis
Maybe related to very poor plaque control
In this case, either porcelain or porcelain fused to metal full coverage restorations that have very
bulky margins, and that may play a role for food to pick up
Pyogenic Granuloma
What is it?
Etiology
Assossiated with which demographics?
Location?
Treatment?
- What is it? Reactive connective tissue hyperplasia - exuberant granulation tissue; Misnomer – not pyogenic and not a true granuloma
- Etiology: Response to injury - calculus or overhang restoration
- Assosiated with? Often occurs in pregnant women (“pregnancy tumor”), also associated with puberty
- Treatment: Excision and removal of irritant (eg calculus, overhanging restorations)
What is the Differential diagnosis of gingival enlargement
Acute Myelogenous Leukemia (AML)
Wegener’s Granulomatosis
Kaposi Sarcoma
Plasma Cell Gingivitis
Generalized gingival enlargement – all different cases and diseases

How to differentiate Pyogenic Granuloma from the other 2Ps ?
(Peripheral ossifying or cementifying fibroma & Peripheral giant cell granuloma)
- They often occur in the gingival, but can occur in multiple areas
- that’s the one thing that distinguishes this from the other 2 P’s: pyogenic granuloma can occur on ANY oral site, most commonly on the gingival tissues
What is this clinical finding?

Hereditary Gingivofibromatosis

Infantile
Hemangioma
(“strawberry” hemangioma).
Infant with two red, nodular masses on
the posterior scalp and neck
Neville Cr
Pyogenic Granuloma
Clinical appearance
Location
Size
Developing rate
Age:
- Clinical appearance
- Usually ulcerated
- Soft exophytic lesion, either sessile or pedunculated
- Deep red to purple in color, bleeds easily
-
Location:
- Most common – gingiva
- Also occurs in other areas of the oral mucosa ( can happen anywhere)
- Size: small to large (millimeters to centimeters)
- Develop rapidly and then remain static
- Age: Any age
How to recogonize a capillary Malformation?
When you apply pressure to it, it evacuates the lesion (disappears!), when you pull away, it refills and you see it again – that tells you it’s a vascular lesion

What is this clinical finding?

Capillary
Malformation (Low
flow)
How to differentiate between
Venous
malformation (low
flow)
from
Arteriovenous or
arteriolar malformations
(High flow)
Venous malformation
(Low flow)
No bruit, non-pulsatile
vs
Arteriovenous or
arteriolar malformations
(High flow)
Bruit and pulsatile
In other word, Venous lesion = Does not have pulse
Histopathologically they look different too
Treatment:
-Don’t biopsy this unless it’s rapidly growing, if it is rapidly growing then suspect ► angiosarcoma? ( unlikely)
-can be surgically treated by oral surgeons -clamping off the blood vessel and dissecting it out, or putting a sclerosis agent

What is this clinical finding?

Venous
malformation (low
flow)
Many pts can live with this without treatment
What are these clinical findings ( which syndrome or complex is this)?

Osler-Weber-Rendu
Syndrome
What are these clinical findings? (What is the syndrome or complex)?

Sturge-Weber
Angiomatosis
Sturge-Weber syndrome
What are these clinical findings (What is the syndrome or complex)?

Sturge-Weber
Angiomatosis
Sturge-Weber syndrome
Notice how the vascular malformation is only one side..
Remember: Vascular changes follow trigeminal nerve, so it doesn’t cross midline
What is this clinical finding?

Lymphangioma
What is this clinical finding?

Cystic Hygroma
a type of Lymphangioma
Peripheral Ossifying or Cementifying Fibroma
What is it?
Clinical appearance
Derived from
Age
Sex
Reccurance rate
Treatment
- a reactive benign soft tissue lesion
- Clinical appearance: Well-demarcated, sessile or pedunculated lesion that appears to originate from the gingival interdental papilla
- Derived from: cells of the periodontal ligament
- Age: children and young adults
- Sex: females more than males
- Recurrence rate – about 16%
- Treatment: Surgical excision
What is this clinical finding?

Neuroma
(Traumatic Neuroma)
Not a benign true neoplasm, it’s reactive lesion
This is an edentulous patient, so resorbed bone, so flange of denture is impinging in the area of mental foramen – develop from repeated trauma
Sometimes have to cut into nerve, peel the neuroma from nerve, careful not to sever nerve

What are these clinical findings (Which syndrome or complex)?

Multiple Endocrine
Neoplasia (MEN)
Syndrome
What is this clinical finding?

neurofibroma
-it looks like lymphoepithelial cyst, but this is further anterior and not where you would get
lymphoid tissue – so it’s not lymphoepithelial cyst, it’s neurofibroma
Yellow – nerves typically yellow
What is this clinical finding?

neurofibroma
Peripheral Giant Cell Granuloma
What is it?
Location?
Age?
Clinical appearance:
Radiographic finding?
- What is it? Probably a reactive lesion due to local irritating factors (giant cells develop inside the lesion which is a benign soft tissue lesion)
- Location: Gingiva, usually anterior to the molars
- Age: Most frequently seen between 40-60 years old
- Clinical appearance: dusky purple, sessile or pedunculated, smooth-surfaced, dome-shaped papule or nodule. Most lesions are less than 1.5 cm in diameter, though infrequently, may grow as large as 5 cm in greatest dimension
- Radiographic Features: Usually none, but superficial destruction of the alveolar bone may occur
What are these clinical findings (which syndrome or complex)?

Neurofibromatosis syndrome
von Recklinghausen’s Disease
- Lisch nodules on iris, pigmented (eye picture)
- Neurofibromatosis in mouth (bottom left picture)
- Café au lait (bottom right picture)

What is the clinical finding?

Schwannoma/ Neurilemoma
What is this clinical finding?

Schwannoma/ Neurilemoma
Schwannoma/ Neurilemoma
Histology
Antoni A and Antoni B.
Streaming fascicles of spindle-shaped Schwann cells characterize Antoni A tissue.
These cells
often form a palisaded arrangement around central acellular, eosinophilic areas known as Verocay bodies. Antoni B
tissue is less cellular and less organized; the spindle cells are randomly arranged within a loose, myxomatous stroma.

What is this clinical finding?

Granular Cell Tumor
What is this clinical finding?

Granular Cell Tumor
Granular Cell Tumor
Histology
Has pseudoepitheliomatus hyperplasia of epithelium (seen on left picture)
Characteristic feature are the granular cells on the right picture
Infiltrate down into the muscle layers, that’s when pathologist confirms granular cell tumor

Diagnosis and Treatment
of the 3Ps
•Diagnosis: All 3 “P” lesions usually occur on gingival interdental papillae ( however pyogenic granuloma can occur anywhere)
• Since they can look similar clinically, excisional biopsy necessary to
determine diagnosis
• Treatment: complete excision and removal of local irritant (scaling
and root planing)
What is this clinical finding?

Congenital Epulis
Gingival Enlargement
Etiology
- Response to chronic inflammation
- Hormonal changes (pregnancy/puberty)
- Immune-mediated/plasma cell gingivitis
- Drug induced
- Genetic/ Inherited
NOTE: Gingival enlargement is not always hyperplastic tissue
What is this clinical finding?

Neuroectodermal tumor of infancy
look how they removed it here surgically
is rare, rapidly growing, pigmented neoplasm of neural crest origin. It is generally accepted as a benign tumour despite of its rapid and locally destructive growth.

Lipoma
What is it?
Location?
Cliniclly?
Histologically?
Treatment?
- What is it: Benign tumor of mature fat cells; Relatively rare
- Location:Won’t see on gingival tissue, will see on buccal mucosa, on the tongue, and floor of the mouth
- Clinically appears as a yellowish mass surfaced by thin overlying epithelium, When you feel it, it’s soft
- Histologically: a well-delineated tumor composed of mature fat cells with a thin capsule
- Treatment: surgical excision,does not recur

What is this clinical finding?

Lipoma
Usually very orange looking lesion in site where there’s adipose tissue
Very obvious, nothing as orange as lipoma
Drug Induced Gingival
Enlargement
What are the famous drugs that are known to cause it?
- Phenytoin: (or Dilantin) – the drug that used to be given to every single
- person that had seizures
- Calcium-channel blockers
- Nifedipine not as prescribed anymore
- Dilitiazem still prescribe
- Amlodipine: is prescribed as one of the first line therapy for hypertension (very commonly prescribed); it doesn’t typically cause gingival overgrowth except in some selected patients, usually
those with pretty poor oral hygiene
- Cyclosporine A (used for for bone marrow transplant, graft vs
host disease, solid organ transplant)- Cyclosporine is universally recognized as causing gingival hyperplasia
- Cyclosporine is largely replaced with Tacrolimus, which typically doesn’t cause gingival overgrowth
- Cyclosporine A is largely replaced with Tacrolimus, which typically doesn’t cause gingival overgrowth
Some drugs have more connective tissue component, others have more epithelial component
Not all identical under the microscope - Cyclosporine provides more epithelial change, Dilantin causes more of a connective tissue change
What is this clinical finding?

Vascular leiomyoma
High-power view showing spindle-shaped cells with bluntended
nuclei. Immunohistochemical analysis shows
strong positivity for smooth muscle actin (inset).

What is this clinical finding?

Rhabdomyoma

Will see the striated muscle
Differential diagnosis… looks like granular cell tumor – don’t know til you remove it
If patient presents with relatively slow growing tumor like this, will I get incisional biopsy or
excisional biopsy? Hard to say
If confident benign tumor and it’s this size and I don’t think it’s vascular (no pulse, can do
aspiration), feels firm – try to excise it
If it looks different, like you think it’s malignant minor salivary gland neoplasm (won’t find it in this
site, but if it’s on hard palate) – incision?
What is this clinical finding?

Leiomyosarcoma
Hereditary Gingivofibromatosis
What causes it?
How common?
what effects on oral cavity?
Treatment?
What causes it?
- Various genes that are implicate (Putative inherited mutations are in the SOS1 or CAMK4 genes.) Linked to both autosomal dominant and recessive patterns of inheritance
How common?
- Very rare
what effects on oral cavity?
- Sometimes gingival overgrowth will completely obliterate the teeth, grow around entire tooth
- Enlargement may be present at birth or may become apparent only with
the eruption of the deciduous or permanent dentitions. - Tooth migration, prolonged retention of the primary dentition, and
diastemata are common, and enlargement may completely cover the
crowns of the teeth, resulting in compromised oral function.
Treatment
- Need surgical (usually laser) treatment – just grows back, so have to get it done periodically
What are these clinical findings?

Rhabdomyosarcoma
In this case, hasn’t broken through epithelium
They don’t all break through
Infantile
Hemangioma
When do they appear?
Rate of Development
Clinical presentation
Treatment
- When do they appear? They are rarely present at birth, infants are Born with this in place.
- Rate of development: the tumor will demonstrate rapid development that occurs at a faster pace than the infant’s overall growth in the first few weeks of life,
-
Clinical presentation: Either superficial or deeper tumors
- Superficial tumors of the skin appear raised and bosselated with a bright-red color (“strawberry” hemangioma); They are firm and rubbery to palpation, and the blood, cannot be evacuated by applying pressure.
- Deeper tumors may appear only slightly raised with a bluish hue.
- May be left with a pink or magenta macule in site where hemangioma occurred after its involute
- Treatment: Typically will involute with time, Some cases don’t involute, so need to be removed
- It is a vascular Anomaly
What is this clinical finding?

Fibrosarcoma

Capillary
Malformation (Low
flow)
- a type of vascular anomaly
- CMs are commonly known as port wine stains.
- They look like a pink, red or purple patch of skin
- occur in 1 in 300 newborns.
What is this clinical finding?

Kaposi Sarcoma
Solitary vascular lesion on hard palate – it was so small so he decided to just excise it in this case^
What are these clinical findings?

Kaposi Sarcoma
- Widespread Kaposi, can see cutaneous lesions
- Oral images of this patient: on palate, starts with macule on patient’s left posterior palate –macular stage
- Then in becomes proliferative – exophytic nodular stage (seen on patient’s right anterior palate,surrounding canine and some incisors)
- Can see engorged blood vessels in area on histology slide
What is this clinical finding?

Plasmacytoma in Multiple Myeloma
- They already had multiple myeloma then developed plasmacytoma
- When you biopsy this, it’s filled with plasma cells bc they’re producing the abnormal immunoglobulins, which are the cause of the devastating issues of multiple myeloma

Acute myelogenous
leukemiawith
granulocytic
sarcoma

- *Complaining of lump inside of her cheek**
- *Notsomuch worried about her gingiva**, despite her overgrowth – leukemic infiltrates that got into gingival tissues
- *Left buccal mucosa**, kept biting on it, feeling incredibly fatigued though she was always working out
- *Oral surgeon biopsied** her buccal mucosa and read by pathologist as pyogenic granuloma
- *Physician** sent her for bloodwork, dental school sent her for bloodwork too
What is this clinical finding?

Lymphoma
- Well circumscribed ulceration in area
- Associated swelling in periphery
- White change in the patient’s left area
- Been there for 3 weeks
- It’s lymphoma
What is this clinical finding?

Looks like it could be a salivary gland neoplasm, but it’s not
It was another lymphoma
Manifest in a number of different ways
Case
40 year old male
Completely healthy otherwise
Not taking any medications
Presents with bump on the tongue
First question: did you do anything that might have led to this? Bite your tongue?
“possible I bit my tongue, or it could be when I had a dental procedure, maybe they accidentally
cut into the side of my tongue” – then it developed
This tells us, is this a reactive lesion?
Is it pedunculated or sessile? It’s pedunculated, larger at the top than the base
Let’s look at the surface: it’s ulcerated
When palpating, it’s only on the surface - don’t feel any submucosal presentation
Tongue underneath feels relatively normal
This bump is kind of firm and it bleeds like crazy when you touch it
When you look at teeth, no area where they’re too sharp

Do you think it’s a fibroma? No. Why?
Fibroma is covered with normal coloring epithelium – sometimes see a little white change on surface or see tiny traumatic ulcer on surface This is not like that, this is completely ulcerated
Not fibroma; fibroma is a chronic bump that patient is aware of
Is it squamous cell carcinoma? Interesting, it is indeed very friable; but no
Sometimes SCC can develop and can be exophytic and don’t have deep invasion, But this is pedunculated, SCC would not be pedunculated
History says there could be some kind of trauma, biting, or nick with bur – not squamous cell
Mucocele? No
Would you typically develop mucocele on lateral border of tongue? No
Not going to be as many mucoceles in this area, but there are the glands of Blandin and Nuhn, so it’s possible to develop on ventral surface of tongue
This bump doesn’t look like a fluid filled bump though, it has surface ulceration, redness ;Mucoceles have intact surface, would not bleed, or be red
Granular cell tumor? No
Granular cell tumor would have normal overlying epithelium (it’s pushing up from underneath)
This does not have normal overlying epithelium
Hemangioma reserved for congenital; not a vascular malformation either
Neurofibroma? No, not the same surface
Salivary gland neoplasms? Possible, there are salivary glands in that area; keep this in differential
The one that this is is pyogenic granuloma: usually red, ulcerated, and bleeds easily

Osler-Weber-Rendu
Syndrome
AKA
What is it and its clinical appearance
Type of Herditary and Etiology
What can it cause?
Location?
AKA
• Hereditary Hemorrhagic Telangiectasia
What is it and its clinical appearance
• disorder of development of the vasculature characterized by telangiectases and
arteriovenous malformations in specific locations. These are essentially endothelial cell issue – get tafted area of abnormal blood vessels multiple different organ systems – causes complications
Type of Herditary and Etiology
•Autosomal dominant with mutations i_n at least five gene_s but mutations in two genes (ENG and ACVRL1/ALK1) cause approximately 85% of cases.
What can it cause?
• Can cause hemorrhage
Location?
often on fingers, lips,tongue, but always look at the fingers!
Sturge-Weber
Angiomatosis
Sturge-Weber syndrome
- Rare, non-hereditary developmental condition
- Vascular proliferation involving tissues of the brain and face
- Face: Unilateral distribution along one or more segments of the trigeminal nerve ( unilateral means don’t cross the midline) known as port wine stain/ nevus flammeus – they are deep-purple color.
- Intracranial calcifications; neurological disorders
- Intraoral involvement is common
Lymphangioma
What is it?
Types
Locations:
Treatment
What is it?
• Benign tumor of lymphatic vessels
Types
- Microcystic
- Mixed
- Cystic hygroma (macrocystic)
Location
- Most frequent extra-oral location: posterior triangle of the neck;
- intraoral location: tongue
Treatment:
monitor, surgery if needed, recurrence common
Neuroma
AKA
What is it?
Clinical presentation
Location
AKA
- traumatic neuroma
What is it?
- Reactive (ie not a true neoplasm) proliferation of nerve tissue after injury, usually extraction or other surgical procedure
Clinical presentation
- They are smooth-surfaced, nonulcerated nodules.
- May be painful (30% of cases) and sometimes associated with altered nerve sensations that can range from anesthesia to dysesthesia to overt pain
Location
- mental foramen area, tongue, lower lip
Multiple Endocrine Neoplasia (MEN) Syndrome
What is it?
Inhertiance type?
Which type is associated with multiple mucosal neruoma?
What other presentations?
Increase risk of which cancer?
What is it?
Group of rare conditions
Inhertiance type?
Autosomal dominant
Which type is associated with multiple mucosal neruoma?
Type 2B associated with multiple mucosal neuromas (one of the first
visual signs)
What other presentations?
• Marfanoid features
• Multiple tumors and hyperplasias of endocrine organs (ie
pheochromocytoma)
Increase risk of which cancer?
• Increased risk for medullary thyroid cancer (prophylactic thyroidectomy)
Common board questions
Neurofibroma
What is it?
Clinical presentation?
Location?
Treatment?
Mailgnancy?
What is it?
- A benign tumor arising from peripheral nerve tissue
Clinical presentation:
- Slow growing, painless lesion
- Smooth-surfaced, nodular mass that varies in size
- Skin more commonly involved than oral mucosa
Location:
- Common oral mucosal sites: tongue and buccal mucosa
- May develop centrally in bone
Treatment: surgical excision
Malignant transformation reported, but rare
Neurofibromatosis syndrome
Most common form?
intheritance type?
Clinical presntation?
Malignant transformation?
Most common form?
Several forms, type I is most common (von Recklinghausen’s Disease)
intheritance type?
• 85-97% of cases inherited as autosomal dominant trait, chromosome 17 (NF1 gene)
Clinical presentations:
- Skin nodules (neurofibromas)
- Café au lait pigmentation on skin
- Lisch nodules very diagnostic (a pigmented hamartomatou in the iris of the eyes)
Malignant transformation
- reported in 5% of cases (neurofibrosarcoma)
Schwannoma/ Neurilemoma
What is it?
Age?
Location?
Clinical presentation?
Treatment?
malignant
transformation ?
What is it?
• Benign neoplasm of Schwann cell origin
• Uncommon lesion: 28-48% occur in the
head and neck
Age?
• Most common in young and middleaged
adults
Location?
• Most common intraoral location:
tongue
Clinical presentation?
• The solitary schwannoma is a slow-growing, encapsulated
tumor that typically arises in association with a nerve trunk.
• May present with pain
• Treatment
• surgical excision
malignant
transformation
reported, but rare
Granular Cell Tumor
What is it?
Location?
Age?
Treatment?
What is it?
Benign tumor derived from
Schwann cells
Location?
• Oral cavity is the most common
location
• Vast majority of cases seen on
dorsal tongue
Clinical presentation?
- Typically an asymptomatic sessile nodule that is usually 2 cm or less in size (firm)
- The mass is typically pink, but some granular cell tumors appear yellow.
- The granular cell tumor is usually solitary, although multiple, separate tumors sometimes occur, especially in black patients.
- The lesion often has been noted for many months or years, although sometimes the patient is unaware of its presence.
Age:
40-60, rare in children
Treatment
• Treated by surgical excision (Be careful with excision! no need
to get all of it out, just most of it)
rarely recurs
Congenital Epulis
AKA
Cell resemble?
Cell origin?
Clinical features & location
Treatment?
• AKA: Congenital epulis of the newborn
• Cells resemble cells of the granular cell tumor
• Cell of origin is unknown, not derived from nerve
• Clinical features:
- Sessile or pedunculated mass, usually found on
- *the anterior** gingiva/ alveolar mucosa
- Almost always occurs in baby girls
- Present at birth
• Treatment:Surgical excision, does not recur
Neuroectodermal tumor of infancy
Location?
Rate of development?
Treatment?
Origin?
Clinical presentation?
Location?
Often occur as soft tissue mass largely in anterior maxilla
Rate of development?
So fast developing that it envelops and moves the teeth
Treatment?
Needs to be surgically excised
Origin?
Thought to be of neuroectodermal source
Clinical presentation?
Pigmented change in tissue
Lipoma vs Lipofibroma
- Sometimes lipomas can be mixed with fibrous tissue, can be lipofibromous
- Two lesions that look almost identical but one is lipoma, one is lipofibroma
- Only difference is that one has fibrous tissue in it, no other difference
Benign Tumors of Muscle
• Leiomyoma
• Benign tumor of smooth muscle
• Vascular Leiomyoma
• Benign tumor of smooth muscle walls of
blood vessels
• Rhabdomyoma
• Benign tumor of skeletal muscle
They are SUPERRR rare
If become malignant, they become leiomyosarcoma or rhabdomyosarcoma – malignant even
more rare
Leiomyosarcoma
- a type of rare cancer that grows in the smooth muscles.
- So, so rare
- Diseases that move rapidly, because they’re malignancies
- You might see surface ulcerations, they’re moving so fast, they break through the epithelium
Rhabdomyosarcoma
- is a type of sarcoma.
- Rhabdomyosarcoma usually begins in muscles that are attached to bones and that help the body move, but it may begin in many places in the body
What is Sarcoma ?
Sarcoma is cancer of soft tissue (such as muscle), connective tissue (such as tendon or cartilage), or bone.
Fibrosarcoma
what is it?
Age?
Rate of growth?
Treatment?
Survival rates?
•What is it? Malignant tumor of fibroblasts
• Age? Most common in young adults and
children
• Rate of growth? Slow growing lesion that is usually not
painful (Can be slow growing, can be rapidly growing – different criteria determining high or low grade)
• Treatment: surgical excision, recurrence is common(Aren’t always easy to surgically remove, because already metastasized into other reservoirs, spread into contiguous areas) Aren’t always radiosensitive, don’t always respond to radiation treatment
• 5-year survival rates range from 40-70%
Vascular Malignant Neoplasms
• Angiosarcoma
• Malignant tumor of blood vessels
• Lymphangiosarcoma
• Malignant tumor of lymphatic vessels
• Kaposi’s sarcoma
- Malignant neoplasm associated with endothelial cells
- Seen predominantly in poorly controlled HIV infected patient population (not exclusively)
- Elderly people can develop Kaposi
Kaposi Sarcoma
Etiology
Types
Treatment
Etiology:Caused by HHV-8 (human herpesvirus 8) /part of herpes family
Types:
- Classic: late adult life, Italian and Jewish men, skin of lower extremities
- Endemic: African form
- Iatrogenic immunosuppression-associated: most often occurs in recipients of organ transplants
- AIDS-related
Treatment
- Surgical excision, radiation therapy or systemic chemotherapy for multiple nonoral lesions, if it gets large, dose-radiation therapy!
Plasmacytoma in Multiple Myeloma
Presents as soft tissue lesion
It is possible that a patient can present with plasmacytoma that would be the first sign of multiple
myeloma (it would be a rare sign, but it can happen)
Lymphoma
- Lymphoma is a general term for a complex group of heterogeneous lymphoreticular malignancies.
- Lymphoma is the sixth most common malignancy and the second most common neoplasm of the head and neck after squamous cell carcinoma and accounts for 50-59% of head and neck neoplasms in children.
- They constitute approximately 3-5% of all known malignancies and are generally divided into two morphologically distinct types: Hodgkin’s lymphoma (HL) and non-Hodgkin’s lymphoma (NHL).
- These malignancies typically arise within the lymphatic tissues and can progress to extranodal disease as in NHL.
- Cervical lymph node involvement can be present in any type of lymphoma.
- HL extends by means of contiguous nodal spread whereas NHL tends to disseminate hematogenously and is typically a systemic diagnosis.
- Within the head and neck, Waldeyer’s ring is the most common site of involvement, accounting for more than half of all extranodal head and neck lymphomas.
- Oral involvement by lymphoma may represent a localized disease process but is more often part of a systemic process that secondarily involves the cervical lymph nodes.
- Lymphoma arising within the oral cavity accounts for less than 5% of all oral malignancies, and approximately 85% of these lesions involve the pharyngeal tonsil and the palate
- Extralymphatic sites include the salivary glands, paranasal sinuses, oral cavity, and larynx.
ADENOMA
benign tumor
of glandular origin
Characteristics of a Benign Tumor:
Encapsulated ‐ distinguishable from surrounding tissues
Freely movable ‐ not fixed
Slow growing
Non tender ‐ patients do not complain of pain
BENIGN SALIVARY GLAND
TUMORS
(list 3)
Pleomorphic adenoma aka mixed tumor
Monomorphic adenomas
o Canalicular adenoma
o Basal cell adenoma
Warthin tumor (papillary cystadenoma lymphomatosum)
PLEOMORPHIC ADENOMA
(MIXED TUMOR)
- This tumor comes in many forms/shapes
- Most common salivary gland tumor
- Painless, slowly growing, firm mass
- Adults (30‐50 years old) ; slight female predilection
- Sites:
- 50% to 77% of parotid tumors (most commonly found in parotid-2/3rd to 3/4th of parotid tumors)
- Minor SG: palate>upper lip>buccal mucosa> other site (most common intraoral site is the palate)
- Malignant transformation possible in long standing lesions (about 5% cases) ‐> called Ca ex PA
What is this clinical finding?

PLEOMORPHIC ADENOMA
(MIXED TUMOR)
What is this clinical finding?

PLEOMORPHIC ADENOMA
Classic presentation: includes swelling in the parotid region
(MIXED TUMOR)
What is this clinical finding?

PLEOMORPHIC ADENOMA
Palatal presentation: since salivary glands are only in lateral sides of the palate, usually
swellings are in one side and not the midline. Lateral swelling is a clue that you are
looking at a salivary gland lesion (left pics)
On the right pic, it involved midline and crossed over to other side, so there are
exceptions. But more commonly found in lateral side of the palate.
(MIXED TUMOR)
What is this clinical finding?

PLEOMORPHIC ADENOMA
- Upper lip presentation: sometimes swelling can be seen extra orally and intraorally.
- Remember the swelling will be movable, not tender, not fixed to underlying structures.
(MIXED TUMOR)
What is this clinical finding?

Untreated pleomorphic adenoma
slow growing, but can grow to enormous sizes
Pleomorphic adenoma
histology
This is a mixed tumor with myxoid component (right) and
fibrous/epithelial component(left)
This type of tumor can produce a lot of different tissues, since the origin is from myoepithelial cells aka plasmacytoid cells, which are pluripotent cells which means they can differentiate into many different lineages of cells such as

What is this clinical finding?

Canalicular Adenoma
What is this clinical finding?

Canalicular Adenoma
- Mucocele might look this way, but what would make it lower on
- differential diagnosis is the location of the swelling. Mucocele is mostly seen on lower lip and this pic shows upper lip. Salivary gland tumors and mucoceles
- can have the same clinical presentation, so always do a biopsy for formal histopathology diagnosis.
Basal Cell Adenoma
- Basaloid appearance of the tumor cells
- Primarily parotid lesion
- predominantly in women over 50 years of age. It is uncommon in young adults.
(Basal cells are located in epithelium that is adjacent to interface with the connective tissue and they are separated from the CT by a basement membrane, stem cells of epithelium are located in basal cell layer)
Basal cells are typically Blue in appearance and cuboidal,

What is this clinical finding?
Basal Cell Adenoma

What is this clinical finding?

PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)
MUCOEPIDERMOID
CARCINOMA
Charcterstics?
Location
Clinical appearance in minor gland
Can be mistaken for
Histopahtology
Most common malignancy of salivary glands
Most common malignant SG tumor in children
Locations
Palate, most common intraoral site
Rare primary intrabony (jaws) tumors
Most common in parotid
Minor SG: palate 2nd
Clinical appearance in minor gland: asymptomatic fluctuant swelling; blue or red colored
Can be mistaken for mucocele
Histopathology: note the cells growing into adjacent tissue, showing infiltration

Monomorphic Adenomas
What is it?
Types?
Treatment?
What is it?
Proliferation of 1 type of cell makes up the tumor.
Types? Includes:
o Canalicular Adenoma
o Basal Cell Adenoma
Treatment for all monomorphic adenomas is surgical excision & diagnosis is done with biopsy
What is this clinical finding?

MUCOEPIDERMOID
CARCINOMA
What is this clinical finding?

MUCOEPIDERMOID
CARCINOMA
Request all for biopsies!
What is this radiographical finding?

CENTRAL
MUCOEPIDERMOID
CARCINOMA
- Intrabony presentations, may have extraoral swelling depending on the stage
- Started as small swelling and progressed rapidly:, need to pick it up early!
- Patient recovered, but might need radiation, lost salivary glands, needed reconstruction of palate
Canalicular Adenoma
- Almost exclusively in minor SG
- Striking predilection for upper lip (>75%)
- Nearly always occurs in older adults
- Slowly growing, painless mass
- One clue for visualization of soft tissue swellings is increased vascularity with blue‐ish tint in the area.
What is the clinical finding?

ACINIC CELL
ADENOCARCINOMA
What is the clinical finding?

ACINIC CELL
ADENOCARCINOMA
blue‐ish tint
What is this clinical finding?

Untreated acinic cell adenocarcinoma
Because it is slow growing, and a low grade tumor, the
patient is alive and not dead with a tumor this size.
Similar presentation to pleomorphic adenomas, but there is a lot of ulceration on the surface and prominent vascularization in acinic cell
adenocarcinoma.
Adenoid Cystic Carcinoma
High grade salivary gland malignancy ( very bad cancer to get)
Adults
Palatal mass; ulcerations
Spread through perineural invasion ‐ tumor wraps itself around nerves and spreads through perineural spaces
Grows slowly in the beginning and then picks up speed
Histology: Duct like proliferation with cystic spaces

What is this clinical finding?

Adenoid Cystic Carcinoma
What are these clinical findings?

Adenoid Cystic Carcinoma
What are these clinical findings?

Adenoid Cystic Carcinoma
Adenoid Cystic Carcinoma
Swiss cheese appearance, cribriform pattern (full of holes aka cystic spaces)

Perineural invasion Histology
Perineural invasion: nerve nuble in the
center and is wrapped by tumor

What is this clinical presentation?

Polymorphous
Adenocarcinoma
What is this clinical presentation?

Polymorphous
Adenocarcinoma
What is this clinical finding?

Carcinoma Ex Pleomorphic
Adenoma
PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)
- finger‐like projections, benign, cystic spaces, aggregates oflymphocytes)
- Vast majority occur within the parotid gland
- Very rare intraorally
- Predominantly in men
- Typically between 5th and 8th decades
- Strong correlation with cigarette smoking
- Most common SG tumor to occur bilaterally (bilateral parotid swelling), but can be unilateral
- Etiology: Thought to arise within lymph nodes as a result of entrapment of
- salivary gland elements early in development
-
Clinical Features:
- swelling that has more subtle presentation
- Doughy to cystic mass
- In the inferior pole of the gland, adjacent and posterior to the angle of the mandible
- Treatment: surgical excision, responds very well to it
Summary for benign
tumors
Encapsulated, freely movable, not fixed to underlying structure, not tender, patients do not complain of pain, slow growing
There is one tumor of the ones discussed that does have a risk of malignant transformation (only 5% and will take many, many years) and that is Pleomorphic adenoma
MALIGNANT SALIVARY
GLAND TUMORS
List 5
Mucoepidermoid carcinoma
Acinic cell carcinoma
Adenoid cystic carcinoma
Carcinoma ex‐mixed tumor/malignant mixed tumor
Polymorphous adenocarcinoma
CLINICAL FEATURES OF
ADENOCARCINOMAS
(malignant gland tumors)
Infiltrative
Fixed to underlying structures, not moveable
Rapid or slow growth, depending on grade and type of malignant salivary
gland tumor
Larger, rapidly growing lesions may cause pain and/or paresthesia
Ulcerated overlying mucosa
MUCOEPIDERMOID
CARCINOMA
What are its compoenents?
Within jaw prognosis
Treatment
Prognosis
Therapy by gene?
What are its compoenents? Mixture of mucus‐producing cells and epidermoid or squamous cells
May arise within jaws from odontogenic epithelium of dentigerous cysts
• More common in the mandible than maxilla
• Molar‐ramus area
Treatment: Usually treated by surgical excision
Prognosis:
• Overall prognosis is fairly good
• 10% of patients die, due to local recurrence or metastasis
Low‐grade tumors have good prognosis (>90% are cured)
High‐grade tumors the prognosis is guarded (Only 30% survive)
Therapy by gene?
CRTC1–MAML2, CRTC3‐MAML2 gene fusions (targeted therapy)
ACINIC CELL
ADENOCARCINOMA
- Occurs predominantly in major SGs,
- Found in all age groups, peak incidence in 5th and 6th grade
- No gender predilection
- Malignancy with serous acinar differentiation
- Most common in the parotid (since 90% serous acini)
- Variable microscopic appearance
- May even appear encapsulated, since it is SLOW growing
- Better prognosis than salivary gland malignancies
Adenoid Cystic Carcinoma
Location
Growth rate
Clinical presentation
Treatment
Prognosis
Location:
Approx. 50% occur within the minor SG ‐ palate most common site
Growth rate
Usually a slowly growing mass
Clinical presentation
Pain is a common and important early finding, occasionally occurring before there is noticeable swelling (described at annoying pain)
Tendency to show perineural invasion, corresponds to pain
Treatment
Excision usually the treatment of choice ‐ but edges of tumor may have perineural invasion and remain undetected ‐ makes tumor dangerous
Prognosis
5‐year survival rate as high as 70% (maybe 90%)
By 20 years, only 20% ‐ poor long term prognosis
Polymorphous
Adenocarcinoma
Location
Gender
Appearance
growth patterns
Treatment
- Location:
- Almost exclusively in the minor SG
- 60% on the hard or soft palate
- Gender”
- 2/3rds in females
- Appearance:
- Tumor cells have deceptively uniform appearance
- Growth patterns:
- Different growth patterns – polymorphous
- Perineural invasion ‐ common ‐ but considered low grade tumor
- Treatment: Wide surgical excision; overall prognosis relatively good, with 80% cure rate
Carcinoma Ex Pleomorphic
Adenoma
What is it?
Mean age?
Growth pattern
Treatment?
Prognosis
What is it? (benign tumors that have underwent malignant transformation‐ takes a lot time, 15 to 20 years)
Mean age about 15 years greater than benign counterpart
Growth patterns: Mass present for many years with recent rapid growth with associated pain or ulceration
Treatment: Best treated by wide excision, with local node dissection and radiation
Prognosis: guarded, with 50% local recurrence or metastases and dying Prognosis is case to case scenario, may transform to high grade tumor
What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION
Lower lip
o Mucocele
o Mucoepidermoid Ca
o Pleomorphic Adenoma
What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION
upper lip
o Canalicular Adenoma
o Salivary Duct Cyst*
o Pleomorphic Adenoma
What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION
Parotid
o Pleomorphic adenoma
o Warthin’s tumor
o Basal cell adenoma
o Mucoepidermoid ca
o Acinic cell ca
o Adenoid cystic ca
o Ca ex mixed tumor
What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION
Palate
o Pleomorphic adenoma
o Adenoid cystic ca
o Mucoepidermoid ca
o PLGA
o Monomorphic adenoma
SG Tumors: Summary of
Key Points
Involve both major and minor glands
Benign and malignant tumors both have similar
clinical presentation
Most malignant salivary gland tumors do not show histopathologic
characteristics associated with malignancy
Most occur in adults
Warthin Tumor seen in parotid, may be bilateral
Mucoepidermoid carcinoma
o Can occur in children
o May occur centrally in bone
Palatine Torus/Torus Palatinus
- Tori are incredibly common, a normal of variant
- Part of physical exam is to visualize as well as running index finger over the hard palate every time
- Sometimes, torus palatinus is quite small and unnoticeable until you touch it (feel a hard bump and it’s just a bony growth)
- Sometimes, they are pedunculated; Sometimes, they get so large they become traumatized; vascular supply on surface can sometimes form ulcerations and even get a little bone exposure.
- If patient with history of use of bisphosphonates (bone modifying agents given to women who have osteoporosis or osteopenia and to prevent metastesis for certain cancers), he will remove that dead bone, and it will slowly heal. That’s one of the perils of having an enlarged palatine torus
What is this clinical finding?

Palatine Torus/Torus Palatinus
What is this clinical finding?

Palatine Torus/Torus Palatinus
What is this clinical finding?

Mandibular Torus:
Torus Mandibularis
What is this clinical finding?

Mandibular Torus:
Torus Mandibularis
What is this clinical finding?

Buccal Exostoses
Mandibular Torus: Torus Mandibularis
- Sometimes pt’s tori are so large that the sublingual frenum gets stuck underneath
- repeated irritation/trauma can create a little white rim on the tori
- these tori are rock hard and may grow overtime, but we don’t really understand why people get them
What is this clinical finding?

Unencapsulated Lymphoid Aggregates
What is this clinical finding?

Lymphoepithelial
cyst
we see a tiny yellowish cyst. we see the blood vessels on the surface; this is quite characteristic.
What is this clinical finding?

Unencapsulated
Lymphoid
Aggregates
Post-tonsillectomy
Can even develop these on area of tonsils.
(left pic) Red/salmon is a lymphoid aggregate (unencapsulated lymphoid tissue). This is someone
who had a tonsillectomy , and you can see these
lymphoid aggregates on posterior pharyngeal wall (salmon color).They move around the area.
(right pic) It grew back even in post-tonsillectomy patients.
What is this clinical finding?

Fordyce Granules
What is this clinical finding?

Fordyce Granules
Buccal Exostoses
- Sometimes patient develops exostoses (another word for torus).
- Can get buccal exostoses, all just bone. Can pick these up on radiograph, the bone is a lot denser.
Why does it happen?
- Maybe it’s related to parafunctional habits – but don’t really understand the
- basis for the exostosis.
- They’re going to be bilateral. If it’s unilateral, we start thinking about other bony diseases
a variant of normal
What is this clinical finding?

Fimbriated
fold/Plica
semiluminaris
What is this clinical finding?

Frenal tag
Unencapsulated Lymphoid Aggregates
- the lymphoid aggregates are part of the foliate papillae (they contain some taste buds as well).
- This is lymphoid tissue -- when you get a cold or upper respiratory tract infection, sometimes these areas can become hyperplastic in response to infection – can become a little enlarged.
- These are usually bilateral.
- a variant of normal
What is this clinical finding?

Sublingual Varices
What is this clinical finding?

Sublingual Varices
What is this clinical finding?

Sublingual Varices
What is this clinical finding?

Circumvallate papillae
What is this clinical finding?

Parotid Papillia (Stenson duct)
What is this clinical finding?

Parotid Papillia (Stenson duct)
What is Lymphoepithelial
cyst?
a cystic structure.develops in that area where there are already unencapsulated lymphoid tissue.
This is not normal – Pathologic
Sometimes when you get a cyst in this area – because of lymphoid tissue, you can develop lymphoepithelial cyst – a tiny yellowish cyst. we see the blood vessels on the surface; this is quite characteristic.
What is this clinical finding?

Linea Alba
What is this clinical finding?

Leukoedema
Fordyce Granules
- Occurs on the buccal labial mucosa, retro molar pad and tonsillar area and lips
- They are white or yellow ectopic sebaceous glands
- They can be present in small or large quantity
- Why do we have sebaceous glands in mouth? we dont know, evolutionary advantage? we don’t really understand.
- a variant of normal
What is this clinical finding?

Palatal Rugae
Fimbriated
fold/Plica
semiluminaris
- Some patients have more obvious fimbriated folds or plica semilunaris in their mouths than others
- When you look at the ventral surface of the tongue, you’ll sometimes be able to pick these up.
- These are duct opening from a series of salivary glands, minor glands, but they’re a little bit different than other minor glands in the mouth.
- They produce more of a viscous type of saliva, and they are the glands of the Blandin and Nuhn
- a variant of normal
What is a Frenal tag?
- Frenal attachments are thin folds of mucous membrane with enclosed muscle fibers that attach the lips to the alveolar mucosa and underlying periosteum.
- Most often, during the oral examination of the patient the dentist gives very little importance to the frenum, for assessing its morpholology and attachment.
- Sometimes occur; essentially normal of varient
Sublingual Varices
- Tortuous dilated vessels (enlarged engourged veins) on the ventral surface of the tongue, and sometimes stretch onto lateral border
- Appears bluish purple in color
- More prominent with increasing age; we don’t see it in younger pts.
- Nothing to be concerned about, a variant of normal
Circumvallate papillae
- Located in the posterior region of the tongue; dividing the body from the base
- They are mushroom shaped and arranged in V-shape formation
- Although they are usually not apparent in most patients, you may be able to visualize them in some
- a variant of normal
Parotid Papillia (Stenson duct)
- Located in right and left buccal mucosa at the level of the occlusal plane close to the maxillary first and second molar.
- This structure may appear as a small dot or have a prominent pink to red papillae presence.
- This is the parotid papilla, and It is the opening of the parotid duct which drains saliva from the parotid gland.
A normal of variant
Linea Alba
•a white line or keratotic area that present along occlusal plane in some patients
- due to some friction In that area. (the buccal mucosa)
- It varies in thickness and opacity
- Can be seen in some patients who have bruxism
- a variant of normal
Leukoedema
- A bluish and white filmy opalescence of the mucosa is observed
- In order to differentiate it from other white lesions à gently stretch the patient’s cheek forward and the leukoedema will disappear or partly fade and appears less apparent
- It is commonly found in people of color and some smokers.
- a variant of normal
Palatal Rugae
- Raised ridges or folds
- Located in the anterior palate on either side of the mid-palatine raphe behind the incisive papilla
- They vary in number and size
- May increase with age
- a variant of normal
Inflammatory/Reactive Lesions of the Salivary Glands
List 5
- mucocele/mucous cyst
- ranula
- necrotizing sialometaplasia
- sialolithiasis
- sialadentitis
Mucocele
Definition
Clinical features
Location
Histological features
Treatment
• definition: a lesion that forms when a salivary gland duct is severed & secretion spills into the adjacent CT
• a pseudocyst (not lined by epithelium) — mucous builds up in the CT & causes a bump
• clinical features:
- swelling in the tissue that may increase & decrease in size
- may have a bluish hue, fluctuant on palpation — fluid filled, soft, compressible
• location: lower lip most common site, but may form in any area where there are minor salivary glands
• histologic features:
- a cyst-like space in soft tissue
- lined by compressed granulation tissue
- lumen filled with mucin, foamy macrophages & inflammatory cells
• treatment: surgical excision, removal of associated minor salivary glands
• may recur if don’t remove all associated injured minor salivary glands

What is this clinical finding?

Mucocele
What is this clinical finding?

Mucous Cyst
What is this clinical finding?

Ranula
Notice how it’s unilateral
on the floor of the mouth
What is this clinical finding?

Ranula
- Notice how it’s unilateral*
- on the floor of the mouth*
Necrotizing Sialometaplasia
Definition
Predisposing factors
Clinical features
Histologic features
Treatment
• Definition: locally destructive inflammatory condition — looks malignant but is benign
• salivary gland ischemia — “heart attack of the palate”; blood flow is interrupted
• predisposing factors:
- local trauma
- palatal injection of local anesthesia
- previous surgery
- many are idiopathic..
• usually a clinical diagnosis based on history & how fast — palate uncommon for SCC
• clinical features:
- initially appears as a non-ulcerated swelling of the palate
- often associated with pain or paresthesia
- within 2-3 weeks, necrotic tissue sloughs off & becomes a crater-like ulcer
- patient may say: “a chunk of the roof of my mouth fell out”
• histologic features:
- necrosis of the salivary glands — coagulative necrosis (green circles in histology —>)
- salivary gland duct epithelium is replaced by squamous epithelium — appear as islands of squamous epithelium deep in the CT & resembles SCC (arrows in histology —>)
• Treatment: no treatment, spontaneously resolves within 6 to 10 weeks
• irrigating & debriding the area can reintroduce vascularity & help healing

What is this clinical finding?

Necrotizing Sialometaplasia
Sialolithiasis
Definition
Location
Origin
Clinical features
Radiological features
Histological features
Treatment
Definition: lith = stone ;; sialolith: a salivary gland stone
Location: occur in both major & minor salivary glands
• floor of the mouth is most common location (Wharton’s duct is a common place)
• often causes obstruction of the duct
Origin: arise from desposition of calcium salts around nidus of debris within the duct lumen
- *clinical features:**- minor glands: hard yellowish structure in soft tissue
- may be visible on a radiograph
- recurrent swelling (due to the obstruction)
- episodic pain & swelling during times of increased salivation
- can be palpated if the stone is located toward the terminal portion of the duct
- *Radiological features** : may be viewed as a radiopacity on an occlusal x-ray–well defined radiopacity
- *Histological features-** concentric rings of calcification, color of it in stain depends on level of calcificatio
- *Treatment**: promote passage of stone (massage, sialogogues, increase fluid intake) or surgical removal

What is this clinical finding?

Sialolithiasis
What is this clinical finding?

Sialolithiasis
Notice how it can appear radiographically as a well defined radiolucency

What is this Radiographical finding?

Sialolithiasis
Mucous Cyst
Definition
Clinical features
Histological features
Treatment
•Definition: a pseudocyst
• microscopicallly appears as an epithelial lined cystic structure that is actually a dilated duct
• clinically you CANNOT tell the difference between a mucocele & mucous cyst
• clinical features:
- same as a mucocele
• histologic features:
- same as mucocele but will see an epithelial lining (but actually a dilated duct)
treatment: same as mucocele; surgical excision
What is this clinical finding?

Sialadenitis
Acute: parotid papilla purulent discharge
What is this clinical finding?

Sialadenitis
Chronic: caused fibrosis

Summery
of inflmattory salivaory conditions
Mucocele
- fluctuant swelling
- bluish hue
- lower lip most common
Ranula
- fluctuant swelling
- floor of mouth
Sialolithisis
• major glands: episodic pain &
swelling of affected gland
• minor glands: asymptomatic/
local swelling or tenderness
• if superficial - firm to palpation
& yellowish color
Necrotizing
Sialometaplasia
• initial painful swelling
• later necrotic ulcer
• posterior lateral hard
palate & soft palate
Sialadenitis
• painful swelling of
affected gland
• purulent discharge if
acute infection

Ranula
Definition
Associated with
Clinical features
Treatment
• Definition: mucocele-like lesion that forms unilaterally on the floor of the mouth
• may break through the mylohyoid muscle & enter neck space = “plunging ranula”
• associated with: the ducts of the sublingual & submandibular glands
• clinical features:
- must be on floor of the mouth for it to be considered a ranula
- big & have deep blue color if exophytic
- sometimes can grow downward/deep & won’t see blue as much
• treatment: surgical excision
Sialadenitis
definition
causes:
clinical features:
histologic features:
Treatment:
• definition: acute or chronic inflammation in major or minor salivary glands
• causes:
• obstruction of a salivary gland duct (sialolith)
• infection (mumps [viral], staph aureus [bacterial, most common], candida [fungal])
• decreased salivary flow (Sjogren’s, sarcoidosis)
• parotid gland = parotitis
• clinical features:
- acute: most common in parotid, swollen & painful gland, erythematous & warm overlying mucosa/skin, purulent discharge, low-grade fever
- chronic: caused by recurrent or persistent ductal obstruction, periodic swelling & pain
• histologic features:
- acute or chronic inflammatory cell infiltrate in the salivary gland
- in chronic cases = salivary gland replaced by fibrous CT & fat
- cells: acute = neutrophils ;; chronic = lymphocytes, plasma cells, macrophages
• Treatment: antibiotics, rehydration, surgical drainage, or surgical removal of gland
Rx Topical
Treatments:
Cautery
‐ Debacterol (sulfonated phenolics; sulfuric acid solution)
o Chemical cautery
o Label: one time application for 5‐10 seconds
‐ NOT recommended to patients with frequent outbreaks
What are the Topical Therapy
Categories to treat ulcers?
Topical anesthetic agents
o To numb the pain
‐ Surface protective agents/bioadhesives
o Cover the ulcer if small enough
‐ Anti‐inflammatory/immunomodulatory agents
o Applied to ulcer surface (corticosteroids)
‐ Anti‐microbials
o Some evidence that topical tetracycline may help
‐ Chemical/physical cautery Lasers
‐ Over‐the‐counter (OTC) versus prescription (Rx
All essentially do the same thing:
o Numbing agent
o Mucosal covering agent
‐ Bottomline:
o ALL canker sores will heal on their on with time
Frequent Minor
RAS or Major RAS
Treatment
‐ Treatment to reduce pain
‐ vs.
‐ Abortive treatment to reduce healing time
‐ vs.
‐ Suppressive treatment to suppress recurrences
‐ Combination of all
Also Consider
- Using Sodium Lauryl Sulfate‐Free Toothpastes
- Remove Obvious Possible Causes
Infrequent Simple
Minor RAS
Treatment
‐ Treatment to reduce pain
Also Consider
- using Sodium Lauryl Sulfate‐Free Toothpastes
- Remove Obvious Possible Causes
- ‐ Repair sharp teeth/restorations
- ‐ Remove plaque
- ‐ Optimize lubrication
Steps in Managing RAS patient
‐ History of RAS
‐ Medical History
o Medications
o Review of Systems
‐ Social History
‐ Dental History
‐ Diet/Nutritional History
‐ Physical Examination
‐ LaboratoryTests
How do we treat this?

‐ Repair sharp teeth/restorations
‐ Remove plaque
‐ Optimize lubrication
Ulcer
What is this clinical finding?

Behcet’s Disease
‐ Recalcitrant oral ulcers associated with Behcet’s Disease
‐ Later developed genital ulcers and other complications
‐ Image:
o Sores in the labial mucosa have classic aphthae appearance
o Other ulcers are major aphthae:
▪ Larger
▪ Irregular borders
▪ Intense proliferative erythema
What is this clinical finding?

Behcet’s Disease
‐ Recurrent inflammatory disorder of unknown cause:
o Bacterial?
‐ Affects:
o Middle Eastern Males
o Asian Females
‐ Onset 3rd – 4th decade
‐ HLA‐B51 association
Recurrent aphthous ulcers generally precede other signs:
o Genital/skin/eye lesions & others (arthritis, Gl lesions, CNS symptoms, vascular lesions)
‐ Diagnosis based upon criteria (point system): no laboratory tests
What is this clinical finding?

Hematinic
Deficiencies
‐ Superficial ulcers
o Not classic aphthous ulcers
‐ Equivocal associations with iron, Vit B1, B2, B6, B12, and folate.
‐ Blood tests are not recommended routinely in all patients with RAS.
‐ Indications for blood work (CBC):
o Older patient with recent RAS history
o Suspicious medical history/review of systems
o Strict vegetarian patients
What is this clinical finding?

HIV‐Associated
Aphthous
- CD4 counts <100 cells/mm3 are predisposed to major RAS
- ‐ Other sites may be affected:
- o Esophagus
- o Genitals
- o Anus/rectum
- ‐ We see this less frequently since ART
- ‐ Diagnosis is important, particularly if no prior history
What are these clinical findings?

Inflammatory
Bowel Diseases
-
Specific lesions:
- o Diffuse labial and buccal swelling
- o Cobblestones
- o Other specific lesions
- ▪ Mucosal tags
- ▪ Deep linear ulcerations
- o Mucogingivitis
- o Granulomatous cheilitis
- Non‐specific lesions:
- o Aphthous ulcerations
- o Pyostomatitis vegetans
- o Dental caries
- o Gingivitis and periodontitis
- o Other non‐specific lesions
What is this clinical finding?

Transient Lingual
Papillitis
- ‐ Relatively rare
- ‐ Canker sore meets fungiform papilla of tongue
- Multiple papilla can become inflamed (above image)
- Very painful
- ‐ Ulcer Appearance:
- Tiny
- Transient
- On fungiform papilla of tongue
- ‐ Typically resolves in 7‐10 days
What is this clinical finding?

Herpetiform aphthous stomatitis
- Apppears like herpesvirus but unrelated to it
- account for 5% of cases (the least common)
Appearance:
- begin as multiple (up to 100) 1- to 3-mm crops of small, painful clusters of ulcers on an erythematous base.
- They coalesce to form larger ulcers that last 2 weeks.
- A bunch of smaller ulcers that coalesce

What is this clinical finding?

‐ Minor Recurrent
Aphthous Ulcers
(RAS)‐ Rare Case
o Keratinized
Mucosal
Site
‐ 11‐year‐old boy
‐ Canine is in process of erupting
‐ Canker sore present on his keratinized mucosa (RARE)
o 99% of canker sores occur on NON-KERATINIZED MUCOSA
What is this clinical finding?

Minor Recurrent
Aphthous Ulcers
(RAS)
- aka‐ “Canker Sores”
- ‐ High prevalence: 5‐25%
- ‐ Comprises the overwhelming majority of cases
- o 75‐85% of ALL RAS cases
- ‐ <10 mm in diameter
- ‐ Ulcer appearance:
- o Shallow
- o Round/Oval Shaped
- o Yellow pseudomembrane
- ▪ Slightly raised margin
- ▪ Erythematous Halo
-
‐ Typically resolves in 7‐10 days
- o *May take longer if in a “high‐traffic” site
- ‐ No scarring
- ‐ Recurrence rates vary
What are the Hallmarks of
Aphthous Ulcers
‐ Hallmarks:
o 1. Central ulceration
o 2. Ring of erythema (erythematous border)
▪ Accentuated in right image

What is this clinical finding?

‐ Aphthous Ulcer of the tongue
‐ Aphthous ulcers can occur on specialized structures of the mouth
What is this clinical finding?

Aphthous ulcer (“The canker sore”)
What would it be like to have a canker sore on your uvula?
o Painful to swallow
‐ The location of the canker sore will predict the symptoms
Rx Topical
Treatments:
Corticosteroid
Rinse‐
‐ Dexamethasone elixir 0.5mg/5ml (ETOH base) or solution (H20 base)
‐ Indicated for difficult to reach lesions to obtain access to all of them
o Disp:600ml
o Label: swish with 5‐10 ml for 5 minutes up to 0.5mg/5mL 4x/day and
expectorate 00s preservalve.) May be used as suppressive therapy in
selected patients with close surveillance
o Prevent recurrences
‐ May buy an EXTRA DAY of healing time
dr. Kerr prefers the elixir

What is this clinical finding?

Major Recurrent
Aphthous Ulcers
(RAS)
- ‐ 10 – 15% of all RAS cases
- ‐ >10 mm in diameter
- ‐ Ulcer Appearance:
- o Deeper
- o Irregular borders (usually)
- ‐ Typically resolves in WEEKS or MONTHS
- ‐ May be associated with fever or malaise
- o The associated cytokine release can induce a fever
- ‐ Predilection for the throat
- ‐ Often DOES leave scarring
- ‐ Recurrence rates vary
Rx Topical
Treatments:
Corticosteroids
for
Ulcers
‐ Triamcinolone acetonide in Orabase 0.1% (intermediate)
o Disp: 5g tube Dental Past
o Label: apply a thin film over ulcer after meals and bedtime APOTHECON
o Do not use for more than 2 weeks
‐ Fluocinonide gel or ointment 0.05% (Potent)
o Disp: 15g tube
o Label: apply a thin film over
o Do not use for more than 2 weeks
‐ Clobetasol ointment 0.05% (Ultra potent)
o Disp: 15gtube Label: apply a thin film over ulcer bid
Problem with topical tx
Topical Treatments
‐ Drug is easily washed away or rubbed off
‐ Topical anesthetics have a short‐lived effect
‐ Often difficult to apply due to location
‐ Cost may be a disincentive to buy OTC
‐ Once ulcers are established, these treatments are not as effective, therefore
abortive treatment early on is preferred
What about
systemic
treatments – taking
pills to treat ulcers?
‐ Prednisone or systemic steroids were the one systemic treatment that Dr. Kerr
has has success with in practice
o 0.5 mg/kg of Prednisone would be prescribed for about 1 week
o Very successful in patients with frequent outbreaks of multiple canker
sores
‐ In some limited cases Dr. Kerr has seen some success with:
o Colchicine
o Pentoxifylline
What is this clinical presentation?

Homogeneous leukoplakia
○ Thickened leathery, White plaque
○ Well-demarcated, Deepened fissures
○ Non-wipeable white patch
What is this clinical presentation?

Homogeneous leukoplakia.
○ Non-wipeable white patch
What is this clinical presentation?

homogenous leukoplakia
Just
white color
What is this clinical presentation?

Non-homogenous leukoplakia
Nodular leukoplakia ~ Largely white
Verrucous leukoplakia ~ Largely white
Erythroleukoplakia ~ Red and white
Speckled and verrucous leukoplakia have a greater risk for malignant
transformation than the homogeneous form
What is this clinical presentation?

Speckled leukoplakia.
Non-homogenous leukoplakia
What is this clinical presentation?

Hairy Leukoplakia
corrugated white lesion on the lateral tongue.
• It only occurs on the lateral tongue
What is this clinical presentation?

Hairy Leukoplakia
What is this clinical presentation?

Proliferative Verrucous Leukoplakia
Patient with proliferative verrucous leukoplakia but manifesting more as
an erythroplakia in multiple sites than a leukoplakia
Proliferative verrucous leukoplakia has very high risk (49.5% in malignant transformation)
almost 10% risk for malignant transformation every year
What is this clinical presentation?

Proliferative Verrucous Leukoplakia
Location
○ Gingiva (Frequent)
○ Buccal Mucosa
○ Palatal Mucosa
What is this clinical presentation?

Proliferative Verrucous Leukoplakia
Multifocal
What is this clinical presentation?

Oral lichen planus
White lacy appearance, with
a network reticular appearance (Wickham’s striae)
sometimes punctate or plaque‐like lesions predominate
o Wickham’s striae→ very characteris► white wispy changes
What is this clinical presentation?

Oral lichen planus
on the buccal mucosa (most common site
reticular form.
What is this clinical presentation?

Oral lichen planus
slightly more red as you move to the left of the picture
● The white lines have small sunburst effect at the periphery
○ Very very characteristic of lichen planus
○ Will never see this in a leukoplakia
What is this clinical presentation?

Oral lichen planus
Lichen planus of the dorsum of the tongue
this is a hypertrophic form.
Leukoplakia
Etiology
Etiology
The exact etiology remains unknown. Tobacco, alcohol,
chronic local friction, and Candida albicans are important predisposing
factors. Human papilloma virus (HPV) may also be involved in the
pathogenesis of oral leukoplakia.
Leukoplakia
Treatment
- Biopsy to rule out malignancy
- Elimination or discontinuation of predisposing factors,
- systemic retinoid compounds.
- Smoking cessation (leukoplakias often disappear or become smaller within first year of smoking cessation)
- Complete removal with surgical excision, electrocautery, cryosurgery, or laser ablation
What is this clinical presentation?

Lichenoid Reactions
Contact Lesions
a sensitivity in contact with a dental amalgam
▪ When you replace these amalgams, the lichenoid reaction will typically
disappear
What is this clinical presentation?

Oral Lichenoid
Contact lesion
chenoid reaction to dental amalgam and cold: white and erythematous
lesions on the buccal mucosa.
What is this clinical presentation?
pts takes Thiazide Diuretic

Oral Lichenoid Drug
Reaction
What is this clinical presentation?
pts takes allopurinol

Oral Lichenoid Drug
Reaction
Oral Lichenoid Drug
Reaction
Etiology
- Lichenoid reactions may develop after exposure to a medication for periods of > 1 year
- May develop very slowly after the problem is initiated so it can be very challenging to connect the dots
Many different medications that can lead to lichenoid reactions
- Beta blockers, ACE inhibitors, Rituxumab etc…
- A number of new targeted agents “mabs” and “nibs” can cause lichenoid reactions
- In cancer centers, this has become quite a problem because they are taking disease‐modifying drugs

What is this clinical presentation?

Nicotinic Stomatitis
also known as
Smoker’s keratosis
smoker’s palate
- the palatal mucosa becomes diffusely gray or white; numerous slightly elevated papules are noted, usually with punctate red centers
What is this clinical presentation?

Nicotinic Stomatitis
These papules represent inflamed minor salivary glands and their ductal orifices.
What is this clinical presentation

Nicotine Stomatitis.
Hairy Leukoplakia
Etiology
Epstein–Barr virus seems to play an important role in the
pathogenesis.
Hairy Leukoplakia
Treatment
- Not required
- however, in some cases aciclovir or valaciclovir
- can be used with success.
- Topical retinoids or podophyllum resin for temporary remission
What is this clinical presentation?

Pseudomembranous candidiasis
on the palate.
usually caused by Candida albicans
Predisposing factors are local
(poor oral hygiene, xerostomia, mucosal
damage, dentures, antibiotic mouthwashes)
What is this clinical presentation?

Geographic tongue/
areata migrans
Multiple, well-demarcated zones of erythema (due to filiform atrophy) surrounded by slightly elevated, yellow-white, serpentine/ scalloped border
annular
- serpiginous
- atrophic
- Fissured
What is this clinical presentation?

Geographic tongue/
areata migrans
What is this clinical presentation?

Geographic tongue/
areata migrans
What is this clinical presentation?

Geographic tongue/
areata migrans
What is this clinical presentation?

Geographic tongue, localized lesion.
What is this clinical presentation?

Fordyce’s granules
on the buccal mucosa.
a normal anatomical variation.
ectopic sebaceous glands of the oral
mucosa.
What is this clinical presentation?

Leukoedema of the buccal mucosa.
Laskaris,
What is this clinical presentation?

White Sponge Nevus
Diffuse, thickened white plaques
of the buccal mucosa
What is this clinical presentation?

White Sponge Nevus
(Canon disease)
Proliferative Verrucous Leukoplakia
Treatment
complete removal: excision, electrocautery, cryosurgery, or laber ablation
Lesions rarely regress despite therapy
What is this clinical presentation?

Verrucous Carcinoma
Early verrucous carcinoma of the buccal mucosa.
What is this clinical presentation?

Verrucous Carcinoma
Large, exophytic, papillary
mass of the maxillary alveolar ridge.
What is this clinical presentation?

Verrucous Carcinoma
Large, exophytic, papillary
mass of the maxillary alveolar ridge.
What is this clinical presentation?

Verrucous Carcinoma
Extensive papillary, white
lesion of the maxillary vestibule

Traumatic Erythema /Traumatic Hematoma
on the lower lip.
What is this clinical presentation?

Geographic tongue: well-demarcated red patch on the tongue.
What is this clinical presentation?

Median rhomboid glossitis.
a Chronic hyperplastic, erythematous candidiasis
what is this clinical presentation?

Denture stomatitis.
Oral lichen planus
Etiology
Although the cause is not well known, T cell-mediated autoimmune
phenomena are involved in the pathogenesis of lichen planus.
What is this clinical presentation?

Erythroplakia
of the buccal mucosa
Well-demarcated erythematous patch or plaque with soft velvety texture
What is this clinical presentation?

Erythroplakia of the buccal mucosa.
What is this clinical presentation?

Erythroplakia
of the lateral margin of the tongue.
Well-demarcated erythematous patch or plaque with soft velvety texture
What is this clinical presentation?

Erythroplakia
Firey red Well-demarcated patch or plaque with soft velvety texture
transformed into SCC
Oral lichen planus
Treatment:
- Incisional biopsy on non-keratinized, non-ulcerated mucosa
○ Asymptomatic → no tx
○ Symptomatic → 0.5mg/ml Dexamethasone Elixir.
What is this clinical presentation?

Erythroplakia.
Well-circumscribed red patch on the
posterior lateral hard and soft palate
What is this clinical presentation?

Erythroplakia.
Erythematous macule on the right
floor of the mouth.
Biopsy–
Turned out to be early invasive squamous cell
carcinoma.
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Smokeless Tobacco–related Gingival Recession.
Extensive recession of the anterior mandibular facial gingiv
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Tobacco Pouch Keratosis, Severe
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Tobacco Pouch Keratosis, Mild. A soft, fissured,
gray-white lesion of the lower labial mucosa located in the area of
chronic snuff placement.
What is this clinical presentation?

Pemphigus Vulgaris.
. Multiple erosions affecting the
marginal gingiva.
What is this clinical presentation?

Pemphigus Vulgaris.
Multiple erosions of the left
buccal mucosa and soft palate.
What is this clinical presentation?

Pemphigus Vulgaris.
Large, irregularly shaped ulcerations
involving the floor of the mouth and ventral tongue.
What is this clinical presentation?

Pemphigus Vulgaris.
Oral Lichenoid
Contact Lesions
Etiology
Hypersensitivity
to
- dental restorative materials, amalgam or other metal, composite resins
- Foods, oral products
- Especially cinnamon
- dental plaque accumulation are the most common
Oral lichenoid reaction
Treatment
Insicional biopsy Mandated to distinguish from OLP
○ Biopsy white areas on non-keratinized mucosa NOT ulcerated OR red areas
Treatment Replacement of the restorative material, polishing and
smoothing, and good oral hygiene are recommended.
Topical steroid
treatment for a short time is also helpful.
Nicotine Stomatitis
Treatment
Smoking Cessation.
- Nicotine stomatitis is completely reversible, even when it has been present for many decades.
- The palate usually returns to normal within 1 to 2 weeks of smoking cessation.
Nicotine Stomatitis.
Etiology
The elevated temperature, rather than the tobacco chemicals,
is responsible for this lesion.
Geographic tongue/
areata migrans
Treatment
- Generally no treatment is indicated
- Reassuring the patient that the condition is completely benign is often all that is necessary.
- In case of tenderness or a burning sensation that is so severe –topical corticosteroids, such as fluocinonide or betamethasone gel, may provide relief
Geographic tongue/
areata migrans
Etiology
The exact etiology remains unknown. It may be genetic.
Leukoedema
Etiology
Treatment
Etiology
It is due to increased thickness of the epitheliumand intracellular
edema of the prickle-cell layer.
Treatment
No treatment required
White Sponge Nevus
Etiology
Autosomal dominant skin disorder
Etiology:
● This condition is due to a defect in the normal keratinization of the oral mucosa in the 30-member family of keratin filaments, the pair of keratins known as keratin 4 and keratin 13 is specifically expressed in the spinous cell layer of mucosal epithelium.
Verrucous Carcinoma
Etiology
a low-grade variant of squamouscell
carcinoma.
Etiology
Leading theories include
- human papillomavirus (HPV) infection
- chemical carcinogenesis induced by smoking and chewing tobacco
- alcohol consumption
- betel nut chewing (oral lesions),
- chronic inflammation
Verrucous Carcinoma
Treatment
○ Surgical Excision
○ Radiotherapy
Median Rhomboid Glossitis
Treatment
No treatment is required.
Median Rhomboid Glossitis
Etiology
Atrophy of central filiform papillae
Presumably developmental. Candida albicans may also be
involved.
but smokers, people with xerostomia , who use inhalation steroids
and denture wearers are at increased risk
Erythroplakia
Malignant transformation
Erythroplakia is a high risk for malignant transformation. So, if you
encounter an erythroplakia, it’s probably already a cancer or it’s fast‐tracking
towards a cancer
Erythroplakia
Treatment
○ Biopsy required for diagnosis
○ If a source of irritation can be identified and removed, biopsy may be delayed for 2 weeks to allow lesion to heal
○ Complete excision
Smokeless tobacco keratosis
Treatment:
typically resolves weeks after cessation
○ if persists 6+weeks -> biopsy to rule out dysplasia + SCC
Erythroplakia
Treatment
○ Biopsy required for diagnosis
○ If a source of irritation can be identified and removed, biopsy may be delayed for 2 weeks to allow lesion to heal
○ Complete excision
What is this clinical presentation?

Erythroplakia.
Well-circumscribed red patch on the
posterior lateral hard and soft palate
What is this clinical presentation?

Erythroplakia.
Erythematous macule on the right
floor of the mouth.
Biopsy–
Turned out to be early invasive squamous cell
carcinoma.
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Smokeless Tobacco–related Gingival Recession.
Extensive recession of the anterior mandibular facial gingiv
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Tobacco Pouch Keratosis, Severe
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Tobacco Pouch Keratosis, Mild. A soft, fissured,
gray-white lesion of the lower labial mucosa located in the area of
chronic snuff placement.
What is this clinical presentation?

Pemphigus Vulgaris.
. Multiple erosions affecting the
marginal gingiva.
What is this clinical presentation?

Pemphigus Vulgaris.
Multiple erosions of the left
buccal mucosa and soft palate.
What is this clinical presentation?

Pemphigus Vulgaris.
Large, irregularly shaped ulcerations
involving the floor of the mouth and ventral tongue.
What is this clinical presentation?

Pemphigus Vulgaris.
What is this clinical presentation?

Pemphigus vulgaris
● Multiple, chronic, mucocutaneous ulcers
● Many patients also have
● Relatively non‐specific
● Very superficial, only in epithelium
● Occur on any mucosal surface: oral, ocular, nasal, GI, esophageal,
genital
What is this clinical presentation?

Pemphigus vulgaris
PV Lesions can affect
virtually any mucosal
surface (oral, nasal,
ocular, pharyngeal,
esophageal, genital)
What is this clinical presentation?

Pemphigus vulgaris
usually suffer from Desquamative
gingivitis (DG)
More superficial erosion of the marginal gingiva, typically with an
intense erythema and inflammation, and very often in the absence of
local factors that would typically cause a gingivitis
o Hurts to brush their teeth
Immediately look for areas where there are no local factors and look for
inflammation there
o To check the possibility of systemic factors causing local
gingivitis
What is this clinical presentation?

Pemphigus vulgaris
Combination of PV
inflammation and
gingival inflammation
accumulating local
factors can result in
advanced loss of
attachment and tooth
loss
What is this clinical presentation?

Mucous membrane pemphigoid
What is this clinical presentation?

Mucous membrane pemphigoid
SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal
can
result in functional
blindness
What is this clinical presentation?

Mucous membrane pemphigoid
Oral Hygiene: Plaque
related gingival
inflammation
contributing to
continued VB
desquamative
gingivitis
What is this clinical presentation?

Mucous membrane pemphigoid
REMEMBER:
▪ Plaque and calculus can be the consequence of painful MMP lesions
▪ When assessing MMP lesions/desquamative gingivitis, look for areas of intense inflammation WITHOUT local factors as evidence of VB disease
MMP & PV BIOPSY
take two different sites
○ For H&E, still must be perilesional
○ If you get only ulcer just because the clinician thinks
○ that is the pathology → there is no epithelium!
○ The sample is useless and no diagnosis can be made

What is this clinical presentation?

Actinic cheilitis
(Solar cheilosis)
Typical presentation of angular cheilitis with erythema, crusting and mild fissuring of the angles of the mouth bilaterally.
What is this clinical presentation?

Actinic cheilitis
(Solar cheilosis)
Early presetation:
Smooth, blotchy, pale, dry areas
Diffuse, irregular white plaque around line of the lip
Crusted, Scaly
Smokeless tobacco keratosis
Treatment:
typically resolves weeks after cessation
○ if persists 6+weeks -> biopsy to rule out dysplasia + SCC
What is this clinical presentation?

SCC
arising from Actinic Cheilitis
What is this clinical presentation?

Oral Melanoma
a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.
What is this clinical presentation?

Oral Melanoma
an ulcerated, blue-black, slightly elevated lesion in the edentulous, posterior right maxilla. The lesion extends across the residual alveolar ridge onto the palate and onto the facial aspect of the ridge.
What is this clinical presentation?

Oral Melanoma
patient with extensive, black-pigmented and irregularly bordered macule in the maxillary labial mucosa and midline facial gingiva, (teeth 8 and 9). (The patient’s fingers are depicted.)
What is this clinical presentation?

Oral Melanoma
Large, blue-black, irregularly bordered lesion on the upper lip of a male Japanese patient. The diagnosis is oral melanoma.
What is this clinical presentation?

Amalgam tattoo
This image depicts two diffusely bordered, dark gray macules in the left posterior buccal mucosa adjacent to molar teeth that have been restored. .
What is this clinica presentation?

Oral melanoacanthoma.
the buccal mucosa of a middle-aged, black woman with a brown-black, irregularly bordered macule that arose suddenly. The patient was unaware of its presence.
What is this clinical presentation?

Oral melanotic macule
an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.
What is this clinical presentation

Oral Melanoma
What is this clinical presentation

Oral Melanoma
What is this clinical presentation

Oral Melanoma
What is this clinical presentation?

Traumatic ulcer
caused by sharp or puncturing food stuff
What is this clinical presentation?

Traumatic ulcer
a chronic ulcer on the left posterior lateral border of the tongue caused by lingually tilted mandibular 3rd molar. Note central ulceration with peripheral keratosis
What is this clinical presentation?

Traumatic ulcer
Post-anaesthesia traumatic ulcer on lower lip.
What is this clinical presentation?

Traumatic ulcer
Most often on tongue, lips, buccal mucosa
Any sites that may be injured by dentition
What is this clinical presentation?

Traumatic
Granuloma
What is this clinical presentation?

Traumatic
Granuloma
(traumatic ulcertaive granuloma)
What is this clinical presentation?

Traumatic Granuloma
( Traumatic Ulcerative Granuloma)
What is this clinical presentation?

Squamous cell carcinoma
on the buccal mucosa)
What is this clinical presentation?

Erythroplakia and Squamous Cell Carcinoma
Erythroplakia is a general term for red, flat, or eroded velvety lesions that develop in the mouth. In this image, an exophytic squamous cell carcinoma on the tongue is surrounded by a margin of erythroplakia
What is this clinical presentation?

Leukoplakia and Squamous Cell Carcinoma
Leukoplakia is a general term for white hyperkeratotic plaques that develop in the mouth. About 80% are benign. However, in this image, squamous cell carcinoma is present in one of the leukoplakic lesions on the ventral surface of the tongue (arrow).
Pemphigus vulgaris
Etiology
Pemphigus vulgaris is not fully understood.
Experts believe that it’s triggered when a person who has a genetic tendency to get this condition comes into contact with an environmental trigger, such as a chemical or a drug.
In some cases, pemphigus vulgaris will go away once the trigger is removed.
What is this clinical presentation?

Graphite tattoo
Most common location on the palate and gingiva
Gray, black, or blue-ish macule
What is this clinical presentation?

Graphite tattoo
Gray, black, or blue-ish macule
Pemphigus vulgaris
Treatment
Treatment has 3 stages:
● Stage 1: Control
○ Suppress inflammation / lesion activity with Systemic Corticosteroid: Remains initial / 1st‐line treatment…
○ Then quickly add steroid‐sparing agents (mycophenolate mofetil) to minimize dose and duration of corticosteroid treatment as well as improve disease control
● Stage 2: Consolidation
○ Reducing auto‐antibody production with the addition of Immunosuppressants
○ Assessed by the lack of development of NEW lesions
● Stage 3. Remission / Maintenance:
○ achieving complete remission of lesion activity OFF medication is the GOAL
○ When lesion activity OFF medications cannot be achieved, principle of MINIMALLY effective therapy is the goal, typically with combination of immunosuppressant medications
○ RITUXIMAB has become the FIRST CHOICE treatment after
○ the consolidation phase to achieve DISEASE REMISSION
● TOPICAL / INJECTABLE CORTICOSTEROID MEDICATIONS
○ o Can be used to help control limited number of lesions resistant to systemic therapy: it treats ONLY the disease
○ outcome (lesions) and not the systemic illness / pathologic antibody production
○ ex:clobetesol 0. 05% , halbetesol 0.05% (most potent)
What is this clinical presentation?

Traumatic ulcer of the tongue.
What is this clinical presentation?

Hemangioma of Infancy
a relatively common benign proliferation of
blood vessels that primarily develops during childhood.
display a rapid growth phase with endothelial
cell proliferation, followed by gradual involution.
What is this clinical finding?

Hemangioma of Infancy
What is this clinical finding?

Necrotizing Sialadenometaplasia
we see two ulcers on the palate
Mostly
● Palatal salivary glands
○ Possible for parotid
● 75% of case on posterior palate
● Hard>Soft palate
● 2/3rd are unilateral
Mucous membrane pemphigoid
Etiology
Mucocutaneous autoimmune disease characterized by sub‐epithelial
blisters (bullae) which ruptures to form large, non‐healing ulcerations
What is this clinical finding?

Frictional Keratosis.
There is a rough, hyperkeratotic change to the posterior mandibular alveolar ridge (“alveolar ridge keratosis”),
because this area is now edentulous and becomes traumatized
from mastication.
Such frictional keratoses should resolve when the
source of irritation is eliminated and should not be mistaken for true
leukoplakia.
What is this clinical finding?

Frictional Keratosis
the white surrounding a a traumatic ulcer
Symptomatic traumatic ulceration of the left mid-ventral tongue associated with a sharp left lower molar. The ulcer has flat edges and is surrounded by an area of frictional keratosis.
Frictional Keratosis.
Differential Diagnosis

Leukoplakia
Linea alba
Chronic cheek chewing (bite injury)
Candidiasis
Oral Lichen planus
Squamous cell carcinoma
What is this clinical finding?

Frictional keratosis
on the tongue
Frictional Keratosis
Etiology

- Trauma from Sharp cusp & ortho appliance
- Chronic mechanical irritation (chronic biting)
- Masticatory function
- Normal hyperplastic response
- Dentures/missing teeth
Frictional Keratosis
Treatment

- Remove the cauative factor that caused the trauma
- observe large lesion regularly
excellent prognosis
What is this clinical presentation?

dry‐mouth
patient
a classic example
• Classic fissuring
• depapillation of the tongue papilla
• some white changes on the tongue.
What is this clinical presentation?

dry‐mouth
from radiation
Note the Ropy, frothiness on the palate.
- The tissues are red and irritated due to candida infection as well.
What is this clinical presentation?

dry Mouth
Cervical caries related
to radiation.
The patient is a smoker and coffee drinker –> explains the staining
What is this clinical presentation?

dry Mouth
Incisal caries in a
radiation patient:
Incisal caries is a sure sign of severe dry mouth/ significant salivary gland hypofunction
Mucous membrane pemphigoid
Treatment
o Approach is similar to PV – but generally not as aggressive unless
hi‐risk areas ( ocular, esophageal ) where more intense immunosuppression indicated
▪ NON‐immunosuppressive treatments uniquely effective:
- *o** Dapsone
- *o Tetracycline + nicotinamide**
Actinic cheilitis
malignant transformation
Actinic cheilitis has 2 times of risk for developing SCC of the lip.
SCC on the lips is 11 times as likely to metastasize compared to SCC found on other parts of the body
Actinic cheilitis
Etiology
due to chronic ultraviolet light exposure.
Actinic cheilitis
Treatment
- avoid sun exposure
- Laser ablation is preferred for severe actinic cheilitis
- surgical excision is recommended for severe actinic cheilitis with evidence of high-grade dysplasia
- Lip Shaving” (Vermilionectomy)
- can also use cryotherapy, electrodesiccation
It requires long term follow up and prognosis is good if caught early
Severity of patients
with xerostomia using
objective measures

What is this clinical presentation?

SJÖGREN’S SYNDROME
Autoimmune exocrinopathy
Marked bilateral parotid gland enlargement in a patient with primary Sjögren syndrome
Dry mouth and eyes resulting from a chronic progressive loss of secretory function (Slowly but surely, the salivary glands and/or lacrimal glands (some cases are more lacrimal & less salivary or vice versa); slow & progressive
Patients with Sjogren’s can have bilateral salivary gland enlargement (parotid) (Sometimes we may see a unilateral enlargement of the salivary
glands due to retrograde infections.)
increased risk of lymphoma (MALT type)
What is this clinical presentation?

SJÖGREN’S SYNDROME
Dry Mouth
very severe
cervical disease & very dry lips
What is this clinical presentation?

Depapillated &
Fissured Tongue
SJÖGREN’S SYNDROME
What is this clinical presentation?

a patient
with a
bacterial sialadenitis
who has
SJÖGREN’S SYNDROME
When we examine such patients and ”milk” the gland ► you actually see a purulent drainage from the gland itself.
SJÖGREN’S SYNDROME
Management

These patients LOW USFR, no response to stimulation (aka abnormal USFR/SFR)
- Rehydrate if dehydrated
- Treat underlying conditions (i.e. DM)
- Salivary substitutes (glycerin)
- Minimize damage to glands from radiation
- Prevention of complications & palliative treatment
- Optimal hygiene
- Restore caries
- Smooth sharp edges in oral cavity
- Fluoride therapy
- Antifungals
- Chlorhexidine rinses w/o alcohol
- Sialendoscopy
- Salitron - salivary pacemaker
- ALTENS (acupuncture like transcutaneous electrical nerve stimulation)
What is this clinical presentation?

Sjögren Syndrome
- bilateral enlargement of the submandibular glands
- angular cheilitis, dry and cracked lips and fissured and despapilated tongue
- severe ocular lesions.
Oral Melanoma
Etiology
Unknown. Ultraviolet radiation is an important causative factor for skin melanoma
Acute sun damage can cause it more than chronic exposure
Oral Melanoma
Risk Factors
Fair skin
A history of sunburn
Excessive ultraviolet (UV) light exposure.
Living closer to the equator or at a higher elevation
Having many moles or unusual moles
A family history of melanoma
Weakened immune system.
Oral Melanoma
Treatment
- Surgical excision
- Radiotherapy
- Chemotherapy
Traumatic ulcer/Traumatic ulcerative granluoma
Etiology
Etiology
- typically caused by trauma. In more than half the cases, the patient does not recall traumatizing the area although this may have occurred during sleep.
- Chronic mucosal trauma from adjacent teeth
- Some adjacent source of irritation
Traumatic ulcer/Traumatic ulcerative granluoma
Treatment
Remove cause of irritation
Topical anesthetic or film for pain relief
If there is no obvious cause then ► biopsy
squamous cell carcinoma
Risk factors
HPV + SCC
Area affected: ( Oropharynx cancers largely involved tonsils, . Posterior 3rd of the Tongue)
Younger pts, 3:1 Males to females ratio, high socio-eco status
Incidence is decreasing
less aggressive → higher survival rates ( Better than HPV negative SCC)
HPV - SCC
The chief risk factors for oral squamous cell carcinoma are
Smoking (especially > 2 packs/day)
Alcohol use
Risk increases dramatically when alcohol use exceeds 6 oz of distilled liquor, 15 oz of wine, or 36 oz of beer/day. The combination of heavy smoking and alcohol abuse is estimated to raise the risk 100-fold in women and 38-fold in men.
( this affects these ares : the tongue, floor of mouth, buccal mucosa, or gingiva)
mostly men, low socio-economic factors
Incidence is decreasing
Very aggressive → lower survival rates
SCC treatment
Early stage: Radiation and/or Surgical removal
Late stage : combination of surgery, radiation therapy, or chemotherapy
Graphite tattoo
Treatment
If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft
Graphite tattoo
Etiology
result from pencil lead that is traumatically implanted, usually during the elementary school years
Hemangioma of Infancy
Treatment
○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”
What is this clinical finding?
Necrotizing Sialadenometaplasia
an uncommon, usually self-limiting, benign inflammatory disorder of the salivary glands.
Here it is on the palate
Necrotizing Sialadenometaplasia
Etiology
The cause is uncertain, although the hypothesis of ischemic
necrosis after vascular infarction seems acceptable.
Necrotizing Sialadenometaplasia
Treatment
No Treatment Needed
but we need to biopsy to rule out other diseases
What is this clinical finding?
Xerostomia-related Caries
Or
Dry Mouth
. Extensive cervical caries of
mandibular dentition secondary to radiation-related xerostomia.
Dry mouth
Subjective vs Objective
Xerostomia
The subjective experience of a dry mouth (ie a symptom)
Salivary Hypofunction
The objective measurement of a reduction in salivary flow (a sign)
What is the normal rate for Stimulated Saliva
Production
Stimulated Saliva
Production
▪ 200+ ml/day
▪ Flow rate: mean 1-2 ml/min, maximum 7 ml/min
o “Normal” range is very wide
What is the normal rate for Unstimulated Saliva
Production
300 ml/day
▪ Flow rate: mean 0.3 ml/min
What are Factors affecting unstimulated flow include?
- Dehydration
- Medical conditions
- Body posture
- Lighting conditions
- Circadian/circannual rhythm (lowest during)
- Medications
Age is an independent factor for whole saliva andsubmandibular/sublingual gland secretion (but notparotid).
What are Factors affecting stimulated flow include:
- Mechanical stimuli
- Vomiting
- Gustatory/olfactory stimuli (acid/smell)
- Gland size
Age is an independent factor for whole saliva (but not
for parotid and minor gland secretions)
What causes
dry mouth?
Central inhibition as a result of connections between the primary salivary centers and the
higher centers of the brain.
● What causes xerostomia in absence of measurable salivary hypofunction?
-
May be a reduction in baseline sialometry which is still above “normal.”
- If they get a decrease in the salivary flow, they still may be in the normal range, but for them the experience is that they have got dry mouth.
-
Saliva film thickness
- Palatal mucous gland secretions?
- Anterior dorsum of tongue?
-
Relative contributions by glands
- Mucins, proteins?
- Alterations in sensory perception?
- Mental status/central inhibition?
What cause
Salivary
Hypofunction?
● Dehydration
● Medications (Rx & OTC)
- Direct damage to glands
- Head and neck radiotherapy
- As a result of radiation it’s irreversible damage to the glands
- Chemotherapy (reversible)
- Autoimmune diseases
- Primary vs Secondary Sjögren’s Syndrome, GVHD
- HIV disease
● Decreased mastication (tooth loss, soft diet)
● Conditions affecting the CNS:
- Psychologic disorders (depression/anxiety?), Alzheimer’s, Parkinson’s, Cerebral palsy
To have dry mouth
xerostomia
what is the rate of Unstimulated and Stimulated Salivary flow
USFR
and
SFR
Abnormal unstimulated USFR= <0.1–0.2ml/min
Abnormal stiumated SFR = <0.5ml/min
How to manage with normal USFR and SFR?
- Salivary stimulation (OTC) to stimulate their glands
- Salivary lubrication ( to improve it)
- Humidification ( like a humidifier in the room at night)
- Hydration/prevent dehydration (ie avoid alcohol, caffeine both will act as a
- diuretic and lead to dehydration).
- Monitor closely to rule out emerging disease ( to see whether they are developing Sjogren’s or something else we want to follow them over time)
How to manage with abnormal USFR and normal SFR?
(respond to stimulated)
Abnormal unstimulated USFR= <0.1–0.2ml/min
- Look for possible causes (major cause will be medications & can dehydration or others)
- Restore chewing function (Masticatory issues)
- Reduce medication‐induced salivary hypofunction
- Prescribe Salivary stimulation OTC, Rx medications, others
- Prescribe Salivary lubrication
- Humidification ‐use humidifiers
- Hydration/prevent dehydration (ie avoid alcohol, caffeine)
- Treat oral consequences (such as candidiasis treated with an antifungal or caries with management of caries).
How to manage with abnormal USFR and abnormal SFR?
Abnormal unstimulated USFR= <0.1–0.2ml/min
Abnormal stiumated SFR = <0.5ml/min
- If dehydrated ► rehydrate or treat underlying condition
- People with uncontrolled diabetes, once you control the diabetes‐ their flow comes back.
- All we can do is offering Salivary substitutes (sprays, gels, rinses )
- For patients with high dose radiation treatment ► makes sure they get the INRT
- Minimizing damage to salivary glands ( there are other strategies for that)
- Prevention and treatment of oral complications
What are the
Prescription
Medications
for people with
low USFR and
some oral signs, but
responds to stimulation ?
(abnormal USFR, Normal/improved SFR)
(include dosage and usage)
– Muscarinic agonists:
– Pilocarpine 5‐7.5mg tid & qhs (can go as
high as 10mg qid)
– Cevimeline 30mg tid (can go as high as
60mg tid)
Contradicated for : CV disease, hepatic, renal or respiratory diseases or narrow angle glaucoma
Pilocarpine affects M1 & M3
side effects (sweating, flushing,
rhinitis, increased urination, weakness and
some experience the shakes. )
Cevimeline affects M3 only
fewer side effects
Erythroplakia
Treatment
○ Biopsy required for diagnosis
○ If a source of irritation can be identified and removed, biopsy may be delayed for 2 weeks to allow lesion to heal
○ Complete excision
What is this clinical presentation?

Erythroplakia.
Well-circumscribed red patch on the
posterior lateral hard and soft palate
What is this clinical presentation?

Erythroplakia.
Erythematous macule on the right
floor of the mouth.
Biopsy–
Turned out to be early invasive squamous cell
carcinoma.
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Smokeless Tobacco–related Gingival Recession.
Extensive recession of the anterior mandibular facial gingiv
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Tobacco Pouch Keratosis, Severe
What is this clinical presentation?

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS
Tobacco Pouch Keratosis, Mild. A soft, fissured,
gray-white lesion of the lower labial mucosa located in the area of
chronic snuff placement.
What is this clinical presentation?

Pemphigus Vulgaris.
. Multiple erosions affecting the
marginal gingiva.
What is this clinical presentation?

Pemphigus Vulgaris.
Multiple erosions of the left
buccal mucosa and soft palate.
What is this clinical presentation?

Pemphigus Vulgaris.
Large, irregularly shaped ulcerations
involving the floor of the mouth and ventral tongue.
What is this clinical presentation?

Pemphigus Vulgaris.
What is this clinical presentation?

Pemphigus vulgaris
● Multiple, chronic, mucocutaneous ulcers
● Many patients also have
● Relatively non‐specific
● Very superficial, only in epithelium
● Occur on any mucosal surface: oral, ocular, nasal, GI, esophageal,
genital
What is this clinical presentation?

Pemphigus vulgaris
PV Lesions can affect
virtually any mucosal
surface (oral, nasal,
ocular, pharyngeal,
esophageal, genital)
What is this clinical presentation?

Pemphigus vulgaris
usually suffer from Desquamative
gingivitis (DG)
More superficial erosion of the marginal gingiva, typically with an
intense erythema and inflammation, and very often in the absence of
local factors that would typically cause a gingivitis
o Hurts to brush their teeth
Immediately look for areas where there are no local factors and look for
inflammation there
o To check the possibility of systemic factors causing local
gingivitis
What is this clinical presentation?

Pemphigus vulgaris
Combination of PV
inflammation and
gingival inflammation
accumulating local
factors can result in
advanced loss of
attachment and tooth
loss
What is this clinical presentation?

Mucous membrane pemphigoid
What is this clinical presentation?

Mucous membrane pemphigoid
SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal
can
result in functional
blindness
What is this clinical presentation?

Mucous membrane pemphigoid
Oral Hygiene: Plaque
related gingival
inflammation
contributing to
continued VB
desquamative
gingivitis
What is this clinical presentation?

Mucous membrane pemphigoid
REMEMBER:
▪ Plaque and calculus can be the consequence of painful MMP lesions
▪ When assessing MMP lesions/desquamative gingivitis, look for areas of intense inflammation WITHOUT local factors as evidence of VB disease
MMP & PV BIOPSY
take two different sites
○ For H&E, still must be perilesional
○ If you get only ulcer just because the clinician thinks
○ that is the pathology → there is no epithelium!
○ The sample is useless and no diagnosis can be made

What is this clinical presentation?

Actinic cheilitis
(Solar cheilosis)
Typical presentation of angular cheilitis with erythema, crusting and mild fissuring of the angles of the mouth bilaterally.
What is this clinical presentation?

Actinic cheilitis
(Solar cheilosis)
Early presetation:
Smooth, blotchy, pale, dry areas
Diffuse, irregular white plaque around line of the lip
Crusted, Scaly
Smokeless tobacco keratosis
Treatment:
typically resolves weeks after cessation
○ if persists 6+weeks -> biopsy to rule out dysplasia + SCC
What is this clinical presentation?

SCC
arising from Actinic Cheilitis
What is this clinical presentation?

Oral Melanoma
a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.
What is this clinical presentation?

Oral Melanoma
an ulcerated, blue-black, slightly elevated lesion in the edentulous, posterior right maxilla. The lesion extends across the residual alveolar ridge onto the palate and onto the facial aspect of the ridge.
What is this clinical presentation?

Oral Melanoma
patient with extensive, black-pigmented and irregularly bordered macule in the maxillary labial mucosa and midline facial gingiva, (teeth 8 and 9). (The patient’s fingers are depicted.)
What is this clinical presentation?

Oral Melanoma
Large, blue-black, irregularly bordered lesion on the upper lip of a male Japanese patient. The diagnosis is oral melanoma.
What is this clinical presentation?

Amalgam tattoo
This image depicts two diffusely bordered, dark gray macules in the left posterior buccal mucosa adjacent to molar teeth that have been restored. .
What is this clinica presentation?

Oral melanoacanthoma.
the buccal mucosa of a middle-aged, black woman with a brown-black, irregularly bordered macule that arose suddenly. The patient was unaware of its presence.
What is this clinical presentation?

Oral melanotic macule
an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.
What is this clinical presentation

Oral Melanoma
What is this clinical presentation

Oral Melanoma
What is this clinical presentation

Oral Melanoma
What is this clinical presentation?

Traumatic ulcer
caused by sharp or puncturing food stuff
What is this clinical presentation?

Traumatic ulcer
a chronic ulcer on the left posterior lateral border of the tongue caused by lingually tilted mandibular 3rd molar. Note central ulceration with peripheral keratosis
What is this clinical presentation?

Traumatic ulcer
Post-anaesthesia traumatic ulcer on lower lip.
What is this clinical presentation?

Traumatic ulcer
Most often on tongue, lips, buccal mucosa
Any sites that may be injured by dentition
What is this clinical presentation?

Traumatic
Granuloma
What is this clinical presentation?

Traumatic
Granuloma
(traumatic ulcertaive granuloma)
What is this clinical presentation?

Traumatic Granuloma
( Traumatic Ulcerative Granuloma)
What is this clinical presentation?

Squamous cell carcinoma
on the buccal mucosa)
What is this clinical presentation?

Erythroplakia and Squamous Cell Carcinoma
Erythroplakia is a general term for red, flat, or eroded velvety lesions that develop in the mouth. In this image, an exophytic squamous cell carcinoma on the tongue is surrounded by a margin of erythroplakia
What is this clinical presentation?

Leukoplakia and Squamous Cell Carcinoma
Leukoplakia is a general term for white hyperkeratotic plaques that develop in the mouth. About 80% are benign. However, in this image, squamous cell carcinoma is present in one of the leukoplakic lesions on the ventral surface of the tongue (arrow).
Pemphigus vulgaris
Etiology
Pemphigus vulgaris is not fully understood.
Experts believe that it’s triggered when a person who has a genetic tendency to get this condition comes into contact with an environmental trigger, such as a chemical or a drug.
In some cases, pemphigus vulgaris will go away once the trigger is removed.
What is this clinical presentation?

Graphite tattoo
Most common location on the palate and gingiva
Gray, black, or blue-ish macule
What is this clinical presentation?

Graphite tattoo
Gray, black, or blue-ish macule
Pemphigus vulgaris
Treatment
Treatment has 3 stages:
● Stage 1: Control
○ Suppress inflammation / lesion activity with Systemic Corticosteroid: Remains initial / 1st‐line treatment…
○ Then quickly add steroid‐sparing agents (mycophenolate mofetil) to minimize dose and duration of corticosteroid treatment as well as improve disease control
● Stage 2: Consolidation
○ Reducing auto‐antibody production with the addition of Immunosuppressants
○ Assessed by the lack of development of NEW lesions
● Stage 3. Remission / Maintenance:
○ achieving complete remission of lesion activity OFF medication is the GOAL
○ When lesion activity OFF medications cannot be achieved, principle of MINIMALLY effective therapy is the goal, typically with combination of immunosuppressant medications
○ RITUXIMAB has become the FIRST CHOICE treatment after
○ the consolidation phase to achieve DISEASE REMISSION
● TOPICAL / INJECTABLE CORTICOSTEROID MEDICATIONS
○ o Can be used to help control limited number of lesions resistant to systemic therapy: it treats ONLY the disease
○ outcome (lesions) and not the systemic illness / pathologic antibody production
○ ex:clobetesol 0. 05% , halbetesol 0.05% (most potent)
What is this clinical presentation?

Traumatic ulcer of the tongue.
What is this clinical presentation?

Hemangioma of Infancy
a relatively common benign proliferation of
blood vessels that primarily develops during childhood.
display a rapid growth phase with endothelial
cell proliferation, followed by gradual involution.
What is this clinical finding?

Hemangioma of Infancy
What is this clinical finding?

Necrotizing Sialadenometaplasia
we see two ulcers on the palate
Mostly
● Palatal salivary glands
○ Possible for parotid
● 75% of case on posterior palate
● Hard>Soft palate
● 2/3rd are unilateral
Mucous membrane pemphigoid
Etiology
Mucocutaneous autoimmune disease characterized by sub‐epithelial
blisters (bullae) which ruptures to form large, non‐healing ulcerations
What is this clinical finding?

Frictional Keratosis.
There is a rough, hyperkeratotic change to the posterior mandibular alveolar ridge (“alveolar ridge keratosis”),
because this area is now edentulous and becomes traumatized
from mastication.
Such frictional keratoses should resolve when the
source of irritation is eliminated and should not be mistaken for true
leukoplakia.
What is this clinical finding?

Frictional Keratosis
the white surrounding a a traumatic ulcer
Symptomatic traumatic ulceration of the left mid-ventral tongue associated with a sharp left lower molar. The ulcer has flat edges and is surrounded by an area of frictional keratosis.
Frictional Keratosis.
Differential Diagnosis

Leukoplakia
Linea alba
Chronic cheek chewing (bite injury)
Candidiasis
Oral Lichen planus
Squamous cell carcinoma
What is this clinical finding?

Frictional keratosis
on the tongue
Frictional Keratosis
Etiology

- Trauma from Sharp cusp & ortho appliance
- Chronic mechanical irritation (chronic biting)
- Masticatory function
- Normal hyperplastic response
- Dentures/missing teeth
Frictional Keratosis
Treatment

- Remove the cauative factor that caused the trauma
- observe large lesion regularly
excellent prognosis
What is this clinical presentation?

dry‐mouth
patient
a classic example
• Classic fissuring
• depapillation of the tongue papilla
• some white changes on the tongue.
What is this clinical presentation?

dry‐mouth
from radiation
Note the Ropy, frothiness on the palate.
- The tissues are red and irritated due to candida infection as well.
What is this clinical presentation?

dry Mouth
Cervical caries related
to radiation.
The patient is a smoker and coffee drinker –> explains the staining
What is this clinical presentation?

dry Mouth
Incisal caries in a
radiation patient:
Incisal caries is a sure sign of severe dry mouth/ significant salivary gland hypofunction
Mucous membrane pemphigoid
Treatment
o Approach is similar to PV – but generally not as aggressive unless
hi‐risk areas ( ocular, esophageal ) where more intense immunosuppression indicated
▪ NON‐immunosuppressive treatments uniquely effective:
- *o** Dapsone
- *o Tetracycline + nicotinamide**
Actinic cheilitis
malignant transformation
Actinic cheilitis has 2 times of risk for developing SCC of the lip.
SCC on the lips is 11 times as likely to metastasize compared to SCC found on other parts of the body
Actinic cheilitis
Etiology
due to chronic ultraviolet light exposure.
Actinic cheilitis
Treatment
- avoid sun exposure
- Laser ablation is preferred for severe actinic cheilitis
- surgical excision is recommended for severe actinic cheilitis with evidence of high-grade dysplasia
- Lip Shaving” (Vermilionectomy)
- can also use cryotherapy, electrodesiccation
It requires long term follow up and prognosis is good if caught early
Severity of patients
with xerostomia using
objective measures

What is this clinical presentation?

SJÖGREN’S SYNDROME
Autoimmune exocrinopathy
Marked bilateral parotid gland enlargement in a patient with primary Sjögren syndrome
Dry mouth and eyes resulting from a chronic progressive loss of secretory function (Slowly but surely, the salivary glands and/or lacrimal glands (some cases are more lacrimal & less salivary or vice versa); slow & progressive
Patients with Sjogren’s can have bilateral salivary gland enlargement (parotid) (Sometimes we may see a unilateral enlargement of the salivary
glands due to retrograde infections.)
increased risk of lymphoma (MALT type)
What is this clinical presentation?

SJÖGREN’S SYNDROME
Dry Mouth
very severe
cervical disease & very dry lips
What is this clinical presentation?

Depapillated &
Fissured Tongue
SJÖGREN’S SYNDROME
What is this clinical presentation?

a patient
with a
bacterial sialadenitis
who has
SJÖGREN’S SYNDROME
When we examine such patients and ”milk” the gland ► you actually see a purulent drainage from the gland itself.
SJÖGREN’S SYNDROME
Management

These patients LOW USFR, no response to stimulation (aka abnormal USFR/SFR)
- Rehydrate if dehydrated
- Treat underlying conditions (i.e. DM)
- Salivary substitutes (glycerin)
- Minimize damage to glands from radiation
- Prevention of complications & palliative treatment
- Optimal hygiene
- Restore caries
- Smooth sharp edges in oral cavity
- Fluoride therapy
- Antifungals
- Chlorhexidine rinses w/o alcohol
- Sialendoscopy
- Salitron - salivary pacemaker
- ALTENS (acupuncture like transcutaneous electrical nerve stimulation)
What is this clinical presentation?

Sjögren Syndrome
- bilateral enlargement of the submandibular glands
- angular cheilitis, dry and cracked lips and fissured and despapilated tongue
- severe ocular lesions.
Oral Melanoma
Etiology
Unknown. Ultraviolet radiation is an important causative factor for skin melanoma
Acute sun damage can cause it more than chronic exposure
Oral Melanoma
Risk Factors
Fair skin
A history of sunburn
Excessive ultraviolet (UV) light exposure.
Living closer to the equator or at a higher elevation
Having many moles or unusual moles
A family history of melanoma
Weakened immune system.
Oral Melanoma
Treatment
- Surgical excision
- Radiotherapy
- Chemotherapy
Traumatic ulcer/Traumatic ulcerative granluoma
Etiology
Etiology
- typically caused by trauma. In more than half the cases, the patient does not recall traumatizing the area although this may have occurred during sleep.
- Chronic mucosal trauma from adjacent teeth
- Some adjacent source of irritation
Traumatic ulcer/Traumatic ulcerative granluoma
Treatment
Remove cause of irritation
Topical anesthetic or film for pain relief
If there is no obvious cause then ► biopsy
squamous cell carcinoma
Risk factors
HPV + SCC
Area affected: ( Oropharynx cancers largely involved tonsils, . Posterior 3rd of the Tongue)
Younger pts, 3:1 Males to females ratio, high socio-eco status
Incidence is decreasing
less aggressive → higher survival rates ( Better than HPV negative SCC)
HPV - SCC
The chief risk factors for oral squamous cell carcinoma are
Smoking (especially > 2 packs/day)
Alcohol use
Risk increases dramatically when alcohol use exceeds 6 oz of distilled liquor, 15 oz of wine, or 36 oz of beer/day. The combination of heavy smoking and alcohol abuse is estimated to raise the risk 100-fold in women and 38-fold in men.
( this affects these ares : the tongue, floor of mouth, buccal mucosa, or gingiva)
mostly men, low socio-economic factors
Incidence is decreasing
Very aggressive → lower survival rates
SCC treatment
Early stage: Radiation and/or Surgical removal
Late stage : combination of surgery, radiation therapy, or chemotherapy
Graphite tattoo
Treatment
If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft
Graphite tattoo
Etiology
result from pencil lead that is traumatically implanted, usually during the elementary school years
Hemangioma of Infancy
Treatment
○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”
What is this clinical finding?
Necrotizing Sialadenometaplasia
an uncommon, usually self-limiting, benign inflammatory disorder of the salivary glands.
Here it is on the palate
Necrotizing Sialadenometaplasia
Etiology
The cause is uncertain, although the hypothesis of ischemic
necrosis after vascular infarction seems acceptable.
Necrotizing Sialadenometaplasia
Treatment
No Treatment Needed
but we need to biopsy to rule out other diseases
What is this clinical finding?
Xerostomia-related Caries
Or
Dry Mouth
. Extensive cervical caries of
mandibular dentition secondary to radiation-related xerostomia.
Dry mouth
Subjective vs Objective
Xerostomia
The subjective experience of a dry mouth (ie a symptom)
Salivary Hypofunction
The objective measurement of a reduction in salivary flow (a sign)
What is the normal rate for Stimulated Saliva
Production
Stimulated Saliva
Production
▪ 200+ ml/day
▪ Flow rate: mean 1-2 ml/min, maximum 7 ml/min
o “Normal” range is very wide
What is the normal rate for Unstimulated Saliva
Production
300 ml/day
▪ Flow rate: mean 0.3 ml/min
What are Factors affecting unstimulated flow include?
- Dehydration
- Medical conditions
- Body posture
- Lighting conditions
- Circadian/circannual rhythm (lowest during)
- Medications
Age is an independent factor for whole saliva andsubmandibular/sublingual gland secretion (but notparotid).
What are Factors affecting stimulated flow include:
- Mechanical stimuli
- Vomiting
- Gustatory/olfactory stimuli (acid/smell)
- Gland size
Age is an independent factor for whole saliva (but not
for parotid and minor gland secretions)
What causes
dry mouth?
Central inhibition as a result of connections between the primary salivary centers and the
higher centers of the brain.
● What causes xerostomia in absence of measurable salivary hypofunction?
-
May be a reduction in baseline sialometry which is still above “normal.”
- If they get a decrease in the salivary flow, they still may be in the normal range, but for them the experience is that they have got dry mouth.
-
Saliva film thickness
- Palatal mucous gland secretions?
- Anterior dorsum of tongue?
-
Relative contributions by glands
- Mucins, proteins?
- Alterations in sensory perception?
- Mental status/central inhibition?
What cause
Salivary
Hypofunction?
● Dehydration
● Medications (Rx & OTC)
- Direct damage to glands
- Head and neck radiotherapy
- As a result of radiation it’s irreversible damage to the glands
- Chemotherapy (reversible)
- Autoimmune diseases
- Primary vs Secondary Sjögren’s Syndrome, GVHD
- HIV disease
● Decreased mastication (tooth loss, soft diet)
● Conditions affecting the CNS:
- Psychologic disorders (depression/anxiety?), Alzheimer’s, Parkinson’s, Cerebral palsy
To have dry mouth
xerostomia
what is the rate of Unstimulated and Stimulated Salivary flow
USFR
and
SFR
Abnormal unstimulated USFR= <0.1–0.2ml/min
Abnormal stiumated SFR = <0.5ml/min
How to manage with normal USFR and SFR?
- Salivary stimulation (OTC) to stimulate their glands
- Salivary lubrication ( to improve it)
- Humidification ( like a humidifier in the room at night)
- Hydration/prevent dehydration (ie avoid alcohol, caffeine both will act as a
- diuretic and lead to dehydration).
- Monitor closely to rule out emerging disease ( to see whether they are developing Sjogren’s or something else we want to follow them over time)
How to manage with abnormal USFR and normal SFR?
(respond to stimulated)
Abnormal unstimulated USFR= <0.1–0.2ml/min
- Look for possible causes (major cause will be medications & can dehydration or others)
- Restore chewing function (Masticatory issues)
- Reduce medication‐induced salivary hypofunction
- Prescribe Salivary stimulation OTC, Rx medications, others
- Prescribe Salivary lubrication
- Humidification ‐use humidifiers
- Hydration/prevent dehydration (ie avoid alcohol, caffeine)
- Treat oral consequences (such as candidiasis treated with an antifungal or caries with management of caries).
How to manage with abnormal USFR and abnormal SFR?
Abnormal unstimulated USFR= <0.1–0.2ml/min
Abnormal stiumated SFR = <0.5ml/min
- If dehydrated ► rehydrate or treat underlying condition
- People with uncontrolled diabetes, once you control the diabetes‐ their flow comes back.
- All we can do is offering Salivary substitutes (sprays, gels, rinses )
- For patients with high dose radiation treatment ► makes sure they get the INRT
- Minimizing damage to salivary glands ( there are other strategies for that)
- Prevention and treatment of oral complications
What are the
Prescription
Medications
for people with
low USFR and
some oral signs, but
responds to stimulation ?
(abnormal USFR, Normal/improved SFR)
(include dosage and usage)
– Muscarinic agonists:
– Pilocarpine 5‐7.5mg tid & qhs (can go as
high as 10mg qid)
– Cevimeline 30mg tid (can go as high as
60mg tid)
Contradicated for : CV disease, hepatic, renal or respiratory diseases or narrow angle glaucoma
Pilocarpine affects M1 & M3
side effects (sweating, flushing,
rhinitis, increased urination, weakness and
some experience the shakes. )
Cevimeline affects M3 only
fewer side effects