STC Flashcards

(496 cards)

1
Q

Irritation Fibromas

Composed of

Etiology

Clinical features ;Color

Location

Treatment

A
  • 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
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2
Q

What is this clinical finding?

A

Irritation Fibromas

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3
Q

What is this clinical finding?

A

Irritation Fibromas

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5
Q

What is this clinical finding?

A

Chronic Hyperplastic Pulpitis (pulp polyp)

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7
Q
A

Giant Cell Fibroma

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8
Q

Chronic Hyperplastic Pulpitis

What is it?

Location?

Age?

Clinical Appearance?

Treatment?

A

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

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10
Q

Giant Cell Fibroma

A
  • 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\
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11
Q

What are these clinical findings (what is the name of the syndrome or complex?)

A

Tuberous sclerosis complex

we see A lot of gingival enlargement – is this overgrowth from disease or from seizure medication? Multi organ system involvement

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13
Q

What is this clinical finding?

A

Epulis Fissuratum

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14
Q

Cowden Syndrome

A
  • (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)
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15
Q

What is this clinical finding?

A

Inflammatory Papillary Hyperplasia of the Palate

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16
Q

What is these clinical findings? (what is the name of the syndrome or complex?)

A

Cowden Syndrome

Very rare!

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17
Q

Tuberous sclerosis complex

A

• 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,

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19
Q

Epulis Fissuratum

AKA

Cause

Location

Clinical presentation

Composed of

Treatment

A

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

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20
Q

What is the clinical finding?

A

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

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22
Q

What is this clinical finding?

A

Pyogenic Granuloma:

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23
Q

Pyogenic Granuloma

Histology

A

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

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24
Q

What is this clinical finding?

A

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

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25
Q

Inflammatory Papillary Hyperplasia of the Palate

Majority occur with what disease?

Associated with what?

Clinical appearance

Treatment

A
  • 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
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26
Q

What is this clinical finding?

A

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

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27
Q

Peripheral Ossifying Fibroma

Histology

A
  • 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
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29
Q

What is this clinical finding?

A

Peripheral Giant Cell Granuloma

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30
Q

Peripheral Giant Cell Granuloma

Histology

A

Giant cells inside the lesion

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31
Q

What are the 3P

or 4P?

A

• Pyogenic granuloma/pregnancy tumor
• Peripheral ossifying**_or_**cementifying fibroma
• Peripheral giant cell granuloma
• Peripheral fibroma (4P)

Memorize these well!

All benign soft tissue lesions

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32
**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
33
**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
34
**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)
35
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**
36
**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
37
What is this clinical finding?
Hereditary Gingivofibromatosis
39
**Infantile Hemangioma** **(“strawberry” hemangioma).** Infant with two red, nodular masses on the posterior scalp and neck *Neville Cr*
40
**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
41
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
42
What is this clinical finding?
**Capillary Malformation (Low flow)**
43
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
44
What is this clinical finding?
Venous malformation (low flow) *Many pts can live with this without treatment*
46
**What are these clinical findings ( which syndrome or complex is this)?**
Osler-Weber-Rendu Syndrome
48
What are these clinical findings? (What is the syndrome or complex)?
Sturge-Weber Angiomatosis Sturge-Weber syndrome
49
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
51
What is this clinical finding?
**Lymphangioma**
52
What is this clinical finding?
**Cystic Hygroma** a type of Lymphangioma
53
**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
54
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
56
What are these clinical findings (Which syndrome or complex)?
Multiple Endocrine Neoplasia (MEN) Syndrome
58
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
59
What is this clinical finding?
neurofibroma
60
**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
61
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)
63
What is the clinical finding?
Schwannoma/ Neurilemoma
64
What is this clinical finding?
Schwannoma/ Neurilemoma
65
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.
67
What is this clinical finding?
Granular Cell Tumor
68
What is this clinical finding?
Granular Cell Tumor
69
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
70
_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)
71
What is this clinical finding?
**Congenital Epulis**
72
**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***
73
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.*
74
**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
75
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
77
**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
78
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).**
79
**What is this clinical finding?**
**Rhabdomyoma** ## Footnote 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?
81
What is this clinical finding?
**Leiomyosarcoma**
82
**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
84
What are these clinical findings?
Rhabdomyosarcoma In this case, hasn’t broken through epithelium They don’t all break through
85
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*
86
What is this clinical finding?
**Fibrosarcoma**
88
**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.
89
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^
90
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
92
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
93
**Acute myelogenous leukemia***with* **granulocytic sarcoma** ## Footnote * *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
95
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
96
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
97
**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 congenita**l; 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
100
**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!
102
**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_
105
**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 nec**k; * intraoral location: **tongue** **Treatment**: monitor, surgery if needed, _recurrence common_
108
**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
110
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_*
112
**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_
115
**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,_ c**hromosome 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**)
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**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
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**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
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Congenital Epulis ## Footnote **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
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**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
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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**
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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
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**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
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**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
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What is Sarcoma ?
Sarcoma is cancer of soft tissue (such as muscle), connective tissue (such as tendon or cartilage), or bone.
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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%
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**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
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**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!
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**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)
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**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.**
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ADENOMA
benign tumor of glandular origin
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Characteristics of a Benign Tumor:
 Encapsulated ‐ distinguishable from surrounding tissues  Freely movable ‐ not fixed  Slow growing  Non tender ‐ patients do not complain of pain
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BENIGN SALIVARY GLAND TUMORS | (list 3)
 **Pleomorphic adenoma** aka mixed tumor  **Monomorphic adenoma**s o **Canalicular adenoma** o **Basal cell adenoma**  **Warthin tumor** (papillary cystadenoma lymphomatosum)
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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
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What is this clinical finding?
PLEOMORPHIC ADENOMA | (MIXED TUMOR)
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What is this clinical finding?
PLEOMORPHIC ADENOMA Classic presentation: includes swelling in the parotid region | (MIXED TUMOR)
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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)
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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)
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What is this clinical finding?
**Untreated pleomorphic adenoma** slow growing, but can grow to enormous sizes
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**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
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What is this clinical finding?
Canalicular Adenoma
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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.
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**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,
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What is this clinical finding?
**Basal Cell Adenoma**
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What is this clinical finding?
PAPILLARY CYSTADENOMA LYMPHOMATOSUM (WARTHIN TUMOR)
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**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
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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
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What is this clinical finding?
MUCOEPIDERMOID CARCINOMA
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What is this clinical finding?
MUCOEPIDERMOID CARCINOMA ## Footnote *Request all for biopsies!*
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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
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**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.**
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What is the clinical finding?
**ACINIC CELL ADENOCARCINOMA**
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What is the clinical finding?
ACINIC CELL ADENOCARCINOMA blue‐ish tint
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What is this clinical finding?
Untreated acinic cell adenocarcinoma ## Footnote  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.
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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
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What is this clinical finding?
Adenoid Cystic Carcinoma
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What are these clinical findings?
Adenoid Cystic Carcinoma
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What are these clinical findings?
Adenoid Cystic Carcinoma
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Adenoid Cystic Carcinoma
Swiss cheese appearance, cribriform pattern (full of holes aka cystic spaces)
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Perineural invasion Histology
Perineural invasion: nerve nuble in the center and is wrapped by tumor
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What is this clinical presentation?
Polymorphous Adenocarcinoma
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What is this clinical presentation?
Polymorphous Adenocarcinoma
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What is this clinical finding?
Carcinoma Ex Pleomorphic Adenoma
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PAPILLARY CYSTADENOMA LYMPHOMATOSUM (WARTHIN TUMOR)
* **finger‐like projections, benign, cystic spaces, aggregates of****lymphocytes)** * 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
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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**
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MALIGNANT SALIVARY GLAND TUMORS List 5
 Mucoepidermoid carcinoma  Acinic cell carcinoma  Adenoid cystic carcinoma  Carcinoma ex‐mixed tumor/malignant mixed tumor  Polymorphous adenocarcinoma
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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
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**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)
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**ACINIC CELL ADENOCARCINOMA**
*  Occurs **predominantly in major SGs,** *  Found in **all age group**s, 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**
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**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
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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
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**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
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What are the **FREQUENCY OF SALIVARY GLAND TUMORS BY LOCATION** _Lower lip_
**o Mucocele o Mucoepidermoid Ca o Pleomorphic Adenoma**
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What are the **FREQUENCY OF SALIVARY GLAND TUMORS BY LOCATION** _upper lip_
**o Canalicular Adenoma o Salivary Duct Cyst\* o Pleomorphic Adenoma**
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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**
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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**
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**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
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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
225
What is this clinical finding?
Palatine Torus/Torus Palatinus
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What is this clinical finding?
Palatine Torus/Torus Palatinus
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What is this clinical finding?
Mandibular Torus: Torus Mandibularis
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What is this clinical finding?
Mandibular Torus: Torus Mandibularis
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What is this clinical finding?
Buccal Exostoses
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**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
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What is this clinical finding?
Unencapsulated Lymphoid Aggregates
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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.
236
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.
238
What is this clinical finding?
Fordyce Granules
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What is this clinical finding?
Fordyce Granules
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**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*
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What is this clinical finding?
**Fimbriated fold/Plica semiluminaris**
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What is this clinical finding?
**Frenal tag**
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**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*
245
What is this clinical finding?
Sublingual Varices
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What is this clinical finding?
Sublingual Varices
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What is this clinical finding?
Sublingual Varices
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What is this clinical finding?
Circumvallate papillae
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What is this clinical finding?
Parotid Papillia (Stenson duct)
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What is this clinical finding?
Parotid Papillia (Stenson duct)
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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.
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What is this clinical finding?
Linea Alba
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What is this clinical finding?
Leukoedema
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**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
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What is this clinical finding?
Palatal Rugae
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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
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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
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**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
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**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
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## Footnote **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 a**s 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*
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**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
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**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
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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
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Inflammatory/Reactive Lesions of the Salivary Glands List 5
* mucocele/mucous cyst * ranula * necrotizing sialometaplasia * sialolithiasis * sialadentitis
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**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
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What is this clinical finding?
**Mucocele**
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What is this clinical finding?
**Mucous Cyst**
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What is this clinical finding?
**Ranula** Notice how it's unilateral on the floor of the mouth
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What is this clinical finding?
Ranula * Notice how it's unilateral* * on the floor of the mouth*
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**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
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What is this clinical finding?
Necrotizing Sialometaplasia
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**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
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What is this clinical finding?
Sialolithiasis
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What is this clinical finding?
**Sialolithiasis** Notice how it can appear radiographically as a well defined radiolucency
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What is this Radiographical finding?
**Sialolithiasis**
293
**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
294
What is this clinical finding?
**Sialadenitis** Acute: parotid papilla purulent discharge
295
What is this clinical finding?
Sialadenitis Chronic: caused fibrosis
296
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
298
**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
307
**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
308
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
309
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**
310
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
311
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
312
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
313
How do we treat this?
‐ Repair sharp teeth/restorations ‐ Remove plaque ‐ Optimize lubrication Ulcer
314
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
315
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
316
What is this clinical finding?
**Hematinic Deficiencies** ## Footnote **‐ 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**
317
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
318
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
319
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**
320
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*
321
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**
322
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
323
What are the Hallmarks of Aphthous Ulcers
**‐ Hallmarks:** o 1. Central ulceration o 2. Ring of erythema (erythematous border) ▪ Accentuated in right image
324
What is this clinical finding?
**‐ Aphthous Ulcer of the tongue** ‐ Aphthous ulcers can occur on specialized structures of the mouth
325
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
327
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_
331
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
341
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
343
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
344
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
345
346
What is this clinical presentation?
**Homogeneous leukoplakia** ○ Thickened leathery, White plaque ○ Well-demarcated, Deepened fissures ○ Non-wipeable white patch
347
What is this clinical presentation?
Homogeneous leukoplakia. *○ Non-wipeable white patch*
348
What is this clinical presentation?
**homogenous leukoplakia** Just white color
349
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
350
What is this clinical presentation?
**Speckled leukoplakia.** **Non-homogenous leukoplakia**
353
What is this clinical presentation?
**Hairy Leukoplakia** corrugated white lesion on the lateral tongue. **• It only occurs on the lateral tongue**
354
What is this clinical presentation?
**Hairy Leukoplakia**
357
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
358
What is this clinical presentation?
**Proliferative Verrucous Leukoplakia** **Location** ○ Gingiva (Frequent) ○ Buccal Mucosa ○ Palatal Mucosa
359
What is this clinical presentation?
**Proliferative Verrucous Leukoplakia** Multifocal
361
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
362
What is this clinical presentation?
**Oral lichen planus** on the buccal mucosa (most common site reticular form.
363
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
364
What is this clinical presentation?
**Oral lichen planus** Lichen planus of the dorsum of the tongue this is a hypertrophic form.
365
**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.
366
**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
367
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
368
What is this clinical presentation?
**Oral Lichenoid** **Contact lesion** chenoid reaction to dental amalgam and cold: white and erythematous lesions on the buccal mucosa.
369
What is this clinical presentation? pts takes *Thiazide Diuretic*
Oral Lichenoid Drug Reaction
370
What is this clinical presentation? pts takes *allopurinol*
Oral Lichenoid Drug Reaction
372
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
374
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
375
What is this clinical presentation?
**Nicotinic Stomatitis** These papules represent _inflamed minor salivary glands_ and their ductal orifices.
376
What is this clinical presentation
Nicotine Stomatitis.
377
Hairy Leukoplakia ## Footnote **Etiology**
Epstein–Barr virus seems to play an important role in the pathogenesis.
378
Hairy Leukoplakia ## Footnote **Treatment**
* Not required * however, in some cases aciclovir or valaciclovir * can be used with success. * Topical retinoids or podophyllum resin for temporary remission
379
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)
380
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
381
What is this clinical presentation?
Geographic tongue/ areata migrans
382
What is this clinical presentation?
Geographic tongue/ areata migrans
383
What is this clinical presentation?
Geographic tongue/ areata migrans
384
What is this clinical presentation?
Geographic tongue, localized lesion.
387
What is this clinical presentation?
**Fordyce’s granules** on the buccal mucosa. a normal anatomical variation. ectopic sebaceous glands of the oral mucosa.
388
What is this clinical presentation?
Leukoedema of the buccal mucosa. Laskaris,
390
What is this clinical presentation?
White Sponge Nevus Diffuse, thickened white plaques of the buccal mucosa
391
What is this clinical presentation?
White Sponge Nevus | (Canon disease)
392
Proliferative Verrucous Leukoplakia ## Footnote **Treatment**
complete removal: excision, electrocautery, cryosurgery, or laber ablation ## Footnote *Lesions rarely regress despite therapy*
393
What is this clinical presentation?
**Verrucous Carcinoma** Early verrucous carcinoma of the buccal mucosa.
394
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
395
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
396
What is this clinical presentation?
Verrucous Carcinoma Extensive papillary, white lesion of the maxillary vestibule
399
Traumatic Erythema /Traumatic Hematoma on the lower lip.
400
What is this clinical presentation?
Geographic tongue: well-demarcated red patch on the tongue.
401
What is this clinical presentation?
Median rhomboid glossitis. a Chronic hyperplastic, erythematous candidiasis
404
what is this clinical presentation?
Denture stomatitis.
405
Oral lichen planus Etiology
Although the cause is not well known, T cell-mediated autoimmune phenomena are involved in the pathogenesis of lichen planus.
406
What is this clinical presentation?
**Erythroplakia** of the buccal mucosa Well-demarcated erythematous patch or plaque with soft velvety texture
407
What is this clinical presentation?
Erythroplakia of the buccal mucosa.
408
What is this clinical presentation?
**Erythroplakia** of the lateral margin of the tongue. Well-demarcated erythematous patch or plaque with soft velvety texture
409
What is this clinical presentation?
Erythroplakia Firey red Well-demarcated patch or plaque with soft velvety texture transformed into SCC
410
Oral lichen planus Treatment:
* Incisional biopsy on non-keratinized, non-ulcerated mucosa ○ Asymptomatic → no tx ○ Symptomatic → 0.5mg/ml Dexamethasone Elixir.
411
What is this clinical presentation?
Erythroplakia. Well-circumscribed red patch on the posterior lateral hard and soft palate
412
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.
413
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Smokeless Tobacco–related Gingival Recession. Extensive recession of the anterior mandibular facial gingiv
414
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Severe
415
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.
417
What is this clinical presentation?
**Pemphigus Vulgaris.** . Multiple erosions affecting the marginal gingiva.
418
What is this clinical presentation?
**Pemphigus Vulgaris.** Multiple erosions of the left buccal mucosa and soft palate.
419
What is this clinical presentation?
**Pemphigus Vulgaris.** Large, irregularly shaped ulcerations involving the floor of the mouth and ventral tongue.
420
What is this clinical presentation?
**Pemphigus Vulgaris.**
424
**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
426
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.
430
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.
431
Nicotine Stomatitis. Etiology
The elevated temperature, rather than the tobacco chemicals, is responsible for this lesion.
438
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
439
Geographic tongue/ areata migrans _Etiology_
The exact etiology remains unknown. It may be genetic.
442
Leukoedema Etiology Treatment
Etiology It is due to increased thickness of the epitheliumand intracellular edema of the prickle-cell layer. Treatment No treatment required
445
**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.
450
**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
451
**Verrucous Carcinoma** Treatment
○ Surgical Excision ○ Radiotherapy
455
Median Rhomboid Glossitis Treatment
No treatment is required.
456
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**
458
**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
463
**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
469
Smokeless tobacco keratosis Treatment:
typically resolves weeks after cessation ○ if persists 6+weeks -\> biopsy to rule out dysplasia + SCC
470
**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
471
What is this clinical presentation?
Erythroplakia. Well-circumscribed red patch on the posterior lateral hard and soft palate
472
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.
473
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Smokeless Tobacco–related Gingival Recession. Extensive recession of the anterior mandibular facial gingiv
474
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Severe
475
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.
477
What is this clinical presentation?
**Pemphigus Vulgaris.** . Multiple erosions affecting the marginal gingiva.
478
What is this clinical presentation?
**Pemphigus Vulgaris.** Multiple erosions of the left buccal mucosa and soft palate.
479
What is this clinical presentation?
**Pemphigus Vulgaris.** Large, irregularly shaped ulcerations involving the floor of the mouth and ventral tongue.
480
What is this clinical presentation?
**Pemphigus Vulgaris.**
481
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
482
What is this clinical presentation?
**Pemphigus vulgaris** PV Lesions can affect virtually any mucosal surface (oral, nasal, ocular, pharyngeal, esophageal, genital)
483
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
484
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
487
**What is this clinical presentation?**
Mucous membrane pemphigoid
488
**What is this clinical presentation?**
Mucous membrane pemphigoid SEVERE/HIGH RISK FORMS OF MMP ▪ Ocular ▪ Esophageal can result in functional blindness
489
**What is this clinical presentation?**
Mucous membrane pemphigoid Oral Hygiene: Plaque related gingival inflammation contributing to continued VB desquamative gingivitis
490
**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
493
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
494
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.
495
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 **​**
496
Smokeless tobacco keratosis Treatment:
typically resolves weeks after cessation ○ if persists 6+weeks -\> biopsy to rule out dysplasia + SCC
499
What is this clinical presentation?
**_SCC_** arising from **Actinic Cheilitis**
500
What is this clinical presentation?
**Oral Melanoma** a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.
501
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.
502
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.)
503
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.
504
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. .
505
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.
506
What is this clinical presentation?
**Oral melanotic macule** an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.
510
What is this clinical presentation
Oral Melanoma
511
What is this clinical presentation
Oral Melanoma
512
What is this clinical presentation
Oral Melanoma
513
What is this clinical presentation?
Traumatic ulcer caused by sharp or puncturing food stuff
514
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
515
What is this clinical presentation?
Traumatic ulcer Post-anaesthesia traumatic ulcer on lower lip.
516
What is this clinical presentation?
Traumatic ulcer Most often on tongue, lips, buccal mucosa Any sites that may be injured by dentition
517
What is this clinical presentation?
Traumatic Granuloma
518
What is this clinical presentation?
Traumatic Granuloma (traumatic ulcertaive granuloma)
519
What is this clinical presentation?
**Traumatic Granuloma** | ( Traumatic Ulcerative Granuloma)
522
What is this clinical presentation?
Squamous cell carcinoma on the buccal mucosa)
523
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
524
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).
526
**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.
527
What is this clinical presentation?
**Graphite tattoo** Most common location on the palate and gingiva Gray, black, or blue-ish macule
528
What is this clinical presentation?
**Graphite tattoo** Gray, black, or blue-ish macule
529
**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)**
531
What is this clinical presentation?
Traumatic ulcer of the tongue.
532
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.
533
What is this clinical finding?
Hemangioma of Infancy
536
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*
538
**Mucous membrane pemphigoid** **Etiology**
Mucocutaneous autoimmune disease characterized by sub‐epithelial blisters (bullae) which ruptures to form large, non‐healing ulcerations
539
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.**
540
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.
541
**Frictional Keratosis.** Differential Diagnosis
Leukoplakia Linea alba Chronic cheek chewing (bite injury) Candidiasis Oral Lichen planus Squamous cell carcinoma
542
What is this clinical finding?
Frictional keratosis on the tongue
543
**Frictional Keratosis** **Etiology**
* Trauma from Sharp cusp & ortho appliance * Chronic mechanical irritation (chronic biting) * Masticatory function * Normal hyperplastic response * Dentures/missing teeth
544
**Frictional Keratosis** **Treatment**
* Remove the cauative factor that caused the trauma * observe large lesion regularly excellent prognosis
545
What is this clinical presentation?
**dry‐mouth** patient a classic example **• Classic fissuring • depapillation of the tongue papilla • some white changes on the tongue.**
546
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.
547
What is this clinical presentation?
**dry Mouth** Cervical caries related to radiation. The patient is a smoker and coffee drinker --\> explains the staining
548
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**
549
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**
553
**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
554
**Actinic cheilitis** Etiology
due to chronic ultraviolet light exposure.
555
**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**
559
Severity of patients with xerostomia using objective measures
564
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)**
565
What is this clinical presentation?
**SJÖGREN’S SYNDROME** _Dry Mouth_ very severe cervical disease & very dry lips
566
What is this clinical presentation?
Depapillated & Fissured Tongue ## Footnote **SJÖGREN’S SYNDROME**
567
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.
568
**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)
569
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.
571
Oral Melanoma ## Footnote **Etiology**
Unknown. Ultraviolet radiation is an important causative factor for skin melanoma **Acute sun damage** can cause it more than chronic exposure
572
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.
573
**Oral Melanoma** Treatment
* Surgical excision * Radiotherapy * Chemotherapy
584
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
585
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**
589
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
590
SCC treatment
Early stage: Radiation and/or Surgical removal Late stage : combination of surgery, radiation therapy, or chemotherapy
593
Graphite tattoo Treatment
If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft
594
Graphite tattoo Etiology
result from pencil lead that is traumatically implanted, usually during the elementary school years
598
**Hemangioma of Infancy** Treatment
○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”
599
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*
601
**Necrotizing Sialadenometaplasia** _Etiology_
*The cause is uncertain, although the hypothesis of ischemic necrosis after vascular infarction seems acceptable.*
602
**Necrotizing Sialadenometaplasia** _Treatment_
No Treatment Needed but we need to biopsy to rule out other diseases
613
What is this clinical finding?
**Xerostomia-related Caries** **Or** **Dry Mouth** . Extensive cervical caries of mandibular dentition secondary to radiation-related xerostomia.
614
**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)
615
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
616
What is the normal rate for Unstimulated Saliva Production
**300 ml/day ▪ Flow rate: mean 0.3 ml/min**
617
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).
618
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)
619
What causes dry mouth?
Central inhibition as a result of connections between the primary salivary centers and the higher centers of the brain.
620
● 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?**
621
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
622
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**
624
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)
625
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).
626
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
627
**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
628
**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
629
What is this clinical presentation?
Erythroplakia. Well-circumscribed red patch on the posterior lateral hard and soft palate
630
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.
631
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Smokeless Tobacco–related Gingival Recession. Extensive recession of the anterior mandibular facial gingiv
632
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Severe
633
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.
635
What is this clinical presentation?
**Pemphigus Vulgaris.** . Multiple erosions affecting the marginal gingiva.
636
What is this clinical presentation?
**Pemphigus Vulgaris.** Multiple erosions of the left buccal mucosa and soft palate.
637
What is this clinical presentation?
**Pemphigus Vulgaris.** Large, irregularly shaped ulcerations involving the floor of the mouth and ventral tongue.
638
What is this clinical presentation?
**Pemphigus Vulgaris.**
639
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
640
What is this clinical presentation?
**Pemphigus vulgaris** PV Lesions can affect virtually any mucosal surface (oral, nasal, ocular, pharyngeal, esophageal, genital)
641
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
642
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
645
**What is this clinical presentation?**
Mucous membrane pemphigoid
646
**What is this clinical presentation?**
Mucous membrane pemphigoid SEVERE/HIGH RISK FORMS OF MMP ▪ Ocular ▪ Esophageal can result in functional blindness
647
**What is this clinical presentation?**
Mucous membrane pemphigoid Oral Hygiene: Plaque related gingival inflammation contributing to continued VB desquamative gingivitis
648
**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
651
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
652
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.
653
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 **​**
654
Smokeless tobacco keratosis Treatment:
typically resolves weeks after cessation ○ if persists 6+weeks -\> biopsy to rule out dysplasia + SCC
657
What is this clinical presentation?
**_SCC_** arising from **Actinic Cheilitis**
658
What is this clinical presentation?
**Oral Melanoma** a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.
659
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.
660
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.)
661
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.
662
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. .
663
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.
664
What is this clinical presentation?
**Oral melanotic macule** an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.
668
What is this clinical presentation
Oral Melanoma
669
What is this clinical presentation
Oral Melanoma
670
What is this clinical presentation
Oral Melanoma
671
What is this clinical presentation?
Traumatic ulcer caused by sharp or puncturing food stuff
672
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
673
What is this clinical presentation?
Traumatic ulcer Post-anaesthesia traumatic ulcer on lower lip.
674
What is this clinical presentation?
Traumatic ulcer Most often on tongue, lips, buccal mucosa Any sites that may be injured by dentition
675
What is this clinical presentation?
Traumatic Granuloma
676
What is this clinical presentation?
Traumatic Granuloma (traumatic ulcertaive granuloma)
677
What is this clinical presentation?
**Traumatic Granuloma** | ( Traumatic Ulcerative Granuloma)
680
What is this clinical presentation?
Squamous cell carcinoma on the buccal mucosa)
681
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
682
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).
684
**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.
685
What is this clinical presentation?
**Graphite tattoo** Most common location on the palate and gingiva Gray, black, or blue-ish macule
686
What is this clinical presentation?
**Graphite tattoo** Gray, black, or blue-ish macule
687
**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)**
689
What is this clinical presentation?
Traumatic ulcer of the tongue.
690
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.
691
What is this clinical finding?
Hemangioma of Infancy
694
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*
696
**Mucous membrane pemphigoid** **Etiology**
Mucocutaneous autoimmune disease characterized by sub‐epithelial blisters (bullae) which ruptures to form large, non‐healing ulcerations
697
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.**
698
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.
699
**Frictional Keratosis.** Differential Diagnosis
Leukoplakia Linea alba Chronic cheek chewing (bite injury) Candidiasis Oral Lichen planus Squamous cell carcinoma
700
What is this clinical finding?
Frictional keratosis on the tongue
701
**Frictional Keratosis** **Etiology**
* Trauma from Sharp cusp & ortho appliance * Chronic mechanical irritation (chronic biting) * Masticatory function * Normal hyperplastic response * Dentures/missing teeth
702
**Frictional Keratosis** **Treatment**
* Remove the cauative factor that caused the trauma * observe large lesion regularly excellent prognosis
703
What is this clinical presentation?
**dry‐mouth** patient a classic example **• Classic fissuring • depapillation of the tongue papilla • some white changes on the tongue.**
704
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.
705
What is this clinical presentation?
**dry Mouth** Cervical caries related to radiation. The patient is a smoker and coffee drinker --\> explains the staining
706
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**
707
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**
711
**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
712
**Actinic cheilitis** Etiology
due to chronic ultraviolet light exposure.
713
**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**
717
Severity of patients with xerostomia using objective measures
722
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)**
723
What is this clinical presentation?
**SJÖGREN’S SYNDROME** _Dry Mouth_ very severe cervical disease & very dry lips
724
What is this clinical presentation?
Depapillated & Fissured Tongue ## Footnote **SJÖGREN’S SYNDROME**
725
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.
726
**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)
727
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.
729
Oral Melanoma ## Footnote **Etiology**
Unknown. Ultraviolet radiation is an important causative factor for skin melanoma **Acute sun damage** can cause it more than chronic exposure
730
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.
731
**Oral Melanoma** Treatment
* Surgical excision * Radiotherapy * Chemotherapy
742
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
743
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**
747
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
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SCC treatment
Early stage: Radiation and/or Surgical removal Late stage : combination of surgery, radiation therapy, or chemotherapy
751
Graphite tattoo Treatment
If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft
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Graphite tattoo Etiology
result from pencil lead that is traumatically implanted, usually during the elementary school years
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**Hemangioma of Infancy** Treatment
○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”
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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*
759
**Necrotizing Sialadenometaplasia** _Etiology_
*The cause is uncertain, although the hypothesis of ischemic necrosis after vascular infarction seems acceptable.*
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**Necrotizing Sialadenometaplasia** _Treatment_
No Treatment Needed but we need to biopsy to rule out other diseases
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What is this clinical finding?
**Xerostomia-related Caries** **Or** **Dry Mouth** . Extensive cervical caries of mandibular dentition secondary to radiation-related xerostomia.
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**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)
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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
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What is the normal rate for Unstimulated Saliva Production
**300 ml/day ▪ Flow rate: mean 0.3 ml/min**
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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).
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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)
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What causes dry mouth?
Central inhibition as a result of connections between the primary salivary centers and the higher centers of the brain.
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● 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?**
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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
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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**
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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)
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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).
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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
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**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