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Module 7 > oral pathology > Flashcards

oral pathology Flashcards

1
Q

. Autosomal Dominant
. May be apparent in infants or not until adolescence
. Ill-defined white patches with ‘shaggy’ surface
. Often bilateral
. Any part of oral mucosa esp buccal mucosa
. Can also affect nose, oesophagus, anogenital region
. Mutations in keratins 4/13

A

White sponge naevus

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2
Q

. Hyperparakeratosis and acanthosis of epithelium
. Marked intracellular oedema of prickle and parakeratinized cells- ‘
. basket-weave’ appearance
. No cellular atypia/dysplasia
. No inflammatory changes in lamina propria

A

white sponge naevus

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3
Q

.White, shaggy appearance on lateral tongue
. Asymptomatic
. Can affect other sites
. Due to EBV infection
. Strongly associated with HIV infection in many cases
. Also seen in immunosuppressed individuals and in some apparently healthy patients

A

oral hairy leukoplakia

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4
Q

. Thickened, hyperparakeratotic epithelium
. Band of ‘ballooned’ pale cells in upper prickle cell layer
. Often superadded candidal infection but without normal inflammatory response

A

Oral hairy leukoplakia

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5
Q

Roughened white patch at site of chronic trauma
. Hyperkeratosis
. Prominent scarring fibrosis within submucosa

A

Frictional Keratosis

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6
Q

> Common chronic inflammatory disease of skin and mucous membranes
Oral lesions in approx 50% of pts with skin lesions, but prevalence of skin lesions in pts primarily seen for oral LP is lower
Mainly affects middle aged and over
F>M
Aetiology unknown
Pathogenesis= T cell-mediated immunological damage to the basal cells of epithelium

A

Lichen Planus (LP)

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7
Q

> Characteristic skin lesion is a violaceous, itchy papule which may have distinctive white streaks on the surface (Wickham’s striae)
Flexor surface of the wrist is the most common site- skin lesions develop slowly and 85% resolve within 18 months
In contrast orally runs a more chronic course, sometimes several years.
Oral lesions usually bilateral and often symmetrical
Buccal mucosa is the most common site, though tongue, gingiva and lips may be affected. FOM and palate rarely affected

A

lichen planus clinical features

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8
Q

what appearances could Lichen planus present in?

A

1- Reticular- most common, lace-like striae
2- Atrophic- diffuse red lesions resembling erythroplakia
3- Plaque-like- white plaques resembling leukoplakia
4- Papular- small white papules that may coalesce
5- Erosive- extensive areas of shallow ulceration
6- Bullous- subepithelial bullae

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9
Q

what is the histopathology of LP?

A

1-Hyperorthokeratosis/hyperparakeratosis of the epithelium which may be acanthotic or atrophic
2- Saw-tooth rete ridges
3- Dense, band-like lymphocytic infiltrate (mostly T cell) hugging epithelial/connective tissue junction
4- Lymphocytic exocytosis
5- Liquefactive degeneration of basal cell layer
6-Degenerating cells appear as hyaline, shrunken/condensed bodies known as ‘Civatte” bodies and represent basal cells undergoing apoptosis
7- Atrophic lesions show severe thinning and flattening of the epithelium
8- Erosive lesions show destruction of the epithelium, leaving fibrin-covered granulation tissue.
9- Lack of cohesion between epithelium and lamina propria as a result of basal cell degeneration and oedema can lead to the formation of subepithelial bullae (blisters) in bullous LP

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10
Q

is lichen planus malignant?

A

Lichen Planus is an Oral Potentially Malignant Disorder (OMPD)

Not all lesions are considered to have equal risk

Not all lesions will undergo malignant transformation

Possible frequency of malignant change in LP is controversial (0.1- 10%) but likely low

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11
Q

What is leukoplakia?

A

Leukoplakia’ is a clinical term used to describe a white plaque of questionable risk after having excluded other known diseases (*WHO 2022)

Can vary in thickness and surface appearance

Risk of malignant transformation is considered to be low

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12
Q

> Older patients, F>M
Gingiva, alveolar ridge, buccal mucosa, tongue, hard palate
Persistent, recurrent and becomes multifocal
Aetiology unknown
Histology shows hyperplastic lesion, hyperkeratosis, often minimal dysplasia
Begins as simple hyperkeratosis that in time becomes exophytic and wart-like
Difficult to completely excise
High risk it may degenerate into oral cancer (verrucous carcinoma or squamous cell carcinoma)

A

Proliferative Verrucous Leukoplakia

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13
Q

Rhomboid red patch on midline of posterior aspect of anterior 2/3 of dorsal tongue

Asymptomatic

Aetiology uncertain, but most cases associated with candida

will have the same leison on the palate in some cases

A

Median rhomboid glossitis

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14
Q

what are the histopathological features of Median rhomboid glossitis? and what is the Tx?

A

Loss of lingual papillae

Parakeratosis and acanthosis of the squamous epithelium

Candidal hyphae in parakeratin and associated neutrophils

Chronic inflammatory infiltrate in connective tissue

Tx: antifungal medications

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15
Q

what is Erythroplakia?

A

1- An oral potentially malignant disorder
2- ‘Erythroplakia is defined as a red patch that cannot be characterized clinically or pathologically as another definable lesion (WHO 2022)
3- Red ‘velvety’ appearance, smooth or nodular
4- Less common than leukoplakia
5- Most frequently seen on palate, floor of mouth and buccal mucosa

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16
Q

What is Erythroleukoplakia?

A

1- Oral potentially malignant disorder

2- Erythroleukoplakia (also called speckled leukoplakia) has both leukoplakia and erythroplakia components

3- Erythroplakias and erythroleukoplakias have high likelihood of malignant transformation

4-On biopsy, greater than 90% will be severe dysplasia or carcinoma

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17
Q

what are oral pigmentation causes?

A

Exogenous

. Superficial staining of mucosa eg. Foods, drinks, tobacco
. Black hairy tongue- papillary hyperplasia + overgrowth of pigment-producing bacteria
. Foreign bodies eg. amalgam tattoo
. Heavy metal poisoning
. Some drugs, NSAIDs, antimalarials, chlorhexidine

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18
Q

What causes black hairy tongue?

A

papillary hyperplasia + overgrowth of pigment-producing bacteria

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19
Q

What causes Amalgam tattoo?

A
  • Amalgam introduced into socket/ mucosa during treatment
    -Presents as symptomless blue/black lesion
    -May be seen on radiograph
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20
Q

. Pigment is present as widely dispersed, fine brown/black granules or solid fragments of varying size
. Associated with collagen and elastic fibres and basement membranes
. OR may be intracellularly within fibroblasts, endothelial cells, macrophages and occasional foreign-body giant cells

A

Histology of Amalgam tattoo

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21
Q

How do we treat an amalgam tattoo?

A

No Tx required
If not obvious in radiograph might need to excise to diagnose

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22
Q

. Well-defined small flat brown/black lesions
. Due to increased activity of melanocytes
. Buccal mucosa, palate and gingiva most common sites
. Benign
. Frequently excised to confirm diagnosis and exclude melanoma

A

Melanotic Macule

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23
Q

. Increased melanin pigment in basal keratinocytes- not increased number of melanocytes
. Melanin pigmentary incontinence in underlying connective tissue

A

Melanotic Macule

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24
Q

What are features of Mucosal melanoma?

A

Mucosal Melanoma
1- Malignant neoplasm of mucosal melanocytes
2- Primary intraoral mucosal melanoma is rare but can occur
3- 40-60 yrs
4- Hard palate and maxillary gingiva most common sites
5- Dark brown or black or, if non-pigmented, red
6- Typically asymptomatic at first
7- May remain unnoticed until pain, ulceration, bleeding or a neck mass
8- Regional lymph node and blood-borne metastases are common
9- Typically very advanced at presentation
10- Very invasive, metastasise early
11- Prognosis is poor
12- Aetiology is unknown
13- Biology of mucosal melanomas is different from skin melanomas

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25
Q

What is the histopathology of Mucosal melanoma?

A

. Melanomas are highly pleomorphic neoplasms, cells appear epithelioid or spindle-shaped
. The amount of melanin pigment is variable and in some may be absent
. Immunohistochemistry using specific markers for malignant melanocytes can be useful in such cases

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26
Q

Tx for a mucosal melanoma?

A

Surgical resection is mainstay treatment
Adjuvant Radiotherapy
? Role of immunotherapy

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27
Q

. Very rare
. Most < 1 yr old
. M>F
. Locally aggressive, rapidly growing pigmented mass
. Most frequently anterior maxillary alveolus

A

Melanotic Neuroectodermal Tumour of Infancy

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28
Q

what is Melanotic Neuroectodermal Tumour of Infancy Histopathology and TX ?

A

Histopathology
Tumour comprises 2 cell population- neuroblastic cells and pigmented epithelial cells

Treatment
. Complete local excision is treatment of choice
. Tumour of uncertain malignant potential
. Can recur
. Small number do metastasise

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29
Q

What is an ulcer?

A

localised surface defect with loss of epithelium exposing underlying inflamed connective tissue

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30
Q

What are the main causes of oral ulceration?

A

Infective
Bacterial, Fungal, Viral (HSV, VZV, CMV, Coxsackie)
Traumatic
Mechanical, Chemical, Thermal, Factitious Injury, Radiation
Drugs
Nicorandil, NSAIDs
Idiopathic
Recurrent Aphthous Stomatitis

Associated with systemic disease
Haematological disease, GI disease, HIV etc

Associated with dermatological disease
Lichen Planus, Discoid Lupus Erythematosus, immunobullous diseases

Neoplastic
Oral Squamous cell carcinoma (SCC), other malignant neoplasms including salivary gland neoplasms or metastases

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31
Q

How does the histopathology of ulcers appear?

A

A large proportion of ulcers will show non-specific features
ulceration with loss of surface epithelium, inflamed fibrinoid exudate and inflamed granulation tissue

Obvious exceptions, eg neoplastic lesions

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32
Q

what are Vesiculobullous Lesions?

A

. Vesicle is a small blister
. Bulla is a blister > 10mm
. Usually present as oral ulceration following rupture of vesicles/bullae
. A subset of lesions are known as immunobullous disorders. .These are autoimmune diseases in which autoantibodies against components of skin and mucosa produce blisters

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33
Q

Disorders which result in vesicles/bullae can be classified histologically depending on the location of the bulla, what are these classifications?

A

1 Intraepithelial

2 Subepithelial

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34
Q

What are intraepithelial bulla further classified into?

A

Non-acantholytic (death and rupture of cells) eg viral infection such as HSV

Acantholytic (desmosomal breakdown: these hold the prickle cells together)

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35
Q

How does a Intraepithelial - Non-acantholytic Eg Herpes simplex virus ulceration form?

A

1-Virus targets and replicates within epithelial cells
2-Leads to cell lysis
3-Groups of infected cells breakdown to form vesicles within the epithelium
4-Infected cells infect nearby normal cells and an ulcer forms when the full thickness of the epithelium is involved and is destroyed

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36
Q

What is an example of Intraepithelial - Acantholytic lesions? and why do they from?

A

example: Pemphigus
>Autoimmune disease
>Vulgaris, Foliaceous, IgA, Drug-induced and paraneoplastic types
>Vulgaris most common and most severe

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37
Q

How do Pemphigus vulgaris lesions form and what is their TX?

A

> Most frequently females, 40-60 years
Autoantibodies to desmosomal protein (desmoglein 1 or 3) produced
Bullae form in skin and mucous membranes then rupture to leave ulcers

Treatment
Steroids

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38
Q

> Characteristic intraepithelial bullae produced by acantholysis (breakdown of desmosomes)
Bullae typically just above basal cells and these form the base of the lesion (tombstones)
Acantholytic cells (Tzanck) cells found lying free within the bulla fluid
Tzanck cells are small, round with enlarged hyperchromatic nuclei unlike normal polyhedral spinous cells
Little inflammation until the lesion ruptures

A

Histopathology of Pemphigus vulgaris

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39
Q

How can we confirm a diagnosis of pemphigus vulgaris?

A

Direct Immunofluorescence (DIF) studies used in conjunction with routine histopathology to confirm diagnosis

Fresh specimen mandatory for DIF

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40
Q

What are examples of subepithelial Vesicularbullous leisons?

A

Examples include
Pemphigoid
Erythema multiforme
Dermatitis herpetiformis
Epidermolysis bullosa acquisita

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41
Q

What are the group of autoimmune diseases under the subepithelial pemphigoid vesicular bullous lesions?

A

Bullous Pemphigoid
Mucous Membrane Pemphigoid
Linear IgA disease
Drug-induced Pemphigoid

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42
Q

> Mostly in females, 50-80 yrs
Oral mucosa almost always involved and usually first affected site. Gingiva, buccal mucosa, tongue, palate
Gingival lesions present as ‘desquamative gingivitis’- clinical description
Eyes, nose, larynx, pharynx, oesophagus and genitalia may be involved
Bullae tend to be relatively tough as the ‘lid’ is full thickness epithelium. When they rupture tend to heal slowly with scarring. Ocular lesions can lead to blindness
Autoantibodies to basement membrane components (usually BP180, less often integrins, laminin and type VII collagen)

A

Mucous Membrane Pemphigoid
Tx: is steriods

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43
Q

> Separation of full thickness epithelium from connective tissue producing subepithelial bulla with a thick roof
Infiltration of neutrophils and eosinophils around and within bulla
Base of bulla is inflamed connective tissue

A

Histopathology of Mucous Membrane Pemphigoid

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44
Q

> Uncommon
Acquired autoimmune blistering dermatosis with subepithelial bullae
Oral lesions in approx 50 % cases
Early stage may mimic pemphigoid and later resembles Epidermolysis Bullosa
Separation occurs in or beneath lamina densa in basement membrane zone

A

Epidermolysis Bullosa Acquisita

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45
Q

> Spontaneous blood-filled bullae, burst to form ulcers and heal uneventfully
Most common on soft palate
Older adults
Subepithelial cleft
Trauma
Not due to systemic or haematological disease

A

Angina Bullosa Haemorrhagica

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46
Q

> Group of rare genetic conditions
Formation of skin bullae which heal with scarring. Variable involvement of oral mucosa

A

Epidermolysis Bullosa

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47
Q

What are the three variations in Epidermolysis Bullosa?

A

> Simplex- intraepithelial, mutations in keratins 5/14
Junctional- subepithelial, separation in lamina lucida, laminin mutations
Dystrophic- subepithelial, separation beneath basal lamina, mutation in type VII collagen gene

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48
Q

. Chronic, progressive, oral potentially malignant disorder
. Associated with betel quid/areca nut
.Clinically pale coloured mucosa, firm to palpate
.Increasing submucosal fibrosis leading to very marked trismus
. Typically fibrous bands which affect buccal mucosa, soft palate and labial mucosa

A

Oral Submucous Fibrosis

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49
Q

What is the histopathological features of oral submucous fibrosis?

A

1-Submucosal deposition of dense collagenous tissue
2-Decreased vascularity
3-Marked epithelial atrophy
4-Variable grades of dysplasia

High risk of malignant transformation

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50
Q

What is epithelial dysplasia?

A

Atypical epithelial alterations limited to the surface squamous epithelium

Architectural changes- maturation and differentiation

Cytological changes- changes in cells

Indicates a risk of developing oral squamous cell carcinoma

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51
Q

Which sites of the oral cavity can be of more risk of epithelial dysplasia?

A

Oral epithelial dysplasia can involve any site in the mouth

Lateral border of tongue, ventral tongue, retromolar area, and floor of mouth are associated with higher risk of malignant transformation than other sites

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52
Q

Histological features of epithelial dysplasia

A

1-Nuclear and cellular pleomorphism
2-Alteration in nuclear/cytoplasmic ratio (invariably an increase)
3-Nuclear hyperchromatism
4-Prominent nucleoli
5-Increased and abnormal mitoses
6-Loss of polarity of basal cells
7-Basal cell hyperplasia
8-Drop-shaped rete pegs ie wider at their deepest part
9-Irregular epithelial stratification or disturbed maturation
10-,Abnormal keratinization ‘Dyskeratosis’- cell starts to keratinize before the surface is reached)
11-Loss/ reduction of intercellular adhesion

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53
Q

What different grades of epithelial dysplasia are there?

A

Mild- disorganisation, increased proliferation and atypia of basal cells

Moderate- more layers of disorganised basaloid cells, atypia, suprabasal mitoses

Severe- very abnormal, affects full thickness of epithelium

  • ‘However, defining dysplasia grade only in this manner oversimplifies the complexity of grading’
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54
Q

What are the differences of epithelial dysplasia and SCC histopathological features?

A

All the features of dysplasia may be seen in oral squamous cell carcinoma, however in dysplasia the atypical cells are confined to the surface epithelium

In squamous cell carcinoma, the atypical cells invade into the underlying connective tissue

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55
Q

How do we mange epithelial dysplasia?

A

Modify risk factors: tobacco and alcohol

High risk sites: FOM and lateral and ventral tongue would be managed less conservatively

Antifungal treatment: hyperplastic candidiasis

Excision/ CO2 Laser Excision

? Topical agents

Close Clinical Review

Rebiopsy: low threshold as they would have multiple sites

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56
Q

What is the most likely type of oral cancers?

A

> 90 % Squamous Cell Carcinoma (SCC)

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57
Q

What are risk factors for Oral cancer?

A

Tobacco
Alcohol
Betel quid/pan/areca nut
Previous oral cancer
Exposure to UV light (lip)
Poor diet
Immune suppression
Oral Potentially Malignant Disorders
Genetics??
Family history
?? HPV- more often associated with Oropharyngeal cancer

58
Q

What testing is done for Oral caners to confirm diagnosis by biopsy?

A

Diagnosis of SCC is confirmed by biopsy

Usually straightforward diagnosis on H & E stained slides

Further investigations usually not required

Very poorly differentiated tumours may require immunohistochemistry to confirm diagnosis

Immunohistochemistry p16 and HPV in situ hybridization used for all Oropharyngeal SCCs

59
Q

What is the histopathology of oral cancers?

A

Considerable variation in appearances, however cytologically malignant squamous epithelium and ALL show invasion and destruction of local tissues

60
Q

What Treatment is available for SCC?

A

Surgery
+/- adjuvant therapy
Monoclonal antibodies

61
Q

What staging system is used for oral cancers and how do they stage?

A

The classification of cancer by anatomic disease extent,TNM components:
T- extent of primary tumour
N- absence or presence and extent of regional lymph node metastasis
M- category describes the absence or presence of distant metastasis

Each component is given a number, the higher the number the more extensive the disease, poorer prognosis.
T1N0M0, T4aN2aM1
Usually no ‘M’ in final Pathological staging
Eg pT3 N1
The most significant prognostic factors for oral cancer are tumour size, depth of invasion, nodal status and distant metastases.

62
Q

What are the core data items to include in the pathology report?

A

Clinical Data-
Site and laterality of Tumour
Type of specimen: partial or full glossectomy

Pathological data –
Maximum diameter of tumour
Maximum depth of invasion
Histological type of carcinoma: (SCC)
Degree of differentiation (grade)
Pattern of invasion
Distance from invasive carcinoma to surgical margins
Vascular invasion
Nerve invasion
Bone invasion
Severe dysplasia

63
Q

History of pain

Grossly carious/heavily restored tooth

Previous trauma

Typically little to see radiographically unless acute exacerbation of chronic lesion

Central collection of pus (neutrophils, bacteria, cellular debris)

Adjacent zone of preserved neutrophils

Surrounding membrane of sprouting capillaries and vascular dilation and occasional fibroblasts (granulation tissue)

A

Acute Periapical Abscess

64
Q

Non-vital tooth, may be previous RCT

Often minimal symptoms

Apical radiolucent lesion may be evident on radiograph

Histopathology:
Lymphocytes
Plasma Cells
Macrophages
Granulation tissue progressing to fibrosis
Resorption of bone
Minimal, if any, tooth resorption

A

Chronic Periradicular Periodontitis

65
Q

what are features of periapical granuloma?

A

a mass of inflamed granulation tissue at the apex of a non-vital tooth
Not a true granuloma
Can transform to abscess
Some may undergo cystic change (radicular cyst)
As for chronic periradicular periodontitis however apical radiolucent lesion typically evident on radiograph

66
Q

> Inflamed granulation tissue- inflammatory component typically lymphocytes, plasma cells, macrophages, neutrophils
Proliferation of cell rests of Malassez, often in long strands and arcades (may ultimately lead to inflammatory radicular cyst formation)
Haemosiderin and cholesterol deposits, from RBC/inflammatory cell breakdown, and associated multinucleate foreign body giant cells
Resorption of adjacent bone+/- tooth

A

Histopathology features of periapical granuloma

67
Q

What is a cyst?

A

A pathological cavity having fluid or semi- fluid content
Lined wholly or in part by epithelium
Not due to accumulation of pus- abscess

68
Q

What are the classifications of the cysts associated to the jaws?

A

odontogenic: Derived from epithelial residues of tooth-forming organ
and non-odontogenic: Derived from sources other than of tooth-forming organ

69
Q

Where do teeth develop from?

A

Teeth develop from odontogenic epithelium and neural crest derived ectomesenchyme

The dental lamina buds down from the ectoderm and becomes the enamel organ

4 layers of the enamel organ-
Inner enamel epithelium (future ameloblasts)
Outer enamel epithelium
Stellate reticulum
Stratum intermedium

The ectomesenchymal cells develop into pulp

Signalling results in the outer cells of the pulp (next to the ameloblasts) differentiating into odontoblasts and laying down dentine
Enamel matrix is then subsequently laid down
After crown formation the enamel organ reduces to form the Root Sheath of Hertwig which grows down to map out the root

70
Q

What odontogenic remnants are there?

A

Remnants of odontogenic epithelium remain in the periodontal ligament and gingiva after tooth development

Remnants of the dental lamina, known as the Glands of Serres

Remnants of the Root Sheath of Hertwig, persist as Cell Rests of Malassez

71
Q

What types of inflammatory odontogenic cysts are there?

A

1 Radicular cyst (apical, lateral, residual)

2 Inflammatory Collateral Cysts
Paradental Cyst: lower 3rd molars
Mandibular Buccal Bifurcation Cyst: lower 1 and 2 molars

72
Q

what are the clinical features of a radicular cyst?

A

1-Most common type of jaw cyst (55 % odontogenic cysts)
2-Arise from epithelial proliferation and cyst formation within some periapical granulomas
3-Anterior maxilla most frequent location
4-Wide age range
5-Slow growing swelling
6-Often no symptoms unless very large
7-Must be associated with a non-vital tooth (usually at the apex, although can be on lateral aspect of root if associated with lateral canal)
6-Typically well-circumscribed unilocular radiolucent lesion seen at apex (although can be on lateral aspect of root if associated with lateral canal)

73
Q

How does the periapical granulomas
transform into a radicular cyst?

A

Proliferation of epithelium (Cell Rests of Malassez) in response to inflammation
Cyst enlarges due to osmotic pressure
Local bone resorption

74
Q

.Chronically inflamed fibrous capsule
.Wholly/partly lined by non-keratinized stratified squamous epithelium of variable thickness
.Hyperplasia of epithelium common, often in arcades
.Mucous metaplasia and ciliated cells may be seen
.Hyaline/Rushton bodies
.Cholesterol clefts and haemosiderin

A

Histopathology of radicular cyst

75
Q

What TX can be provided to resolve a radicular cyst?

A

Small cysts may resolve after: RCT/extraction/periradicular surgery
Enucleation
Marsupialisation for very large lesions

76
Q

Aetiology- inflammation associated with pericoronitis
May be enamel spur on buccal aspect of involved tooth
Exacerbated by impaction of food
Proliferation of sulcular or junctional epithelium derived from reduced enamel epithelium
Associated with vital tooth
Well-demarcated radiolucency

A

Inflammatory Collateral Cysts

77
Q

Often painless swelling
Associated tooth usually tilted buccally with deep perio pocket
Well-demarcated buccal radiolucency

A

Mandibular Buccal Bifurcation Cyst

78
Q

What are the different types of developmental odontogenic cysts present?

A

Odontogenic keratocyst
Dentigerous cyst/ Eruption cyst
Lateral periodontal cyst and Botryoid odontogenic cyst
Glandular odontogenic cyst
Gingival cysts
Calcifying odontogenic cyst
Orthokeratinized odontogenic cyst

79
Q

> 3rd most common cyst of the jaws
Occur over a wide age range, peaks in 2nd- 3rd and 6th-8th decades
Slight male predilection
Majority (80% arise) in mandible (esp posteriorly)
Symptomless unless infected or when cortical bony expansion (often late as enlarges in Anterior-Posterior direction)
Well-defined radiolucent uni- or multilocular lesion

A

Odontogenic keratocyst

80
Q

What is the mode of action for the formation of an odontogenic keratocyst?

A

Arise from remnants of the dental lamina (Glands of Serres)
Associated with mutation or inactivation of PTCH1 gene, chromosome 9, activates SHH signalling pathway resulting in aberrant cell proliferation of epithelium
Sporadic and syndromic patients

81
Q

what is Naevoid Basal Cell Carcinoma Syndrome (Gorlin Syndrome)?

A

1- Multiple odontogenic keratocysts
2- Occur at younger age than sporadic cases
3- Basal cell naevi, multiple, recurring odontogenic keratocysts, skeletal abnormalities, multiple basal cell carcinomas
4- AD inheritance
5- PTCH 1 gene mutations

82
Q

> Cystic lesion
Keratinized stratified squamous epithelial lining, 5- 10 cells thick
Corrugated appearance of surface parakeratin layer
Well-defined, palisaded basal cell layer
Keratin debris in lumen
Thin fibrous cyst wall with no inflammation, unless secondary infection
May be daughter/satellite cysts in wall

A

histopathology of odontogenic keratocyst

83
Q

> Benign developmental cyst
High recurrence rate (25%) if incompletely removed- thin capsule/daughter cysts*
Recurrence rate varies with treatment
No evidence to support a difference in behaviour between sporadic lesions and those of NBCCS(syndromic patients)

A

Odontogenic Keratocyst Behaviour

84
Q

what are TX options for a odontogenic keratocyst?

A

Marsupialization

Enucleation

Marsupialization + Enucleation

Enucleation + Carnoy’s solution (modified Carnoy’s)

Enucleation + Cryotherapy

Resection

85
Q

> 2nd most common odontogenic cyst
Encloses all or part of crown of unerupted tooth
Attached to Amelocemental junction
Impacted teeth or late to erupt; 3, 5, 8 s
Mandible > Maxilla, 20-50yrs
Symptom-free until significant swelling or if infected
Ballooning expansion
Well-circumscribed unilocular radiolucency associated with crown of unerupted tooth

A

Dentigerous Cyst

86
Q

> Thin non-keratinized stratified squamous epithelial lining, 2-5 cells thick
Mucous metaplasia common
Fibrous capsule
No inflammation, unless secondary infection
May be odontogenic epithelium remnants, calcification, Rushton Bodies

A

Histopathology of a dentigerous cyst

87
Q

Uncommon
Arise adjacent to vital tooth
Canine and premolar region of mandible
Wide age range
Usually symptom-free, incidental finding
Well-circumscribed radiolucency in PDL

A

Lateral Periodontal Cyst

88
Q

Likely arises from cell rest of Malassez
Histopathology
Thin, non-keratinized squamous or cuboidal epithelium
Focal thickenings/plaques
Uninflamed fibrous wall

A

Lateral Periodontal Cyst

89
Q

Very rare multicystic variant of lateral periodontal cyst (same histological features)
‘Bunch of grapes’- polycystic appearance
Typically multilocular radiolucency
Mandibular premolar =canine region
Adult
Can recur

A

Botryoid Odontogenic Cyst

90
Q

Very rare cyst
Anterior mandible
Wide age range
Multilocular radiolucency
Strong tendency to recur

A

Glandular Odontogenic Cyst

91
Q

> Cystic lumen lined by epithelium of various thickness with mucous cells and glandular structures (crypts/ cyst-like spaces)
Focal epithelial plaques/thickenings
Must be differentiated from central mucoepidermoid carcinoma

Treatment
Enucleation but high recurrence rate (up to 50%)

A

histopathology of Glandular Odontogenic Cyst

92
Q

Seen as Bohn’s nodules, superficial keratin-filled cysts in the gingivae of newborns
??Due to proliferation of dental lamina remnants (Glands of Serres)
Present as white nodules in gingivae
Very rare
Middle-aged adults
Painless dome-shaped swelling in gingiva
Majority in Mandibular canine-premolar region
May be superficial erosion of underlying alveolar bone
???Derived from dental lamina remnants

A

gingival cysts

93
Q

Rare

Wide age range, average 30 yrs

Painless swelling of jaw

Well-defined radiolucency

Tooth displacement and resorption common

Either jaw, often anterior

Minority can be in soft tissues

A

Calcifying Odontogenic Cyst (COC)

94
Q

Unicystic
Lined by epithelium which is ameloblastoma-like
Palisaded basal layer with overlying stellate reticulum-like layer
Focal ‘Ghost cells’, which may calcify

A

Histopathology of Calcifying odontogenic cyst

95
Q

Actual prevalence uncertain, rare

Wide age range, peak 3rd-4th decade

Male predilection

90% mandible

Typical presentation is painless swelling of jaw

Well-defined unilocular radiolucency

A

Orthokeratinised Odontogenic Cyst

96
Q

Uninflamed fibrous wall
Lined by stratified squamous epithelium
Prominent granular cell layer and orthokeratinized
No basal palisading, no corrugated parakeratin

A

histopathology of Orthokeratinised Odontogenic Cyst

97
Q

What types of non odontogenic cysts are there?

A

Nasopalatine Duct Cyst
Surgical Ciliated Cyst
Nasolabial Cyst

98
Q

> Uncommon

Originates from epithelium of nasopalatine duct in incisive canal

Occur anywhere in nasopalatine canal, most frequently palatal end

Any age but frequently 5th and 6th decades
Slow growing

Swelling in midline of anterior palate

May complain of ‘salty’ taste

Rounded or heart-shaped radiolucency in midline of anterior hard palate

A

Nasopalatine duct cyst

99
Q

Epithelial lining can be stratified squamous, respiratory, cuboidal or columnar

Fibrous connective tissue capsule

Neurovascular bundles may be seen in capsule

Mucous glands may also be seen in capsule

Often chronically inflamed

A

Histopathology of Nasopalatine duct cyst

100
Q

cyst:
Rare
F =M
Peak incidence in 5th – 6th decades
Most in posterior maxilla
May be asymptomatic or present with pain and swelling
Develop after sinus/nasal mucosa implanted in the jaw following trauma or surgery

Cyst lined by respiratory epithelium (ie pseudostratified columnar epithelium)

Fibrous connective tissue capsule which may be inflamed

A

surgical ciliated cyst

101
Q

Very rare
F >M,
Peak incidence in 4th – 5th decades
Arise in upper lip below nose, lateral to midline
Slow growing, distorts nostril
Painless unless infected
10% Bilateral
Now considered to likely derive from remnants of the embryonic nasolacrimal duct or the lower anterior portion of the mature duct
Cystic lesion with fibrous capsule
Usually pseudostratified columnar epithelium lining

A

Nasolabial cyst

102
Q

What are soft tissue cysts?

A

Salivary mucocoele (Extravasation and Retention types and Ranula)
Epidermoid Cyst
Dermoid Cyst
Lymphoepithelial Cyst
Thyroglossal Cyst

103
Q

cyst which is:
Painless swelling
Often following trauma or surgery
More common on skin
Cystic lesion with thin cyst wall
Keratinizing stratified squamous epithelium lining
Abundant keratin debris in lumen
No skin appendages in cyst wall

A

Epidermoid cyst

104
Q

Developmental lesion
Various locations in head and neck
Floor of mouth is most common oral site
Presents as painless swelling in midline
keratinized stratified squamous lining
Keratin debris within cyst lumen
Must also have skin appendage(s) (eg sebaceous gland, hair follicle) in cyst wall

A

Dermoid cyst

105
Q

Developmental lesions
Uncommon but do occur in oral cavity
Floor of mouth and tongue most common intraoral sites
Painless small swelling
May be yellowish in colour
Thin keratinized stratified squamous epithelium lining
Keratin debris in cyst lumen
Lymphoid tissue in cyst wall

A

lymphoepithelial cysts

106
Q

Developmental cyst derived from embryonic thyroglossal duct
Intraoral lesions very rare
Most arise near hyoid bone
Present as midline swelling, wide age range
Usually painless
Symptoms if infected, or very large
May have functioning thyroid tissue
Cystic lesion lined by stratified squamous epithelium/ciliated columnar epithelium/ nonciliated columnar epithelium
Fibrous wall which typically contains thyroid tissue
Can find incidental thyroid carcinoma

A

Thyroglossal duct cyst

107
Q

what types of Non-epithelialised Primary Bone Cysts are there and what are their two main features?

A

Simple (or Solitary) bone cyst
Aneurysmal bone cyst

Almost exclusively involve mandible
Not true cysts

108
Q

What are the clinical features of Simple (Solitary) Bone Cyst?

A

Peak incidence 2nd decade

Premolar/molar regions of mandible

May be asymptomatic swelling or often incidental finding

Large radiolucency on radiograph

Not a true cyst

? cause

109
Q

Bony cavity with no epithelial lining
May be thin fibrovascular tissue lining with haemosiderin, RBCs or giant cells covering bony walls
Usually no cyst contents

A

Histopathology of a solitary (Simple) cyst

110
Q

What are features of aneurysmal bone cysts?

A

Very rare in jaws
Usually mandible
Young people
? Cause
Painless swelling
Radiolucency on radiograph

111
Q

Blood-filled spaces separated by cellular fibrous tissue

No lining of spaces

Multinucleated giant cells in fibrous band

A

Histopathology of a aneurysmal bone cyst

112
Q

2nd most common odontogenic tumour
30-60 yrs
Usually posterior mandible
Swelling
Radiolucent lesion on imaging
Slow growing, locally aggressive

A

Ameloblastoma, conventional

113
Q

2 types of tumour cells

well-organized peripheral single layer of tall, columnar, pre-ameloblast-like cells, which have nuclei at the opposite pole to the basement membrane (reversed polarity)
core of loosely arranged cells resembling stellate reticulum

2 patterns
follicular (islands of epithelial cells)
plexiform (long strands of epithelial cells)

Set in fibrous stroma

A

Histopathology of ameloblastoma

114
Q

What Tx can be carried out for ameloblastoma?

A

Complete excision with margin of uninvolved tissue
If excision incomplete, it will recur
Long-term follow-up

115
Q

Most in 2nd decade, 90% before 30yrs
Females>males
Maxilla>mandible
Majority in canine region
Often associated with unerupted permanent tooth
Unilocular radiolucency, may mimic dentigerous cyst
Most are asymptomatic

A

Adenomatoid Odontogenic Tumour

116
Q

Odontogenic epithelium arranged in solid nodules or rosette-like structures

Duct-like structures

Eosinophilic amorphous material

Minimal fibrous stroma

A

Histopathology of adenomatoid odontogenic tumours

117
Q

Developmental malformations (hamartomas) of dental tissues
Once fully calcified do not develop further
Young patients
Painless slow growing lesions
Contain enamel, dentine and sometimes cementum
it has two types.

A

Odontoma

118
Q

Most common odontogenic tumour
Esp Anterior maxilla
Lots of tooth-like structures on imaging
Fibrous capsule enclosing many separate, small, tooth-like structures (denticles/ odontoids)
Aetiology???

A

compound odontoma

119
Q

Commonly posterior mandible
Radiopaque mass on imaging
Consist of an irregular mass of hard and soft dental tissues, haphazard arrangement with no resemblance to a tooth and often forming a cauliflower-like mass
Cementum is often very scant

A

Complex odontoma

120
Q

What Tx is available for odontoma?

A

Enucleation
Mature lesions completely enucleated do not recur
Incompletely enucleated developing lesions may recur

121
Q

Formation of cementum-like tissue in connection with root of tooth
10- 40 yrs
Mandible> maxilla, esp associated with 6s
Painful swelling
Tooth remains vital
Well-defined radiopaque or mixed-density lesion

A

Cementoblastoma

122
Q

what are the TX and histopathological features of cementoblastoma?

A

Dense masses of acellular cementum-like material
Fibrous, sometimes vascular stroma
Tumour blends with root of tooth- helps distinguish lesion from bone tumours

Treatment
Complete excision and removal of tooth
Commonly recur if incompletely excised

123
Q

How is bone disease diagnosed?

A

Serum levels of calcium, phosphorus and alkaline phosphatase are principal biochemical investigations

124
Q

What types of Giant cell and bone cysts are there?

A

Central giant cell granuloma
Peripheral giant cell granuloma
Cherubism
Aneurysmal bone cyst
Simple bone cyst

125
Q

Localized benign (but can be aggressive) lesion
Most < 30 years
Mandible > Maxilla
F > M
Often asymptomatic
If cortical plate perforates lesion can present as a peripheral giant-cell granuloma (giant cells epulis)

A

Central giant cell granuloma

126
Q

Large numbers of multi-nucleate, osteoclast-like giant cells
Set in a vascular fibrous stroma
Areas of haemorrhage and haemosiderin

A

Histopathology of giant cell lesions

127
Q

Rare inherited, AD, causing distension of jaws
M>F
Mandible often more extensively involved
Normal at birth but painless swelling, usually bilateral, symmetrical, of jaws appear between 2-4 yrs
Enlarge until ~7yrs
May regress by adulthood
Lesions cause fullness of cheeks and in severe cases maxillary swellings cause eyes to look upward giving ‘Cherub-like” appearance
May be dental anomalies

A

Cherubism

127
Q

Lesions consist mainly of cellular and vascular fibrous tissue containing varying numbers of multinucleate giant cells
As activity decreases lesions become progressively more fibrous and numbers of giant cells decreases

A

Histopathology of Cherubism

128
Q

what are soft tissue hyperplastic lesions?

A

Common in the oral cavity

Usually a response to chronic trauma/inflammation

Can originate anywhere in the oral cavity

Known as an ‘epulis’ only if located on the gingiva

129
Q

What types of localised soft tissue hyperplastic lesions are there?

A

Epulides- Fibrous Epulis
Pyogenic Granuloma/ Pregnancy Epulis
Giant-Cell Epulis (Peripheral

Giant Cell Granuloma)

Pyogenic Granuloma

Fibroepithelial Polyp (Giant Cell Fibroma)

Denture Irritation Hyperplasia

Papillary Hyperplasia of the Palate

130
Q

What are clinical features of a fibrous epulis?

A

Pedunculated( something that sits on a wide base) or sessile firm mass on gingiva, often between 2 teeth

Pink in colour

Wide age range

131
Q

Nodular lesion
Hyperplastic surface epithelium
Cellular fibroblastic granulation tissue + collagen bundles
Variable inflammation
Calcification or metaplastic bone formation can be seen (‘Mineralising’ or ‘Ossifying Fibrous Epulis’)

A

Histopathology of the fibrous epulis

132
Q

What are clinical features of Pyogenic Granuloma/ Pregnancy Epulis?

A

Soft red/purple swelling
Often ulcerated
Wide age range
Pregnancy epulis is pyogenic granuloma in specific patient group

133
Q

Nodular lesion
Surface epithelium often ulcerated
Underlying vascular proliferation- either solid sheets of endothelial cells or small and large vascular spaces
Oedematous fibrous stroma
Variable inflammation- often acute and chronic

A

Histopathology of Pyogenic Granuloma/ Pregnancy Epulis

134
Q

What are clinical features of Giant-Cell Epulis/ Peripheral Giant-Cell Granuloma?

A

Soft purplish gingival swelling
Mostly on gum of teeth anterior to molars
F>M
Wide age range, esp 30-40 yrs

135
Q

Collections of lots of multinucleated osteoclast giant cells in rich vascular and cellular stroma

Narrow zone of fibrous tissue with dilated blood vessels separates lesion from overlying epithelium

A

Histopathology of Giant-Cell Epulis/ Peripheral Giant-Cell Granuloma

136
Q

Clinical Features:

Pink smooth mucosal polyp

Very common

Wide age range

Buccal mucosa, lip, tongue

FEP under denture = leaf fibroma

A

Fibroepithelial Polyp

137
Q

Polypoid lesion with core of dense scar-like fibrous tissue

Overlying stratified squamous epithelium may be hyperplastic

Typically little inflammation

A

Histopathology of fibroepithelial polyp

Nb. Giant Cell Fibroma is a variant of fibroepithelial polyp, often seen on the gingivae and tongue

138
Q

Hyperplastic fibrous connective tissue
Hyperplasia of the overlying epithelium
May show focal ulceration
Variable inflammation, often acute and chronic
May be superadded candida infection

A

Histopathology of Denture irritation Hyperplasia

139
Q

Numerous, small, tightly packed, nodular lesions
Involves all or part of denture bearing area of palate
Typically older patients, ill-fitting dentures
Can be seen in non-denture wearers
May be superadded candidal infection (not causative)

A

Papillary Hyperplasia of the Palate

140
Q

Papillary/nodular projections
Underlying hyperplastic, chronically-inflamed vascular fibrous tissue
Hyperplastic overlying epithelium
Fungal organisms with acute inflammation may be seen (Periodic Acid Schiff (PAS) special stain to highlight fungi

A

PAlpillary hyperpa

Module 7 (9 decks)

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