oral pathology Flashcards
(141 cards)
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
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
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
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
5
Q
Roughened white patch at site of chronic trauma
. Hyperkeratosis
. Prominent scarring fibrosis within submucosa
A
Frictional Keratosis
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)
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
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
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
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
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
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
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
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
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
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
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
18
Q
What causes black hairy tongue?
A
papillary hyperplasia + overgrowth of pigment-producing bacteria
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
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
21
Q
How do we treat an amalgam tattoo?
A
No Tx required
If not obvious in radiograph might need to excise to diagnose
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
23
Q
. Increased melanin pigment in basal keratinocytes- not increased number of melanocytes
. Melanin pigmentary incontinence in underlying connective tissue
A
Melanotic Macule
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
25
What is the histopathology of Mucosal melanoma?
. 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
26
Tx for a mucosal melanoma?
Surgical resection is mainstay treatment
Adjuvant Radiotherapy
? Role of immunotherapy
27
. Very rare
. Most < 1 yr old
. M>F
. Locally aggressive, rapidly growing pigmented mass
. Most frequently anterior maxillary alveolus
Melanotic Neuroectodermal Tumour of Infancy
28
what is Melanotic Neuroectodermal Tumour of Infancy Histopathology and TX ?
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
29
What is an ulcer?
localised surface defect with loss of epithelium exposing underlying inflamed connective tissue
30
What are the main causes of oral ulceration?
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
31
How does the histopathology of ulcers appear?
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
32
what are Vesiculobullous Lesions?
. 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
33
Disorders which result in vesicles/bullae can be classified histologically depending on the location of the bulla, what are these classifications?
1 Intraepithelial
2 Subepithelial
34
What are intraepithelial bulla further classified into?
Non-acantholytic (death and rupture of cells) eg viral infection such as HSV
Acantholytic (desmosomal breakdown: these hold the prickle cells together)
35
How does a Intraepithelial - Non-acantholytic Eg Herpes simplex virus ulceration form?
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
36
What is an example of Intraepithelial - Acantholytic lesions? and why do they from?
example: Pemphigus
>Autoimmune disease
>Vulgaris, Foliaceous, IgA, Drug-induced and paraneoplastic types
>Vulgaris most common and most severe
37
How do Pemphigus vulgaris lesions form and what is their TX?
>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
38
>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
Histopathology of Pemphigus vulgaris
39
How can we confirm a diagnosis of pemphigus vulgaris?
Direct Immunofluorescence (DIF) studies used in conjunction with routine histopathology to confirm diagnosis
Fresh specimen mandatory for DIF
40
What are examples of subepithelial Vesicularbullous leisons?
Examples include
Pemphigoid
Erythema multiforme
Dermatitis herpetiformis
Epidermolysis bullosa acquisita
41
What are the group of autoimmune diseases under the subepithelial pemphigoid vesicular bullous lesions?
Bullous Pemphigoid
Mucous Membrane Pemphigoid
Linear IgA disease
Drug-induced Pemphigoid
42
>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)
Mucous Membrane Pemphigoid
Tx: is steriods
43
>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
Histopathology of Mucous Membrane Pemphigoid
44
>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
Epidermolysis Bullosa Acquisita
45
>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
Angina Bullosa Haemorrhagica
46
>Group of rare genetic conditions
>Formation of skin bullae which heal with scarring. Variable involvement of oral mucosa
Epidermolysis Bullosa
47
What are the three variations in Epidermolysis Bullosa?
>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
48
. 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
Oral Submucous Fibrosis
49
What is the histopathological features of oral submucous fibrosis?
1-Submucosal deposition of dense collagenous tissue
2-Decreased vascularity
3-Marked epithelial atrophy
4-Variable grades of dysplasia
High risk of malignant transformation
50
What is epithelial dysplasia?
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
51
Which sites of the oral cavity can be of more risk of epithelial dysplasia?
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
52
Histological features of epithelial dysplasia
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
53
What different grades of epithelial dysplasia are there?
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’
54
What are the differences of epithelial dysplasia and SCC histopathological features?
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
55
How do we mange epithelial dysplasia?
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
56
What is the most likely type of oral cancers?
>90 % Squamous Cell Carcinoma (SCC)
57
What are risk factors for Oral cancer?
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
What testing is done for Oral caners to confirm diagnosis by biopsy?
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
What is the histopathology of oral cancers?
Considerable variation in appearances, however cytologically malignant squamous epithelium and ALL show invasion and destruction of local tissues
60
What Treatment is available for SCC?
Surgery
+/- adjuvant therapy
Monoclonal antibodies
61
What staging system is used for oral cancers and how do they stage?
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
What are the core data items to include in the pathology report?
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
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)
Acute Periapical Abscess
64
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
Chronic Periradicular Periodontitis
65
what are features of periapical granuloma?
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
>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
Histopathology features of periapical granuloma
67
What is a cyst?
A pathological cavity having fluid or semi- fluid content
Lined wholly or in part by epithelium
Not due to accumulation of pus- abscess
68
What are the classifications of the cysts associated to the jaws?
odontogenic: Derived from epithelial residues of tooth-forming organ
and non-odontogenic: Derived from sources other than of tooth-forming organ
69
Where do teeth develop from?
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
What odontogenic remnants are there?
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
What types of inflammatory odontogenic cysts are there?
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
what are the clinical features of a radicular cyst?
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
How does the periapical granulomas
transform into a radicular cyst?
Proliferation of epithelium (Cell Rests of Malassez) in response to inflammation
Cyst enlarges due to osmotic pressure
Local bone resorption
74
.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
Histopathology of radicular cyst
75
What TX can be provided to resolve a radicular cyst?
Small cysts may resolve after: RCT/extraction/periradicular surgery
Enucleation
Marsupialisation for very large lesions
76
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
Inflammatory Collateral Cysts
77
Often painless swelling
Associated tooth usually tilted buccally with deep perio pocket
Well-demarcated buccal radiolucency
Mandibular Buccal Bifurcation Cyst
78
What are the different types of developmental odontogenic cysts present?
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
>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
Odontogenic keratocyst
80
What is the mode of action for the formation of an odontogenic keratocyst?
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
what is Naevoid Basal Cell Carcinoma Syndrome (Gorlin Syndrome)?
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
>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
histopathology of odontogenic keratocyst
83
>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)
Odontogenic Keratocyst Behaviour
84
what are TX options for a odontogenic keratocyst?
Marsupialization
Enucleation
Marsupialization + Enucleation
Enucleation + Carnoy’s solution (modified Carnoy’s)
Enucleation + Cryotherapy
Resection
85
>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
Dentigerous Cyst
86
>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
Histopathology of a dentigerous cyst
87
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
Lateral Periodontal Cyst
88
Likely arises from cell rest of Malassez
Histopathology
Thin, non-keratinized squamous or cuboidal epithelium
Focal thickenings/plaques
Uninflamed fibrous wall
Lateral Periodontal Cyst
89
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
Botryoid Odontogenic Cyst
90
Very rare cyst
Anterior mandible
Wide age range
Multilocular radiolucency
Strong tendency to recur
Glandular Odontogenic Cyst
91
>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%)
histopathology of Glandular Odontogenic Cyst
92
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
gingival cysts
93
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
Calcifying Odontogenic Cyst (COC)
94
Unicystic
Lined by epithelium which is ameloblastoma-like
Palisaded basal layer with overlying stellate reticulum-like layer
Focal ‘Ghost cells’, which may calcify
Histopathology of Calcifying odontogenic cyst
95
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
Orthokeratinised Odontogenic Cyst
96
Uninflamed fibrous wall
Lined by stratified squamous epithelium
Prominent granular cell layer and orthokeratinized
No basal palisading, no corrugated parakeratin
histopathology of Orthokeratinised Odontogenic Cyst
97
What types of non odontogenic cysts are there?
Nasopalatine Duct Cyst
Surgical Ciliated Cyst
Nasolabial Cyst
98
>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
Nasopalatine duct cyst
99
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
Histopathology of Nasopalatine duct cyst
100
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
surgical ciliated cyst
101
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
Nasolabial cyst
102
What are soft tissue cysts?
Salivary mucocoele (Extravasation and Retention types and Ranula)
Epidermoid Cyst
Dermoid Cyst
Lymphoepithelial Cyst
Thyroglossal Cyst
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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
Epidermoid cyst
104
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
Dermoid cyst
105
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
lymphoepithelial cysts
106
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
Thyroglossal duct cyst
107
what types of Non-epithelialised Primary Bone Cysts are there and what are their two main features?
Simple (or Solitary) bone cyst
Aneurysmal bone cyst
Almost exclusively involve mandible
Not true cysts
108
What are the clinical features of Simple (Solitary) Bone Cyst?
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
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
Histopathology of a solitary (Simple) cyst
110
What are features of aneurysmal bone cysts?
Very rare in jaws
Usually mandible
Young people
? Cause
Painless swelling
Radiolucency on radiograph
111
Blood-filled spaces separated by cellular fibrous tissue
No lining of spaces
Multinucleated giant cells in fibrous band
Histopathology of a aneurysmal bone cyst
112
2nd most common odontogenic tumour
30-60 yrs
Usually posterior mandible
Swelling
Radiolucent lesion on imaging
Slow growing, locally aggressive
Ameloblastoma, conventional
113
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
Histopathology of ameloblastoma
114
What Tx can be carried out for ameloblastoma?
Complete excision with margin of uninvolved tissue
If excision incomplete, it will recur
Long-term follow-up
115
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
Adenomatoid Odontogenic Tumour
116
Odontogenic epithelium arranged in solid nodules or rosette-like structures
Duct-like structures
Eosinophilic amorphous material
Minimal fibrous stroma
Histopathology of adenomatoid odontogenic tumours
117
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.
Odontoma
118
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???
compound odontoma
119
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
Complex odontoma
120
What Tx is available for odontoma?
Enucleation
Mature lesions completely enucleated do not recur
Incompletely enucleated developing lesions may recur
121
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
Cementoblastoma
122
what are the TX and histopathological features of cementoblastoma?
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
How is bone disease diagnosed?
Serum levels of calcium, phosphorus and alkaline phosphatase are principal biochemical investigations
124
What types of Giant cell and bone cysts are there?
Central giant cell granuloma
Peripheral giant cell granuloma
Cherubism
Aneurysmal bone cyst
Simple bone cyst
125
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)
Central giant cell granuloma
126
Large numbers of multi-nucleate, osteoclast-like giant cells
Set in a vascular fibrous stroma
Areas of haemorrhage and haemosiderin
Histopathology of giant cell lesions
127
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
Cherubism
127
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
Histopathology of Cherubism
128
what are soft tissue hyperplastic lesions?
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
What types of localised soft tissue hyperplastic lesions are there?
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
What are clinical features of a fibrous epulis?
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
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’)
Histopathology of the fibrous epulis
132
What are clinical features of Pyogenic Granuloma/ Pregnancy Epulis?
Soft red/purple swelling
Often ulcerated
Wide age range
Pregnancy epulis is pyogenic granuloma in specific patient group
133
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
Histopathology of Pyogenic Granuloma/ Pregnancy Epulis
134
What are clinical features of Giant-Cell Epulis/ Peripheral Giant-Cell Granuloma?
Soft purplish gingival swelling
Mostly on gum of teeth anterior to molars
F>M
Wide age range, esp 30-40 yrs
135
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
Histopathology of Giant-Cell Epulis/ Peripheral Giant-Cell Granuloma
136
Clinical Features:
Pink smooth mucosal polyp
Very common
Wide age range
Buccal mucosa, lip, tongue
FEP under denture = leaf fibroma
Fibroepithelial Polyp
137
Polypoid lesion with core of dense scar-like fibrous tissue
Overlying stratified squamous epithelium may be hyperplastic
Typically little inflammation
Histopathology of fibroepithelial polyp
Nb. Giant Cell Fibroma is a variant of fibroepithelial polyp, often seen on the gingivae and tongue
138
Hyperplastic fibrous connective tissue
Hyperplasia of the overlying epithelium
May show focal ulceration
Variable inflammation, often acute and chronic
May be superadded candida infection
Histopathology of Denture irritation Hyperplasia
139
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)
Papillary Hyperplasia of the Palate
140
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
PAlpillary hyperpa
