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Module 7 > Oral Pathology > Flashcards

Oral Pathology Flashcards

Topics covered: An introduction to oral and maxillofacial pathology, white lesions, red lesions, pigmented lesions, ulcerated lesions, non-cystic dental inflammatory lesions, odontogenic cysts, non-odontogenic cysts, odontogenic tumours, soft tissue hyperplastic lesions, soft tissue neoplasms

1
Q

What are the different types of biopsy and when are each of the types used?

A

Excisional - clinical diagnosis usually matches the definitive diagnosis therefore specimen is removed for definitive diagnosis and treatment is given at the same time.

Incisional - small piece of tissue is taken from a representative area of the lesion to obtain diagnosis of the condition

Surgical resection - usually carried out after incisional biopsy if further histopathological assessment is required.

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2
Q

When would you send a fresh biopsy sample?

A

In cases where urgent diagnosis is required or for specimens where further investigations are required (immunofluorescent studies).

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3
Q

Why are fixed biopsy samples placed in a 10% neutral buffered formalin when sent to the lab?

A

As it stops the tissues from breaking down
And allows cross-linking of proteins which helps to preserve the tissue histology.

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4
Q

What should be sent to the lab along with the specimen?

A
  • Correct patient details on specimen tube
  • Correctly filled out pathology request form (including accurate details that may help with diagnosis)
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5
Q

What happens when the pathology lab receives the specimen?

A

The specimen and the form will be checked to ensure the patient details are correct.

Once this has been checked the specimen will be logged into the pathology system and assigned a unique pathology number.

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6
Q

How long must a specimen be fixed for before undergoing macroscopic description and dissection by the pathologist?

A

24 hours for small non high risk specimens
4-5 days for larger resections

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7
Q

What do larger biopsy specimens often require before significant dissection?

A

They often require to be inked in different colours to mark the surgical margins prior to dissection

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8
Q

What happens to the specimens following dissection?

A

Once dissected the specimens are normally photographed to help relay information to the surgeons.

The tissue will then be embedded in hot paraffin wax to form tissue blocks.

4 micrometres thick sections are then cut from the tissue blocks using a microtome.

Sections are then floated in a water bath, mounted on a glass slide, stained using H&E stain and a coverslip is placed.

The slides are then examined by a pathologist - additional stains/investigations may be required.

A pathology report is issued following examination and interpretation of macroscopic and microscopic features.

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9
Q

What stain is most commonly used?

A

H&E (haematoxylin and eosin) stain

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10
Q

Other than H&E stain, what other special histochemical stains are available?

A

Periodic Acid-Schiff (PAS)
Trichromes
Gram

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11
Q

In addition to light microscopy with routine special stains and immunohistochemistry, what other investigations may be used to aid diagnosis?

A
  1. Immunofluorescence
  2. In situ hybridisation
  3. Electron microscopy
  4. Cytogenetic and molecular genetic analysis
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12
Q

What does digital pathology include?

A

Acquisition, management, sharing and interpretation of pathology information including slides and data in a digital environment

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13
Q

How are digital slides created?

A

Glass slides are captured with a scanning device to provide a high-resolution image that can be viewed on a computer screen or mobile device.

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14
Q

What does hyperplasia mean?

A

The abnormal multiplication or increase in number of normal cells in normal arrangement in a tissue.

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15
Q

What does hypertrophy mean?

A

The enlargement or overgrowth of an organ or part due to an increase in size of its constituent cells.

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16
Q

What does atrophy mean?

A

A decrease in cell size by loss of cell substance.

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17
Q

What is metaplasia?

A

Reversible change in which one adult cell type is replaced by another adult cell type

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18
Q

What does hyperkeratosis mean?

A

That there is a thickening of the stratum corneum

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19
Q

What is orthokeratosis?

A

The formation of an anuclear keratin layer, as found in normal keratinised stratified squamous epithelium.

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20
Q

What is parakeratosis?

A

The persistence of nuclei in the cells of a keratin layer

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21
Q

What is dyskeratosis?

A

Premature keratinisation of epithelial cells that have not reached the keratinising surface layer.

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22
Q

What is acanthosis?

A

Increased thickness of the prickle cell layer

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23
Q

What is acantholysis?

A

The loss of intercellular adhesion between keratinocytes

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24
Q

What is epithelial dysplasia?

A

Alteration in differentiation, maturation, and architecture of adult epithelial cells.

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25
Q

What is ulceration?

A

Mucosal/skin defect with complete loss of surface epithelium

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26
Q

What is apoptosis?

A

Programmed cell death

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27
Q

What is necrosis?

A

Cell death by injury or disease

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28
Q

List 8 causes of white lesions:

A
  1. Developmental
  2. Normal variation
  3. Hereditary
  4. Traumatic
  5. Dermatological
  6. Infective
  7. Idiopathic
  8. Neoplastic
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29
Q

Give an example of a developmental white patch seen in the mouth.

A

Fordyce spots

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30
Q

Give an example of a white patch seen in the mouth that is of normal variation?

A

Leukoedema

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31
Q

Give 3 examples of hereditary white lesions seen in the mouth?

A
  1. White sponge naevus
  2. Pachyonychia congenita
  3. Dyskeratosis congenita
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32
Q

List some typical features that may be seen in white sponge naevus:

A

Ill-defined white patches with shaggy surface
Often bilateral
Any part of oral mucosa, especially buccal mucosa
Can also affect nose, oesophagus, and anogenital region

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33
Q

What histopathological features can be seen in white sponge naevus?

A
  1. Hyperparakeratosis of the epithelium
    - thickening of the stratum corneum composed of parakeratin
  2. Acanthosis of the epithelium
    - Increased thickness of the prickle cell layer
  3. Marked intracellular oedema of prickle and parakeratinised cells - ‘basket weave’ appearance
  4. No cellular atypia/dysplasia
  5. No inflammatory changes in lamina propria
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34
Q

Does white sponge naevus require treatment?

A

No

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35
Q

What 3 types of trauma may cause a white lesion to form in the mouth?

A
  1. Mechanical/frictional trauma
  2. Chemical trauma
  3. Thermal trauma
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36
Q

What histopathological features can be seen in a white lesion that has occurred as a result of mechanical/frictional trauma?

A
  1. Hyperkeratosis
  2. Prominent scarring fibrosis with submucosa
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37
Q

Name 2 dermatological conditions that can present as white patches in the mouth?

A
  1. Lichen planus
  2. Lupus erythematosus
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38
Q

What is important about oral lichen planus?

A

Because it is an oral potentially malignant disorder - 0.1-10% (low risk) of developing into an oral squamous cell carcinoma.

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39
Q

List some clinical features of oral lichen planus:

A
  1. Violaceous, itchy papule that may present with distinctive white streaks on the surface (Wickham’s striae)
  2. More chronic than skin lichen planus - sometimes can last several years.
  3. Usually bilateral and symmetrical
  4. Buccal mucosa is most commonly affected site although tongue, gingiva and lips my be affected.
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40
Q

What are the 6 different appearances of lichen planus?

A
  1. Reticular
  2. Atrophic
  3. Plaque-like
  4. Papular
  5. Erosive
  6. Bullous
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41
Q

What can plaque-like lichen planus be mistaken for?

A

Leukoplakia

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42
Q

What does bullous lichen planus look like and how does it get its appearance?

A

Presence of subepithelial blisters that form as a result of basal cell degradation and oedema.

This is due to lack of cohesion between the epithelium and lamina propria.

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43
Q

What 6 histopathological features can be seen in lichenoid inflammation*?

**(this includes lichen planus, lichenoid reactions to drugs/restorative material, lupus erythematosus, graft versus host disease, lichenoid inflammation associated with dysplasia.)

A
  1. Hyperorthokeratosis/hyperparakeratosis of the epithelium which may be acanthotic.
  2. Saw-tooth rete ridges
  3. Dense band-like lymphocytic infiltrate (mostly T-cell) hugging epithelial/connective tissue junction
  4. Lymphocytic exocytosis
  5. Liquefaction degeneration of basal cell layer
  6. Degenerating cells appear as hyaline, shrunken/condensed bodies known as ‘Civatte’ bodies and represent basal cells undergoing apoptosis.
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44
Q

How can symptomatic lichen planus be treated?

A

Steroids

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45
Q

Which 3 infective conditions can result in white patches?

A
  1. Candidosis
  2. Syphilitic Leukoplakia
  3. Oral Hairy Leukoplakia
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46
Q

List the clinical features associated with Oral Hairy Leukoplakia:

A
  1. White, shaggy appearance on lateral tongue
  2. Asymptomatic
  3. Can affect other sites - e.g. buccal mucosa
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47
Q

Which infections are associated with Oral Hairy Leukoplakia?

A

EBV
Strong association with HIV
Also seen in immunocompromised patients and in some apparently healthy patients

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48
Q

What histopathological features can be seen in oral hairy Leukoplakia?

A
  1. Thickened, hyperparakeratotic epithelium
  2. Band of ballooned pale cells in upper prickle cell layer
  3. Often superadded candidal infection but without normal inflammatory response
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49
Q

What test is carried out to confirm the presence of EBV in oral hairy leukoplakia?

A

In situ hybridisation (ISH)

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50
Q

What treatment is carried out for oral hairy leukoplakia?

A

No treatment.

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51
Q

Name 2 conditions that may present as a white patch in the mouth that have no known cause (idiopathic):

A
  1. Leukoplakia
  2. Proliferative Verrucous Leukoplakia
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52
Q

What is important about leukoplakia?

A

It is important as leukoplakia is classified as an oral potentially malignant disorder (although considered low risk).

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53
Q

What is proliferative verrucous leukoplakia?

A

A clinico-pathological variant of oral leukoplakia that is multifocal, persistent, and progressive with a high rate of recurrence

HIGH risk of progression to cancer (SCC or verrucous carcinoma!!)

It begins as normal hyperkeratosis that in time becomes exophytic and wart-like.

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54
Q

Where is proliferative verrucous leukoplakia most commonly seen?

A

Gingiva, alveolar ridge, buccal mucosa, tongue, hard palate.

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55
Q

Name 2 neoplastic conditions that can present as a white patch in the mouth:

A
  1. Dysplastic lesions (abnormal cell growth in a tissue)
  2. Squamous Cell Carcinoma
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56
Q

What histological features can be seen in proliferative verrucous leukoplakia?

A
  1. Hyperplastic lesion (abnormal increase in normal cells)
  2. Hyperkeratosis (thickening of the stratum corneum)
  3. Often minimal dysplasia
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57
Q

List 4 causes of red patches in the mouth:

A
  1. Infective - bacterial, viral, fungal
  2. Associated with dermatological disorders
  3. Idiopathic
  4. Neoplastic
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58
Q

List 3 infections (bacterial, fungal or viral) that may result in red patches in the mouth?

A
  1. Periodontal disease
  2. Median rhomboid glossitis
  3. HIV gingivitis
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59
Q

What is median rhomboid glossitis?

A

An asymptomatic rhomboid shaped red patch on the midline of the posterior aspect of the anterior 2/3 of the dorsal tongue

Can present with a reciprocal lesion on the palate

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60
Q

What causes median rhomboid glossitis?

A

Aetiology is uncertain, but most cases are associated with candida

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61
Q

How would you diagnose median rhomboid glossitis?

A

Usually diagnosed clinically, however some do go on to get biopsied.

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62
Q

What histological features can be seen in median rhomboid glossitis?

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

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63
Q

How would you treat median rhomboid glossitis?

A

Anti-fungals

  • even with successful treatment, papillae on the tongue do not grow back.
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64
Q

Name 2 dermatological conditions that may present as a red patch in the mouth:

A
  1. Erosive lichen planus
  2. Discoid Lupus Erythematosus
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65
Q

Name 2 conditions that may present as a red patch in the mouth that have no known cause (idiopathic):

A
  1. Geographic tongue
  2. Erythroplakia
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66
Q

What is the importance of erythroplakia?

A

It is an oral potentially malignant disorder that has a HIGH likelihood of malignant transformation

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67
Q

What does erythroplakia look like and where is it commonly found?

A

It has a red velvety appearance, smooth or nodular.

It is most frequently seen on the palate, FOM, and buccal mucosa.

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68
Q

What is erythroleukoplakia (speckled leukoplakia) ?

A

An oral potentially malignant disorder.
Has both leukoplakia (white) and erythroplakia (red) components
On biopsy >90% will show severe dysplasia or carcinoma!!

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69
Q

List 5 exogenous (out with the body) causes of oral pigmentation?

A
  1. Superficial staining of mucosa from food, drinks, tobacco
  2. Black hairy tongue - papillary hyperplasia and overgrowth of pigment producing bacteria - more common in smokers.
  3. Foreign bodies - amalgam tattoo
  4. Heavy metal poisoning
  5. Some drugs - NSAIDs, antimalarials, chlorhexidine
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70
Q

How would you confirm diagnosis of amalgam tattoo?

A

May be seen on a radiograph.

May excise lesion to confirm diagnosis.

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71
Q

List 9 endogenous (within the body) causes of oral pigmentation:

A
  1. Normal variation in pigmentation similar to that seen in skin
  2. Melanotic macule
  3. Pigmented naevi
  4. Peutz-Jeghers Syndrome
  5. Smoker’s Melanesia
  6. HIV infection
  7. May be a manifestation of systemic disease (Addison’s), malignancy
  8. Mucosal melanoma
  9. Melanotic neuroectodermal tumour of infancy
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72
Q

What is a melanotic macule?

A

A benign, well-defined small flat brown/black lesion that occurs due to an increased activity of melanocytes.

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73
Q

Where would a melanotic macule commonly be found?

A

Buccal mucosa, palate, gingiva

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74
Q

Why would you excise a melanotic macule?

A

To confirm diagnosis and exclude melanoma

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75
Q

What histopathological features would be seen in a melanotic macule?

A

Increased melanin pigment in basal keratinocytes (NOT an increased number of melanocytes!!)

Melanin pigmentary incontinence in underlying connective tissue

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76
Q

What is a mucosal melanoma?

A

A dark brown, black or red (if not pigmented) malignant neoplasm of mucosal melanocytes.

Typically asymptomatic at first, however can progress and present with pain, ulceration, bleeding, or neck mass

Regional lymph node and blood borne metastases are common

Very invasive lesions that metastasise early

Typically very advanced at presentation - prognosis is poor

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77
Q

What are the most common sites for a mucosal melanoma?

A

Hard palate and maxillary gingiva

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78
Q

What causes mucosal melanoma?

A

Aetiology is unknown

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79
Q

What histopathological features can be seen in melanomas?

A

Cells appear epithelioid or spindle shaped
Amount of melanin pigment varies

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80
Q

What diagnostic aid can be useful in the diagnosis of melanomas?

A

Immunohistochemistry using specific markers for malignant melanocytes.

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81
Q

What is the treatment for mucosal melanoma?

A

Surgical resection is mainstay treatment
Adjuvant radiotherapy
Potential role in immunotherapy

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82
Q

What is melanotic neuroectodermal tumour of infancy?

A

A very rare condition affecting <1yr olds
Locally aggressive, rapidly growing pigmented mass
Arises most frequently in the anterior maxillary alveolus

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83
Q

What histopathological features can be seen in neuroectodermal tumour of infancy?

A

Neuroblastic cells and pigmented epithelial cells

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84
Q

How would you treat neuroectodermal tumour of infancy?

A

Complete local excision (treatment of choice)
Tumour of uncertain malignant potential
Some can recur
Small number do behave in a malignant behaviour and metastasise

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85
Q

List 7 causes of oral ulceration:

A
  1. Infective
  2. Traumatic
  3. Drugs
  4. Idiopathic
  5. Associated with systemic disease
  6. Associated with dermatological disease
  7. Neoplastic
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86
Q

List some infections that may be responsible for oral ulceration:

A
  1. Bacterial
  2. Fungal
  3. Viral:
    - Herpes Simplex Virus
    - Varicella zoster virus
    - Cytomegalovirus
    - Coxsackie virus
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87
Q

What types of trauma can cause oral ulceration?

A

Mechanical
Chemical
Thermal
Factitious injury
Radiation

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88
Q

Which drugs can cause oral ulceration?

A

Nicorandil
NSAIDs

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89
Q

Name a condition that results in oral ulceration that can have no known cause (idiopathic)?

A

Recurrent aphthous stomatitis

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90
Q

Name 3 systemic diseases that may result in oral ulceration:

A
  1. Haematological disease
  2. GI disease
  3. HIV (immunosuppressed)
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91
Q

Name 3 different types of dermatological diseases that can result in oral ulceration:

A
  1. Lichen planus
  2. Discoid lupus erythematosus
  3. Immunobullous diseases
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92
Q

List some neoplastic lesions of the mouth than can result in oral ulceration?

A
  1. Oral squamous cell carcinoma
  2. Other malignant neoplasms including salivary gland neoplasms or metastasis
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93
Q

What histopathological features may you see in an ulcer?

A
  1. Non-specific features of ulceration with loss of surface epithelium.
  2. Inflamed fibrinoid exudate and inflamed fibrinoid exudate and inflamed granulation tissue

** It can be difficult to differentiate between the different causes using histopathology, however, Neoplastic lesions are an exception as they would have an ulcerated tumour

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94
Q

What is the difference between a vesicle and a bulla?

A

Vesicles are small blisters

Whereas bulla are large blisters (>10mm)

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95
Q

How do vesiculobullous lesion present?

A

As oral ulceration following rupture of vesicles/bullae.

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96
Q

What are Immunobullous disorders?

A

Immunobullous disorders are autoimmune diseases in which antibodies against components of the skin and mucosa produce blisters.

These disorders are a subset of vesiculobullous lesions.

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97
Q

How are vesicles/bullae classified histologically?

A

They are classified histologically depending on the location of the bulla.

Different classification categories include:
- Intraepithelial (non-acantholytic or acantholytic)
- Subepithelial

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98
Q

How do non-acantholytic intraepithelial vesiculobullous lesions form?

A

By death and rupture of cells by viral infection (e.g. HSV in primary hermetic stomatitis and herpes labialis).

Groups of infected cells break down to form vesicles within the epithelium - infection can spread infecting nearby normal cells.

Ulcer forms when full thickness epithelium is involved and destroyed.

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99
Q

How do acantholytic intraepithelial vesiculobullous lesions form?

A

By desmodermal breakdown as a result of autoimmune disease

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100
Q

Name one autoimmune disease that can result in the formation of an acantholytic intraepithelial vesiculobullous lesion:

A

Pemphigus

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101
Q

What are the different types of pemphigus and identify which type is the most common and most severe?

A

Types:
- Vulgaris (most common, most severe)
- Foliaceous
- IgA
- Drug-induced
- Paraneoplastic

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102
Q

How do you treat pemphigus vulgaris?

A

Steroids

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103
Q

List some histopathological features of pemphigus vulgaris:

A
  1. Intraepithelial bullae produced by acantholysis (desmodermal breakdown)
  2. Bullae just above basal cells that form base of the lesion (tombstones)
  3. Acantholytic cells (Tzanck) found lying free within the bulla fluid
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104
Q

What can be used to aid diagnosis of Pemphigus vulgaris?

A

Direct immunofluorescence and histopathology to confirm diagnosis - fresh specimen is mandatory for direct immunofluorescence!!

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105
Q

List 4 examples of subepithelial vesiculobullous lesions?

A
  1. Pemphigoid
  2. Erythema multiforme
  3. Dermatitis herpetiform
  4. Epidermolysis bullosa
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106
Q

What is pemphigoid?

A

A group of autoimmune diseases including:
- Bullous pemphigoid
- Mucous membrane pemphigoid
- Linear IgA disease
- Drug induced pemphigoid

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107
Q

How does mucous membrane pemphigoid present?

A

Oral mucosa almost always involved and usually first affected site - gingiva, buccal mucosa, tongue, palate

Gingival lesions present as desquamative gingivitis

Eyes, nose, larynx, oesophagus and genitalia may be involved

Bullae tend to be relatively tough as the lid is full thickness epithelium - when they rupture, they tend to heal slowly with scarring

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108
Q

How do you treat mucous membrane pemphigoid?

A

Steroids

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109
Q

What histopathological features can be seen in mucous membrane pemphigoid?

A

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 has inflamed connective tissue

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110
Q

What can be used to aid diagnosis of mucous membrane pemphigoid?

A

Direct Immunofluorescence and histopathology to confirm diagnosis - fresh specimen is mandatory for direct immunofluorescence!!

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111
Q

What is the difference between pemphigoid and pemphigus?

A

Pemphigus:
- Affects outer layer of skin
- Intraepithelial Vesiculobullous lesion
- Fragile shallow blisters - rupture easily

Pemphigoid:
- Affects deeper layer of skin
- Subepithelial Vesiculobullous lesion
- Stronger tense blisters - Hard to burst
Commonly present with red itchy hives

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112
Q

What is epidermolysis bullosa acquisita?

A

A acquired autoimmune condition resulting in subepithelial vesiculobullous lesions.

Presents as blistering dermatosis with subepithelial bulllae.

Oral lesions in approximately 50% cases.

Early stage mimics pemphigoid and later resembles epidermolysis bullosa.

Separation occurs in or beneath lamina densa in basement membrane zone.

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113
Q

What is epidermolysis bullosa?

A

A group of rare genetic conditions

Formation of skin bullae which heal with scarring - variable involvement with oral mucosa

3 variants:
- Simplex (intraepithelial)
- Junctional (subepithelial)
- Dystrophic (subepithelial)

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114
Q

Which variant of epidermolysis bullosa is caused by mutations in keratins 5/14?

A

Simplex

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115
Q

Which variant of epidermolysis bullosa is caused by mutation in type VII collagen gene?

A

Dystrophic

116
Q

What is the scientific name given to oral blood blisters?

A

Angina Bullosa Haemorrhagica

117
Q

Where do oral blood blisters most commonly occur?

A

Soft palate

118
Q

What is the most common cause of blood blisters?

A

Secondary to trauma

(NOT caused by systemic reasons or haematological disease)

119
Q

What is oral submucous fibrosis?

A

A chronic progressive oral potentially malignant disorder resulting in:
- Pale mucosa that is firm to palpate
- Fibrous bands of tissue affecting the buccal/labial mucosa, and soft palate.
- Marked trismus

120
Q

Name a common cause of submucous fibrosis:

A

Betel quid/areca nut

121
Q

What histopathological features can be seen in oral submucous fibrosis?

A
  1. Submucosal deposition of dense collagenous tissue
  2. Decreased vascularity
  3. Marked epithelial atrophy
  4. Variable grades of epithelial dysplasia
  5. High risk of malignant transformation
122
Q

What is epithelial dysplasia?

A

Atypical epithelial changes to the surface squamous epithelium
- architectural changes: maturation and differentiation
- cytological changes: change in cells

Risk of developing oral SCC - if the atypical cells invade the underlying connective tissue (not all epithelial dysplasia’s progress to cancer - high grade epithelial dysplasia’s have a higher risk)

123
Q

Where does epithelial dysplasia commonly affect?

A

Can affect anywhere in the mouth, however lateral/ventral surfaces of the tongue, retromolar area, and FOM are areas associated with higher risk of malignant change

124
Q

What histological features are associated with Epithelial Dysplasia?

A
  • Nuclear and cellular pleomorphism
  • Alteration in nuclear/cytoplasmic ratio (invariably an increase)
  • Nuclear hyperchromatism
  • Prominent nucleoli
  • Increased and abnormal mitoses
  • Loss of polarity of basal cells
  • Basal cell hyperplasia
  • Drop-shaped rete pegs - i.e. wider at their deepest part
  • Irregular epithelial stratification or disturbed maturation
  • Abnormal keratinisation ‘dyskeratosis’ - cell starts to keratinise before the surface is reached
  • Loss/reduction of intracellular adhesion
125
Q

How is epithelial dysplasia graded?

A
  1. Using the basic grading system:

Mild - disorganisation, increased proliferation, atypia of basal cells
Moderate - more layers of disorganised basaloid cells, atypia. suprabasal mitoses
Severe - very abnormal, affects full thickness of epithelium

  1. Using the binary system:
  • Low grade
  • High grade
126
Q

How would you manage epithelial dysplasia?

A
  1. Modify risk factors - tobacco, alcohol
  2. Manage high risk areas (lateral, ventral, FOM) less conservatively
  3. Antifungal treatment - if superadded candidal infection
  4. Excision/CO2 laser excision
  5. Topical agents - Imiquimod (immunotherapy cream - typically used for dysplasia in the lip)
  6. Close clinical review
  7. Re-biopsy - pts will likely have multiple sites of dysplasia
127
Q

What is classified as an oral cancer?

A

Any cancer that is present in the oral cavity and the external lip up to the vermillion border.

128
Q

What % of oral cancers present as SCCs?

A

> 90%

129
Q

What are the risk factors for oral cancer?

A

Tobacco
Alcohol
Betel quid/pan/areca nut
Previous oral cancer
Exposure to UV light (lip)
Poor diet
Immunosuppression
OPMDs
Genetics - genetic predisposition
FH
Human papilloma virus - more often associated with oropharyngeal cancer

130
Q

Name some high risk sites and some low risk sites of oral cancer:

A

High risk sites:
- Lateral/ventral tongue
- FOM
- Retromolar region
(tonsils/soft palate - oropharyngeal cancer)

Low risk sites:
- Hard palate
- Dorsal of tongue

131
Q

List some signs and symptoms of oral cancer:

A
  1. Lumps and bumps
  2. Ulcers
  3. White patches
  4. Red patches
  5. Speckled patches
  6. Non-healing socket
  7. Tooth mobility not associated with periodontal disease
  8. Induration/fixation of mucosa
  9. Dysphasia
  10. Pain/paraesthesia
  11. Bleeding
132
Q

What should you do if you suspect that your patient has oral cancer?

A

Refer them to a specialist management team (the local Oral and Maxillofacial surgery department) under the ‘Urgent 2-week suspicion of cancer’ referral pathway.

133
Q

What exact presentations would elicit the need for referral due to suspected oral cancer?

A
  1. Persistent unexplained head and neck lumps >3 weeks
  2. Unexplained ulceration or unexplained swelling/induration of the oral mucosa persisting > 3 weeks
  3. All unexplained red or mixed red/white patches in the oral mucosa persisting >3 weeks
  4. Persistent (non-intermittent) hoarseness lasting >3weeks
  5. Persistent pain in the throat/pain on swallowing lasting for >3 weeks
134
Q

Which tumours require immunohistochemistry to aid diagnosis?

A

Very poorly differentiated tumours

Immunohistochemistry is not used routinely for diagnosis of all oral cancers - however it is used routinely for all oropharyngeal SCCs.

135
Q

Which staging system is used to stage most cancers (including lip and oral cavity carcinomas)?

A

TNM Staging

136
Q

How are tumours staged in the TNM staging system?

A

Staged depending on the anatomical extent of disease
Staged clinically, radiologically and pathologically

137
Q

What are the TNM components of TNM staging?

A

T - extent of primary tumour
N - absence or presence and extent of regional lymph node metastasis
M - absence or presence of distant metastasis

138
Q

What does the number given to each component in TNM staging of cancer indicate?

A

The greater the number= the larger the extent of disease

139
Q

What are the most significant prognostic factors for oral cancer?

A

Tumour size
Depth of invasion
Nodal status
Distant metastasis

140
Q

How are SCCs graded?

A

By degree of differentiation
- Well-differentiated: very obviously squamous with prickles and keratinisation
- Moderately differentiated
- Poorly differentiated: may be difficult to identify tumour cells as epithelial

**grading alone does not correlate with prognosis

141
Q

How do you treat oral cancer?

A

Surgery +/- adjuvant therapy - radiochemotherapy
Monoclonal antibodies - can be used in advanced H&N cancers

142
Q

What is the survival rate for oral cancer?

A

5 year survival rate - early detection is crucial in optimising treatment outcomes

143
Q

What core data items are included in a histopathology report when reporting oral cancers?

A
  1. Clinical data - site and laterality of the tumour, type of specimen
  2. Pathological data:
    - max diameter of tumour
    - max depth of invasion
    - type of carcinoma
    - grade of tumour
    - pattern of invasion
    - distance from invasive carcinoma to surgical margins
    - vascular invasion
    - nerve invasion
    - bone invasion
    - severe dysplasia
144
Q

List 5 examples of non-cystic dental inflammatory lesions:

A
  1. Acute periradicular periodontitis
  2. Acute periapical abscess
  3. Chronic periradicular periodontitis
  4. Periapical granuloma
  5. Pericoronitis
145
Q

What is the most common reason for periradicular/periapical inflammation?

A

Bacterial infection following pulpal death - this may be due to caries or trauma

146
Q

What can acute and chronic periradicular periodontitis lead to?

A

Periapical abscess

147
Q

What can chronic periradicular periodontitis lead to?

A

Periapical granuloma

148
Q

What can periapical granuloma lead to?

A

Radicular cyst formation
OR
Can become acutely inflamed and develop an acute abscess

149
Q

What can an acute abscess result in?

A

Chronic abscess formation
OR
Cellulitis

150
Q

What are the clinical features of an acute periradicular periodontitis?

A

Pain
Grossly carious/heavily restored tooth
Previous trauma
Typically little to see radiographically unless acute exacerbation of chronic lesion

151
Q

What histopathological features might you see in an acute periradicular periodontitis?

A

Acute inflammatory changes:
- vascular dilation
- neutrophils
- oedema

152
Q

What treatment options are there for an acute periradicular periodontitis?

A
  • Extract
  • RCT
153
Q

What are the clinical features of acute periapical abscess?

A

Pain
Swelling/sinus

154
Q

What histopathological features can be seen with an acute periapical abscess?

A

Central collection of pus (neutrophils, bacteria, cellular debris)
Adjacent zone of preserved neutrophils
Surrounding membrane of sprouting capillaries, vascular dilation, and occasional fibroblasts (granulation tissue).

155
Q

What are the treatment options for an acute apical abscess?

A

Drainage of abscess and extraction or RCT of associated tooth

156
Q

What are the clinical features of chronic periradicular periodontitis?

A

Non-vital tooth (may be previous RCT)
Often minimal symptoms
Apical radiolucent lesion may be evident on radiograph

157
Q

What histopathological features can be seen in chronic periradicular periodontitis?

A

Chronic inflammatory changes - seen by the presence of:
- Lymphocytes
- Plasma cells
- Macrophages
- Granulation tissue progressing to fibrosis - predominantly by lymphocytes and plasma cells
- Resorption of bone
- Minimal, if any, tooth resorption

158
Q

What are the treatment options for chronic periradicular periodontitis?

A

Extraction. RCT, endodontic retreatment, periradicular surgery
Does NOT resolve spontaneously

159
Q

What is a periapical granuloma?

A

A mass of inflamed granulation tissue at the apex of a non-vital tooth, that can arise as a result of chronic periradicular periodontitis or from an acute abscess.

Not a true granuloma - i.e. not a collection of macrophages

Can transform to an abscess

Some may undergo cystic change to become a radicular cyst (odontogenic inflammatory cyst)

160
Q

What are the clinical features of a periapical granuloma?

A

Same features as chronic periradicular periodontitis, however apical radiolucency is typically evident on radiograph.

161
Q

What histopathological features can be seen in a periapical granuloma?

A

Inflamed granulation tissue - lymphocytes, plasma cells, macrophages and neutrophils

Proliferation of cell rests of Malassez - often in long strands and arcades (may ultimately lead to inflammatory radicular cyst formation

Hemosiderin and cholesterol deposits from RBC/inflammatory cell breakdown, with multi-nuclear foreign body giant cells

Resorption of adjacent bone +/- tooth

162
Q

What are the treatment options for periapical granuloma?

A
  1. Extraction
  2. RCT
  3. Endodontic re-treatment
  4. Peri-radicular surgery
163
Q

What is pericoronitis?

A

Inflammation of soft tissues around PE tooth
Frequently lower 8s
Often exacerbated by trauma from opposing tooth

164
Q

What are the clinical features of pericoronitis?

A

Pain
Swelling/tenderness of operculum
Bad taste
Trismus

165
Q

What histopathological features can be seen in pericoronitis?

A

Acute and chronic inflammatory changes including oedema, inflammatory cells, vascular dilation, fibrotic connective tissue.

Paradental cyst (type of odontogenic cyst) may arise in chronic pericoronitis.

166
Q

How can you treat pericoronitis?

A

Irrigation
Consider extraction of opposing tooth
Antibiotics (only if systemically unwell)

167
Q

What is a cyst?

A

A pathological cavity having fluid or semi-fluid contents
Lined wholly or partly in epithelium
Not due to accumulation of pus

168
Q

What are the 2 different types of cysts that are classified in the WHO 2022 Classification of Cysts of the Jaws?

A

Odontogenic cysts - derived from epithelial residues of tooth forming organ. Can be inflammatory or developmental

Non-odontogenic cysts - derived from sources other than tooth forming organ

169
Q

What components combine to form a tooth?

A

Odontogenic epithelium and neural crest derived ectomesenchyme

170
Q

What forms the enamel organ?

A

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

171
Q

What are the 4 layers that make up the enamel organ?

A
  1. Inner enamel epithelium (future ameloblasts)
  2. Outer enamel epithelium
  3. Stellate reticulum
  4. Status intermedium
172
Q

Which types of cells develop into pulpal tissue?

A

Ectomesenchymal cells

173
Q

How is dentine and the enamel matrix formed?

A

Signalling causes the outer cells of the pulp (next to ameloblasts) to differentiate into odontoblasts and lay down dentine.

Enamel matrix is then subsequently laid down.

174
Q

What happens after crown formation?

A

The enamel organ reduces to form the Root Sheath of Hertwig which grows down to map out the root.

175
Q

What remnants can be left behind following odontogenesis?

A
  1. Remnants of odontogenic epithelium
    - will remain in PDL and gingiva after tooth development
  2. Remnants of dental lamina (known as Glands of Serres)
  3. Remnants of Root Sheath of Hertwig (known as cell Rests of Malassez)
176
Q

What are the 2 different types of odontogenic cyst?

A
  1. Inflammatory odontogenic cyst
  2. Developmental odontogenic cyst
177
Q

What are the 2 types of inflammatory odontogenic cyst?

A
  1. Radicular cyst (apical, lateral, residual)
  2. Inflammatory collateral cyst (paradental cyst or mandibular buccal bifurcation cyst)
178
Q

Where does a lateral radicular cyst arise from?

A

Lateral root canal branch of a non-vital tooth

179
Q

Where does a residual radicular cyst arise from?

A

Persists after extraction of the associated non-vital tooth

180
Q

What are the clinical features of a radicular cyst?

A

Most common type of jaw cyst
Anterior maxilla most frequent location
Can occur over a wide age range
Slow growing swelling
Often asymptomatic unless very large
Must be associated with a non-vital tooth (usually at the apex, although can be on a lateral aspect of root if associated with lateral canal.
Typically well-circumscribed unilocular radiolucent lesion seen at the apex, although can be on lateral aspect of root if associated with lateral canal.

181
Q

What is happening pathologically in the presence of a radicular cyst?

A

There is proliferation of the epithelium (Cell Rests of Malassez) in response to inflammation.

Cyst enlarges due to osmotic pressure

Local bone resorption

182
Q

What histopathological features can be seen in a radicular cyst?

A

Chronically inflamed fibrous capsule

Central cystic lumen surrounded by a non-keratinised stratified squamous epithelium lining of variable thickness

Beyond the epithelial lining lies fibrous connective tissue cyst wall - areas of this cyst wall are densely packed with chronic inflammatory infiltrate

May also see hyperplasia of epithelium, mucous metaplasia, ciliated cells, Hyaline/Rushton bodies (secreted by cyst lining - indicates odontogenic origin), cholesterol clefts and hemosiderin

183
Q

How would a radicular cyst be treated?

A

Small cysts may resolve after RCT/extraction/periradicular surgery.

Larger lesions may require enucleation - entire removal of lesion

Very large lesions may require marsupialisation prior to enucleation - small pouch made into cyst to allow decompression of the lesion prior to enucleation.

184
Q

What is the cause for inflammatory collateral cysts?

A

Inflammation associated with pericoronitis
May be enamel spur on buccal aspect of involved tooth
Exacerbated by impact action of food
Proliferation of sulcular or junctional epithelium derived from reduced enamel epithelium.

185
Q

What are the 2 different types of inflammatory collateral cyst and which teeth are affected by each of the cysts?

A
  1. Paradental cyst - lower third molars
  2. Mandibular buccal bifurcation cyst - lower 1st and 2nd molars
186
Q

Which type of inflammatory collateral cyst can arise from chronic pericoronitis?

A

Paradental cyst

187
Q

What radiological features are associated with a paradental cyst?

A

Well-demarcated radiolucency

188
Q

What are the clinical and radiological features associated with a mandibular buccal bifurcation cyst?

A
  • Often painless swelling
  • Associated tooth usually tilted buccally with deep perio pocket
  • Well demarcated buccal radiolucency
189
Q

What histopathological features can be seen associated with a inflammatory collateral cyst?

A

Same histopathological features that are associated with radicular cysts.

190
Q

How would you treat mandibular buccal bifurcation cysts?

A

By enucleation (complete removal)

191
Q

How would you treat paradental cysts?

A

Removal of 8s and paradental cyst

192
Q

List the 7 different developmental odontogenic cysts:

A
  1. Odontogenic keratocyst
  2. Dentigerous cyst/Eruption cyst
  3. Lateral periodontal cyst and botryoid odontogenic cyst
  4. Glandular odontogenic cyst
  5. Gingival cysts
  6. Calcifying odontogenic cysts
  7. Orthokeratinised odontogenic cyst
193
Q

What are OKCs?

A

A benign developmental odontogenic cyst that has a high recurrence rate (25%) if incompletely removed.

194
Q

Why was the 2005 term ‘Keratocystic Odontogenic tumour’ (KCOT) more recently changed to ‘Odontogenic Keratocyst’ (OKC)?

A

Because there was insufficient evidence to suggest a neoplastic origin.

195
Q

What are the clinical/radiographic features of an OKC?

A

3rd most common cyst in the jaw
Occurs over a wide age range
80% arise in the mandible (especially posteriorly)

Symptomless unless infected or when cortical bony expansion is evident (often late as enlarges in anterior-posterior direction) - can reach considerable size before detection.

Well-defined radiolucent uni- or multilocular lesion

196
Q

What is the aetiology of OKC?

A

Arise from remnants of the dental lamina (Glands of Serres)

Associated with mutation or inactivation of the PTCH1 gene (found in chromosome 9) - this activates SHH signalling pathway resulting in aberrant cell proliferation of epithelium.

OKCs can be sporadic or associated with a particular syndrome
- Naevoid basal cell carcinoma syndrome (Gorlin syndrome) - multiple recurring OKCs, skeletal abnormalities, multiple basal cell carcinomas, associated with autosomal dominant PTCH1 gene mutations

197
Q

What histopathological features can be seen in OKCs?

A

Cystic lesion
Keratinised 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.

198
Q

What happens to the histopathological features in OKCs if secondary infection in present?

A

Typical features are lost - in these circumstances it is hard to distinguish OKC from other inflammatory cysts using histology alone.

199
Q

Why do OKCs have a high recurrence rate?

A

Due to thin capsule/daughter cysts

200
Q

What are the treatment options for OKCs?

A
  • Marsupialisation
  • Enucleation
  • Marsupialisation and enucleation
  • Enucleation and Carnoy’s solution (modified Carnoy’s) - used to eliminate any remaining cyst/daughter cyst, <10% recurrence rate
  • Resection - involves removal of whole lesion and margin of normal bone (2% recurrence rate, has increased morbidity)
201
Q

What is a dentigerous cyst?

A

Accumulation of fluid between the reduced enamel epithelium of the dental follicle and the crown of the unerupted tooth

202
Q

What are the clinical features of a dentigerous cyst?

A

2nd most common odontogenic cyst
Encloses all or part of crown of unerupted tooth
Attached to ACJ
Associated with impacted teeth or late to erupt teeth (3, 5, 8s)
Higher occurrence in the mandible, 20-50 years
Symptom-free until significant swelling or if infected
Ballooning expansion
Well-circumscribed unilocular radiolucency associated with crown of unerupted tooth.

203
Q

What histopathological features can be seen in dentigerous cysts?

A

Thin non-keratinised stratified squamous epithelial lining (2-5 cells thick)
Mucous metaplasia is common
Fibrous capsule
No inflammation, unless secondary infection
May be odontogenic epithelium remnants, calcification, Rushton bodies

204
Q

What happens to the histopathological features in dentigerous cysts if secondary infection in present?

A

They are lost which makes it difficult to distinguish dentigerous cysts from other inflammatory cysts.

205
Q

What should you include on the pathology request form to aid diagnosis of dentigerous cysts?

A

The attachment of the lesion to the ACJ of the unerupted tooth.

206
Q

How are dentigerous cysts treated?

A

By enucleation of the cyst with exposure/transplantation/extraction of associated tooth

207
Q

What is an eruption cyst?

A

A dentigerous cyst arising in an extra-alveolar location

208
Q

What are the clinical features of an eruption cyst?

A

Typically seen in children
Deciduous and permanent molars
Presents as a bluish swelling

209
Q

What is the histopathology of an eruption cyst?

A

Same as dentigerous cyst

210
Q

How would you treat a dentigerous cyst?

A
  1. No treatment - the unerupted tooth should naturally erupt through the cyst
  2. Exposure of erupting tooth
211
Q

What are the clinical features of a lateral periodontal cyst?

A

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

212
Q

What is the aetiology of a lateral periodontal cyst?

A

Likely arises from cell rest of Malassez

213
Q

What histopathological features can be seen with lateral periodontal cysts?

A

Thin non-keratinised squamous or cuboidal epithelium
Focal thickenings/plaques
Uninflamed fibrous wall

214
Q

How would you treat a lateral periodontal cyst?

A

Enucleation

*Recurrence is RARE.

215
Q

What is a Botryoid Odontogenic Cyst?

A

Very rare, multi-cystic variant of lateral periodontal cyst - has the same histopathological features as a lateral periodontal cyst.

Botryoid = ‘bunch of grapes’ - polycystic appearance
Typically multilocular radiolucency
Affects the mandibular premolar to canine region
Frequent in adults
Can recur

216
Q

What are the clinical features of a glandular odontogenic cyst?

A

Very rare
Occur over wide age range
Anterior mandible
Multilocular radiolucency
Strong tendency to recur

217
Q

What histopathological features can be seen in a glandular odontogenic cyst?

A

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!

218
Q

How would you treat a glandular odontogenic cyst?

A

Enucleation but high recurrence rate (up to 50%)

219
Q

What clinical features are associated with gingival cysts in children?

A

Seen as Bohn’s nodules - superficial keratin-filled cysts in the gingivae of newborns

Present as white nodules in gingivae

220
Q

How do you treat gingival cysts in children?

A

No treatment - usually disappear within a few weeks.

221
Q

What clinical features are associated with gingival cysts in adults?

A

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

222
Q

What histopathological features can be seen in gingival cysts in adults?

A

Cyst just below oral epithelium
Un-inflamed fibrous wall
Lined by thin epithelium, cuboidal to squamous

223
Q

How would you treat gingival cyst in adult?

A

Simple excision

224
Q

What is the cause of a calcifying odontogenic cyst?

A

Arises from dental lamina
Currently classified as a benign lesion

225
Q

What are the clinical features of a calcifying odontogenic cyst?

A

Rare
Wide age range
Painless swelling of jaw
Well-defined radiolucency
Tooth displacement and resorption common
Either jaw, often anterior
Minority can be in soft tissues

226
Q

What histopathological features can be seen in calcifying odontogenic cysts?

A

Uni-cystic
Lined by epithelium which is ameloblast-like
Palisaded basal cell layer with overlying stellate reticulum-like layer
Focal ‘ghost cells’ which may calcify

227
Q

How would you treat a calcifying odontogenic cyst?

A

Enucleation
Recurrence is rare

228
Q

What causes Orthokeratinised odontogenic cysts?

A

Likely derived from dental lamina

229
Q

What are the clinical features of an orthokeratinised odontogenic cyst?

A

Rare
Wide age range
90% mandible
Painless swelling of the jaw
Well defined uni-locular radiolucency

230
Q

What histopathological features can be seen in orthokeratinised odontogenic cysts?

A

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

231
Q

How would you treat orthokeratinised odontogenic cysts?

A

Enucleation
Recurrence is rare

232
Q

Name 5 types of Non-Odontogenic cysts:

A
  1. Nasopalatine duct cyst
  2. Surgical ciliated cyst
  3. Nasolabial cyst
  4. Soft tissue cyst
  5. Non-epithelialised primary bone cyst
233
Q

What are the clinical features of Nasopalatine Duct Cysts?

A

Uncommon
Originates from the nasopalatine duct in the incisive canal
Swelling in the midline of the anterior palate
Pt may complain of a salty taste
Rounded heart-shaped radiolucency in the midline of the anterior hard palate
Often chronically inflamed

234
Q

List 3 different presentations of Nasopalatine Duct Cyst:

A
  1. Median palatine cyst
  2. Incisive canal cyst
  3. Median alveolar cyst
235
Q

How would you treat a nasopalatine duct cyst?

A

Enucleation
Recurrence is unlikely

236
Q

What are the clinical features of a surgical ciliated cyst?

A

Rare
Most are found in the posterior maxilla
May be asymptomatic or present with pain and swelling
Develop after sinus/nasal mucosa implanted in the jaw following trauma or surgery

237
Q

How are surgical ciliated cysts treated?

A

Enucleation
Recurrence is rare

238
Q

What is enucleation of a cyst?

A

Enucleation is a type of excision carried out which involves removing a cyst along with the cyst lining to prevent recurrence.

239
Q

What is marsupilisation of a cyst?

A

Marsulipilisation is a procedure used to decompress large cystic lesions prior to enucleation.

240
Q

Name the 5 types of soft tissue cysts:

A
  1. Salivary mucocele (extravasation/retention types, ranula)
  2. Epidermoid cyst
  3. Dermis cyst
  4. Lymphoepithelial cyst
  5. Thyroglossal cyst
241
Q

Where is an oral dermoid cyst most commonly found?

A

FOM

242
Q

What distinct/identifiable histopathological feature can be in dermoid cysts?

A

Skin appendages in the cyst wall - e.g. hair follicle, sebaceous gland etc.

243
Q

How are all soft tissue cysts treated?

A

By excision

244
Q

What type of procedure would be followed when excising a thyroglossal duct cyst?

A

A ‘Sistrunk’ procedure - involves the removal of the mid-third of the hyoid bone as well as the cystic lesion, to prevent the chance of recurrence

245
Q

Are non-epithelialised primary bone cysts true cysts?

A

No - as they are not lined by epithelium

246
Q

List 2 examples of non-epithelialised primary bone cysts:

A
  1. Simple solitary bone cyst
  2. Aneurysmal bone cyst
247
Q

When do simple solitary bone cysts often arise?

A

Premolar/molar regions of mandible.

248
Q

How do you treat simple solitary bone cysts?

A

They resolve spontaneously and after opening of cavity

249
Q

Which developmental anomaly appears cyst-like on the radiograph?

A

Stafne’s duct

250
Q

List 4 different odontogenic tumours:

A
  1. Ameloblastoma
  2. Ademomatoid odontogenic tumour
  3. Odontoma
  4. Cementoblastoma
251
Q

Which odontogenic tumour has the following features:

  • Usually found in the posterior mandible
  • Slow-growing, locally aggressive
A

Ameloblastoma

252
Q

What is important to note about maxillary ameloblastomas?

A
  • They are rare but readily spread through thin bones and base of the skull
  • Difficult to completely excise
  • Potentially lethal!!
253
Q

How are ameloblastomas treated?

A

Complete excision with a margin of uninvolved tissue + long-term follow-up
(if excision is incomplete then it will recur)

254
Q

Which odontogenic tumour has the following features:

  • Found most commonly in the maxillary canine region
  • Often associated with UE permanent tooth
  • Unilocular radiolucency
  • Arranged in solid nodules or rosette-like structures
A

Adenomatoid Odontogenic Tumour

**(i dont know ma toid)

255
Q

How are Adenomatoid odontogenic tumours treated?

A

Local excision
Recurrence is rare

256
Q

What are the 2 different types of odontoma?

A
  1. Compound type
  2. Complex type
257
Q

Out of the 2 types of odontomas (compound and complex) which type is known as the most common odontogenic tumour?

A

Compound type

258
Q

Where are odontomas (compound type) most frequently found?

A

Anterior maxilla

259
Q

What does a compound type odontodoma look like?

A

Lots of tooth-like structures enclosed in a fibrous capsule (bag of teeth)

260
Q

Where are odontomas (complex type) most frequently found?

A

Posterior mandible

261
Q

How does a complex type odontoma appear radiographically?

A

Radiopaque mass (irregular mass of hard and soft dental tissues)
Haphazard arrangement with no resemblance to tooth
Often forming a cauliflower-like mass
Cementum is often very scant

262
Q

How are odontomas treated?

A

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

263
Q

Which odontogenic tumour has the following features:

  • formation of cementum-like tissue in connection with root of a tooth
  • most commonly found in the mandible - especially associated with 6s
  • painful swelling
  • tooth remains vital
  • well defined radiopaque or mixed density lesion
A

Cementoblastoma

264
Q

How do you distinguish a cementoblastoma from a bone tumour?

A

As the cementoblastoma blends with the roots of the tooth

265
Q

How do you treat cementoblastoma?

A

By complete excision and removal of the tooth - common recurrence rate if incompletely excised.

266
Q

What are soft tissue hyperplastic lesions known as if they are found on the gingiva?

A

An epulis

267
Q

List 5 different types of soft tissue hyperplastic lesion:

A
  1. Epulides
  2. Pyogenic granuloma
  3. Fibroepithelial polyp
  4. Denture irritation hyperplasia
  5. Papillary hyperplasia of the palate
268
Q

Name 3 different types of epulides:

A
  1. Fibrous Epulis
  2. Pyogenic Granuloma/Pregnancy Epulis
  3. Giant Cell Epulis (Peripheral Giant Cell Granuloma)
269
Q

List some clinical features of a fibrous epulis?

A

Pedunculated or sessile firm mass on the gingiva
Often between 2 teeth
Pink in colour

270
Q

How do you treat a fibrous epulis?

A

Excision
Remove the source of irritation (e.g. ill-fitting crown, restoration overhang etc.) - if not removed then irritation is likely to recur.

271
Q

List some clinical features of a pyogenic granuloma/pregnancy epulis?

A

Soft red/purple swelling
Often ulcerated
Can occur in gingiva (epulis) or other places of the mouth

*pregnancy epulis is a pyogenic granuloma in a pregnant woman

272
Q

How would you treat pyogenic granuloma/pregnancy epulis?

A

Pyogenic granuloma - local excision, remove source of irritation
Pregnancy epulis - Good OH and periodontal treatment (lesion typically regresses post-partum)

273
Q

List some clinical features of a Giant cell epulis (peripheral giant cell granuloma)?

A

Soft purplish gingival swelling
Mostly on gum of teeth anterior to molars
Caused by local irritation
Must differentiate from central giant cell granuloma, hyperparathyroidism

274
Q

How would you treat a Giant cell epulis (peripheral giant cell granuloma)?

A

Excision of lesion
Remove source of irritation
Curettage of underlying bone to reduce chance of recurrence

275
Q

Which soft tissue hyperplastic lesion has these features?

  • Pink smooth mucosal polyp
  • Very common
  • Most common sites: buccal mucosa, lip, tongue
  • FEP under denture is known as a ‘leaf fibroma’
A

Fibroepithelial polyp

276
Q

How would you treat a fibroepithelial polyp?

A

Excision

277
Q

What is a giant cell fibroma?

A

A variant of fibroepithelial polyp often seen on the gingivae and tongue
In this lesion, there are more conspicuous larger stellate fibroblasts.

278
Q

Which soft tissue hyperplastic lesion has these features?

  • Broad-based, leaf-like folds of tissue related to periphery of badly fitting dentures
  • Typically pale, fibrous swelling
  • May be ulcerated
A

Denture irritation hyperplasia

279
Q

What is also commonly found in patients that have denture irritation hyperplasia?

A

Superadded candida infection

280
Q

How would you treat denture irritation hyperplasia?

A

Excision
New dentures

281
Q

Which soft tissue hyperplastic lesion has these features?

  • 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

282
Q

How do you treat papillary hyperplasia of the palate?

A

Good denture hygiene
Anti-fungals if indicated
Rarely surgery

283
Q

Name an intraoral soft tissue tumour that:

  • is most commonly found on the palate or gingivae
  • is purple/red
  • becomes increasingly nodular
  • frequently bleeds
A

Kaposis sarcoma

284
Q

Which viral infection is associated with Kaposis sarcoma?

A

HHV-8 infection

285
Q

How is kaposis sarcoma treated?

A

By anti-retroviral therapy/chemotherapy

Module 7 (14 decks)

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