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Module 7 > Oral Pathology > Flashcards

Oral Pathology Flashcards

1
Q

What is oral and maxillofacial pathology?

A

A LABORATORY based clinical specialty concerned with diagnosis and assessment of diseases of the ORAL and MAXILLOFACIAL region (mouth, jaws, nose, ear, throat, neck).

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2
Q

3 reasons why knowing about oral and maxillofacial pathology is important?

A
  • Diagnosis.
  • Treatment.
  • Prevention.
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3
Q

What is an incisional biopsy?

A

Small piece of tissue taken from a REPRESENTATIVE area of the lesion to obtain a DIAGNOSIS and influence the treatment.

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4
Q

What kind of specimen do you take when a patient presents with a sinister lesion but you are unsure of the diagnosis?

A

Incisional biopsy.

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5
Q

Excisional biopsy?

A

Clinical diagnosis is usually the definitive diagnosis, specimen removed for DIAGNOSIS and TREATMENT at the same time.

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6
Q

Resection?

A
  • Usually after INCISIONAL BIOPSY.
  • Surgical resection sent to pathology for further HISTOPATHOLOGICAL ASSESSMENT.
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7
Q

How are most specimens sent to pathology?

A
  • FIXED with 10% NEUTRAL BUFFERED FORMALIN.
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8
Q

Why are specimens fixed (2)?

A
  • To prevent tissue breakdown.
  • Crosslink proteins to preserve tissue histology.
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9
Q

2 reasons why a specimen may be sent fresh to pathology?

A
  • Urgent diagnosis needed.
  • Further investigations (immunofluorescent studies).
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10
Q

2 requirements when sending a specimen to pathology?

A
  • Patient details on specimen pot.
  • Histopathology request form.
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11
Q

10 things that occur once pathology receives a specimen?

A
  1. Check details on pot and request form.
  2. Specimen logged into system and assigned unique pathology number.
  3. Specimen macroscopic description and cut-up by pathologist (photos, decalcification if needed).
  4. All biopsy/ appropriate blocks taken from larger resection specimen and placed in cassettes.
  5. Processing - further fixation then dehydration of tissue in ethanol.
  6. Embedding - in hot paraffin wax to form tissue blocks.
  7. Microtome used to cut sections from tissue block - 4µm.
  8. Sections floated in waterbath, mounted on glass slide, stained and coverslip placed.
  9. Slides examined by pathologist.
  10. (additional stains/ investigations may be required).
  11. Pathology report issued following examination and interpretation of the macroscopic and microscopic features.
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12
Q

Why is decalcification sometimes needed?

A
  • Bones and teeth need to be softened (using acid) until they are able to be cut through with a scalpel.
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13
Q

What is done during the processing stage?

A

Processing - further fixation then dehydration of tissue in ethanol.

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14
Q

What happens during embedding?

A

Specimen embedded in hot paraffin wax to form tissue blocks.

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15
Q

How are sections cut from tissue blocks?

A

Using MICROTOME.

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16
Q

What thickness do the blocks cut from tissue blocks have?

A

4µm thickness (thickness of a single cell).

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17
Q

What is the most commonly used stain for sections in oral pathology?

A

Haematoxylin and Eosin (H and E).

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18
Q

3 different types of stain?

A
  • Haematoxylin and Eosin.
  • Special histochemical stains (periodic acid schiff - PAS, trichomes, gram).
  • Immunohistochemistry - antibodies.
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19
Q

3 types of special histochemical stains?

A
  • Periodic acid schiff - PAS.
  • Trichomes.
  • Gram.
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20
Q

4 different extra investigations to aid diagnosis?

A
  • immunofluorescence
  • in situ hybridisation
  • electron microscopy
  • cytogenetic and molecular genetic analysis
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21
Q

Hyperplasia?

A

The abnormal multiplication or INCREASE in the NUMBER of NORMAL cells in NORMAL ARRANGEMENT in a tissue.

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22
Q

Hypertrophy?

A

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

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23
Q

Atrophy?

A

A decrease in cell size by loss of cell substance.

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24
Q

Metaplasia?

A

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

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25
Q

Hyperkeratosis?

A

Thickening of the stratum corneum.

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26
Q

Orthokeratosis?

A

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

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27
Q

Parakeratosis?

A

The persistence of nuclei in the cells of a keratin layer.

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28
Q

Dyskeratosis?

A

Premature keratinization of epithelial cells that have not reached the keratinizing surface layer.

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29
Q

Acanthosis?

A

increased thickness of prickle cell layer

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30
Q

Acantholysis

A

the loss of intercellular adhesion between keratinocytes.

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31
Q

Epithelial dysplasia

A

alteration in differentiation, maturation and architecture of adult epithelial cells

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32
Q

Ulceration

A

mucosal/skin defect with complete loss of surface epithelium

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33
Q

Apoptosis

A

programmed cell death

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34
Q

Example of developmental white lesion?

A

Fordyce granules.

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35
Q

Necrosis

A

cell death by injury or disease

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36
Q

Leukoedema? what? where?

A
  • Milky white coloration
  • Usually over buccal mucosa.
  • Normal variation.
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37
Q

3 hereditary white spot lesions?

A
  • White sponge naevus.
  • Pachyonychia congenita.
  • Dyskeratosis congenita.
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38
Q

3 traumatic white spot lesions?

A
  • Mechanical/ friction.
  • Thermal.
  • Chemical.
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39
Q

2 dermatological causes of white spot lesions?

A
  • Lichen planus.
  • Lupus erythematosus.
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40
Q

Example of normal variation white lesion?

A

Leukoedema

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41
Q

3 types of infective white lesions?

A
  • Candidiasis.
  • Oral hairy leukoplakia.
  • Syphilitic leukoplakia.
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42
Q

Fordyce granules? What? Where?

A
  • Ectopic sebaceous glands.
  • Lips and buccal mucosa.
  • Become more prominent with age.
  • Developmental.
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43
Q

2 types of idiopathic white lesions?

A
  • Leukoplakia.
  • Proliferative verrucous leukoplakia.
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44
Q

2 types of neoplastic leukoplakia?

A
  • Dysplastic lesions.
  • Squamous cell carcinoma.
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45
Q

How is white sponge naevus inherited?

A
  • Autosomal dominant.
  • Mutations in keratins 4/13.
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46
Q

When does white sponge naevus present?

A

May be apparent in infants or not until adolescence.

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47
Q

What is the presentation of white sponge naevus?

A
  • Ill defined white patches with ‘shaggy’ surface.
  • Often BILATERAL.
  • Any part of oral mucosa, especially BUCCAL MUCOSA.
  • Other mucosa: nose, oesophagus, anogenital region.
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48
Q

What is a characteristic histopathological appearance of white sponge neavus?

A

BASKET WEAVE APPEARANCE.
due to intracellular edema of prickle and parakeratinized cells.

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49
Q

Histopathology of white sponge nevus?

A
  • Hyperparakeratosis and acanthosis of epithelium.
  • Basket weave apperance (intracellular edema of prickle and parakeratinized cells).
  • No cellular atypia/ dysplasia.
  • No inflammatory changes in lamina propria.
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50
Q

Treatment of white sponge nevus?

A

No treatment needed.

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51
Q

Presentation of oral hairy leukoplakia?

A
  • White, shaggy appearance on LATERAL BORDER OF TONGUE
  • Can affect other sites - can also be seen on buccal mucosa.
  • Asymptomatic
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52
Q

What causes oral hairy leukoplakia?

A
  • Due to EBV infection.
  • Strongly associated with HIV (pathognomonic).
  • Seen in immunosuppressed individuals and is some apparently healthy patients.
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53
Q

What is a characteristic histopathological appearance of oral hairy leukoplakia?

A

Band of BALLOONED PALE CELLS in the UPPER PRICKLE CELL LAYER.

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54
Q

Histopathology of oral hairy leukoplakia?

A
  • Thickened, hyperparakeratotic epithelium.
  • Band of ballooned pale cells in upper prickle cell layer.
  • Often superadded candidal infection but without normal inflammatory response.
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55
Q

How is the presence of EBV in oral hairy leukoplakia confirmed?

A

By in situ hybridisation (ISH).

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56
Q

Treatment for oral hairy leukoplakia?

A

No treatment needed.

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57
Q

presentation of frictional keratosis?

A

Roughened white patch at site of chronic trauma.

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58
Q

Histopathology of frictional keratosis?

A
  • Hyperkeratosis.
  • Prominent scarring fibrosis within submucosa.
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59
Q

Treatment for frictional keratosis?

A

Resolves once the source of friction is removed.

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60
Q

What is lichen planus?

A

Common CHRONIC INFLAMMATORY DISEASE of SKIN and MUCOUS MEMBRANES.

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61
Q

Who is affected by lichen planus?

A
  • Mainly affects middle aged and over.
  • F > M.
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62
Q

What is the cause of lichen planus?

A

Cause unknown.

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63
Q

What is the pathogenesis of lichen planus?

A

T cell-mediated immunological damage to the basal cells of epithelium.

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64
Q

Relationship between oral and skin lesions in patients with lichen planus?

A
  • Oral lesions in approximately 50% of patients with skin lesions.
  • Prevalence of skin lesions in patients primarily seen for oral LP lower.
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65
Q

Skin presentation of lichen planus?

A
  • Violaceous, itchy papule which may have distinctive white streaks (wickham’s striae).
  • Flexor of the wrist most common site.
  • Develop slowly and 85% resolve within 18 months.
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66
Q

What are the white streaks on lichen planus skin lesions called>

A

Wickham’s striae.

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67
Q

Oral presentation of lichen planus?

A
  • BUCCAL MUCOSA most common site.
  • Tongue, gingiva and lips may be affected.
  • FOM and palate rarely affected.
  • Oral LP runs a more chronic course - sometimes several years.
  • Usually BILATERAL and SYMMETRICAL.
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68
Q

6 different presentations of oral lichen planus?

A
  • Reticular.
  • Atrophic.
  • Plaque-like.
  • Papular.
  • Erosive.
  • Bullous.
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69
Q

Most common oral appearance of LP?

A

Reticular.

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70
Q

Reticular LP

A

Most common, lace-like striae.

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71
Q

Atrophic LP

A

Diffuse red lesions resembling erythroplakia.

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72
Q

Plaque-like LP

A

White plaques resembling leukoplakia.

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73
Q

Papular LP

A

Small white papules that may coalesce.

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74
Q

Erosive LP

A

Extensive areas of shallow ulceration.

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75
Q

Bullous LP

A

Subepithelial bullae.

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76
Q

Characteristic histopathology presentation of LP?

A
  • SAW-TOOTH RETE RIDGES.
  • CIVATTE BODIES (basal cells undergoing apoptosis).
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77
Q

Histopathological presentation of LP

A
  • Saw-tooth rete ridges.
  • Dense band-like infiltrate of lymphocytes hugging epithelial/ connective tissue junction.
  • Lymphocytic exocytosis.
  • Civatte body (basal cells undergoing apoptosis).
  • Hyperkeratosis/ hyperparakeratosis.
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78
Q

How do atrophic LP lesions present histopathologically?

A

Severe THINNING and FLATTENING of the epithelium.

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79
Q

How do erosive LP lesions present histopathologically?

A

Destruction of the epithelium, leaving fibrin-covered granulation tissue.

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80
Q

4 conditions that have similar histopathology to lichenoid inflammation?

A
  • Lichenoid reaction
  • Lupus erythematosus.
  • Graft vs host disease.
  • Lichenoid inflammation with associated dysplasia.
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81
Q

Treatment for LP?

A

If symptomatic, STEROIDS.

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82
Q

What are oral potentially malignant disorders?

A

Heterogenous group of clinically-defined conditions associated with a variable risk of progression to oral squamous carcinoma.

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83
Q

Lichen planus and malignant transformation?

A
  • Not all lesions are considered to have equal risk.
  • Not all lesions will undergo malignant transformation.
  • Malignant change of LP 0.1-10% (likely low).
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84
Q

Leukoplakia?

A
  • ORAL POTENTIALLY MALIGNANT LESION.
  • A white plaque of questionable risk after excluding other known diseases.
  • Can vary in thickness and surface appearance.
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85
Q

Risk of malignant transformation of leukoplakia?

A

Low.

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86
Q

What is proliferative verrucous leukoplakia?

A

PVL is a variant of oral leukoplakia that is multifactorial, persistent and progressive with a high rate of recurrence and a high risk of progression to squamous cell carcinoma.

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87
Q

Who is most affected by proliferative verrucous leukoplakia?

A

Older patients, F>M.

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88
Q

Oral presentation of proliferative verrucous leukoplakia?

A
  • Gingiva, alveolar ridge, buccal mucosa, tongue, hard palate.
  • Persistent, recurrent, become multi-focal.
  • Begins as simple hyperkeratosis that in time becomes exophytic and wart-like.
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89
Q

Cause of proliferative verrucous leukoplakia?

A

Unknown.

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90
Q

2 concerns with proliferative verrucous leukoplakia?

A
  • Difficult to completely excise.
  • High risk of degenerating to ORAL CANCER –> VERRUCOUS CARCINOMA or SQUAMOUS CELL CARCINOMA.
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91
Q

Histology of proliferative verrucous leukoplakia?

A

Hyperplastic lesion, hyperkeratosis, often minimal dysplasia.

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92
Q

3 examples of infective red patches?

A
  • Periodontal disease.
  • Median rhomboid glossitis.
  • HIV gingivitis.
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93
Q

2 dermatological disorders that can manifest as red oral patches?

A
  • Erosive lichen planus.
  • Discoid lupus erythematosus.
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94
Q

2 idiopathic examples of red patches?

A
  • Erythroplakia.
  • Geographic tongue.
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95
Q

2 neoplastic red patches?

A
  • Dysplastic lesions.
  • Squamous cell carcinoma.
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96
Q

Presentation of median rhomboid glossitis (3)?

A
  • Rhomboid red patch on midline of posterior aspect of anterior 2/3rds of dorsal tongue.
  • Asymptomatic.
  • May be a ‘kissing lesion’ - reciprocal lesion on palate opposing tongue.
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97
Q

Aetiology of median rhomboid glossitis?

A

Most cases associated with candida.

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98
Q

How is median rhomboid glossitis diagnosed?

A
  • Usually diagnosed CLINICALLY (no need for biopsy).
  • Sometimes get biopsy.
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99
Q

Histopathology of median rhomboid glossitis?

A
  • Loss of lingual papillae.
  • Thickened epithelium.
  • Parakeratosis and acanthosis.
  • CANDIDAL HYPHAE and neutrophils in parakeratin.
  • Chronic inflammatory infiltrate in connective tissue.
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100
Q

Treatment for median rhomboid glossitis?

A

Antifungal medication.

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101
Q

What stain is used to highlight candida?

A

periodic acid Schiff (PAS).

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102
Q

What is erythroplakia?

A
  • A red patch that cannot be characterized clinically or pathologically as another definable lesion.
  • An ORAL POTENTIALLY MALIGNANT DISORDER.
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103
Q

Presentation of erythroplakia?

A
  • Red ‘velvety’ appearance, smooth or nodular.
  • Most frequently seen on palate, FOM and buccal mucosa.
  • Less common than leukoplakia.
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104
Q

What is erythroleukoplakia?

A
  • Speckled leukoplakia.
  • Has both leukoplakia and erythroplakia components.
  • ORAL POTENTIALLY MALIGNANT DISORDER.
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105
Q

Malignancy and erythroleukoplakia and erythroplakia?

A
  • HIGH likelihood of malignant transformation.
  • Greater than 90% will be SEVERE DYSPLASIA or CARCINOMA.
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106
Q

Exogenous sources of oral pigmentation? (5)

A
  • Superficial staining of mucosa (foods, drinks, tobacco).
  • Black hairy tongue.
  • Foreign bodies (ex. amalgam tattoo).
  • Heavy metal poisoning.
  • Some drugs, NSAIDs, antimalarials, chlorhexidine.
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107
Q

What results in black hairy tongue?

A

Papillary hyperplasia + overgrowth of pigment producing bacteria.

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108
Q

Who is most affected by black hairy tongue? Treatment?

A
  • Much more common in SMOKERS.
  • No IMMEDIATE treatment but good OH should help reduce appearance.
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109
Q

What causes amalgam tattoo? Presentation?

A
  • Amalgam introduced into SOCKET/ MUCOSA during treatment.
  • SYMPTOMLESS blue/black lesion.
  • May be seen on radiograph.
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110
Q

Histopathology of amalgam tattoo?

A

Pigment dispersed in connective tissue as fine black/ brown granules.

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111
Q

Treatment for amalgam tattoo?

A
  • None required.
  • Patient may request removal for aesthetics.
  • If not seen on radiograph, may be excised to confirm diagnosis.
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112
Q

9 ENDOGENOUS causes of oral pigmentation?

A
  • Normal variation in pigmentation similar to that seen in skin.
  • Melanotic macule.
  • Pigmented naevi.
  • Peutz_Jeghers syndrome.
  • Smoker’s melanosis.
  • HIV infection.
  • Manifestation of systemic disease (ex. addison’s disease, malignancy).
  • Mucosal melanoma.
  • melanotic neuroectodermal tumor of infancy.
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113
Q

Pigmented naevi?

A

Developmental lesions with proliferation of melanocytes.

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114
Q

Peutz-jeghers syndrome?

A

Multiple pigmented lesions on skin/mucosa, LIPS, tongue, palate, buccal mucosa, intestinal polyposis.

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115
Q

Smoker’s melanosis?

A

pigmentary incontinence.

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116
Q

HIV infection?

A

numerous melanotic macules in some individuals.

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117
Q

Melanotic macule presentation?

A
  • Well defined small brown/black lesions.
  • Buccal mucosa, palate and gingivae.
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118
Q

Cause of melanotic macule?

A

Due to INCREASED ACTIVITY OF MELANOCYTES.
- Benign.

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119
Q

Treatment for melanotic macule?

A

frequently excised to confirm diagnosis and exclude melanoma.

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120
Q

Histopathology of melanotic macule?

A
  • Increased melanin pigment in basal keratinocytes, NOT increased number of melanocytes.
  • Melanin pigmentary incontinence in connective tissue.
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121
Q

What is mucosal melanoma?

A

MALIGNANT NEOPLASM of mucosal MELANOCYTES.

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122
Q

Most common sites for mucosal melanoma in the head and neck? (2)

A
  • Nose.
  • Maxillary sinus.
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123
Q

Presentation of mucosal melanoma (7)?

A
  • Primary intraoral mucosal melanoma is rare but can occur.
  • HARD PALATE and MAXILLARY GINGIVAE most common intraoral sites.
  • Dark brown, black or red.
  • Typically ASYMPTOMATIC at first.
  • May remain unnoticed until pain, ulceration, bleeding or a neck mass.
  • Regional lymph node and blood-borne metastases are common
  • Typically very advanced at presentation
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124
Q

Who does mucosal melanoma most often affect?

A

40-60 years.

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125
Q

Progression of mucosal melanoma?

A
  • Typically very advanced at presentation.
  • Very invasive, metastasize early.
  • Prognosis is POOR.
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126
Q

Aetiology of mucosal melanomas?

A

Unknown.

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127
Q

Histopathology of mucosal melanoma?

A
  • Pleomorphic neoplasms, cells appear epithelioid or spindle-shaped.
  • Amount of melanin pigment is variable and may be absent.
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128
Q

What special histopathological investigation can be used to help DIAGNOSE mucosal melanoma?

A

Immunohistochemistry using specific markers for malignant melanocytes.

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129
Q

Treatment for mucosal melanoma (3)?

A
  • SURGICAL RESECTION.
  • Adjuvant radiotherapy.
  • Immunotherapy.
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130
Q

Who is most often affected by melanotic neuroectodermal tumor of infancy?

A
  • Very rare.
  • most < 1 years old.
  • M >F.
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131
Q

Presentation of melanotic neuroectodermal tumor of infancy?

A
  • Locally aggressive, rapidly growing pigmented mass.
  • Most often ANTERIOR MAXILLARY ALVEOLUS.
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132
Q

Origin and pathogenesis of melanotic neuroectodermal tumor of infancy?

A
  • ?neural crest cell origin.
  • Pathogenesis is unknown.
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133
Q

histopathology of melanotic ectodermal tumor of infancy?

A

Tumor comprises 2 types of cells:
- Neuroblastic.
- Pigmented epithelial cells.

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134
Q

treatment of melanotic neuroectodermal tumor of infancy?

A
  • Complete local excision is treatment of choice.
  • Tumor of uncertain malignant potential
  • Can recur.
  • Small number do metastasise.
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135
Q

what is an ulcer?

A

Localized surface defect with LOSS OF EPITHELIUM, exposing underlying INFLAMED CONNECTIVE TISSUE.

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136
Q

infective causes of oral ulceration?

A
  • Bacterial.
  • Fungal.
  • Viral (HSV, VZV, CMV, Coxsackie).
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137
Q

5 traumatic causes of oral ulceration?

A
  • Mechanical.
  • Chemical.
  • Thermal.
  • Factitious injury.
  • Radiation.
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138
Q

Drugs that can cause oral ulceration? (2)

A
  • NSAIDs.
  • Nicorandil.
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139
Q

Idiopathic causes of oral ulceration (1)?

A

Recurrent aphthous stomatitis.

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140
Q

3 systemic disease causes of oral ulcers?

A
  • Hematological disease.
  • GI disease.
  • HIV.
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141
Q

3 dermatological disease causes of oral ulcers?

A
  • Lichen planus.
  • Discoid lupus erythematosus.
  • Immunobullous diseases.
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142
Q

3 neoplastic causes of oral ulcers?

A
  • Oral squamous cell carcinoma.
  • Salivary gland neoplasms.
  • metastases.
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143
Q

Histopathology of ulcers?

A

Most ulcers will show NON SPECIFIC FEATURES OF ULCERATION:
- loss of surface epithelium.
- Inflamed fibrinoid exudate.
- Inflamed granulation tissue.

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144
Q

How do vesiculobullous lesions usually present?

A
  • vesicle is a small blister.
  • Bulla is a blister >10mm.
  • Presents as ORAL ULCERATION following rupture of vesicles/ bullae.
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145
Q

What are immunobullous disorders?

A
  • Subset of vesiculobullous disorders.
  • AUTOIMMUNE diseases in which autoantibodies against components of skin and mucosa produce BLISTERS.
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146
Q

2 ways to classify disorders which result in vesicles/ bullae histologically?

A

Based on the LOCATION of the bulla:
1. Intraepithelial.
2. Subepithelial.

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147
Q

2 types of intraepithelial bullous disorder?

A
  1. Non -acantholytic (death and rupture of cells, ex. viral infection as HSV).
  2. Acantholytic (desmosomal breakdown).
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148
Q

Give an example of intraepithelial non- acantholytic pathogen and diseases (2)?

A
  • HERPES SIMPLEX VIRUS.
  • Primary herpetic stomatitis.
  • Herpes labialis.
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149
Q

Primary herpetic stomatitis?

A

Intra epithelial, non acantholytic vesiculobullous condition.

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150
Q

herpes labialis?

A

Intra epithelial, non acantholytic vesiculobullous condition.

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151
Q

How do intraepithelial, NON acantholytic pathogens cause ulceration (4)?

A
  • Virus targets and replicates within epithelial cells.
  • Leads to cell lysis.
  • Groups of infected cells breakdown to form vesicles within the epithelium.
  • Infected cells infect nearby normal cells and an ulcer forms when the full thickness of the epithelium is involved and is destroyed.
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152
Q

Example of intra epithelial acantholytic lesion?

A

PEMPHIGUS

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153
Q

What is pemphigus? Types (5)? Most common type?

A
  • AUTOIMMUNE disease.
  • Vulgaris, folicaceous, IgA, drug-induced and paraneoplastic.
  • VULGARIS MOST COMMON AND SEVERE.
154
Q

Who is most often affected by pemphigus vulgaris?

A
  • Most frequently FEMALES, 40-60 years.
155
Q

Pathogenesis and presentation of pemphigus vulagaris?

A
  • AUTOANTIBODIES to desmosomal protein (desmoglein 1 or 3).
  • BULLAE form in skin and mucous membranes then rupture to leave ulcers.
156
Q

Treatment for pemphigus vulgaris?

157
Q

histopathology of pemphigus vulgaris (4)?

A
  • INTRAEPITHELIAL BULLAE.
  • Tombstone basal cells remain attached to basement membrane.
  • Acantholytic Tzanck cells found in the bulla fluid.
  • Little inflammation until lesion ruptures.
158
Q

2 methods used to confirm diagnosis of pemphigus vulgaris?

A
  • Routine histopathology.
  • Direct immunofluorescence (DIF).
159
Q

important consideration about direct immunofluorescence studies?

A

FRESH SPECIMEN MANDATORY!!!!!

160
Q

6 steps to direct immunofluorescence.

A
  1. Fix patient tissue/cells containing target antigen.
  2. Wash.
  3. Add the fluorescence conjugated antibody specific for the target antigen in the cell/tissue into the slide.
  4. Wash.
  5. Conjugated antibodies bind to target antigen (if present).
  6. Analyze using fluorescent microscope.
161
Q

4 examples of subepithelial vesiculobullous conditions?

A
  • Pemphigoid.
  • Erythema multiforme
  • Dermatitis herpetiformis.
  • Epidermolysis bullosa acquisita.
162
Q

What is pemphigoid?

A

Group of AUTOIMMUNE DISEASES:
- Bullous pemphigoid.
- Mucous membrane pemphigoid.
- Linear IgA disease.
- Drug-induced pemphigoid.

163
Q

Which pemphigoid is most common in the oral cavity?

A

Mucous membrane pemphigoid.

164
Q

Who is most often affected by mucous membrane pemphigoid?

A
  • Mostly females.
  • 50 -80 years.
165
Q

Presentation of mucous membrane pemphigoid?

A
  • Oral mucosa almost always involved and usually FIRST AFFECTED SITE.
  • Gingiva (desquemative gingivitis), buccal mucosa, tongue, palate.
  • Bullae are tough as lid is full thickness epithelium.
  • Tend to heal SLOWLY with SCARRING after rupture. Ocular lesions can lead to blindness.
  • Eyes, nose, larynx, pharynx, oesophagus and genitalia.
166
Q

3 conditions which may present as desquemative gingivitis.

A
  • Mucous membrane pemphigoid.
  • Pemphigus vulgaris.
  • Lichen planus.

CLINICAL DESCRIPTION.

167
Q

Pathology of mucous membrane pemphigoid?

A

Autoantibodies to basement membrane components (BP180).

168
Q

Treatment for mucous membrane pemphigoid?

169
Q

Histopathology of mucous membrane pemphigoid?

A
  • Separation of full thickness epithelium from connective tissue producing subepithelial bulla with a thick roof.
  • Neutrophils and eosinophils around and within bulla.
  • Base of bulla is inflamed connective tissue.
170
Q

2 methods used to confirm diagnosis of mucous membrane pemphigoid?

A
  • Routine histopathology.
  • Direct immunofluorescence (DIF).
171
Q

What is epidermolysis bullosa acquisita?

A
  • Uncommon
  • Acquired autoimmune blistering dermatosis with subepithelial bullae.
172
Q

Presentation of epidermolysis bullosa acquisita?

A
  • Oral lesions in approx 50 % cases. (desquamative gingivitis).
  • Early stage may mimic pemphigoid and later resembles Epidermolysis Bullosa
173
Q

Histopathology of epidermolysis bullosa acquisita?

A

Separation occurs in or beneath lamina densa in basement membrane zone

174
Q

What is epidermolysis bullosa? 3 types?

A

Group of rare genetic conditions

  • simplex.
  • junctional.
  • dystrophic.
175
Q

Simplex epidermolysis bullosa?

A

intraepithelial, mutations in keratins 5/14

176
Q

Junctional epidermolysis bullosa?

A

subepithelial, separation in lamina lucida, laminin mutations

177
Q

dystrophic epidermolysis bullosa?

A

subepithelial, separation beneath basal lamina, mutation in type VII collagen gene

178
Q

Presentation of epidermolysis bullosa?

A

Formation of skin bullae which heal with scarring. Variable involvement of oral mucosa.

179
Q

What are oral blood blisters? Proper name?

A
  • Spontaneous blood-filled bullae, burst to form ulcers and heal uneventfully.
  • Angina bullosa haemorrhagica.
180
Q

Who is most often affected by angina bullosa haemorrhagica?

A

Older adults.

181
Q

Oral presentation of angina bullosa haemorrhagica?

A

Most common on soft palate.

182
Q

Histopathology of angina bullosa haemorrhagica?

A

Subepithelial cleft.

183
Q

In what condition may Tznack cells be seen? What are they?

A
  • Acantholytic cells.
  • Pemphigous vulgaris
184
Q

What is submucous fibrosis (3)? What is it associated with?

A
  • Chronic, progressive, OTAL POTENTIALLY MALIGNANT DISORDER.
  • Associated with BETEL QUID/ ARECA NUT.
185
Q

Clinical features of oral submucous fibrosis (3)?

A
  • Clinically pale coloured mucosa.
  • Firm to palpate.
  • Increased submucosal fibrosis leads to VERY MARKED TRISMUS.
  • Usually FIBROUS BANDS that affect the BUCCAL MUCOSA, SOFT PALATE & LABIAL MUCOSA.
186
Q

histopathology of oral submucous fibrosis (4)?

A
  • Submucosal deposition of dense collagenous tissue
  • Decreased vascularity
  • Marked epithelial atrophy
  • Variable grades of dysplasia
187
Q

What is epithelial dysplasia?

A

Atypical epithelial alterations limited to the surface squamous epithelium.
- Architectural changes: maturation and differentiation.
- Cytological changes: changes in cells.

188
Q

Submucous fibrosis risk of malignancy?

A

HIGH RISK OF MALIGNANT TRANSFORMATION.

189
Q

What does epithelial dysplasia indicate?

A

Indicates a risk of developing oral squamous cell carcinoma.

190
Q

WHO definition of epithelial dysplasia?

A

Oral epithelial dysplasia (OED) is a spectrum of architectural and cytological epithelial changes resulting from accumulation of genetic alterations, usually arising in a range of oral potentially malignant disorders (OPMD) and indicating a risk of malignant transformation to squamous cell carcinoma (SCC).

191
Q

Which areas of the mouth may epithelial dysplasia affect?

A
  • Oral epithelial dysplasia can involve any site in the mouth
  • Lateral border of tongue, ventral tongue, retromolar area, and floor of mouth are associated with higher risk of malignant transformation than other sites.
192
Q

11 histological features of epithelial dysplasia?

A
  1. Nuclear and cellular pleomorphism
  2. Alteration in nuclear/cytoplasmic ratio (invariably an increase)
  3. Nuclear hyperchromatism
  4. Prominent nucleoli
  5. Increased and abnormal mitoses
  6. Loss of polarity of basal cells
  7. Basal cell hyperplasia
  8. Drop-shaped rete pegs ie wider at their deepest part
  9. Irregular epithelial stratification or disturbed maturation
  10. Abnormal keratinization ‘Dyskeratosis’- cell starts to keratinize before the surface is reached
  11. Loss/ reduction of intercellular adhesion
193
Q

What is the grading of epithelial dysplasia?

A
  • Mild: disorganisation, increased proliferation and atypia of BASAL cells
  • Moderate: more layers of disorganised basaloid cells, atypia, suprabasal mitoses (about 2/3rds of epithelium).
  • Severe: very abnormal, affects FULL THICKNESS of epithelium.

moderate, severe (carcinoma in situ - old fashion term).
- SUBJECTIVE.

194
Q

Relation of epithelial dysplasia to cancer?

A
  • Not all epithelial dysplasias progress to cancer.
  • Higher grade epithelial dysplasia has a higher risk of malignant transformation.
195
Q

Epithelial dysplasia vs oral squamous cell carcinoma?

A
  • All features of dysplasia may be seen in oral squamous cell carcinoma HOWEVER IN DYSPLASIA THE ATYPICAL CELLS ARE CONFINED TO THE SURFACE EPITHELIUM.
  • In SCC the ATYPICAL CELLS INVADE INTO THE UNDERLYING CONNECTIVE TISSUE.
196
Q

7 ways to manage epithelial dysplasia?

A
  • Modify risk factors (tobacco and alcohol).
  • High risk sites (lateral &ventral border of tongue, FOM may be managed less conservatively).
  • Antifungal treatment.
  • Excision/ CO2 laser excision.
  • Topical agents.
  • Close clinical review.
  • Rebiopsy.
197
Q

What is oral cancer?

A

Cancer of the ORAL CAVITY and EXTERNAL LIP (up to vermillion border).

198
Q

What is the most common type of oral cancer?

A
  • More than 90% is SQUAMOUS CELL CARCINOMA.
199
Q

What is the 5 year survival for oral cancer?

A

5 year survival is around 55%.
- often advanced at detection.

200
Q

What is a risk factor

A

factors that can increase your RISK of getting a disease.

201
Q

11 Risk factors for oral cancer?

A
  • Tobacco
  • Alcohol
  • Betel quid/pan/areca nut
  • Previous oral cancer
  • Exposure to UV light (lip)
  • Poor diet
  • Immune suppression
  • Oral Potentially Malignant Disorders
  • Genetics??
  • Family history
  • ?? HPV- more often associated with Oropharyngeal cancer
202
Q

Why is early detection of oral cancer important?

A

Greater chance of:
- CURE
- QOL
- FUNCTION.

203
Q

Low risk sites for oral cancer?

A
  • Hard palate.
  • Dorsum of tongue.
204
Q

High risk sites for oral cancer?

A
  • Lateral/ ventral tongue.
  • FOM.
205
Q

11 signs and symptoms of oral cancer?

A
  • Lumps and bumps
  • Ulcers
  • White patches
  • Red patches
  • Speckled patches
  • Non-healing socket
  • Tooth mobility not associated with periodontal disease
  • Induration/fixation of mucosa
  • Dysphagia
  • Pain/paraesthesia
  • Bleeding
206
Q

4 additional tests for detection of oral cancer?

A
  • Toludine Blue
  • Autofluorescence
  • Chemiluminescence
  • Vizlite Plus®

Sensitivity/ specificity issues, should NOT replace thorough visual examination.

207
Q

2 GUIDELINES FOR ORAL CANCER?

A
  • Scottish Referral Guidelines for Suspected Cancer.
  • NICE (National Institute for Health and Care Excellence)
    Referral for Suspected Oral Cancer
208
Q

What type of referral is sent for suspected oral cancer?

A
  • URGENT.
  • Patient to be seen in 2 WEEKS.
209
Q

5 scottish referral guidelines for suspected cancer?

A
  • Persistent unexplained head and neck lump > 3 weeks.
  • Unexplained ulceration or unexplained swelling/induration of the oral mucosa persisting > 3 weeks
  • All unexplained red or mixed red and white patches of the oral mucosa persisting > 3 weeks
  • Persistent (not intermittent) hoarseness lasting for > 3 weeks
  • Persistent pain in the throat or pain on swallowing lasting for > 3 weeks
210
Q

How is diagnosis of oral cancer usually done?

A

By INCISIONAL BIOPSY of the lesion.

211
Q

Diagnosis of oral squamous cell carcinoma (4)?

A
  • 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
212
Q

What special investigation is done for the diagnosis of oropharyngeal cancers?

A

Immunohistochemistry for p16 and HPV in situ hybridization used for all oropharyngeal SCCs.

213
Q

What may be of therapeutic use in advanced oral cancer?

A

Can use tissue from FFPE (formalin fixed paraffin embedded) tissue blocks for molecular testing to see if MONOCLONAL ANTIBODIES maybe of therapeutic use in advanced oral cancer.

214
Q

Histopathology of oral cancer (2)?

A
  • Considerable variation in appearances, however
  • cytologically malignant squamous epithelium and ALL show invasion and destruction of local tissues
215
Q

How is SCC graded?

A

By degree of DIFFERENTIATION.
- Well-differentiated tumour cells very obviously squamous with ‘prickles’ and keratinization.
- Moderately differentiated
- Poorly differentiated, may be difficult to identify tumour cells as epithelial

216
Q

What does the grade of SCC tell us (2)?

A
  • Degree of differentiation.
  • GRADING ALONE DOES NOT CORRELATE WELL WITH PROGNOSIS.
217
Q

Treatment for oral cancer (3)?

A
  • Surgery
  • +/- adjuvant therapy (chemotherapy/ radiotherapy)
  • Monoclonal antibodies (for advanced cancers).
218
Q

How has the 5 year survival for oral cancer changed in the last few decades?n

A
  • 5yr survival not improved over last few decades.
  • Need to detect tumours early!!!!
219
Q

Define staging?

A

The anatomical extent of the disease aka HOW FAR THE DISEASE HAS SPREAD.

220
Q

What does staging include? Why is it important?

A
  • Clinical and radiological (preoperative)
  • Pathological (postoperative from resection spacing and neck dissection) findings.
  • Major determinant of APPROPRIATE TREATMENT and PROGNOSIS.
221
Q

How is cancer classified?

A

TNM STAGING/ TNM CLASSIFICATION OF MALIGNANT TUMOR.
- classification of cancer by anatomic disease extent (stage) is the major determinant of appropriate TREATMENT and PROGNOSIS.

222
Q

6 advantages of TNM staging?

A
  • Aid treatment planning.
  • Provide an indication of prognosis.
  • Assist in the evaluation of treatment results.
  • Facilitate the exchange of information between treatment centres.
  • Contribute to continuing investigations of human malignancies.
  • Support cancer control activities, including through cancer registries.
223
Q

What do the TNM components stand for?

A
  • T: extend of primary tumor.
  • N: absence or presence and extent of regional lymph node metastasis.
  • M: category described the absence or presence of distant metastasis.
224
Q

How are different stages differentiated in TNM staging?

A
  • Each component is given a number.
  • The higher the number, the more extensive the disease, POORER PROGNOSIS.
225
Q

4 most significant prognostic factors for oral cancer?

A
  • Tumor size.
  • Depth of invasion.
  • Nodal status.
  • Distant metastases.
226
Q

What core data items should be included in a histopathology report of carcinomas of the oral cavity?

A

Clinical and pathological data.

227
Q

What clinical data items should be included in a histopathology report of carcinomas of the oral cavity (2)?

A
  • Site and laterality of tumor.
  • Type of specimen.
228
Q

11 pathological data items should be included in a histopathology report of carcinomas of the oral cavity?

A
  • Maximum dimension of tumour.
  • Histological tumour type.
  • Histological tumour grade.
  • Depth of invasion.
  • Pattern of invasive front.
  • Bone invasion.
  • Perineural invasion.
  • Lymphovascular invasion.
  • Margin status- invasive carcinoma.
  • Margin status- carcinoma in situ/high-grade dysplasia.
  • Pathological staging.
229
Q

What clinical data items should be included in a histopathology report of nodal excisions and neck dissection specimens associated with head and neck carcinomas (2)?

A
  • Laterality of nodes and anatomical levels of nodes present.
  • Details of any extranodal structures removed.
230
Q

What pathological data items should be included in a histopathology report of nodal excisions and neck dissection specimens associated with head and neck carcinomas (5)?

A
  • Total number of lymph nodes at each anatomic level.
  • Number of nodes involved by metastatic carcinoma.
  • Size of the largest metastatic deposit.
  • Extracapsular spread.
  • Pathological staging.
231
Q

Fill in the sentence: the more ______ the tumor, the ______ the stage.

A

Tumor, stage.

232
Q

What do we use for staging of lip and oral cavity carcinomas?

A

TNM 8th edition.

233
Q

What is the highest T stage there is?

234
Q

What are the criteria for a T4a oral oral cavity cancer?

A

Tumour invades through cortical bone of the mandible or maxillary sinus, or invades skin of face.

235
Q

What happens as you increase in the pN staging?

A
  • Increased number of nodes.
  • Laterality of nodes involved (ipsi vs bilateral).
  • Size of nodes.
  • Extranodal extension.
236
Q

What is the higher pN regional lymph node stage?

A

pN3 (extranodal extension).

237
Q

What is the most common cause of periradicular/ periapical pathology?

A

Bacterial infection following pulpal death.

238
Q

4 clinical features of acute periapical periodontitis?

A
  • History of pain.
  • Grossly carious/ heavily restored tooth.
  • Previous trauma.
  • Typically little to see radiographically unless acute exacerbation of a chronic lesion.
239
Q

3 histopathology features of acute periapical pathology?

A

Acute inflammatory changes:
- Vascular dilation.
- Neutrophils.
- Edema.

240
Q

what is the key acute inflammatory cell?

A

Neutrophil.

241
Q

2 clinical features of acute periapical abscess?

A
  • Pain.
  • Swelling/ sinus.
242
Q

What pathways from the chart can lead to acute periapical abscess?

A

Acute and chronic periodontitis.

243
Q

3 components of pus?

A
  • Neutrophils.
  • Bacteria.
  • Cellular debris.
244
Q

4 histopathology features of acute periapical abscess?

A
  • 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).
245
Q

Treatment options for acute periapical abscess?

A
  • Drainage
    AND
  • Extraction OR RCT.
246
Q

What pathways from the chart can lead to chronic periapical abscess?

A

May follow acute periodontitis or be chronic from the onset.

247
Q

3 clinical features of chronic periradicular periodontitis?

A
  • Non vital tooth, may be previous RCT.
  • Often minimal symptoms.
  • Apical radiolucent lesion may be evident on radiographs.
248
Q

6 histopathology features of chronic periradicular periodontitis?

A

Chronic inflammatory changes.
- Lymphocytes.
- Plasma cells.
- Macrophages.
- Granulation tissue progressing to fibrosis.
- Resorption of bone.
- Minimal, if any, tooth resorption.

249
Q

Treatment options for chronic periradicular periodontitis?

A
  • Extraction.
  • RCT.
  • reRCT
  • Periradicular surgery.
  • Will NOT resolve spontaneously.
250
Q

What pathways from the chart can lead to periapical granuloma?

A

Chronic periapical periodontitis or acute abscess.

251
Q

What is a periapical granuloma (2)? What are its sequelae (2)?

A
  • A mass of inflamed granulation tissue at the apex of a non-vital tooth.
  • Not a true granuloma.
  • Can transform to abscess.
  • Some may undergo cystic change (radicular cyst)
252
Q

Clinical features of periapical granuloma?

A
  • Non vital tooth, may be previous RCT.
  • Often minimal symptoms.
  • Apical radiolucent lesion TYPICALLY EVIDENT on radiographs.

(as of chronic periodontitis - excl radiograph).

253
Q

4 histopathological features of periapical granuloma?

A
  • Inflamed granulation tissue (lymphocytes, plasma cells, macrophages, neutrophils).
  • Proliferation of cell rests of malassez (may ultimately lead to inflammatory radicular cyst formation).
  • Haemosiderin and chlolesterol deposits (from RBC/ inflammatory cell breakdown) and associated multinucleate foreign body giant cells.
  • Resorption of adjacent bone +/- tooth.
254
Q

Treatment options for periradicular granuloma?

A
  • Extraction.
  • RCT.
  • reRCT
  • Periradicular surgery.
255
Q

What is pericoronitis?

A
  • Inflammation of soft tissues around partially erupted tooth, frequently lower 8s.
  • Often exacerbated by trauma from opposing tooth.
256
Q

4 clinical features of pericoronitis?

A
  • Pain
  • Swelling/Tenderness of operculum
  • Bad taste
  • Trismus
257
Q

6 histopathological features of pericoronitis?

A

Acute and chronic inflammatory changes:
- Edema.
- Inflammatory cells.
- Vascular dilation.
- Fibrotic connective tissue.

  • PARADENTAL cyst may arise in chronic pericoronitis.
258
Q

Treatment of pericoronitis?

A
  • Irrigation.
  • Consider XLA of opposing tooth.
  • Antibiotics (if systemically unwell).
259
Q

What is a cyst? (3)

A
  • A PATHOLOGICAL cavity having FLUID or SEMI-FLUID content.
  • Lined wholly or in part by epithelium.
  • NOT due to accumulation of pus (abscess).
260
Q

How are cysts of the jaws classified?

A
  • Odontogenic (derived from epithelial residues of the tooth-forming organ - can be inflammatory or developmental).
  • Non odontogenic (derived from sources other than tooth-forming organ).
261
Q

Odontogenic cyst?

A
  • Derived from epithelial residues of tooth-forming organ.
  • Can be inflammatory or developmental
262
Q

Non odontogenic cyst?

A

Derived from sources other than tooth-forming organ.

263
Q

From what tissue do teeth develop?

A
  • Odontogenic epithelium + neural crest derived ectomesenchyme.
264
Q

How does the enamel organ form? What are its 4 layers?

A
  • The DENTAL LAMINA buds down from the ECTODERM and becomes the ENAMEL ORGAN.
    4 layers:
  • Inner enamel epithelium (future ameloblasts).
  • Outer enamel epithelium.
  • Stellate reticulum.
  • Stratum intermedium.
265
Q

Which tissues form each dental tissue: enamel, dentine, pulp.

A
  • Enamel: inner enamel epithelium (future ameloblasts).
  • Pulp: ectomesenchymal cells.
  • Dentine: signalling results in the outer cells of the pulp next to the ameloblasts differentiating into odontoblasts and laying down dentine.
266
Q

5 steps to crown formation?

A
  1. Inner enamel epithelium become ameloblasts.
  2. Ectomesenchymal cells become pup cells.
  3. Signalling results in the outer cells of the pulp next to the ameloblasts differentiating into odontoblasts and laying down dentine.
  4. Enamel matrix is laid down.
  5. After crown formation, enamel organ forms the Sheath of Hertwig which maps out the root.
267
Q

3 types of odontogenic remnants?

A
  • Remnants of ODONTOGENIC EPITHELIUM in the PDL and gingiva after tooth development.
  • Remnants of the DENTAL LAMINA known as the GLANDS OF SERRES.
  • Remnatns of the ROOT SHEATH OF HERTWIG, persist as CELL RESTS OF MALASSEZ.
268
Q

Remnants of the dental lamina?

A

Glands of Serres

269
Q

Remnants of Root Sheath of Hertwig?

A

Cell rests of malassez

270
Q

2 types of inflammatory odontogenic cysts?

A
  1. Radicular cyst (apical, lateral, residual).
  2. Inflammatory Collateral Cysts (paradental, mandibular buccal bifurcation cyst).
271
Q

What is the most common type of jaw cyst?

A

Radicular cyst (inflammatory odontogenic cyst).
- Accounts for 55% of odontogenic cysts.

272
Q

What causes radicular cysts?

A

Arise from EPITHELIAL PROLIFERATION and CYST FORMATION within SOME PERIAPICAL GRANULOMAS.

273
Q

6 clinical features of radicular cysts?

A
  • Most common in the ANTERIOR MAXILLA.
  • WIDE age range.
  • SLOW GROWING swelling.
  • Often NO SYMPTOMS unless very large.
  • MUST BE ASSOCIATED WITH A NON-VITAL TOOTH.
  • Typically WELL CIRCUMSCRIBED, UNILOCULAR, RADIOLUCENT lesion seen at APEX (can be lateral if lateral canal).
274
Q

pathogenesis of radicular cyst (3)?

A
  • Proliferation of epithelium (cell rests of malassez) in response to inflammation.
  • Cyst enlarges due to osmotic pressure.
  • Local bone resorption.
275
Q

What is the typical structure of cysts?

A
  • Central cystic lumen
  • Lined by epithelium of varying type
  • In turn is surrounded by a connective tissue cyst wall/ capsule.
276
Q

6 histopathology characteristics of radicular cysts?

A
  • Central cystic lumen.
  • Wholly/ partly lined by NON KERATINIZED, STRATIFIED SQUAMOUS epithelium of varbiable thickness, hyperplasia common.
  • Chronically inflamed fibrous connective tissue capsule.
  • Mucous metaplasia and ciliated cells may be seen.
  • Hyaline/Rushton bodies.
  • Cholesterol clefts and haemosiderin.
277
Q

What are hyaline/ rushton bodies (3)?

A
  • Pink structures.
  • Secreted by the cyst lining.
  • Indicate the cyst is ODONTOGENIC origin but not specific to radicular cysts.
278
Q

What is enucleation?

A

Entire lesion is removed.

279
Q

What is marsupialisation?

A

Small pouch is made into the cyst to allow it to decompress prior to marsupialisation.

280
Q

Treatment for radicular cysts (3)?

A
  • Small cysts may resolve after RCT, extraction, periradicular surgery.
  • Enucleation (removal).
  • Marsupialisation for very large lesions (prior to enucleation).
281
Q

Lateral radicular cyst?

A

Radicular cyst arising from a lateral root canal branch of a non-vital tooth.

282
Q

Residual cyst?

A

Radicular cyst that persists after extraction of the associated non-vital tooth.

283
Q

2 types of inflammatory collateral cysts?

A
  • Paradental (associated with lower 3rd molars).
  • Mandibular Buccal Bifurcation Cyst (lower 1st or 2nd molars).
284
Q

Aetiology of inflammatory collateral cysts? (4)

A
  • Inflammation associated with pericoronitis.
  • Exacerbated by impaction of food.
  • May be enamel spur on buccal aspect of involved tooth.
  • Proliferation of sulcular or junctional epithelium derived from reduced enamel epithelium.
285
Q

What type of inflammatory collateral cyst is most common?

A

More than 60% of inflammatory collateral cysts are paradental cysts.

286
Q

Clinical features of paradental cysts (3)?

A
  • Arise from chronic pericoronitis/ long standing pericoronitis.
  • Associated with a vital tooth.
    -Well-demarcated radiolucency.
287
Q

3 clinical features of mandibular bifurcation cyst?

A
  • Often painless swelling.
  • Tooth usually TILTED BUCCALLY with DEEP PERIO POCKET.
  • Well-demarcated buccal radiolucency.
288
Q

Histopathology of paradental cysts?

A

Same as radicular cysts.

289
Q

Histopathology of mandibular buccal bifurcation cysts?

A

The same as in radicular cysts.

290
Q

Treatment of mandibular buccal bifurcation cyst?

A

Enucleation

291
Q

Treatment of paradental cyst?

A

Removal of 8s and paradental cyst.

292
Q

6 types of developmental odontogenic cysts?

A
  • Odontogenic keratocyst.
  • Dentigerous cyst/ Eruption cyst.
  • Lateral periodontal cyst and Botryoid odontogenic cyst.
  • Glandular odontogenic cyst
  • Gingival cysts
  • Calcifying odontogenic cyst
  • Orthokeratinized odontogenic cyst
293
Q

How common is odontogenic keratocyst (OKC)?

A

3rd most common cyst of the jaws.

294
Q

5 clinical features of odontogenic keratocyst (OKC).

A
  • Wide age range.
  • Slight male.
  • Majority in POSTERIOR MANDIBLE (80%).
  • **Symptomless* unless infection or when cortical bony expansion (often late as enlarges A-P).
  • Well defined radiolucent uni or multilocular lesion.
295
Q

Aetiology of odontogenic keratocyst (3)?

A
  • Arise from remnants of dental lamina (glands of serres).
  • Associated with mutation & inactivation of PTCH1 gene (chromosome 9, SHH signalling, aberrant cell proliferation of epithelium).
  • Sporadic and syndromic patients.
296
Q

Is OKC neoplastic?

A

Insufficient evidence to support a neoplastic origin of OKC.

297
Q

What syndrome may odontogenic keratocysts be associated with?

A

Naevoid basal cell carcinoma syndrome/ Gorlin syndrome.

298
Q

7 clinical features of naevoid basal cell carcinoma syndrome/ Gorlin syndrome?

A
  • Multiple recurring odontogenic keratocysts.
  • Occur at younger age than sporadic cases.
  • Basal cell naevi.
  • Skeletal abnormalities.
  • Multiple basal cell carcinomas.
  • AD inheritance.
  • PTCH1 gene mutations.
299
Q

7 histopathological features of odontogenic keratocyst?

A
  • Cystic lesion.
  • Keratinized stratifies squamous epithelial lining (5-10 cells thick).
  • Thin, fibrous cyst wall with no inflammation unless secondary infection.
  • Corrugated appearance of surface parakeratin layer.
  • Well-defined, palisaded basal cell layer.
  • Keratin debris in lumen.
  • May be daughter/ satellite cysts in wall.
300
Q

How is diagnosis of odontogenic keratocyst made?

A

Usually via CHARACTERISTIC HISTOPATHOLOGY.

301
Q

Effect of secondary infection on odontogenic keratocyst?

A
  • The characteristic histopathological features typically lost if secondary infection.
  • Thus unable to distinguish from inflammatory cyst on histology alone.
302
Q

Behavior of odontogenic keratocyst (4)?

A
  • BENIGN developmental cyst.
  • High recurrence rate in incompletely removed (25% - thin capsule, daughter cysts).
  • Recurrence rate varies with treatment.
  • No evidence to support a difference in behaviour between sporadic lesions and those of NBCCS.
303
Q

Why is it believed that odontogenic keratocysts have a high recurrence rate?

A

If incompletely removed:
- Thin capsule.
- Daughter cysts.

304
Q

6 treatment options for odontogenic keratocyst?

A
  • Marsupialization
  • Enucleation
  • Enucleation + marsupialization
  • Enucleation + Carnoy’s solution (modified Carnoy’s)
  • Enucleation + Cryotherapy
  • Resection
305
Q

Which treatment options are considered better for odontogenic keratocyst?

A

Some evidence to support a lower recurrence rate with:
- Enucleation + Carnoy’s solution (<10%)
- Resection (2%) but increased morbidity.

306
Q

What is the second most common odontogenic cyst?

A

Dentigerous cyst

307
Q

7 clinical features of dentigerous cyst?

A
  • 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
308
Q

Histopathology of dentigerous cyst (4)?

A
  • Thin non-keratinized stratified squamous epithelial lining, 2-5 cells thick.
  • Uninflammed fibrous capsule, unless secondary infection.
  • Mucous metaplasia common
  • May be odontogenic epithelium remnants, calcification, Rushton Bodies.
309
Q

What is the pathogenesis of dentigerous cyst (2)?

A
  • Pathogenesis unclear.
  • Accumulation of fluid between the reduced enamel epithelium of the dental follicle and the crown of unerupted tooth.
310
Q

Treatment of dentigerous cyst?

A
  • Enucleation
  • Exposure/ transplantation/ extraction of associated tooth.
311
Q

Effect of secondary infection on dentigerous cyst?

A
  • The characteristic histopathological features typically lost if secondary infection.
  • Thus unable to distinguish from inflammatory cyst
312
Q

What must we include on the pathology request form for dentigerous cyst?

A
  • Include information regarding clinical attachment of lesion to ACJ of unerupted tooth.
313
Q

What is an eruption cyst?

A

A dentigerous cyst arising in extra-alveolar location.

314
Q

3 clinical features of eruption cyst?

A
  • Typically seen in children.
  • Deciduous and permanent molars.
  • Presents as bluish swelling.
315
Q

Histopathology of eruption cyst?

A

As dentigerous cyst.

316
Q

Treatment options of eruption cyst?

A
  • None (tooth usually erupts through cyst).
  • Exposure of erupting tooth.
317
Q

Clinical features of lateral periodontal cyst (6)?

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.
318
Q

Aetiology of lateral periodontal cyst?

A

Likely arises from cell rest of Malassez.

319
Q

Histopathology of lateral periodontal cyst (3)?

A
  • Thin, non-keratinized squamous or cuboidal epithelium.
  • Focal thickenings/plaques in epithelium.
  • Uninflamed fibrous wall.
320
Q

Treatment of lateral periodontal cyst (2)?

A
  • Enucleation.
  • Reccurence rare.
321
Q

What is botryoid odontogenic cyst?

A
  • Very rare multicystic variant of lateral periodontal cyst (same histological features).
  • Botryoid= ‘Bunch of grapes’- polycystic appearance
322
Q

4 clinical features of botryoid odontogenic cyst?

A
  • Typically multilocular radiolucency
  • Mandibular premolar =canine region
  • Adult
  • Can recur
323
Q

Clinical features of glandular odontogenic cyst (5)?

A
  • Very rare.
  • Anterior mandible.
  • Wide age range.
  • Multilocular radiolucency.
  • Strong tendency to recur.
324
Q

Etiology of glandular odontogenic cyst?

A

Remnants of the dental lamina.

325
Q

Histopathology of glandular odontogenic cyst (5)?

A
  • Cystic lumen
  • Lined by epithelium of various thickness with mucous cells and glandular structures (crypts/ cyst-like spaces).
  • Focal epithelial plaques/thickenings.
  • Uninflamed fibrous wall.
  • Must be differentiated from central mucoepidermoid carcinoma.
326
Q

Treatment of glandular odontogenic cyst?

A

Enucleation but high recurrence rate (up to 50%)

327
Q

Clinical features of gingival cysts in infants?

A
  • Seen as Bohn’s nodules, superficial keratin-filled cysts in the gingivae of newborns.
  • Present as white nodules in gingivae.
328
Q

What is the cause of gingival cysts in infants and adults?

A

??Due to proliferation of dental lamina remnants (Glands of Serres).

329
Q

What is the treatment for gingival cysts in infants?

A

None, usually disappear in a few weeks.

330
Q

Clinical features of gingival cysts in adults (6)?

A
  • Very rare
  • Middle-aged adults
  • Painless
  • Dome-shaped, translucent swelling in gingiva
  • Majority in Mandibular canine-premolar region
  • May be superficial erosion of underlying alveolar bone
331
Q

histopathology of gingival cysts in adults (3)?

A
  • Cyst just below oral epithelium.
  • Uninflamed fibrous wall.
  • Lined by thin epithelium, cuboidal to squamous
332
Q

Treatment of gingival cysts in adults?

A

Simple Excision.

333
Q

Clinical features of calcifying odontogenic cyst (7)?

A
  • Rare
  • Wide age range, average 30 yrs
  • Painless swelling of jaw
  • Tooth displacement and resorption common
  • Either jaw, often anterior
  • Minority can be in soft tissues
  • Well-defined radiolucency
334
Q

Etiology of calcifying odontogenic cyst?

A
  • Arises from dental lamina
  • (controversy neoplasm - still classified as DEVELOPMENTAL).
335
Q

Histopathology of calcifying odontogenic cyst (4)?

A
  • Unicystic.
  • Lined by epithelium which is ameloblastoma-like.
  • Palisaded basal layer with overlying stellate reticulum-like layer.
  • Focal ‘Ghost cells’, which may calcify.
336
Q

Treatment of calcifying odontogenic cyst?

A
  • Enucleation
  • Recurrence is rare
337
Q

Clinical features of orthokeratinized odontogenic cyst (6)?

A
  • 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.
338
Q

Etiology of orthokeratinized odontogenic cyst?

A

Pathogenesis uncertain but likely derives from dental lamina.

339
Q

Histopathology of orthokeratinized cyst (4)?

A
  • Uninflamed fibrous wall
  • Lined by stratified squamous epithelium
  • Prominent granular cell layer and orthokeratinized.
  • No basal palisading, no corrugated parakeratin (as seen in odontogenic keratocyst).
340
Q

Treatment of orthokeratinized odontogenic cyst (2)?

A
  • Enucleation
  • Recurrence is rare.
341
Q

What is a non odontogenic cyst?

A

Derived from sources OTHER THAN TOOTH-FORMING ORGAN.

342
Q

3 non odontogenic cysts?

A
  • Nasopalatine duct cyst.
  • Surgical ciliated cyst.
  • Nasolabial cyst.
343
Q

8 clinical features of nasopalatine duct cyst?

A
  • 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.
344
Q

Where does the nasopalatine duct cyst originate from?

A

Originates from epithelium of nasopalatine duct in incisive canal.

345
Q

3 other names for nasopalatine duct cyst?

A
  • Median palatine cyst.
  • Incisive canal cyst.
  • Median alveolar cyst.
346
Q

What is a strong histopathological clue to the diagnosis of nasopalatine duct cyst?

A

Neurovascular bundles in the capsule.

347
Q

5 histopathological characteristic of nasopalatine duct cyst?

A
  • 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.
348
Q

Treatment for nasopalatine duct cyst?

A
  • Enucleation.
  • Recurrence unlikely.
349
Q

6 clinical features of surgical ciliated cyst?

A
  • Rare.
  • M = F
  • Peak in 5-6th decades.
  • Most common in posterior maxilla (rare in mandible).
  • May be asymptomatic or present with pain and swelling.
  • Develop after sinus/ nasal mucosa implanted in the jaw following trauma or surgery.
350
Q

Histopathology of surgical ciliated cyst?

A
  • Cyst lined by respiratory epithelium (pseudostratified columnar epithelium).
  • Fibrous connective tissue capsule which may be inflamed.
351
Q

What is respiratory epithelium?

A

Pseudostratified columnar epithelium.

352
Q

Treatment of surgical ciliated cyst?

A
  • Enucleation.
  • Recurrence is rare.
353
Q

5 clinical features of nasolabial cyst?

A
  • Very rare.
  • F>M
  • 4th-5th decades.
  • Arise in UPPER LIP BELOW NOSE, lateral to the MIDLINE.
  • Slow growing, distorts nostril.
  • Painless unless infected.
  • 10% bilateral.
  • Likely to derive from remnants of the embryonic nasolacrimal duct or the lower anterior portion of the mature duct.
354
Q

Where does nasolabial cyst derive from?

A

Likely to derive from remnants of the embryonic nasolacrimal duct or the lower anterior portion of the mature duct.

355
Q

Histopathology of nasolabial cyst (2)?

A
  • Cystic lesion with fibrous capsule.
  • Usually pseudostratified columnar epithelium lining.
356
Q

Treatment of nasolabial cyst?

357
Q

5 types of soft tissue cysts?

A
  • Salivary mucoceles.
  • Epidermoid cyst.
  • Dermoid cyst.
  • Lymphoepithelial cyst.
  • Thyroglossal duct cyst.
358
Q

3 types of salivary mucoceles?

A
  • Extravasation.
  • Retention.
  • Ranula.
359
Q

3 clinical features of epidermoid cyst?

A
  • Painless swelling.
  • Often following trauma or surgery.
  • More common on the skin (less common in OC).
360
Q

4 histopathological features of epidermoid cyst?

A
  • Thin cyst wall.
  • Keratinizing stratified squamous epithelium lining.
  • Abundant keratin debris in lumen.
  • No skin appendages in cyst wall.
361
Q

Treatment of epidermoid cyst?

362
Q

4 clinical features of dermoid cyst?

A
  • Developmental lesion.
  • Various location in the head and neck.
  • Floor of mouth is most common oral site.
  • Presents as painless swelling in midline.
363
Q

4 histopathological features of dermoid cyst?

A
  • Same as for epidermoid cyst BUT MUST HAVE SKIN APPENDAGES IN THE CYST WALL (ex. sebaceous gland, hair follicle) in cyst wall.
  • Thin cyst wall.
  • Keratinizing stratified squamous epithelium lining.
  • Abundant keratin debris in lumen.
364
Q

Treatment of dermoid cyst?

365
Q

5 clinical features of lymphoepithelial cyst?

A
  • Developmental lesions.
  • Uncommon but do occur in oral cavity.
  • FOM and TONGUE most common intraoral sites.
  • PAINLESS small swelling.
  • May be YELLOWISH in colour.
366
Q

3 histopathological characteristics of lymphoepithelial cyst?

A
  • Thin keratinized stratified squamous epithelium lining.
  • Keratin debris in cyst lumen.
  • LYMPHOID TISSUE in CYST WALL.
367
Q

Treatment of lymphoepithelial cyst?

368
Q

7 clinical features of thyroglossal duct cyst?

A
  • Developmental cyst derived from embryonic thyroglossal duct.
  • Intraoral lesions very rare.
  • Most arise near hyoid bone.
  • Present as midline swelling.
  • Usually painless.
  • Symptoms if infected, or very large.
  • May have functioning thyroid tissue.
369
Q

3 histopathological features of thyroglossal duct cyst?

A
  • 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.
370
Q

Treatment of thyroglossal duct cyst?

A

EXCISION
- SISTRUNK PROCEDURE - remove cyst + mid third of hyoid bone.
- Lower chance of recurrence.

371
Q

What procedure is used to treatment thyroglossal duct cyst? What does it involve.

A
  • SISTRUNK PROCEDURE.
  • Removal of cyst + mid third of hyoid bone.
372
Q

2 types of non-epithelialised primary bone cysts?

A
  • Simple/ Solitary bone cyst.
  • Aneurysmal bone cyst.
373
Q

What do non epithelialized primary bone cysts most often affect? What are they?

A
  • Almost exclusively involve MANDIBLE.
  • Not true cysts.
374
Q

5 clinical features of simple/ solitary bony cyst?

A
  • Peak incidence 2nd decade.
  • Premolar/molar regions of mandible.
  • May be asymptomatic swelling or incidental finding.
  • Large radiolucency on radiograph.
  • Not a true cyst.
375
Q

3 histopathological features of simple/ solitary bone cysts?

A
  • 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.
376
Q

Treatment of simple/ solitary bone cyst (2)?

A
  • Resolve spontaneously.
  • Resolve after opening a cavity.
377
Q

6 clinical features of aneurysmal bone cysts?

A
  • Very rare in jaws (more common in long bones).
  • Usually MANDIBLE.
  • Young.
  • Benign neoplasms.
  • Painless swelling.
  • Radiolucency on radiograph.
378
Q

3 histopathological features of aneurysmal bone cysts?

A
  • Blood filled spaces separated by cellular fibrous tissue.
  • No lining of spaces.
  • Multinucleated giant cells in fibrous bands.
379
Q

Treatment of aneurysmal bone cysts?

A
  • Curettage.
  • May recur.
380
Q

4 clinical features of Stafne’s defect/ stafne’s idiopathic bone cavity?

A
  • NOT a true lesion.
  • Developmental anomaly.
  • Due to part of submandibular gland indenting lingual mandible.
  • Appears cyst-like on radiograph and be mistaken for a cyst.

Module 7 (9 decks)

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