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Module 9 > Oral Pathology > Flashcards

Oral Pathology Flashcards

1
Q

What types of specimen are sent for histopathological investigation?

A
  1. Incisional
  2. Excisional
  3. Resection
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2
Q

What does the specimen journey through the pathology laboratory involve?

A
  1. Most specimens are sent to pathology as fixed specimens (placed in 10% neutral buffered formulin). A small number can be sent as fresh specimens (such as when patient is in theatre, and immunofluoresense dyes require fresh specimens).
  2. Specimens arrived at pathology lab with correctly filled out pathology request form.
  3. The details on specimen pot and request form are logged into pathology system and assigned a unique pathology number.
  4. Specimen is fixed for suitable length of time (can be 24hours to several days depending on size). Specimen has a macroscopic description and then cut-up by pathologist.
  5. All tissue blocks taken from a resection will be placed into cassettes.
  6. Tissues are processed and dehydrated with alcohol.
  7. After tissues are dehydrated the tissues are embedded in hot paraffin wax.
  8. Microtome cuts sections from the tissue block. Thickness is normally 4 micronanometers.
  9. Sections are floated in warm water bath and mounted onto glass slide where they are stained and cover slip placed on slide.
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3
Q

What is the most commonly used staining for specimens?

A

H&E.

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4
Q

What are additional stains that can be done in addition to H&E staining?

A
  • Special histochemical stains e.g PAS, trichromes, Gram
  • Immunohistochemistry - antibodies.
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5
Q

What other special investigations can be carried out as opposed to light microscopy?

A
  • in situ hybridization
  • immunofluorescence
  • electron microscopy
  • cytogenetic and molecular genetic analysis
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6
Q

Define hyperplasia

A

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

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7
Q

Define 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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8
Q

Define atrophy

A

A decrease in cell size by loss of cell substance

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9
Q

Define metaplasia

A

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

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10
Q

Define hyperparakeratosis

A

Thickening of the stratum corneum.

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11
Q

Define orthokeratosis

A

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

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12
Q

Define parakeratosis.

A

The persistence of nuclei in the cells of keratin layer.

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13
Q

Define dyskeratosis.

A

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

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14
Q

Define acanthosis.

A

Increased thickness of prickle cell layer

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15
Q

Define acantholysis.

A

The loss of intercellular adhesion between keratinocytes.

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16
Q

Define epithelial dysplasia.

A

alteration in differentiation, maturation and architecture and adult epithelial cells.

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17
Q

Define ulceration

A

Mucosal/skin defect with complete loss of surface epithelium.

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18
Q

Define apoptosis.

A

Programmed cell death.

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19
Q

Define necrosis

A

Cell death by injury or disease.

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20
Q

Name 1 white lesion that is developmental.

A

Fordyce spots

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21
Q

Name 1 white lesion that is seen with normal variation.

A

Leukodaema.

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22
Q

Name 3 white lesions that are of hereditary causes.

A
  1. White sponge naevus
  2. Pachyonychia congenita
  3. Dyskeratosis congenita.
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23
Q

Name 2 white lesions that are of dermatological causes.

A
  1. Lichen Planus
  2. Lupus erythematosus
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24
Q

Name 3 white lesions that are of infective causes.

A
  1. Candidiosis
  2. Syphilitic Leukoplakia
  3. Oral hairy leukoplakia
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25
Q

Name 2 white lesions that are of idiopathic causes.

A
  1. Leukoplakia
  2. Proliferative verrucous leukoplakia
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26
Q

Name 2 white lesions that are of neoplastic causes.

A
  1. Dysplasia
  2. Oral squamous cell carcinoma
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27
Q

Describe the clinical features of white sponge naevus.

A
  • Autosomal dominant
  • May be apparent in infants or not until adolescents
  • Ill-defined white patches with “shaggy” surface.
  • Often bilateral
  • Any part of oral mucosa esp buccal mucosa
  • Can also effect nose, oesophagus, anogenital region,
  • Mutations in keratin 4 + 13
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28
Q

What is the histopathological appearance of white sponge naevus.

A
  • hyperparakeratosis and acanthosis of epithelium
  • Marked intracellular oedema of prickle and parakeratinized cells - “basket weave” appearance.
  • No cellular atypia/dysplasia
  • No inflammatory changes in lamina propria.
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29
Q

What treatment is required for white sponge naevus?

A

None.

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30
Q

What is frictional keratosis?

A

Traumatic lesion where roughened white patch at site of chronic trauma.

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31
Q

What is the histopathology of frictional keratosis?

A
  • hyperkeratosis
  • prominent scarring fibrosis with submucosa.
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32
Q

Describe lichen planus

A
  • Common chronic inflammatory disease of skin and mucous membranes
  • Oral lesions in approx 50% of pt with skin lesions, but prevalence of skin lesions in pts primarily seen for oral LP is lower.
  • Mainly affects middle aged and over.
  • Females > Males
  • Aetiology unknown
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33
Q

Describe the pathogenesis of lichen planus.

A

T cell mediated immunological damage to the basal cells of epithelium

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34
Q

What are clinical features of lichen planus?

A
  • Characteristic skin lesion is a violaceous, itchy papule which may have distinctive white streaks on the surface
  • Flexor surface of the wrist is the most common site - skin lesions develop slowly and 85% resolve within 18 months.
  • In contrast oral LP runs a more chronic course, sometimes several years. Oral lesions are usually bilateral and often symmetrical
  • Buccal mucosa is the most common site, though tongue lips, and gingivae may be affected. FOM and palate rarely affected.
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35
Q

Name the different types of lichen planus.

A

Reticular
Papular
Atrophic
Erosive
Bullous
Plaque-like

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36
Q

Describe the histopathological features of lichen planus.

A
  • Hyperparakeratosis of the epithelium which may be acanthotic or atrophic
  • Saw tooth rete ridges
  • Dense, band like lymphocytic infiltrate (mostly T cell mediated)
  • Degenerative cells appear as hyaline/condensed bodies known as “Civatte” bodies. These represent cells in the basal cell layer undergoing apoptosis.
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37
Q

What other lesions give a similar histopathological appearance as lichen planus?

A

-Lichenoid reaction
- Lupus erythematosus
- Graft-versus-host disease
- Lichenoid inflammation associated with dysplasia.

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38
Q

What is the possible frequency of malignant change in lichen planus?

A

0.1% over 10 years.

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39
Q

What is the clinical features of oral hairy leukoplakia?

A
  • White shaggy appearance on lateral tongue.
  • Asymptomatic
  • Can affect other sites.
  • Due to EBV infection
  • Strongly associated with HIV in many cases
  • Also seen in immunosuppressed individuals and in some apparently healthy patients.
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40
Q

What is the histopathological features 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.
  • Presence of EBV confirmed by in situ hybridization
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41
Q

What is proliferative verrucous leukoplakia?

A
  • Older patients, F>M
  • Gingival, buccal mucosa, tongue
  • Persistent, recurrent and becomes multifactorial
  • Difficult to completely excise
  • Histology shown hyperplastic lesion, hyperparakeratosis, often minimal dysplasia
  • Begins as simple hyperkeratosis that in time becomes exophytic and wart like
  • High risk that it may degenerate into oral cancer (verrucous carcinoma or squamous cell carcinoma).
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42
Q

Name 3 red patches that is due to infective causes

A
  1. Periodontal disease
  2. Median rhomboid glossitis
  3. HIV gingivitis
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43
Q

Name 2 red patches that is due to dermatological causes.

A
  1. Erosive lichen planus
  2. Discoid Lupus erythematosus
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44
Q

Name 2 red patches that is of idiopathic cause.

A
  1. Geographic tongue
  2. Erythroplakia
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45
Q

Name 2 red patches that are of neoplastic causes.

A
  1. Dysplastic lesions
  2. Squamous cell carcinoma.
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46
Q

Describe median rhomboid glossitis

A

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

Asymptomatic

Aetiology uncertain but associated with candidal infection.

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47
Q

What is the histopathological features of 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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48
Q

What is erythroplakia?

A

An oral potentially malignant disorder​

‘A clinical term used to describe a red patch of questionable risk, once other specific conditions and other OPMDs have been ruled out’. WHO 2017​

Red ‘velvety’ appearance, smooth or nodular​

Most common on soft palate, floor of mouth and buccal mucosa​

Erythroleukoplakia (speckled leukoplakia) = leuko and erythroplakia​

Erythroplakia and speckled leukoplakias have high likelihood of malignant transformation (50%)​

On biopsy, often severe dysplasia or early invasive SCC

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49
Q

Name some exogenous causes of oral pigmentation

A
  1. Superficial staining of mucosa - foods, drinks, tobacco
  2. Black hairy tongue - papillary hyperplasia, overgrowth of pigment containing bacteria
  3. Foreign bodies e.g amalgam tattoo
  4. Heavy metal poisoning
  5. Some drugs e.g NSAIDS, antimalarials, chlorohexidine
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50
Q

Describe the histopathology of an amalgam tattoo.

A
  • Pigment is present as widely dispersed, fine brown/black granules or as solid fragments of varying in size
  • Associated with collagen and elastic fibres and basement membranes
  • OR may be intracellularly within fibroblasts, endothelial cells, macrophages, and occasional foreign-body giant cells
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51
Q

Name endogenous causes of pigmentation.

A
  • normal variation in pigmentation similar to that seen in skin
  • melanotic macule
  • pigmented naevi (developmental lesions with proliferation of melanocytes).
  • Peutz Jeghers syndrome (multiple pigmented lesion on skin/mucosa, lips, tongue, palate, buccal mucosa, intestinal polyps
  • Smokers melanosis
  • HIV infection
  • May be a manifestation of systemic disease (Addisons disease), malignancy
  • Melanotic neuroectodermal tumour of infancy
  • Mucosal melanoma
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52
Q

Describe a melanotic macule.

A

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

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53
Q

What is the histopathology of a melanotic macule?

A
  • Increased melanin pigment in basal keratinocytes - not increase number of melanocytes
  • Melanin pigmentary incontinence in underlying connective tissue
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54
Q

Describe a melanotic melanoma?

A
  • Malignant neoplasm of melanocytes
  • Primary intraoral mucosal melanoma is rare but can occur
  • 40-60 years
  • Hard palate and maxillary gingivae most common sites
  • Dark brown or black or, if non-pigmented, red
  • Typically asymptomatic at first, may remain unnoticed until pain, ulcerated, bleeding or neck mass
  • Regional lymph node and blood-borne metastases are common
  • Typically very advanced at presentation
  • Very invasive, ,metastasis early
  • Prognosis is poor
  • Aetiology is unknown
  • Biology of mucosal melanoma is different from skin melanoma
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55
Q

What is the histopathology of mucosal melanoma?

A

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

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56
Q

What is the treatment for mucosal melanoma?

A
  • Resection is mainstay treatment
  • Adjuvant radiotherapy
  • ? Role of immunotherapy
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57
Q

Give a definition of an ulcer.

A

Localised surface defect with loss of epithelium exposing underlying inflammed connective tissue

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58
Q

Name 2 drugs that can cause oral ulceration

A
  • Nicorandil
  • NSAID’s
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59
Q

Name 3 systemic diseases that can cause oral ulceration

A
  • Haematological disorders
  • GI disorders such as Crohn disease
  • HIV
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60
Q

Name 3 dermatological conditions that can cause oral ulceration.

A
  1. Lichen Planus
  2. Discoid Lupus Erythematosus
  3. Immunobullous diseases
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61
Q

What are other causes of oral ulceration apart from dermatological, systemic or drugs.

A
  • neoplastic
  • infective
  • traumatic
  • idiopathic
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62
Q

What is the histopathology of an ulcer?

A
  • A large proportion of ulcers will show non-specific features ulceration with loss of surface epithelium, inflammed fibrinoid exudate and inflammed granulation tissue.
  • Obvious exceptions are neoplasms.
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63
Q

What is a vesicle?

A

A small blister

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64
Q

What is a bulla?

A

Blister >10mm

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65
Q

Describe immunobullous disorders.

A

A subset of lesions, these are autoimmune diseases in which auto-antibodies against components of skin and mucosa produce blisters

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66
Q

What 2 categories can immunobullous disorders be categorised by?

A
  1. Intra-epithelial
  2. Sub-epithelial
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67
Q

What further 2 sub-categories can intra-epithelial immunobullous disorder be categorised by?

A
  1. Non-acantholytic
  2. Acantholytic
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68
Q

Name an example of an non-acantholytic intraepithelial immunobullous disorder.

A

Herpes simplex virus in primary herpetic stomatitis and herpes labialis.
1. Virus targets and replicates within epithelial cells
2. Leads to cell lysis
3. Groups of infected cells breakdown to form vesicles within the epithelium
4. Infected cells infect nearby normal cells and an ulcer forms when the full thickness of the epithelium is involved and destroyed.

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69
Q

Name an example of an acantholytic intra-epithelial immunobullous disorder.

A

Pemphigus vulgaris.

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70
Q

Describe pemphigus vulgaris and the treatment normally required for this.

A
  • Most frequently affect females, 40-60 years
  • Autoantibodies to desmosomal protein (desmoglein 1 and 3 produced).
  • Bullae form in skin and mucous membranes then rupture to leave ulcers.
    Treatment : steroids
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71
Q

What is the histopathology of pemphigus vulgaris?

A
  • Characteristic intra-epithelial bullae produced by acantholysis (breakdown of desmosomes)
  • Bullae typically just above basal cells and these form the base of the lesion (tombstones)
  • Acantholytic cells (Tzank cells) found lying free within the bullae fluid
  • Tzank cells are small, round and enlarged hyperchromatic nuclei unlike normal polyhedral spinous cells
  • Little inflammation until the lesion ruptures
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72
Q

What is used to diagnose pemphigus vulgaris?

A

DIF in addition to normal histochemical staining. Fresh specimen mandatory for DIF.

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73
Q

Name 4 examples of subepithelial immunobullous diseases.

A
  1. Pemphigoid
  2. Erythema multiforme
  3. Dermatitis herpetiformis
  4. Epidermolysis bullosa acquisita
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74
Q

Describe mucous membrane pemphigoid

A
  • Mostly in females 50-80 years
  • Oral mucosa almost always involved and usually first affected site. Gingivae, tongue, buccal mucosa, and palate
  • Gingival lesions present as “desquamative gingivitis”clinical description,
  • Eyes, nose, larynx, pharynx, oesophagus and genitalia may be involved
    -Bullae tend to be relatively tough as the ‘lid’ is full thickness epithelium. When they rupture tend to heal slowly with scarring. Ocular lesions can lead to blindness
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75
Q

What is the histopathology of mucous membrane pemphigoid?

A
  • Separation of full thickness of epithelium from connective tissue producing subepithelial bulla with a thick roof
  • Infiltration of neutrophils and eosinphils around within bulla.
  • Base of bulla is inflammed connective tissue.
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76
Q

What is epidermolysis bullosa acquisita?

A
  • Uncommon
  • Acquired autoimmune blistering dermatosis with subepithelial bullae
  • Oral lesions in approx 50% cases
  • Early stage may mimic pemphigoid and later resembles epidermolysis bullosa
  • Separation occurs in or beneath lamina densa in basement membrane zone.
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77
Q

What is epidermolysis bullosa?

A
  • Group of rare genetic conditions
  • Formation of skin bullae which heal with scarring. Variable involvement of oral mucosa.
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78
Q

What are the 3 variants of epidermolysis bullosa?

A

3 variants:​

Simplex- intraepithelial, mutations in keratins 5/14 ​

Junctional- subepithelial, separation in lamina lucida, laminin mutations​

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

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79
Q

What is angina bullosa haemorrhagica?

A

Spontaneous blood-filled bullae, burst to form ulcers and heal uneventfully​

Most common on soft palate​

Older adults​

Subepithelial cleft​

? Trauma​

Not due to systemic or haematological disease

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80
Q

Describe oral submucous fibrosis

A

Chronic, progressive, oral potentially malignant condition​

Associated with betel quid/areca nut​

Clinically pale coloured mucosa, firm to palpate​

Increasing submucosal fibrosis leading to very marked trismus​

Typically fibrous bands which affect buccal mucosa, soft palate and labial mucosa

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81
Q

What is the histopathology for oral submucous fibrosis?

A

Submucosal deposition of dense collagenous tissue​

Decreased vascularity​

Marked epithelial atrophy​

Variable rates of dysplasia ​

High risk of malignant transformation

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82
Q

Describe chronic candidiasis/chronic hyperplastic candidiasis.

A

Persistent white patch on oral mucosa, cannot be removed by scraping​

Buccal mucosa adjacent to commissure of lips most common site​

Triangular, often bilateral, white plaque tapering posteriorly​

Palate or tongue can be involved​

Often associated with angular cheilitis​

Degree of risk of malignancy controversial?? Likely low
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83
Q

What is the histopathology of chronic candidiasis?

A

Hyperparakeratosis​

Prominent, irregular acanthosis​

Numerous neutrophils in parakeratin, forming microabscesses​

Candidal hyphae in parakeratin​

Acute and chronic inflammation in prickle cell layer​

Mixed chronic inflammatory infiltrate in lamina propria​

Varying degrees of cellular atypia

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84
Q

What is epithelial dysplasia?

A

​

Atypical epithelial alterations limited to the surface squamous epithelium​

Architectural changes- maturation and differentiation​

Cytological changes- changes in cells​

Indicates a risk of developing carcinoma

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85
Q

What are 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​
  3. Drop-shaped rete pegs ie wider at their deepest part​
    9.Irregular epithelial stratification or disturbed maturation​
  4. Abnormal keratinization ‘Dyskeratosis’- cell starts to keratinize before the surface is reached)​
  5. Loss/ reduction of intercellular adhesion
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86
Q

What is the difference between mild, moderate and severe epithelial dysplasia?

A

Mild- disorganisation, increased proliferation and atypia of basal cells​

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

Severe- very abnormal, affects full thickness of epithelium

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87
Q

What is the difference in diagnosing epithelial dysplasia from sqaumous cell carcinoma?

A

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

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

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88
Q

What is the management of epithelial dysplasia?

A

Modify risk factors
High risk sites - lateral border of tongue and FOM managed less conservatively
Antifungal treatment?
Excision/CO2 laser
? Topical agents
Close clinical review
Biopsy

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89
Q

What % of oral cancers are squamous cell carcinomas?

A

> 90%

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90
Q

How many mouth and oropharyngeal cancers are diagnosed per year?

A

8500

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91
Q

What is the year survival rate of oral cancer?

A

55%

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92
Q

Name risks factors for oral cancer?

A

Tobacco​

Alcohol​

Betel quid/pan/areca nut​

Previous oral cancer​

Exposure to UV light (lip)​

Poor diet​

Immune suppression​

Genetics??​

Social deprivation​

?? HPV- Oropharyngeal cancer

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93
Q

What are high risk sites for oral cancer?

A

Lateral/ventral tongue
FOM
retromolar trigone (tonsils/soft palate/oropharyngeal).

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94
Q

Name some signs and symptoms for 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

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95
Q

What are the guidelines you would follow for a suspected cancer

A

Scottish Referral Guidelines for Suspected Cancer and NICE guidelines e.g:
Persistent unexplained head and neck lumps for >3 weeks
Unexplained ulceration or unexplained swelling/induration of the oral mucosa persisting for >3 weeks
All unexplained red or mixed red and white patches of the oral mucosa persisting for >3 weeks
Persistent (not intermittent) hoarseness lasting for >3 weeks. If other symptoms are present to suggest suspicion of lung cancer, refer via lung cancer guideline
Persistent pain in the throat or pain on swallowing lasting for >3 week

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96
Q

When should the patient expect to get an appointment if following the urgent suspected cancer referral pathway?

A

2 weeks

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97
Q

How is diagnosis of SCC carried out?

A

Incisinal biopsy:
Usually straightforward diagnosis on H & E stained slides​

Further investigations usually not required​

Very poorly differentiated tumours may require immunohistochemistry to confirm diagnosis​

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

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98
Q

What is the histopathology of squamous cell carcinoma?

A

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

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99
Q

What is the TNM staging in oral cancer?

A

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

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100
Q

Name examples of core data that must be included in the pathological report when staging and grading tumours.

A
  • maximum diameter of tumour
  • maximum depth of invasion
  • Type of carcinoma
  • Degree of differentiation
  • Distance of carcinoma from surgical margins
  • Any bone/vascular/nerve invasion
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101
Q

The depth of invasion of the tumour is critical to the staging of the tumour. True or false?

A

Trueee.

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102
Q

What factors contribute to a higher “N” stage/grade?

A
  • increase no of nodes
  • size of nodes involved
  • whether or not there is extranodal extension
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103
Q

Why can you not include “M” stage and grade in pathological reports?

A

Because you cant tell from a bipsy/resection if there are any metastases elsewhere in the body.

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104
Q

What is the clinical features of acute periradicular periodontitis?

A
  • History of pain
  • Grossly carious or heavily restored tooth
  • Previous trauma
  • Typically little to see radiographically unless acute exacerbation of chronic lesion
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105
Q

What would be the histopathology of periradicular periodontitis?

A
  • Acute inflammatory changes
  • Vascular dilation
  • Neutrophils
  • Oedema
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106
Q

What is the treatment options for periradicular periodontitis?

A
  • Extraction or endodontic treatment
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107
Q

What is the clinical features of acute periapical abscess?

A

Pain and swelling/sinus

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108
Q

What is the histopathology of acute periapical abscess?

A
  • Central collection of pus (comprises neutrophils, bacteria and cellular debris)
  • Adjacent zone of preserved neutrophils
  • Surrounding membranes of sprouting capillaries and vascular dilation and occasional fibroblasts (granulation tissue).
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109
Q

What is the treatment options for acute periapical abscess?

A
  • Drainage and XLA
  • Endo
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110
Q

What are the clinical features of a chronic periradicular periodontitis?

A

May follow acute periodontitis or be chronic from onset
- Non-vital tooth, may be previous RCT
- Often minimal symptoms
- Apical radiolucent lesion may be evident on radiograph

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111
Q

What is the histopathology of chronic periradicular periodontits?

A

Chronic inflammatory changes
- lymphocytes
-plasma cells
- macrophages
- granulation tissue
- resorption of bone
- minimal if any tooth resorption

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112
Q

What is the treatment options for chronic periradicular periodontitis?

A
  • XLA
  • Endo
  • Endro retreatment if applicable
  • peri-radicular surgery
    Chronic periradicular periodontitis will not resolve spontaneously.
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113
Q

What is a peri-apical granuloma?

A

A mass of inflammed granulation tissue at the apex of non-vital tooth. Not a true granuloma. Can transform to abscess. Some may undergo cystic changes e.g to form a radicular cyst.

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114
Q

What are the clinical features of a periapical granuloma?

A

The same as chronic periradicular periodontitis however apical radiolucent lesion typically evident on radiograph

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115
Q

What is the histopathology of periapical granuloma?

A
  • Inflammed granulation tissue- inflammatory component typically lymphocytes, plasma cells, macrophages and neutrophils
  • Proliferation of cell rests of Malassez, often in long strands and arcades (may ultimately lead in inflammatory cyst formation)
  • Haemosiderin and cholesterol deposits from RBC/inflammatory cell breakdown, and associated multinucleate foreign giant body cells
  • Resorption of adjacent tooth/bone.
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116
Q

What are the treatment options for periapical granuloma?

A
  • Extraction
  • Endodontic treatment
  • Endodontic re-treatment
  • Periradicular surgery
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117
Q

What is the clinical feature of pericoronitis?

A

Inflammation of soft tissues around partially erupted tooth, frequently lower 8’s. Often exacerbated by trauma from opposing tooth.
- Pain
- swelling/tenderness of operculum
- Bad taste
- Trismus

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118
Q

What is the histopathology of pericoronitis?

A

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

Paradental cyst may arise in chronic pericoronitis.

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119
Q

What is the treatment for pericoronitis?

A
  • Irrigation
  • Consider extraction of opposing tooth
  • Antibiotics (only if systemically unwell)
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120
Q

What is a cyst?

A

A pathological cavity with fluid or semi-fluid contents. Lined wholly or in part by epithelium. Not due to accumulation of pus as this is an abscess.

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121
Q

Cysts of the jaw can either be derived by odontogenic or non-odogentic causes. Name 2 classifications of odontogenic cysts.

A
  1. Inflammatory
  2. Developmental
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122
Q

What are the 5 stages of odontogenesis?

A
  1. Initiation
  2. Bud stage
  3. Bell stage
  4. Cap stage
  5. Maturation stage
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123
Q

What happens in the initiation stage of odontogenesis (6 week embryonic stage)

A

Tissues such as primitive oral epithelium and ectomesechymal cells that are derived from neural crest cells. These tissue form a dental lamina, from here the dental lamina proliferates to form a bud.

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124
Q

What happens in the bud stage of odontogenesis?

A

A tooth bud is formed which is attached to the oral epithelium by the dental lamina. Differential proliferation of cells (cells inside the bud grow at a different rate) cause the formation of a cap shape.

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125
Q

What happens in the cap stage of odontogenesis?

A

Here the cap forms an enamel organ which has different types of epithelial cells. The enamel organ has 4 layers such as the inner and outer enamel epithelium, the stellate reticulum and the stratum intermediate.

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126
Q

What happens at the bell stage?

A

The cap changes shape to form an invagination of the inner and outer epithelium which forms the dental papillae. A sac forms around the tooth germ which forms the dental follicle.

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127
Q

What do the inner enamel epithelium and the dental papillae histodifferentiate into creating?

A

Ameloblasts - create enamel
Odontoblasts - create dentine

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128
Q

What occurs after maturation occurs and the crown has developed?

A

The dental lamina (connecting the tooth germ to the oral epithelium) disintegrates. However sometimes remnants of the dental lamina can remain forming issues in the future (such as supernumerary, cysts or odontoma)

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129
Q

What does the inner and outer enamel epithelium form as it grows apically and derives root formation?

A

Hertwigs epithelial root sheath

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130
Q

What is the function of the dental follicle?

A

Histodifferentiation into osteooblasts and fibroblasts which form form and the PDL.

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131
Q

Name 2 inflammatory odontogenic cysts.

A
  1. Radicular cysts
  2. Inflammatory collateral cysts
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132
Q

Name 2 types of inflammatory collateral cysts.

A
  1. Buccal bifurcation cysts
  2. Paradental cysts.
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133
Q

Can a periapical granuloma undergo cystic change to form a radicular cyst?

A

Yep

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134
Q

What are some clinical features of radicular cysts?

A
  • Most common type of cyst in jaw (55% of jaw cysts)
  • Arise from epithelial proliferation and cyst formation within some periapical granulomas
  • Anterior maxilla most frequent location
  • Wide age range
  • Slow growing swelling
  • Often no symptoms unless very large
  • Must be associated with an non-vital tooth
  • Radiographically appears as well-circumscribed, unilocular radiolucent lesion seen at apex
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135
Q

What is the pathogenesis of radicular cyts?

A

Arises from proliferation of epithelium (cell rests of Malassez) in response to inflammation
- Cysts enlarges due to osmotic pressure
- Local bone resorption

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136
Q

What is the histopathology of a radicular cysts?

A
  • Chronically inflammed fibrous capsule
  • Wholly-partly lined non-keratinized stratified squamous epithelium of variable thickness
  • Hyperplasia of epithelium common, often in arcades
  • Mucous metaplasia and ciliated cells may be seen
  • Hyaline/Rushton bodies
  • Cholesterol clefts and haemosiderin
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137
Q

What is the treatment for radicular cyst?

A
  • Small cysts may resolve after RCT/Extraction/Periradicular surgery
  • Enucleation
  • Marsupialisation
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138
Q

What does a lateral radicular cyst arise from?

A

A lateral root canal branch of a non vital tooth.

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139
Q

What does a residual radicular cyst arise from?

A

Persists after extraction of the associated non-vital tooth.

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140
Q

What teeth are paradental cysts most common in ?

A

Lower 3rd molars

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141
Q

What teeth are mandibular buccal bifurcation cysts most common in?

A

Lower 1st-2nd molars.

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142
Q

> 60% of inflammatory collateral cysts are paradental cysts. What are the clinical features of a paradental cyst?

A
  • Long standing peri-coronitis
  • Associated with vital tooth
  • Well-demarcated radiolucency.
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143
Q

What is the clinical features of a mandibular buccal bifurcation cysts?

A
  • Often painless swelling
  • Associated tooth is tilted buccally with a deep perio pocket
  • Well-demarcated buccal radiolucency.
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144
Q

What is the histopathology of a mandibular buccal bifurcation cyst?

A
  • Essentially the same as a radicular cyst.
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145
Q

What is the treatment for a mandibular buccal bifurcation cyst?

A

Enucleation.

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146
Q

Name 8 developmental odontogenic cysts.

A
  1. Odontogenic keratocyst
  2. Dentigerous cyst
  3. Eruption cyst
  4. Lateral periodontal cyst and Botryoid odontogenic cyst
  5. Glandular odontogenic cysts
  6. Gingival cysts
  7. Calcifying odontogenic cyst
  8. Orthokeratinized odontogenic cyst.
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147
Q

What are the clinical features of an odontogenic keratocyst?

A
  • 3rd most common cyst of the jaws
  • Occurs over a wide age range. Peaks in 2nd-3rd then 6th-8th decade
  • Slight male predilection
  • Majority (80%) arise in mandible esp posteriorly
  • Often symptom free unless infected or have bony expansion
  • Well defined uni or multilocular lesion.
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148
Q

What is the aetiology of odontogenic keratocysts.

A
  • Arise from remnants of the dental lamina
  • Associated with mutation or inactivation of PTCH 1 gene, chromosome 9, activates SHH pathway resulting in aberrant cell proliferation of epithelium.
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149
Q

What is naevoid basal cell carcinoma syndrome?

A
  • Multiple odontogenic keratocysts
  • Occur at a younger age than sporadic cases
  • Basal cell naevi, multiple, recurring odontogenic keratocysts, skeletal abnormalities, multiple basal cell carcinomas.
  • AD inheritance
  • PTCH1 gene mutation
150
Q

What is the histopathology of odontogenic keratocysts?

A
  • cystic lesion
  • keratinized stratified squamous epithelial lining, 5-10 cells thick.
  • Corrugated appearance of surface parakeratin layer
  • Well-defined, palisaded basal cell layer
  • Keratin debris in the lumen
  • Thin fibrous cyst wall with no inflammation, unless secondary infection
  • May be daughter/satellite cysts in wall.
151
Q

What happens histopathologically in odontogenic keratocysts if secondary infection?

A
  • Histopathological features are lost therefore cannot distinguish between other inflammatory cysts.
152
Q

What is the difficulty in treating odontogenic keratocysts?

A
  • High recurrence rate (25%) if incompletely removed - has thin capsule and daughter cysts.
153
Q

What are the treatment options for odontogenic keratocysts?

A

​

-Marsupialization ​
-Enucleation​
-Marsupialization + Enucleation​
-Enucleation + Carnoy’s solution (modified
Carnoy’s)​
-Enucleation + Cryotherapy​
- Resection
no evidence to support best treatment

154
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 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

155
Q

What is the histopathology of a dentigerous cyst?

A

Thin non-keratinized stratified squamous epithelial lining, 2-5 cells thick​

Mucous metaplasia common​ feature

Fibrous capsule​- No inflammation, unless secondary infection​

May be odontogenic epithelium remnants, calcification, Rushton Bodies

156
Q

What is the treatment for dentigerous cysts?

A
  • Enucleation
  • Exposure/transplantation/extraction of associated tooth.
157
Q

What is the clinical features of an eruption cyst?

A

Typically seen in children​

Deciduous and permanent molars​

Presents as bluish swelling

158
Q

What is the histopathology of an eruption cyst?

A

Same as dentigerous cyst:

Thin non-keratinized stratified squamous epithelial lining, 2-5 cells thick​

Mucous metaplasia common​ feature

Fibrous capsule​- No inflammation, unless secondary infection​

May be odontogenic epithelium remnants, calcification, Rushton Bodies

159
Q

What is the treatment for an eruption cyst?

A

None- exposure of erupting tooth.

160
Q

What are 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

161
Q

What is the histopathology of a lateral periodontal cyst?

A

Thin, non-keratinized squamous or cuboidal epithelium​

Focal thickenings/plaques​

Uninflamed fibrous wall

162
Q

What is the treatment for a lateral periodontal cyst?

A

Excision- recurrence is rare.

163
Q

What is Botryoid odontogenic cyst?

A

Very rare multicystic variant of lateral periodontal cyst​

Botryoid= ‘Bunch of grapes’- polycystic appearance​

Typically multilocular radiolucency ​

Mandibular premolar =canine region​

Adult​

Can recur

164
Q

What are the clinical features of Glandular odontogenic cyst?

A

Very rare​

Anterior mandible ​

Wide age range​

Multilocular radiolucency​

Strong tendency to recur

165
Q

What is the histopathology of glandular odontogenic cysts?

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

166
Q

What is the treatment/recurrence rate for a glandular odontogenic cyst?

A

Enucleation/55%

167
Q

What is the clinical features of gingival cysts in infants?

A

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

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

​Present as white nodules in gingivae

168
Q

What is the treatment for gingival cysts in infants?

A

None - usually go away within weeks.

169
Q

What are the clinical features of gingivae 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​

???Derived from dental lamina remnants

170
Q

What is the histopathology of gingival cysts in adults?

A

Cyst just below oral epithelium​

Uninflamed fibrous wall​

Lined by thin epithelium, cuboidal to squamous​

171
Q

What is the treatment for gingival cysts in adults?

A

Simple excision

172
Q

What are the clinical features for a calcifying odontogenic keratocyst?

A

Rare​

Wide age range, average 30 yrs​

Painless swelling of jaw​

Well-defined radiolucency​

Tooth displacement and resorption common​

​Either jaw, often anterior​

​Minority can be in soft tissues

173
Q

What is the histopathology of calcifying odontogenic keratocyst?

A

Unicystic​

Lined by epithelium which is ameloblastoma-like​

Palisaded basal layer with overlying stellate reticulum-like layer​

Focal ‘Ghost cells’, which may calcify

174
Q

What is the treatment for odontogenic keratocyst?

A

Enucleation- recurrence is rare.

175
Q

What is the clinical features of an orthokeratinised odontogenic cyst?

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

176
Q

What is the histopathology of an orthokeratinised odontogenic cyst?

A

Uninflamed fibrous wall​

Lined by stratified squamous epithelium​

Prominent granular cell layer and orthokeratinized​

No basal palisading, no corrugated parakeratin

177
Q

Name 3 non-odontogenic cysts

A
  1. Nasopalatine cyst
  2. Nasolabial cyst
  3. Surgical ciliated cyst.
178
Q

What are the clinical feature of nasopalatine duct cyst?

A

-Uncommon
-Originate from epithelium of nasopalatine duct in incisive canal
-Occur anywhere in the nasopalatine canal but most frequently at the palatal end.
- Any age but frequently 5th and 6th decades.
- Slow growing
- Swelling in midline of anterior hard palate
- May complain of salty taste
- Rounded or heart shaped radiolucency in midline of anterior hard palate

179
Q

What is the histopathology of a nasopalatine duct cyst?

A
  • Epithelial lining can either be stratified squamous, respiratory, columnar or cuboidal
  • Fibrous connective tissue capsule
  • Neurovascular bundles may be seen in capsule
  • Mucous glands may be seen in capsule
  • Often chronically inflammed
180
Q

What is the treatment for a nasopalatine duct cyst?

A

Enucleation- recurrence is unlikely

181
Q

What are the clinical features of a surgical ciliated cyst?

A
  • Rare
  • F = M
  • Peak incidence in 5th and 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 surgery
182
Q

What is the histopathology of surgical ciliated cyst?

A
  • Cyst lined by respiratory epithelium (ie pseudostratified columnar epithelium)
  • Fibrous connective tissue capsule may be inflammed
183
Q

What is the treatment for surgical ciliated cysts?

A

Enucleation - recurrence is rare.

184
Q

What are clinical features of a nasolabial cyst?

A
  • Very rare
  • F>M
  • Peak incidence in 4th-5th decades
  • Arise in upper lip below nose, lateral to midline
  • Slow growing, distorts nostril
  • Painless unless infected
  • 10% bilateral
  • Now considered to likely derive from remnants of the embryonic nasolacrimal duct or the lower anterior portion of the mature duct.
185
Q

What is the histopathology of a nasolabial cyst?

A

Cystic lesion with fibrous capsule
Usually pseuodocolumnar epithelial lining.

186
Q

What is the treatment for a nasolabial cyst?

A

Excision.

187
Q

Name 5 soft tissue cysts.

A
  1. Salivary mucoceale
  2. Epidermoid cyst
  3. Dermoid cyst
  4. Lymphoepithelial cysts
  5. Thyroglossal cysts
188
Q

What are the clinical features of an epidermoid cyst?

A
  • More common on the skin
  • Painless swelling
  • Often following trauma or surgery
189
Q

What is the histopathology of an epidermoid cyst?

A
  • Cystic lesion with thin cyst wall
  • Lined by keratinizing stratified squamous epithelium
  • Abundant keratin debris in the lumen
  • No skin appendages in cyst wall
190
Q

What is the treatment for an epidermoid cyst?

A

Local excision

191
Q

What are the clinical features of a dermoid cyst?

A
  • Development lesion
  • Arise at various locations of the head and neck
  • Most common site is FOM
  • Presents as painless swelling in the midline
192
Q

What is the histopathology of a dermoid cyst?

A
  • As epidermoid cyst with keratinizing stratified squamous lining
  • Keratin debris within cyst lumen
  • MUST have skin appendages e.g sebbaceous glands, hair follicle in cyst wall.
193
Q

What is the treatment for a dermoid cyst?

A

Excision

194
Q

What are the clinical features of an lymphoepithelial cyst?

A
  • Development lesions
  • Uncommon but do occur in the oral cavity
  • FOM most common intra-oral site
  • Typically present as painless small swelling which may be yellowish in colour
195
Q

What is the histopathology of a lymphoepithelial cyst?

A
  • Thin keratinized stratified squamous epithelium lining
  • Keratin debris in lumen
  • Lymphoid tissue in cyst wall
196
Q

What is the treatment for lymphoepithelial cyst?

A

Excision.

197
Q

What are the clinical features of an thryoglossal cyst?

A
  • Development cyst derived from embryonic thyroglossal duct
  • Intraoral lesions are very rare
  • Most arise near hyoid bone
  • Present as midline swelling, wide age range
  • Usually painless
  • Symptoms if infected, or very large
  • May have functioning thyroid tissue
198
Q

What is the histopathology of a thyroglossal duct cyst?

A
  • Cystic lesion lined by stratified squamous epithelium/ciliated columnar epithelium/noncilated columnar epithelium
  • Fibrous wall which typically contains thyroid tissue
  • Can find incidental thyroid carcinoma
199
Q

What is the treatment for a thyroglossal duct cyst?

A

Excision- “Sistrunk procedure” which involves removing middle third of hyoid bone along with lesion which reduces the chance of recurrence.

200
Q

Name 2 non-epithelialised primary bone cysts.

A
  1. Simple/Solitary lesion
  2. Aneurysmal bone cyst

Almost exclusively mandible

201
Q

Name clinical features of a solitary bone cyst

A
  • Peak incidence is 2nd decade
  • Typically seen in premolar/molar region of mandible
  • May be incidental finding or present as asymptomatic swelling.
  • Large radiolucency on radiographs
  • Not true cysts (cavities that are empty)
  • Cause is unknown
202
Q

What is the histopathology of solitary bone cysts?

A
  • Bony cavity with no epithelial lining
  • May be thin fibrovascular tissue lining with haemosiderin, RBC’s or giant cells covering bony walls
  • Usually no cystic contents
203
Q

What is the treatment for a solitary bone cyst?

A

No treatment - usually resolves spontaneously.
If not may resolve after opening investigation of lesion

204
Q

What are the clinical features of an aneurysmal bone cyst?

A
  • Very rare in jaws
  • Usually mandible
  • Young people more commonly
  • Painless swelling
  • Radiolucent lesion on radiograph
  • unknown cause
205
Q

What is the histopathology of anerysmal bone cyst?

A
  • Blood filled spaces separated by cellular fibrous tissue
  • No lining of spaces
  • Multinucleate giant cells in fibrous band
206
Q

What is the treatment for an aneurysmal bone cyst?

A
  • Curettage
  • May recur
207
Q

What is Stafnes Defects?

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

208
Q

Name 5 odontogenic carcinomas.

A
  1. Ameloblastic carcinoma
  2. Primary intraosseous squamous cell carcinoma
  3. Sclerosing odontogenic carcinoma
  4. Clear cell odontogenic carcinoma
  5. Ghost cell odontogenic carcinoma
209
Q

Name 3 odontogenic sarcomas.

A
  1. Ameloblastic sarcoma
  2. Ameloblastic fibrodentinosarcoma
  3. Ameloblastic fibrodontosarcoma
210
Q

Name 4 benign epithelial odontogenic tumours.

A
  1. Ameloblastoma
  2. Squamous odontogenic tumour
  3. Calcifying epithelial odontogenic tumour
  4. Adenomatoid odontogenic tumour
211
Q

What are the 3 different forms/types of ameloblastoma?

A
  • unicystic
  • peripheral
  • metastazing
212
Q

What are the clinical features of ameloblastoma?

A

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

213
Q

What is the histopathology of an ameloblastoma?

A

2 types of tumour cells​:

1.well-organized peripheral single layer of tall, columnar, pre-ameloblast-like cells, which have nuclei at the opposite pole to the basement membrane (reversed polarity)​

  1. core of loosely arranged cells resembling stellate reticulum​

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

tumour regardless of pattern is set in fibrous stroma

214
Q

What is the treatment for an ameloblastoma?

A
  • complete excision with a margin of uninvolved tissue.
  • If excision incomplete then it will recur
  • Follow up required
215
Q

What are the clinical features of an adenomatoid odontogenic tumour?

A

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

216
Q

What is the histopathology of an adenomatoid odontogenic tumour?

A

-Odontogenic epithelium arranged in solid nodules or rosette-like structures​

-Duct-like structures​

-Eosinophilic amorphous material​

-Minimal fibrous stroma

217
Q

What is the treatment for an adenomatoid odontogenic tumour?

A

Local excision​
Recurrence is rare

218
Q

Name 4 benign mixed epithelial and mesenchymal odontogenic tumours

A
  1. Ameloblastic fibroma
  2. Primordial odontogenic tumour
  3. Odontoma
  4. Dentinogenic ghost tumour
219
Q

What are odontomas?

A

​Developmental malformations (hamartomas) of dental tissues​

Once fully calcified do not develop further​

Young patients​

Painless slow growing lesions​

Contain enamel, dentine and sometimes cementum

220
Q

Describe the compound type of odontoma.

A

Most common odontogenic tumour
Esp anterior maxilla
Lots of tooth like structures on imaging
Fibrous capsule
“Bag of teeth”

221
Q

Describe the complex type of odontoma.

A

Commonly posterior mandible​

Radiopaque mass on imaging​

Consist of an irregular mass of hard and soft dental tissues, haphazard arrangement with no resemblance to a tooth and often forming a cauliflower-like mass ​

Cementum is often very scant

222
Q

What is the treatment for odontomas?

A

Enucleation​

Mature lesions completely enucleated do not recur​

Incompletely enucleated developing lesions may recur

223
Q

Name 4 benign mesenchymal odontogenic tumours.

A
  1. Cementoblastoma
  2. Odontogenic fibroma
  3. Cemento-ossifying fibroma
  4. Odontogemic myxoma
224
Q

What are the clinical features of cementoblastoma?

A

Formation of cementum-like tissue in connection with root of tooth​

10- 40 yrs​

Mandible> maxilla, esp associated with 6s​

Painful swelling​

Tooth remains vital​

Well-defined radiopaque or mixed-density lesion

225
Q

What is the histopathology of a cementoblastoma?

A

Dense masses of acellular cementum-like material ​

Fibrous, sometimes vascular stroma​

Tumour blends with root of tooth- helps distinguish lesion from bone tumours

226
Q

What is the treatment for cementoblastoma?

A

Complete excision and removal of tooth​

Commonly recur if incompletely excised

227
Q

Name 3 malignant maxillofacial bone and cartilage tumours

A
  1. Chondrosarcoma
  2. Mesenchymal chrondrosarcoma
  3. Osteosarcoma
228
Q

Name 8 benign maxillofacial bone and cartilage tumours

A

Chondroma​

Osteoma​

Melanotic neuroectodermal tumour of infancy​

Chondroblastoma​

Chondromyxoid fibroma​

Osteoid osteoma​

Osteoblastoma​

Desmoplastic fibroma​

229
Q

Describe an osteoma?

A
  • Benign slow-growing tumour consisting of well-differentiated mature bone
  • Occur mostly in adults, M>F
  • Mandible>Maxilla
  • Usually solitary lesions, although multiple lesions can occur as a feature of Gardner Syndrome
230
Q

What is Gardner Syndrome?

A

Rare Autosomal dominant disorder, features include multiple osteomas, polyposis coli (which shows a marked tendency to undergo malignant change), and multiple fibrous tumours and epidermal/sebaceous cysts of skin.

231
Q

What are the 2 types of osteoma?

A

Compact type- mass of dense lamellar bone with few marrow spaces
Cancellous type- interconneting trabeculae enclosing fatty or fibrous tissue.

232
Q

What is the treatment for osteoma?

A
  • Lesions is removed if asymptomatic or causing problems with fit of denture.
  • Recurrence is rare.
233
Q

What is a melanotic neuroectodermal tumour of infancy?

A

Very rare​ tumour (most are benign)

Most < 1 yr old​

M>F​

Locally aggressive, rapidly growing pigmented mass​

Most frequently anterior maxillary alveolus

234
Q

What is the histopathology of a melanotic neuroectodermal tumour of infancy?

A

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

235
Q

What is the treatment of melanotic neuroectodermal tumour of infancy?

A
  • Complete local excision of treatment of choice
  • Most are benign but small number do metastasize.
  • Can recur
236
Q

Name 5 fibro-osseous and osteochrondromatous lesions.

A
  1. Cemento-osseous dysplasia
  2. Osteochrondroma
  3. Fibrous dysplasia
  4. Familial gigantiform cementoma
  5. Ossifying fibroma
237
Q

Name 5 giant cell lesions and bone cysts.

A
  1. Solitary bone cyst
  2. Aneurysmal bone cyst
  3. Cherubism
  4. Peripheral giant cell granuloma
  5. Central giant cell granuloma
238
Q

Describe haematolymphoid tumours

A
  • Solitary plasmacytoma of bone
  • Localized proliferation of monoclonal plasma cells involving bone
    -Mandible>Maxilla
  • No other bony lesions, no clinical features of plasma cell myeloma.
239
Q

What do all fibro-osseous lesions have in common?

A

All histologically characterised by replacement of normal bone by cellular fibrous tissue within which islands and trabeculae of metaplastic bone develop

Cannot be diagnosed by histology alone, need clinical/radiographic features

240
Q

What are the clinical features of an ossifying fibroma?

A

Slow, painless expansion of bone- jaws and craniofacial skeleton​

Peak incidence 3rd- 4th decades​

F>M​

Different variants- cemento-ossifying fibroma occurs exclusively in the tooth-bearing regions of the jaws​

Mandible > maxilla

241
Q

What is histopathological features of ossifying fibroma?

A

Well-demarcated or rarely encapsulated benign lesion ​

Fibrous tissue containing varying amounts of metaplastic bone and mineralised masses resembling cementum​

Demarcated nature is an important feature distinguishing it from fibrous dysplasia

242
Q

What is the treatment for ossifying fibroma?

A

Complete excision​

Ossifying Fibroma continues to enlarge if left untreated​

Must be distinguished from fibrous dysplasia

243
Q

What is familial gigantiform cementoma?

A

Rare form of fibro-osseous lesion of jaws​

Early onset of fast growing multifocal/multiquadrant expansive lesions​

May be massive with ++ facial deformity​

Inheritance in some not all cases

244
Q

What is the treatment of familial gigantiform cementoma?

A

Surgery- difficult!

245
Q

What is fibrous dysplasia of bone?

A

​Fibro-osseous lesion of growing bones​

May involve one (monostotic) or several bones (polyostotic)​

Sporadic condition​

GNAS1 mutations identified

246
Q

Describe monostotic fibrous dysplasia.

A

Gives rise to painless bony swelling, facial asymmetry​

Usually starts in childhood and arrests in adulthood​

M=F​

Jaws most frequent head + neck site​

Radiographically -orange-peel/ground glass effect​

Maxilla>mandible​

Maxillary lesions often involve adjacent bones- Craniofacial fibrous dysplasia

247
Q

Describe polystotic fibrous dysplasia.

A

Rare​

F>M​

Affects several bones ​

Skin pigmentation and endocrine abnormalities also associated​

Albright’s syndrome comprises polyostotic fibrous dysplasia, skin pigmentation and sexual precocity​

Head + neck involved in ~50% of cases

248
Q

What is the histopathology for both types of fibrous dysplasia (both are the same)

A

Irregularly shaped slender trabeculae of woven (immature) bone lying in a very cellular fibrous tissue​

Fuses directly with normal bone at edges of lesion

249
Q

What is the treatment for fibrous dysplasia?

A

Aesthetic surgery​

Rarely, malignant change, typically osteosarcoma, can occur in FD

Lesions stabilise as skeleton matures.

250
Q

Describe clinical features of cemento-osseous dysplasia

A

​-Fibro-osseous lesion occurring in tooth-bearing areas of jaws​

​-Most common fibro-osseous lesion of jaws​

-Often asymptomatic​

-Involved teeth remain vital​

-Characterized by replacement of normal bone by fibrous tissue and metaplastic bone​

-Predilection for middle-aged African/ African-American females

251
Q

Name the 3 forms of cemento-osseous dysplasia.

A
  1. Peri-apical cemento-osseous dysplasia
  2. Focal cemento-osseous dysplasia
  3. Florid cemento-osseous dysplasia
252
Q

Describe the differences clinically between each type of cemento-osseous dysplasia.

A

Periapical cemento-osseous dysplasia—>Involves apical incisor region of mandible, several adjacent teeth involved​

​
Focal cemento-osseous dysplasia​–>Associated with a single tooth​

​
Florid cemento-osseous dysplasia –>Multifocal/multiquadrant

253
Q

What is the treatment for cemento-osseous dysplasia?

A

Surgery only if symptomatic

254
Q

Describe an osteochondroma

A

​-Bony projection with a cap of cartilage​

-Continuous with underlying bone​

-Rare in maxillofacial bones (occurs at sites of endochondral ossification)​

-Symptoms depend on site of lesion

255
Q

What is the treatment for an osteochondroma?

A

Complete excision

256
Q

Describe clinical features of a central giant cell granuloma.

A

Localized benign (but can be aggressive) lesion​

Most < 30 years​

Mandible > Maxilla​

F > M​

Often asymptomatic​

If cortical plate perforates lesion can present as a peripheral giant-cell granuloma

257
Q

What is the histopathology of central giant cell granuloma?

A

Large numbers of multi-nucleate, osteoclast-like giant cells​

Set in a vascular fibrous stroma​

Areas of haemorrhage and haemosiderin

258
Q

Describe clinical features of cherubism.

A

Rare inherited, AD, causing distension of jaws​

M>F​

Mandible often more extensively involved​

Normal at birth but painless swelling, usually bilateral, symmetrical, of jaws appear between 2-4 yrs​

Enlarge until ~7yrs​

May regress by adulthood​

Lesions cause fullness of cheeks and in severe cases maxillary swellings cause eyes to look upward giving ‘Cherub-like” appearance​

May be dental anomalies

259
Q

What is the histopathology of cherubism?

A

-Lesions consist mainly of cellular and vascular fibrous tissue containing varying numbers of multinucleate giant cells​

-As activity decreases lesions become progressively more fibrous and numbers of giant cells decreases

260
Q

Histologically what is cherubism similar to and hence would require further clinical and radiological correlation.

A
  • central giant cell granuloma
  • brown tumour of hyperparathyroidism
  • giant-cell tumour
  • aneurysmal bone cyst
261
Q

Name 4 inherited disorders of the bone.

A
  1. Osteogenesis Imperfecta
  2. Osteopetrosis (marble bone disease)
  3. Cleidocranial Dysplasia
  4. Achondroplasia
262
Q

Describe osteogenesis imperfecta

A

​-Hereditary disease, AD and AR and sporadic ​

-Heterogeneous group of related disorders characterized by impairment of collagen maturation​

-Collagen is component of bone, ligaments, sclerae, dentine, skin​

-Several different types of OI, type I most common and mild​

​
Variety of clinical features:​

Easily fractured, osteoporotic bone​

Affected teeth appear as in dentinogenesis imperfecta​

Malocclusion may be a problem

263
Q

Describe osteopetrosis (marble bone disease)

A

​-Group of rare genetic diseases in which there is marked increase in bone density- infantile and adult forms​

-Due to failure of normal osteoclast activity and absence of normal modelling resorption​

-Cortices are thickened and sclerosis of cancellous bone​

-Anaemia is common due to marrow space deficiency​

-Osteomyelitis is a recognized complication and prevention of dental infections important

264
Q

Describe cleidocranial dysplasia

A

Rare genetic disorder, AD and sporadic​

Characterized by abnormalities of many bones but most notably there is defective formation of the clavicles, delayed closure of fontanelles and sometimes retrusion of the maxilla ​

Partial or complete absence of clavicles allows patient to bring shoulders together in front of the chest​

Dental anomalies are common, particularly delayed eruption of permanent dentition and supernumerary teeth (often numerous)​

Narrow, high-arched palate

265
Q

Describe achondroplasia

A

​May be AD inheritance or spontaneous​

Associated with an abnormality in endochondral ossification​

Head and trunk of normal size but limbs are excessively short​

Defective growth at base of skull leads to a retrusive maxilla, often resulting in severe malocclusion

266
Q

Name 4 metabolic and endocrine disorders.

A
  1. Osteoporosis
  2. Hyperparathyroidism
  3. Rickets/osteomalacia
  4. Acromegaly
267
Q

Describe osteoporosis

A

Results when bone loss is excessive or when apposition of bone is reduced​

Most common in postmenopausal women​

Also accentuated in other diseases including Cushing syndrome, thyrotoxicosis and primary hyperparathyroidism​

Osteoporotic bone is of normal composition but is reduced in quantity​

There is increased radiolucency of bone, cortex is thinned, and there are more marrow spaces in the cancellous bone associated with thin trabeculae​

Both jaws may be affected​

Nb Bisphosphonates

268
Q

Describe hyperparathyroidism.

A

​-Overproduction of parathormone, PTH​
-Mobilises calcium and raises the plasma calcium level​
-Primary hyperparathyroidism usually due to hyperplasia or adenoma of the parathyroids​
-Most patients are female and postmenopausal​
-Secondary hyperparathyroidism develops when PTH produced in response to chronic low calcium levels, often seen in chronic renal disease​

269
Q

What clinical symptoms do patients present with in hyperparathyroidism.

A

-Patients present with ‘stones, bones and abdominal groans’​

-Stones- renal calculi and other calcifications​

-Bones- various bone lesions including ‘brown tumour’ of hyperparathyroidism​

-Abdominal groans- tendency to develop duodenal ulcers​

-May present in dental patients as a cyst-like swelling of the jaw which displays the histological features of a giant-cell lesion

270
Q

Describe clinical features of rickets/osteomalacia.

A

Rickets and its adult counterpart osteomalacia are due to deficiency of, or resistance to the action of, vitamin D​

Failure of mineralization of osteoid and cartilage​

Dental defects rarely seen except in very severe cases when hypocalcification of dentine and enamel hypoplasia may occur​

May also be a delay in tooth eruption​

Dental defects also seen in hypophosphataemia (Vitamin-D resistant rickets)

271
Q

Decribe acromegaly.

A

Caused by prolonged and excessive secretion of growth hormone​

Usually due to anterior pituitary tumour developing after epiphyses have closed ​

There is renewed growth of the bones of the jaws, hands and feet with soft tissue overgrowth also​

Activation of condylar growth centre of mandible causes jaw to become enlarged and protrusive with increased spacing between teeth​

Thickening of facial soft tissues

272
Q

Name examples of inflammatory diseases of bone.

A
  1. Alveolar osteitis
  2. Osteomyelitis
  3. Radiation injury and osteoradionecrosis
  4. MRONJ
  5. Pagets disease of bone
273
Q

What is alveolar osteitis?

A

Unpredictable complication of extractions, particularly lower molars​

Due to failure of blood clot to form or dislodgment or breakdown of clot.​

Bone of socket becomes infected and necrotic and very painful!​

Inflammatory reaction in adjacent marrow localises the infection to the walls of the socket, otherwise osteomyelitis would ensue​

Dead bone is separated by osteoclasts and small sequestra form and are shed

274
Q

What is osteomyelitis?

A

Spectrum of inflammatory and reactive changes in bone and periosteum​

Typically in mandible of adults​

Reflects a balance between the nature and severity of the irritant, the host defences, and local and systemic predisposing factors​

Acute and chronic suppurative and non-suppurative and sclerotic forms

275
Q

What is radiation injury and osteoradionecrosis?

A

Radiation affects the vascularity of bone by causing proliferation of the intima of the blood vessels (endarteritis obliterans)​

Potentially serious in mandible with its end artery supply​

ID artery or its branches may become thrombosed​

The non-vital bone which results is sterile and asymptomatic but very susceptible to infection and trauma​

Infection can spread rapidly through irradiated bone, resulting in extensive osteomyelitis and painful necrosis of bone​

Can be very difficult to treat

276
Q

What is the definition for a diagnosis of MRONJ?

A

MRONJ defined as’ exposed bone, or bone that can be probed through an intraoral or extraoral fistula, in the maxillofacial region that has persisted for more than eight weeks in patients with a history of treatment with anti-resorptive or anti-angiogenic drugs, and where there has been no history of radiation therapy to the jaw or no obvious metastatic disease to the jaws’

277
Q

What patients are at higher risk of MRONJ?

A

IV bisphosphonates
Patients taking anti-resorptive medications for cancer.

278
Q

What is Pagets disease of bone?

A

Form of osteodystrophy characterised by disorganised formation and remodelling of bone unrelated to functional requirements​

Aetiology unknown ?? Paramyxovirus ??Genetic Factors ? endocrine​

Relatively common​

Often subclinical​

40yrs​

?M>F​

Geographic variation in incidence​

Chronic slowly progressing condition

279
Q

What are clinical features Pagets Disease of bone?

A

-Single or multiple bones can be affected​
-Sacrum, spine, skull, femora and pelvis most common sites​
-Can be asymptomatic or be painful​
-Maxilla more often affected than mandible​
-Patients show varying degrees of bony deformation and distortion of weight-bearing portions of skeleton ​
-Affected bones are thickened but weaker and pathological fractures occur​
-Progressive enlargement of skull and facial bones- hats don’t fit, dentures don’t fit ​
- Narrowing of foramina can cause cranial nerve deficits
-In dentate, derangement of occlusion and spacing of the teeth can occur​
-Also may be hypercementosis and ankylosis of teeth leading to extraction difficulties​
-Development of osteosarcoma is a recognised, rare complication of Paget’s disease of bone​
-Giant cell tumours may also arise in bones affected by Paget’s​
-Characteristic radiographic ‘cotton-wool’ appearance

280
Q

What are the 3 phases of Pagets disease of bone?

A
  1. Initial predominantly osteolytic phase
  2. Active stage of mixed osteolysis and osteogenesis
  3. Predominantly osteoblastic or sclerotic phase
281
Q

What is the histopathology of Pagets disease of bone?

A

-varies with phase​

-Main features are irregular pattern of reversal lines, many osteoblasts and osteoclasts, fibrosis of marrow spaces and increased vascularity​

-Destruction and new bone formation may alternate rapidly, marked histologically by haemotoxylin-staining reversal lines Their irregular pattern produces a ‘Mosaic’ appearance in the bone
-Early phase there is typically more resorption than osteoblastic activity​

-Late stage bones are thick, cortex and medulla are obliterated and the whole bone is spongy in texture

282
Q

What would you find in the biochemistry for Pagets disease?

A

Serum calcium and phosphorus levels are usually normal but alkaline phosphatase level is very high

283
Q

What is normally the treatment for Pagets disease?

A

Calcitonin​

Bisphosphonates (nb MRONJ!)

284
Q

What is a tori?

A

Exostoses are localised bony protuberances​

Non-neoplastic lesion that may be developmental in origin or may be a response to a stimulus such as chronic trauma​

A torus is an exostosis which occurs at a characteristic site, either in the midline of the palate (torus palatinus) or on the lingual surface of the mandible, usually premolar region above the mylohyoid line (torus mandibularis)​

Mandibular tori often bilateral​

Typically seen in adults​

Their aetiology is unknown

285
Q

what are the most common primary tumours which metastasise to bone, including the jaws?

A

breast, bronchus, prostate, thyroid, kidney

286
Q

Where are the most common sites for metastases to occur in the mouth?

A

the gingiva or alveolar mucosa, followed by the tongue

287
Q

What is an epulis?

A

Soft tissue hyperplastic lesion located on the ginigvae

288
Q

Name examples of soft tissue hyperplastic lesions.

A
  • Fibrous epulis
  • Pyogenic granuloma/Pregnancy epulis
  • Giant-cell epulis
  • Fibroepithelial polyp
  • Denture irritation hyperplasia
  • Papillary hyperplasia of the palate
289
Q

What are the clinical features of a fibrous epulis?

A

Pedunculated or sessile firm mass on gingiva, often between 2 teeth​

Pink in colour​

Wide age range

290
Q

What is the histopathology of a fibrous epulis?

A

Nodular lesion​

Hyperplastic surface epithelium​

Cellular fibroblastic granulation tissue + collagen bundles​

Variable inflammation​

Calcification or metaplastic bone formation can be seen (‘Mineralising’ or ‘Ossifying Fibrous Epulis’)​

291
Q

What is the treatment for fibrous epulis?

A
  • Excision
  • Remove source of infection
292
Q

What are the clinical features of a pyogenic granuloma?

A

Soft red/purple swelling ​

Often ulcerated​

Wide age range​

Pregnancy epulis is pyogenic granuloma in specific patient group​

293
Q

What is the histopathology of a pyogenic granuloma?

A

Nodular lesion​

Surface epithelium often ulcerated​

Underlying vascular proliferation- either solid sheets of endothelial cells or small and large vascular spaces​

Oedematous fibrous stroma​

Variable inflammation- often acute and chronic

294
Q

What is the treatment for a pyogenic granuloma?

A

Local excision
Good OH and periodontal treatment and lesions typically regress post-partum.

295
Q

What are the clinical features of a giant cell epulis?

A

Soft purplish gingival swelling​

Mostly on gum of teeth anterior to molars​

F>M​

Wide age range, esp 30-40 yrs

296
Q

What is the histopathology of a giant cell epulis?

A

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

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

297
Q

What is the treatment for a giant cell epulis?

A
  • Excision of lesion
  • Curettage of underlying bone to reduce chance of recurrence
298
Q

What is the clinical features of a fibroepithelial polyp?

A

-Pink smooth mucosal polyp​
-Very common​
-Wide age range​
-Buccal mucosa, lip, tongue​

-FEP under denture = leaf fibroma

299
Q

What is the histopathology of a fibroepithelial polyp?

A

​Polypoid lesion with core of dense scar-like fibrous tissue​

Overlying stratified squamous epithelium may be hyperplastic​

​Typically little inflammation

300
Q

What is the treatment for a fibroepithelial polyp?

A
  • Excision

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

301
Q

What is the clinical features for denture irritation hyperplasia

A
  • Broad based, leaf-like folds of tissue related to periphery of badly fitting dentures.
  • Typically pale, fibrous swelling
  • May be ulcerated
302
Q

What is the histopathology of denture irritation hyperplasia?

A
  • hyperplastic fibrous connective tissue
  • Hyperplasia of the overlying epithelium
  • May show focal ulceration
  • Variable inflammation
303
Q

What is the treatment for denture irritation hyperplasia?

A

Excision and new dentures

304
Q

What are some clinical features of papillary hyperplasia of the palate?

A
  • 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)
305
Q

What is the histopathology of papillary hyperplasia of the palate?

A

Papillary/nodular projections ​

Underlying hyperplastic, chronically-inflamed vascular fibrous tissue​

Hyperplastic overlying epithelium​

Fungal organisms with acute inflammation may be seen

306
Q

What is the treatment for papillary hyperplasia of the palate?

A
  • Good denture hygiene
  • Antifungals if needed
  • Rarely surgery
307
Q

Most intraoral fibrous lesions are benign overgrowths, not tumours​ - true or false?

A

True

308
Q

Name a malignant tumour of fibrous tissue

A

Fibrosarcoma

  • Rare in the oral cavity
  • Neoplastic fibroblasts with variable amount of collagen
  • Radical excision
  • Can recur, rarely metastasise
309
Q

Name a benign and malignant tumour of adipose tissue

A
  1. Lipoma (benign)
  2. Liposarcoma (malignant)
310
Q

What are the clinical features of a lipoma?

A

Soft smooth swelling​

Pedunculated or sessile​

Asymptomatic​

Can be yellowish or pink​

Buccal mucosa most common intraoral site​

Patients typically adults 40+ yrs

311
Q

What is the histopathology and treatment of a lipoma?

A

Histopathology: Well-circumscribed lesion​

Thin capsule​

Lobules of mature fat cells​

Bands (septa) of fibrous tissue

Treatment: Excision

312
Q

Name 4 tumours of vascular tissue.

A
  1. Haemangioma
  2. Lymphangioma
  3. Karposi’s sarcoma
  4. Angiosarcoma
313
Q

What are the clinical features of haemangioma?

A

Vascular hamartomatous lesion/ developmental lesions/benign neoplasm​

Wide age range, common in children esp Females​

Dark red/purple swelling​

Blanch on pressure​

Usually solitary though can be part of angiomatous syndrome- Sturge-Weber Syndrome

314
Q

What is the histopathology of a haemangioma?

A

Juvenile haemangioma very cellular endothelial proliferation ​

Capillary and Cavernous depending on size of vascular spaces​

Spaces are endothelium lined and contain red blood cells​

Capillary-lots of small blood vessels​

Cavernous- large blood-filled spaces​

Oral haemangiomas may also involve muscle, bone and salivary glands

315
Q

What is the clinical features of lymphangioma?

A

Rare​

Pale swelling​

Often present in childhood​

Malformation of lymphatic vessels​

May be bleeding into lesion​

Can be localised or diffuse lesion​

May present in neck (cystic hygroma)

316
Q

What is the histopathology of lymphangioma?

A

Subepithelial collection of dilated lymphatic channels​

Vessels contain lymph

317
Q

What is Karposi’s sarcoma?

A

Locally aggressive (intermediate grade) tumour of endothelial cells

318
Q

What infection is Karposi’s sarcoma associated with?

A

HHV8

319
Q

What are the 4 variants of Karposi’s sarcoma?

A

Classic ​

Endemic​

AIDS-associated​

Iatrogenic (Immunosuppression associated)

320
Q

What are the clinical feature of Karposi’s Sarcoma?

A

Palate and gingivae most common intraoral sites​

Purplish/red lesion​

Becomes increasingly nodular ​

Lesions frequently bleed

321
Q

What is the treatment for Karposi’s sarcoma?

A

Antiretroviral therapy/chemotherapy

322
Q

What is angiosarcoma?

A

Malignant tumour of vascular endothelium​

Very rare in the oral cavity​

Forehead and Scalp of older male patients​

Excision +/- radiotherapy​

Prognosis poor

323
Q

Name 4 tumours of peripheral nerves.

A
  1. Neurofibroma
  2. Neurilemmoma
  3. “Traumatic neuroma
  4. Malignant peripheral nerve sheath tumours (MPNST)
324
Q

What are the clinical features of a neurofibroma?

A

-Benign peripheral nerve sheath tumour​

-Arises from mixture of cell types​

-Rare in the mouth​

-Smooth painless swelling​

-Affects tongue, gingivae, salivary glands or rarely intraosseous​

-Solitary or multiple, associated with Neurofibromatosis-1​

-NF-1 type significant risk of malignant transformation

325
Q

What is the histopathology of neurofibroma?

A

Mixed cellular components including Schwann cells and intraneural fibroblasts​

Spindle cells with wavy, dark-staining nuclei and scanty cytoplasm ​

Background of collagen fibres, myxoid stroma and occasional mast cells

326
Q

What is the clinical features of a neurilemmoma?

A
  • Benign peripheral nerve sheath tumour
  • Schwann cell origin
  • Slow growing painless swelling
  • Tongue most common site
327
Q

What is the histopathology of a neurilemmoma?

A
  • Encapsulated tumour
  • Spindle cells with palisaed nuclei (Antoni A areas)
  • Loose, cellular connective tissue (Antoni B areas)
328
Q

What is a traumatic neuroma and what is the clinical features??

A
  • Reactive lesion after nerve damage, not a tumour!
  • Smooth nodule
  • Tongue, lower lip, saliva gland most common sites
  • History of trauma/surgery
  • Uncommon
  • May be painful
329
Q

What is the histopathology of traumatic neuroma?

A
  • proliferation of nerve bundles
  • Random arrangement
330
Q

What is a Malignant Peripheral Nerve Sheath tumour?

A

​Accounts for 2-4% Head and Neck Sarcomas​

May be associated with NF-1​

Adults, young adults in NF-1​

Painful quickly growing mass​

Mandible, lips, buccal mucosa​

Radical Excision +/- adjuvant therapy​

Prognosis poor, esp in NF-1

331
Q

Name 2 smooth muscular tumours.

A
  1. Leiomyoma (benign)
  2. Leiomyosarcome (malignant)
332
Q

What are clinical features of leiomyoma?

A
  • Rare in the oral cavity
  • Most arise from vascular smooth muscle
  • Slow growing nodule
  • Sometimes painful
  • Lips, tongue, palate, buccal mucosa most common sites
333
Q

What is the histopathology of a leiomyoma?

A
  • Well circumscribed proliferation of smooth muscles cells
  • May be multiple vessels with thickened walls in angioleiomyoma).
334
Q

What is the clinical feautres of leiomyosarcoma?

A

Very rare in the oral cavity​

Older patients​ when does arise

Enlarging mass which may be painful ​

Treatment: Radical excision +/- adjuvant therapy​

Variable behaviour​

May recur locally ​

Can metastasise

335
Q

Name 2 tumours of skeletal muscle.

A
  1. Rhabdomyoma (benign)
  2. Rhabdosarcoma (malignant)
336
Q

What are 2 sub-categories of rhabdomyoma?

A
  • Foetal
  • Adult
337
Q

Describe foetal rhabdomyoma

A

-Young children (some adults)​

-Very rare​

-Male​ more common

-Swelling face and ear region​

-Proliferation of immature muscle cells​

-Must distinguish from rhabdomyosarcoma​

  • Treatment: Local excision
338
Q

Describe adult rhabdomyosarcoma.

A

-Older male patients​

-Floor of mouth, tongue, soft palate​ most common sites

-Often large slow growing mass​

-Histology shows lobules of closely packed more mature muscle cells​

-Can be multifocal​

-Local excision, can recur

339
Q

What are clinical features of rhabdomyosarcoma?

A

​-More frequent in young children​

-Often painless rapidly growing mass​

-Head and neck most common site​

-Various histological patterns including embryonal and alveolar​

-Prognosis varies between types​

-Specific genetic alterations identified​

  • Treatment : Radical excision +/- adjuvant therapy
340
Q

What is a granular cell tumour and what are the clinical features?

A

Benign tumour, ? Schwann cell origin​

Clinical Features​:

Tongue, buccal mucosa, floor of mouth, palate​

Wide age range, rare in children​

Females>males​

Submucosal, smooth, painless swelling

341
Q

What is the histopathology of a granular cell tumour?

A

Large eosinophilic cells with granular cytoplasm in subepithelial tissue​

Unencapsulated​

Tend to merge with underlying skeletal muscle fibres​

Marked hyperplasia of overlying epithelium

342
Q

What is a congenital epulis?

A

-Uncommon​

-Pink polypoid mass on alveolus of newborns​

(very rarely on tongue- not epulis!)​

-Can be quite large​

-Anterior maxilla most frequent site​

-Females»> males​

-Origin ?

343
Q

What is the histology of a congenital epulis?

A

Mass of large eosinophilic granular cells similar to those seen in granular cell tumour​

Hyperplasia of overlying epithelium not seen​

Immunohistochemistry different from granular cell tumour

344
Q

What is the treatment for a congenital epulis?

A

Excision, esp if breathing or feeding difficulties​

Spontaneous regression in some cases​

Should not recur

345
Q

What types of acini are in the parotid, submandibular and sublingual salivary glands?

A

Parotid - mainly serous acini
Submandibular- Mixed serous (90%) and mucous acini (10%)
Sublingual - mucous acini.

346
Q

Are tumours more common in the major salivary glands or minor salivary glands?

A

More common in major.

347
Q

What % of all salivary glands tumours are in the minor salivary glands?

A

15-20%

348
Q

What % of salivary glands tumours occur in the parotid gland?

A

90%

349
Q

In minor salivary gland tumours, what % occur in the palate, and what % occur in the upper lip?

A

55% occur in the palate
20% occur in the upper lip
lower lip is rare

350
Q

Is the proportion of carcinomas higher in major or minor salivary glands?

A

Minor salivary glands

351
Q

How is salivary glands tumours diagnosed?

A

Clinical and radiographic findings are very important in terms of diagnosis.

Biopsys are carried out to get a definite diagnosis such as:
- Fine needle aspiration (FNA)
- Core biopsy
- Open biopsy
- Excisional biopsy

352
Q

What is the disadvantage of carrying out a core biopsy when diagnosing salivary gland tumours?

A

Can be given limited sampling which can be non diagnostic. Salivary gland tumours are often heterogenous and frequently all of the tumour requires to be examined histologically to reach a definitive diagnosis.

353
Q

Name 3 malignant tumours of salivary glands.

A
  1. Mucoepidermoid carcinoma
  2. Acinic cell carcinoma
  3. Adenoid cystic carcinoma
354
Q

What is the clinical features of mucoepidermoid carcinoma?

A
  • It is the most common primary epithelial salivary gland malignant tumour
  • It most frequently affects the parotids but can occur in others including the minor salivary glands
  • Can be seen in children and young adults
  • More common in females than in males
  • It is locally invasive, it can recur and metastasise
355
Q

What is the histology of mucoepidermoid carcinoma?

A
  • The tumour is unencapsulated and displays an infiltrative pattern of growth.
356
Q

What is the 3 variable types of cells in mucoepidermoid carcinoma?

A
  1. Mucous-secreting cells
  2. Epidermoid (squamous) cells
  3. Intermediate cells

Tumours with high mucous cell numbers tend to be more cystic whereas mainly epidermoid lesions tend to be more solid and often aggressive

357
Q

What is the treatment for mucoepidermoid carcinoma?

A

Complete excision of the tumour.

358
Q

What is the clinical features of adenoid cystic carcinoma?

A
  • Esp middle-aged or elderly patients
  • Found in parotid, submandibular and minor salivary glands
  • Found in 30% of minor salivary gland tumours esp palate
  • Slow growing, painful, tends to be ulceration of overlying skin/mucosa.
  • Tendency to infiltrate and spread along nerve sheaths
  • May also infiltrate along marrow spaces
  • Metastases usually appear late, prognosis is poor.
359
Q

What is the histology of adenoid cystic carcinoma?

A
  • Tumour consists of epithelial and myoepithelial cells in variable configurations in scanty connective tissue stroma
  • Characteristic feature is the presence of numerous microscopic cyst-like spaces within the epithelial islands, producing a cribiform, lace-like or “Swiss-cheese” pattern.
  • Less frequently tubular or solid patterns are seen
  • Perineural invasion frequently observed.
360
Q

What are clinical features of acinic cell carcinoma?

A
  • Most arise as swelling (sometimes cystic) in parotid
  • F>M
  • Wide age range including children
  • Unpredictable behaviour - can be invasive and can metastasise.
361
Q

What is the histology of acinic cell carcinoma?

A

Non-encapsulated and may have pushing or infiltrative pattern of growth​

Almost uniform pattern of large tumour cells, similar to serous cells, with granular cytoplasm, often in acinar arrangement​

Can show other patterns with other non-acinar cells​

Less well-differentiated lesions show obvious features of malignancy

362
Q

Name 3 benign salivary gland tumours

A
  1. Pleomorphic adenoma
  2. Warthin tumour
  3. Canalicular adenoma
363
Q

What are some clinical features of pleomorphic adenoma?

A
  • Most common type of salivary gland tumours
  • Accounts for approximately 60% of all parotid tumours
  • Slightly more common in females than in males
  • Occur at any age, peak incidence 5th and 6th decades.
  • Benign, painless, slow growing “rubbery” lump
  • Usually solitary although recurrences may be multifocal
    -Most are associated with gene rearrangements in PLAG1 or HMGA2
364
Q

What is the histology of pleomorphic adenoma?

A
  • Well-circumscribed tumour
  • Incomplete fibrous capsule (tumour nodules can extend through capsule).
  • May be cystic
  • Variety of histological appearances with a complex intermingling of epithelial and myoepithlial components. Tumour epithelial cells differentiate to connective tissue type and can form connective tissue e.g cartilage and bone
365
Q

What is the treatment for pleomorphic adenoma?

A
  • Complete excision
  • If incompletely excised pleomorphic adenoma has a high recurrence rate
  • Malignant transformation can occur in pleomorphic adenoma, usually in long standing lesions.
  • Transformed tumours, called ex pleomorphic adenoma, are typically high grade malignancies with poor prognosis.
366
Q

What is the clinical features of Warthins tumour?

A
  • Almost exclusively in the parotid
  • Bilateral lesions in 5-10% of cases
  • M>F
  • > 50years
  • Painless swelling
  • Strong link with cigarette smoking
  • Radiation
  • Increased frequency in pts with autoimmune disorder?
367
Q

What is the histology of Warthins tumour?

A
  • Well circumscribed with thin capsule
  • Tumour tissue comprised of epithelial and lymphoid elements
  • Papillary (finger-like) processes of tumour tissue project into irregular cystic spaces containing mucoid material
  • Double layer of epithelial cells covers projections (basal cuboidal cells below columnar cells)
  • Stroma contains a variable amount of lymphoid tissue, often with germinal centres evident
368
Q

What are the clinical features of canalicular adenoma?

A
  • Almost exclusively (80%) in the upper lip
  • Can be multifocal
  • Typically painless slow growing nodule
  • > 50years
  • F>M
369
Q

What is the histology of a canalicular adenoma?

A

-Well-circumscribed​

-Two rows of columnar epithelial cells which are alternately closely opposed and widely separated​

​-Minimal vascular stroma​

​-May be cystic​

-Can sometimes resemble adenoid cystic carcinoma but no evidence of invasion

370
Q

Name 4 non-neoplastic epithelial lesions (tumours of salivary glands)

A
  • sclerosing polycystic adenosis
  • Nodular oncocytic hyperplasia
  • Lymphoepithelial sialadenitis
  • Intercalated duct hyperplasia
371
Q

Name 3 benign soft tissue lesions (tumours of salivary glands)

A

Haemangioma​

Lipoma/sialolipoma​

Nodular fasciitis

Module 9 (20 decks)

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