Oral Pathology: Bacterial Infections Flashcards

1
Q

What are the symptoms of congenital syphilis?

A
  • Notched permanent incisors
  • Hypoplastic first molars or mulberry first molars
  • Nasal bone deformities (saddle/concave shaped nose)
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2
Q

What are the symptoms of (acquired) primary syphilis?

A
  • Development of infectious chancre (painless ulcerated localised lesion) in area of infection
  • Heals within 2-8 weeks
  • Regional lymphadenopathy (enlarged lymph nodes)
  • Possibly negative serology
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3
Q

What are the signs and symptoms of (acquired) secondary syphilis?

A
  • Develop 6-8 weeks after initial lesion
  • Positive serology
  • Rash or skin macules (flat skin spots)
  • Infectious Oral mucous patches
  • Condyloma latum (raised warty lesion)
  • Duration: weeks to months
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4
Q

What are the signs and symptoms of (acquired) tertiary syphilis?

A
  • Can develop 3-10 years after secondary stage
  • Positive serology
  • Gumma (slow, persistent, ulcerated granulomatous inflammation that can be destructive and lead to perforations), can involve any organ
  • CV problems
  • Neurosyphilis: can affect mental health
  • Syphilitic glossitis: potential increased risk for squamous cell carcinoma
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5
Q

What are some histological features of syphilis?

A
  • Chancre will appear as non-specific lesion
  • May cause peri-vascular changes/inflammation with lymphocytes and macrophages
  • Proliferative endarteritis: proliferation of endothelial wall may result in smaller lumen
  • Gumma: appears as a localised area of necrosis and granulomatous inflammation (macrophages + giant cells)
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6
Q

What are the classic signs of leprosy (oral manifestations)?

A
  • Caused by mycobacterium leprae
  • Red macule
  • Purple papules
  • Nodules and papules on tongue
  • Soft+hard palate ulceration
  • Histological chronic inflammation (some cases mononuclear macrophage type)
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7
Q

What is the pathogenesis of tuberculosis?

A

Infection:

  • Inhalation of droplet nuclei
  • Larger nuclei lodge in upper respiratory tract
  • Smaller nuclei may reach alveoli

Proliferation
-Bacteria multiply rapidly within inactivated macrophages–>form ghon foci

Granuloma
-T Cells surround macrophages to form granuloma/tubercles
-Secrete cytokines to induce infected macrophages to kill bacteria
-Sometimes directly kill infected macrophages
-Centre of granuloma has casseous consistency
(Disease may arrest here)

Miliary TB

  • Some poorly activated macrophages at periphery of tubercle
  • Allows spread of TB and growth of tubercle, resulting in spread to other areas of lung and potential spread to extra pulmonary areas via blood and lymphatic vessels (Miliary TB)

Liquefaction

  • Centre of granuloma liquefies: resulting in faster growth + spread extracellularly
  • Antigen load causes lung tissue to breakdown and rupture–> allowing spread to other areas and causing bloody sputum

Key histological feature: giant cells

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8
Q

What are the signs and symptoms of gonorrhea?

A

Bacteria: N gonorrhoeae

  • Pharyngitis
  • Oral ulceration (rare and if occur non-specific)
  • Mucosal erythema
  • Cervical lymphadenopathy
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9
Q

What are some predisposing features of NUG?

A
  • Smoking
  • Stress
  • Fatigue
  • Poor OH
  • Decreased immunity/host response
  • Usually occurs in younger patients
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10
Q

What is Cancrum oris?

A
  • Severe localised destruction of jaws and bone
  • Thought to arise due to spread of NUG to nearby tissues
  • At risk groups are malnourished children
  • Treatable though facial deformities can be severe
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11
Q

What is actinomyces?

A

-Infection with actinomyces due to lowered immunity
Characterised by:
-Localised foci of chronic suppuration (pus drainage)
-Firm swellings, usually in submandibular region
-Pus contains small granules representing different colonies of actinomyces

Histology:

  • Characterised by granulomatous inflammation and radiating mass of bacteria
  • Contains tangled organisms
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12
Q

What are the causes of osteomyelitis?

A
Periapical infection
Periodontal infection
Fractures/penetrating wounds
NUG
Periocoronitis (infection around crown of tooth, usually caused by operculum/flap due to P/E tooth)
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13
Q

What are some pre-disposing factors for osteomyelitis?

A

Local
Fractures/injury
Radiation
Paget’s disease (increased turnover rate of bone)

Systemic:

  • Immune suppression
  • Diabetes
  • Malnutrition
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14
Q

What are some signs of acute osteomyelitis?

A
  • Pain
  • Swelling
  • Pus
  • Gingival Inflammation
  • Subperiosteal bone formation
  • Tooth tenderness and mobility
  • Trismus/swallowing difficulty
  • Systemic symptoms of acute inflammation
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15
Q

What are some signs of chronic osteomyelitis?

A
  • Variable pain
  • Swelling
  • Loose teeth

Radiographic Changes:

  • Moth eaten appearance
  • Focal zones of sclerosis
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16
Q

What are some histological signs of acute osteomyelitis?

A
  • Pus in bone marrow spaces
  • Increased osteoclastic activity
  • Decreased osteoblastic activity
  • Areas of bone necrosis
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17
Q

How is osteomyelitis managed?

A
  • Bacterial culture + sensitivity testing
  • Antibiotics
  • Drainage of pus
  • Pain control
  • Debridement/removal of infection source
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18
Q

How can acute hypertrophic candidiasis be diagnosed?

A
  • White patched
  • Can be scraped off
  • Can have some areas of redness/inflammation

Note: most common form for people who are immunosuppressed but may have other systemic risk factors

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19
Q

How can acute atrophic candidiasis be diagnosed?

A
  • Sudden onset
  • Generalised or localised red patches of inflammation, however not as distinct as the chronic form
  • Can also present with non-specific pain (burning sensation)
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20
Q

How can chronic hypertrophic candidiasis be diagnosed?

A
  • White patch that can not be removed
  • Usually on tongue and buccal mucosa, but can occur anywhere
  • Requires a biopsy as appearance is similar to lichenoid reactions/ squamous cell carcinoma
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21
Q

How can chronic atrophic candidiasis be diagnosed?

A
  • Usually occurs overtime due to non-removal of denture/build up of fungi underneath
  • Distinct red patch, will follow shape of denture if denture induced
  • Usually asymptomatic/painless, though can present with pain in some cases

May also present with:

  • Non-specific red areas
  • Denture stomatitis
  • Median rhomboid glossitis (loss of lingual papillae in midline in front of circumvillate papilla)
  • Papillary hyperplasia of hard palate
  • Angular chelitis
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22
Q

What are some pre-disposing factors for candidiasis?

A
  • Poor denture hygiene
  • Reduced OVD (folding of mucosa creates niche)
  • If poor fitting can cause accumulation/affect gingiva
  • Porosity from not cleaning properly
  • Reduced salivary flow
  • Extremes of age
  • Immunosuppression
  • Endocrine disturbances
  • Advanced malignancies
  • Malnutrition
  • Antibiotic therapy
  • Blood dyscrasias: vitamin B-12/iron deficiency
  • Post-operative state
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23
Q

What is the progression of Herpes Simplex virus infection?

A

Seronegative individual
Primary disease
Latent disease
Secondary disease (may regress to latent which can then reactivate)

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24
Q

What are the signs and symptoms of the primary infection of Herpes Simplex?

A

Usually subclinical (assymptomatic)

If symptomatic, usually consists of:

  • Generalised gingivostomatitis
  • Widespread vesicular eruptions that can burst and leave ulcers (painful)
  • Prodromal symptoms: may get tingling sensation where vesicles are about to erupt
  • Systemic signs: fever, arthralgia, malaise, headache, cervical lymphadenopathy
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25
Q

What are the signs and symptoms of secondary herpes simplex virus?

A
  • Localised vesicular eruptions/ulcers compared to the more widespread lesions in primary disease, generally affect attached mucosa (palate, gingiva)
  • Development of vesicular lesions on peri-oral tissues, particularly herpes labialis
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26
Q

What can trigger reactivation of latent herpes simplex infection?

A
  • Sunlight
  • Stress
  • Immunosuppression
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27
Q

What are some histological features of herpes simplex virus infection?

A
  • Acantholysis
  • Intraepithelial vesicle formation
  • Viral inclusions
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28
Q

What effects can immunosuppression/deficiency have on herpes infections?

A
  • Increased pain/discomfort
  • Increased risk of fungal/bacterial infections
  • More widespread mucosal lesions
  • Can present as chronic infections rather than self limiting
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29
Q

What are some possible differential diagnoses for primary and secondary herpes simplex?

A

Primary:

  • ANUG
  • Streptococcus pharyngitis
  • Erythema multiforme

Secondary:

  • Aphthous ulcer
  • Developmental (e.g. epidermolysis bullosa)
  • Other vesicular (e.g. pemphigus)
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30
Q

What is a common name for the primary infection of varicella-zoster virus and what are the signs and symptoms?

How can it spread?

A

Chicken pox

-spread via direct contact or droplet inhalation

  • Itchy rash which can develop into vesicles, may affect the oral mucosa
  • Lesions may result in secondary skin infections
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31
Q

Where can herpes virus lay dormant?

A

Sensory ganglia

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32
Q

What is the common name for secondary/recurrent varicella-zoster virus disease and what are the signs and symptoms?

A

Shingles

  • Vesicular eruptions corresponding to dermatomes of infected sensory nerve where virus laid dormant (e.g. trigeminal nerve dermatomes)
  • May have prodromal symptoms of pain/paraesthesia where vesicles are about to arupt
  • May also develop further complications such as post-herpatic neuralgia and secondary infections

Differential diagnosis: vesicles stop in the midline as follow nerve dermatome distribution

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33
Q

What can Epsten-Barr Virus cause?

A
  • Oral hairy leukplakia
  • Nasopharyngeal carcinoma
  • Burkitts lymphoma
  • Infective mononucleosis (glandular fever)
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34
Q

What can coxsackie virus cause?

A

Herpangina

Hand foot mouth disease

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35
Q

What are the signs and symptoms of hand foot mouth disease?

How is it spread?

A
  • Oral mucosa ulceration
  • Vesicular rash on extremities
  • Resolves within 1-2 weeks (self-limiting infection)
  • Systemic symptoms: lymphadenopathy, fever, malaise
  • Airborne or oro-faecal transmission
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36
Q

What are the signs and symptoms of herpangina?

How is it transmitted?

A
  • Vesicular eruptions on soft palate, fauces, diffuse pharyngitis
  • Systemic symptoms: fever, malaise, sore throat
  • Resolves within 1 week
  • Transmitted via saliva or oro-faecal transmission
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37
Q

What is HPV and what diseases can be caused by it?

A

Human papilloma virus, typically affects epithelium particularly basal cells

  • Squamous papilloma
  • Condyloma accuminatum
  • Oropharyngeal carcinoma
  • Focal epithelial hyperplasia
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38
Q

What are the signs and symptoms of squamous papilloma?

A
  • Hyperkeratinised, hyperplastic exophitic growth of oral mucosa, usually cauli-flower shaped
  • Slow growing
  • White coloured due to keratinisation
  • Asymptomatic
  • Usually solitary
  • Surface is corrugated (has many grooves/ridges)
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39
Q

What are the histological features of squamous papilloma?

A
  • Papillary/finger-like projections of epithelium with central core of fibro-vascular tissue
  • Can be dysplastic (in HIV lesions)
  • Exophytic
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40
Q

What are possible differential diagnoses of squamous papilloma?

A
  • Condyloma accuminatum
  • Verruciform xanthoma
  • Papillary hyperplasia (of hard palate)
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41
Q

What are the signs and symptoms of condyloma accuminatum?

How is the disease transmitted?

A
  • Pink, broad based nodules that grow and coalesce forming an exophytic lesion
  • Less keratinised and faster growing than squamous papilloma
  • Does not have cauliflower appearance of squamous papilloma

Transmitted through direct contact

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42
Q

What are the histological features of condyloma accuminatum?

A
  • Papillary/finger-like projections of hyperplastic epithelium but with no dysplasia
  • May see koilocytic cells in upper layers
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43
Q

What are some features of focal epithelial hyperplasia?

A
  • Multiple nodular, squamous papilloma like lesions over mucosa
  • Assymptomatic
  • Histological acanthosis and parakeratosis
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44
Q

What are the signs and symptoms of leukoedema?

A
  • Bilateral
  • Assymptomatic
  • Diffuse, translucent white/grey patch
  • Poorly defined margins
  • Disappears upon being stretched
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45
Q

What are some histological features of leukoedema?

A
  • Intracellular edema of superficial half of oral mucosa
  • Pyknotic nuclei
  • Vacuolated cells
  • Thickened, broad based rete tags
  • Acanthosis
  • Thickened parakeratin layer
  • Hyperkeratinisation
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46
Q

What are the signs and symptoms of white sponge nevus?

A
  • Diffuse, irregular, opaque white thickening of mucosa
  • Early onset (ask patient if had lesion for entire life)
  • No well defined borders
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47
Q

What are some histological features of white sponge nevus?

A
  • Extensive edema of superfical half of epithelial layer, particularly prickle cell layer
  • Pyknotic nuclei
  • Vacuolated cells
  • Acanthosis
  • Hyperkeratinisation
  • Thicked parakeratin layer
  • Few cells undergoing mitosis, no dysplasia
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48
Q

What are the signs and symptoms of gingival fibromatosis?

A
  • Diffuse, painless enlargement of gingiva
  • Non-drug induced
  • Solitary
  • Other than excess tissue, generally healthy gingiva (no redness, no bleeding, no exudate, quite firm/hard)
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49
Q

What are the histological features of gingival fibromatosis?

A
  • Dense, avascular, fibrous CT
  • Some inflammation due to overgrowth onto crown making it difficult to clean
  • Elongated rete pegs
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50
Q

What are some differential diagnosis of gingival fibromatosis?

A
  • Drug induced hyperplasia
  • Neoplastic disease
  • Granulomatous disease
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51
Q

What is a haemangioma?

A
  • Localised proliferation of endothelial cells
  • Can have bony involvement
  • May have single or multiple
  • Can cause excessive bleeding when cut
  • Presents as a localised, bluish purple swelling that can go white when pressure applied (due to squeezing blood out of it)
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52
Q

What are the histological features of haemangioma?

A
  • Normal epithelium
  • Lobules of proliferation of capillaries
  • Can have capillary or cavernous types (dilated vessels), but clinical behaviour much the same
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53
Q

What is a lymphangioma?

A
  • Localised proliferation of lymphoid tissue
  • Usually present as small swellings, classically on the tongue, may get macroglossia
  • Histologically can see proliferation and enlargement of lymph vessels
  • Usually occur superficially
  • Different for haemangiomas in that vessels lack red blood cells, instead have VERY pale pink fluid
  • Can have occasional lymphocytes
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54
Q

What is cystic hygroma?

A
  • Large lymphangioma affecting the cervical region
  • Life threatening
  • Can have respiratory distress, intralesional haemorrhage, disfigurement
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55
Q

What is calibre persistent labial artery?

A
  • Mental artery retains normal size after leaving mental foramen (i.e. inferior alveolar artery does not shrink)
  • Results in palpable, pulsatile, sessile (broad based), nodule in lower lip
  • May increase risk of trauma
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56
Q

What are fordyce spots?

A
  • Ectopic sebaceous glands growing in the oral cavity (this is abnormal as sebaceous glands are usually associated with skin/hair)
  • Present as slightly elevated, small, yellow-ish or white nodules (about 1-3mm)
  • Can be discrete or confluent (if confluent may be mistaken for pathology)
  • Appear histology like sebaceous glands (collections of sebaceous cells): foamy cytoplasm, dark nucleus, occasionally hyperplastic mass
  • Ducts don’t communicate with mucosa
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57
Q

What is lingual thyroid tissue?

A
  • Nodular mass of thyroid tissue at the foramen caecum area
  • Caused by incomplete descent of thyroid to neck
  • May be the only thyroid tissue present: do not remove
  • Can manifest during pregnancy or puberty
  • May cause dysphagia
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58
Q

What can occur in ectopic/hyperplastic lingual tonsil?

A
  • Present as lymphoid aggregates, usually affecting posterior lateral of tongue
  • Variable clinical appearance, usually results in development of folds of tissue which leads to formation of crypt
  • Usually occur in response to infection, will reduce after infection subsides
  • Sometimes if tonsils become inflamed can lead to blockage of crypts: present as yellow nodule
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59
Q

What is benign migratory glossitis?

A
  • Also known as geographic tongue
  • Loss of areas of filiform papillae with associated inflammatory erythema
  • Sometimes thickened white border
  • Denuded areas regenerate, but new areas develop
  • May persist for months to years
  • More florid presentations may be associated with increased candidiasis /burning mouth syndrome risk
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60
Q

What causes pigmented gingiva?

A

-Normal number of melanocytes but increased melanin production

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61
Q

What are oral melanotic macules?

A
  • Localised, uniform brown pigmentation of mucosa with clearly defined margins
  • Assymptomatic
  • Flat lesion
  • Histologically increased melanin deposition but same number of melanocytes; may also get melanin incontincence/phagocytosis of melanin in adjacent tissue (if melaine released into CT);
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62
Q

What is mucosal melanocytic nevus?

A
  • Benign proliferation of nevus cells/melanocytes resulting in dark brown/black lesion
  • Usually (but not always) slightly raised lesion compared to macule which is flat (if macule=freckle, nevi=mole)
  • Non-neoplastic, grow at the same rate as surrounding tissue, stays within tissue of origin, simply more cells in that area, as such can be described as harmartomatous
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63
Q

What is a harmartoma?

A
  • Non-neoplastic proliferation of tissue
  • Located at tissue/site of origin
  • Grow at same rate as surrounding tissue, simply more cells
  • example is oral melanocytic nevus
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64
Q

What are the different types of nevi?

A

Junctional: confined to basal cell layer at junction of epithelium/CT
Intramucosal: Proliferation of cells below basement membrane
Compound: combined junctional and intramucosal
Blue: Proliferation of melanocyte like cells but these are spindle shaped rather than normal

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65
Q

What are amalgam tattoos?

A
  • Pigmented lesion caused by uptake of amalgam into tissues
  • Characterised histologically by black amalgam granules in tissue
  • May have radiopaque areas in radiogrpah in soft tissue that have no other explanation
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66
Q

Where are melanocytes derived from?

A

Neural crest cells

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67
Q

What is hyperplasia?

A

Increase in tissue size via increase in cell numbers

  • Caused by increased mitosis and/or decreased apoptosis
  • Reversible
  • Stimulus dependant
  • Usually concomitant inflammation that may contribute to cause
68
Q

What is a polyp? What are the different types?

A

Small growth projecting into a cavity

Papillary: Any small growth projecting into cavity (think of this as a classic polyp)
Verrucous: Warty surface appearance, small hyper keratinised projections
Epulis: Lump on gum

69
Q

What is an exophytic lesion?

A

Lesion that grows out from a surface

70
Q

What is a sessile lesion?

A

Broad based

71
Q

What is a pedunculated lesion?

A

Lesion attached to surface by a stalk, easier to remove than sessile lesions

72
Q

What is a linea alba?

A

-Hyperplastic lesion occurring on buccal mucosa due to mechanical trauma
-Presents as a white, narrow lesion
-Symptomless
Histologically:
-Acanthosis
-Hyperkeratosis

73
Q

What is smoker’s keratosis?

A
  • Diffuse, white, moderately thickened palate
  • Affects the entire palate
  • Characterised by 1-2mm diameter red dots that represent salivary gland openings/peri-ductal inflammation
  • Sometimes roughened
74
Q

What is the histopathology of smoker’s keratosis?

A
  • Hyperkeratosis
  • Acanthosis
  • Subepithelial chronic inflammation
  • Periductal inflammation
75
Q

What is fibroepithelial hyperplasia/fibroepithelial polyp?

A

-Usually occur in response to trauma (e.g. cheek/tongue biting, irritation from broken teeth/restorations)
-Exophytic lesions
-Growth rate: slow
-Surface: smooth, slightly pebbly, may have ulcerations
Extra features
-Sessile or pedunculated
-Coloured same as normal mucosa with or without inflammation
-Firm consistency

  • Histologically:
  • Hyperkeratosis, acanthosis of white areas, however epithelium is variable
  • Bulk of lesion is fibrous tissue with some chronic inflammatory infiltrates, may get calcification of the polyp form
76
Q

What is papillary hyperplasia of the hard palate?

A
  • Nodular overgrowth of palate (usually by formation of multiple nodules)
  • Usually associated with dentures/candidiasis/low grade trauma
  • Histologically: nodular overgrowth with central areas of vascular fibrous tissue + chronic inflammatory cell infiltrate,
77
Q

What is a pyogenic granuloma?

A
-Localised exophytic soft tissue lesion
Growth rate: Sudden onsent, rapid growth (distinguishing feature from fibroepithelial hyperplasia)
Surface: usually ulcerated surface
Extra features:
-Usually sessile
-Bright red, haemorrhagic

Histopathology

  • Granulation tissue: large number of thin walled dilated endothelial cells/blood vessels
  • Stroma (area surrounding vessels) is edematous, accollagenous, usually inflamed
  • Can have epithelial hyperplasia at non-ulcerated areas

Eitology largely unknown, but often associated with pregnancy/puberty

78
Q

What are some differential diagnosis for pyogenic granuloma?

A
  • Haemangioma
  • Neoplasm
  • Calcifying fibroblastic granuloma
  • Peripheral giant cell granuloma
79
Q

What is a peripheral giant cell granuloma?

A

-Similar to pyogenic granuloma
-Exophytic
-Growth rate: Rapid onset
-Surface: Can be ulcerated
Extra features:
-Vascular
-Can have radiographic evidence of bone involvement
-Usually relatively large

Histologically:

  • Well vasculated cellular tissue with thin walled vessels
  • Can have haemorrhage
  • Mononuclear cells + multinucleated giant cells (granulomatous inflammation)–>key feature differentiating from pyogenic granuloma
  • Haemosiderin pigment (byproduct of RBC breakdown)
80
Q

What is a calcifying fibroblastic granuloma?

A

-Appear histologically similar to other oral polyps i.e.
-Presents as localised exophytic lesion
-Surface: Can be ulcerated
-Growth rate: in between pyogenic granuloma and fibroepithelial hyperplasia
Extra features:
-Painless
-Smaller than peripheral giant cell granuloma

Histologically:

  • Very cellular lesion (differentiates it from fibroepithelial hyperplasia as the other one is not as cellular)
  • Well vascularised and collagenous
  • Areas of calcification
81
Q

What is a giant cell fibroma?

A
  • Small, assymptomatic lesion
  • Logan describes as just a type of fibroepithelial polyp

Histologically:
-Characterised by large fibroblasts which have multiple nuclei

82
Q

What is traumatic neuroma?

A
  • Nerve damage
  • When nerve repairs itself it becomes obstructred, resulting it proliferating into a disorganised bulbous mass
  • Digital pressure causes pain
83
Q

What is verruciform xanthoma?

A
  • Hyperplasia of epithelium
  • Localised
  • Have warty appearance (corrugated surface)

Histologically
Characteristic change in epithelium re
-Elongated/broad rete pegs
-Hyperkeratosis (white lesion)
-Elongated CT papillae filled with cells with foamy (pale coloured) cytoplasm
-May have keratin plugging (keratin plugs up gap between soft tissue papillae), usually causes orange clinical appearance

84
Q

What happens to CD4+ cells in HIV?

A

Decrease rapidly, increase as immune response mounted, then continue to decrease overtime; viral cells follow opposite pattern

85
Q

What are the stages of HIV?

A

Primary:

  • Rash
  • Myalgia (muscle pain)
  • Pharyngitis
  • Adenopathy
  • Mouth ulcers

Early:
-Asymptomatic

Intermediate:

  • Minor infections
  • Skin conditions
  • Fever and weight loss
  • TB
  • Pneumonia

Late:
Severe, life threatening Infections
Can have lymphomas

86
Q

What are some possible changes to oral disease presentation caused by HIV?

A
  • Longer healing times (cold sores may take 2-3 weeks rather than 1-2 days)
  • Repeated viral infections for no apparent reason (e.g. in young person who has no risk factors)
  • Presence of disease that normally does not occur without specific triggers (e.g. NUG)
87
Q

How is fungal infection presentation described in HIV? How may the infection differ?

A
  • Described as pseudomembranous, erythamatous or angular chelitis
  • Presentation much the same
  • May have longer time course
  • May have no specific reason for infection (e.g. if in young patient with no risk factors)
  • May have more widespread, florid presentation
88
Q

What can be a sign of epstein barr infection with HIV? What can it be an indication of? What is the histological appearance?

A
  • Oral hairy leukoplakia
  • Diffuse, white thickening affecting lateral surface of tongue, but may spread to other areas
  • Corrugated surface
  • Often bilateral
  • Indication that there is high viral load: patient may not be taking medications or may have become resistant

Histology:

  • Epithelial hyperplasia
  • Acanthosis
  • Hyperkeratosis
  • Koilocyte-like cells in prickle layer
89
Q

What are koilocytic cells?

A

Cells surrounded by white halo–>indication that it has been infected by virus

90
Q

What are the main viral infections associated with HIV?

A
Epstein Barr
HPV
Human Herpes Virus 8 (Kaposi's sacrcoma)
Herpes Simplex
Varicella Zoster
91
Q

How can HIV affect presentation of herpes simplex?

A
  • More intraoral symptoms
  • More long term disease rather than self limiting
  • Pattern of disease the same
92
Q

How does HIV affect presentation of varicella zoster virus?

A
  • More at risk of recurrent disease (shingles), which may occur more often
  • May cause recurrent disease in younger patients if not well controlled
93
Q

What are the signs of NUG?

A
  • Pain
  • Halitosis
  • Red, velvety gingiva
  • Punched out interdental papillae
  • Ulceration/necrosis of gingival tissue
  • Grey pseudomembrane consisting of dead cells/bacteria/fibrin
94
Q

What are the signs of NUP?

A
Severe, progressive bone loss
Severe pain
Halitosis
Loosening of teeth
Exposed bone
Minimal pocketing due to gingiva dropping away from bone
95
Q

What are the signs of symptoms of Kaposi’s sarcoma?

A
Vascular sarcoma
Bleeds easily
Purplish area or nodule
Associated with human herpes virus 8
Can result in development of nodules
Histologically proliferation of endothelial cells/blood vessels, spindle cells, haemosiderin

Non-exophytic

96
Q

What issues can HIV cause with salivary gland disease?

A
  • Sjogren syndrome like disease (autoimmune destruction of salivary gland due to virus or due to treatment)
  • Can lead to salivary stones–>swelling of gland
  • Increased risk of caries and other infections
97
Q

What type of ulcers can HIV cause?

A

Major aphthous ulcers

98
Q

What is the surgical sieve for ulcers?

A
Reactive
Idiopathic/Iatrogenic
Inflammatory/immunogenic
Infective
Neoplasm
Developmental

(RIIIND)

99
Q

What is the main type of reactive ulcer?

What are some subtypes?

A

Traumatic ulcer

  • Mechanical
  • Chemical
  • Radiation
  • Thermal
100
Q

What are the characteristics of acute traumatic lesions?

A
  • Acute inflammation (associated with pain, erythema, swelling)
  • Surface covered by yellow fibrinous exudate
  • Erythamatous border or halo
  • Well defined margins
101
Q

What are some signs and symptoms of chronic traumatic lesions?

A

Minimal pain
Induration
Elevated margins, fibroepithelial hyperplasia, hyperkeratosis
(Beware as may appear malignant)

102
Q

What is a traumatic eosinophilic ulcer?

A

Benign chronic ulcer
Usually history of trauma/has not resolved

  • Margins: Big rolled margins
  • Healing time:Extended healing time (months), but heals faster after biopsy
  • Surface: May have epithelial hyperkeratosis + yellowish coloured areas + red dots representing granulation tissue capillaries
  • Induration: indurated

Characterised by histological presence of eosinophils

  • Inflammation also deep/extends down to skeletal muscle
  • Loss of epithelial layer also present
103
Q

What are the indicators of granulation tissue?

A

Non specific inflammation
Immature fibroblasts (large nucleus)
Immature endothelium
Lots of inflammation

104
Q

What are minor aphthous ulcers?

A
  • Rounded 5-7mm ulcers
  • Affect non-keratinised mucosa
  • Margin: Erythematous margin, well defined borders
  • Surface: yellow-ish floor
  • Healing time: Heal up in 7-10 days
  • Induration: shallow

Histologically:
-Similar to eosinophilic ulcers: loss of epithelium + development of inflammation / granulation tissue but inflammation not as deep

105
Q

What are major aphthous ulcers?

A

-Large ulcers, centimeters across (clinically similar to traumatic eosinophilic ulcers but do not have
eosinophils histologically)
-Can involve keratinised mucosa
-Scarring following healing (can be debilitating if occur in the wrong spot, e.g. base of tongue)

-Margin: elevated margin
Healing speed: Persistent ulcers, last for months
-Induration: Somewhat indurated
-Surface: Yellow-ish base

-Usually biopsied as appearance similar to malignant lesion: method of differentiating=apply topical steroid and should see signs of healing within 3 days

106
Q

What are herpetiform aphthous ulcers?

A
  • Characterised by many small ulcers that can coalesce to form one large irregular ulcer
  • Generally affect non-keratinised mucosa but can affect keratinised mucosa
  • Painful
  • Tend to heal up on their own (behave similarly to minor aphthous ulcers)
107
Q

What are possible causes of aphthous ulcer? (Just know a few of these)

A
Genetic
Exaggerated trauma response (not caused by trauma, ulcer may develop later down the track)
Infections (minimal evidence)
Immunological abnormalities (cell/Ig mediated)
Gastro disorder (strong link)
Haematological disorders
Hormonal disturbance
Stress
108
Q

What GI disease is associated with aphthous ulcers? What are the signs and symptoms?

A

Crohns disease

  • Malabsorption may lead to B12 or folate or iron deficiency–>increased ulcer risk
  • Thickening + ulceration of ileocaecal region
  • Abdominal pain
  • Constipation/diarrhoea

Oral signs:

  • Diffuse lip swelling (may develop folds/ridges/cobblestone appearance)
  • Gingival erythema and swelling
  • Ulcers
  • Fibroepithelial hyperplasia (with evidence of granulomatous inflammation histologically)
  • Glossitis
109
Q

What are some haematological diseases that can pre-dispose to abscess ulcers? What are possible signs and symptoms?

A

Anaemias resulting in Folate, iron or B12 deficiency

  • Pallor
  • Breathlessness
  • Fatigue
  • Tachycardia
  • Glossitis + increased infection risk
  • Mucosal lesions/ulcers

Be careful as risks associated with GA

110
Q

What is Becet’s disease?

A

Multisystem disorder
Characterised by aphthous ulcers, genital ulcers, uveitis (eye ulceration)
Genetic distribution

111
Q

What risk factors can predispose to premalignant lesion becoming malignant?

A

History:

  • Tobacco
  • Alcohol
  • UV light exposure

Clinical features

  • Age
  • Gender
  • Type of lesion (colour, ulceration, speckling)
  • Location

Histological features:
-Degree of dysplasia

112
Q

What are some examples of epithelial architectural atypia?

A
  • Drop shaped rete pegs
  • Irregular stratification with early keratinisation
  • Loss of basal cell polarity
  • Increased numbers of mitotic figures
  • Superficial mitosis
  • Single cell keratinisation (prickle cell layer may keratinise)
113
Q

What are some examples of epithelial cytologic atypia?

A
  • Nuclear pleomorphism (abnormal size + shape)
  • Cellular pleomorphism (abnormal size + shape)
  • Increased nuclear size + nuclear: cytoplasm ratio
  • Hyperchromasia (increased stainign for nuclei acids)
  • Increased number + size of nucleoli
  • Abnormal mitotic figures (cell tries to divide into 3-4 rather than 2)
114
Q

What is the difference between carcinoma and dysplasia?

A

Dysplasia has not yet broken through basement membrane: only involves epithelium

115
Q

What are the grades of severity of dysplasia?

A

Mild: 1/3 or less thickness of epithelium
Moderate: 2/3
Severe: full thickness, also known as carcinoma in situ

116
Q

What is a sign of sun damge?

A

Pale skin

117
Q

What lesions have a high risk of developing into a malignant lesion?

A
  • Dysplastic leukoplakia
  • Dysplastic erythroplakia
  • Speckled leukoplakia: intermingling red and white areas (get this biopsied immediately)
  • Tertiary syphilis
  • Oral submucous fibrosis
118
Q

What is a leukoplakia?

A

Fixed white patch: clinical term only, do not call it a leukoplakia after it has been diagnosed

119
Q

What are the high risk sites for leukoplakia developing into carcinoma?

A
  • Buccal mucosa including commissure
  • Alveolar ridge
  • Retromolar area
  • Anterior floor of mouth and ventral tongue (sublingual keratosis–>extremely high risk)
  • Tongue
120
Q

What is oral submucous fibrosis?

A
Thinning of mucosa
Fibrotic change in CT
Scarring can cause immobility of tissues thus reducing opening
Associated with betel quid use
High risk of malignant transformation
121
Q

What are the three types of lichen planus? What are some common features? What are some common sites? What is the histology like?

A
  • Erosive
  • Atrophic
  • Striated
  • Commonly bilateral
  • Will commonly affect skin as well presenting as purple papules/scaly lesions: ask patient if any itchy skin rashes, forearms most common site
  • When occur on gingiva have both striated and atrophic areas

Common sites buccal mucosa, dorsal surface of tongue, gingiva

Histology:
-Hyperkeratosis, saw-tooth appearance of rete pegs, doesn’t have acanthosis, inflammation

122
Q

What are some differential diagnosis of lichen planus?

A
  • Lichenoid drug reaction
  • Lupus erythematosus
  • cheek biting
  • Graft vs host
  • Cadidiasis
  • Idiopathic leukoplakia
  • SCC
123
Q

T/F: lichen planus is at high risk of malignant transformation

A

F

However ensure patient has no risk factors (smoking, alcohol, wears sun protection)

124
Q

What is a squamous cell carcinoma?

A
  • Invasive epithelial neoplasm
  • Various degrees of squamous differentiation
  • Propensity to early and extensive lymph node metastisis
  • Main risk factors alcohol and tobacco use
  • Mainly occur with 50-60 years old
125
Q

What are some risk factors for SCC?

A

Tobacco use:

  • Smoking
  • Chewing
  • Snuff
  • Betel Quid

Alcohol
HPV (better prognosis than smoking)

126
Q

What are some clinical presentations of squamous cell carcinoma?

A
  • Red, speckled or white patches
  • Raised nodule
  • Non-healing ulcer
  • Rolled borders
127
Q

What are some common sites for squamous cell carcinoma?

A
  • Lower lip
  • Tongue
  • Geographical variation linked to habitats
128
Q

What is the pathophysiology of squamous cell carcinoma?

A
  • Invasion of malignant epithelial cells
  • Local tissue destruction
  • Spread to lymph nodes
  • Distant metastasis
129
Q

What type of inflammation is generally present around squamous cell carcinomas? How does this influence prognosis?

A
  • Acute if ulcer
  • Chronic around tumour

Presence of inflammation generally means better prognosis

130
Q

How does the degree of differentiation of tumour cells influence prognosis? What are the degrees of differentiation? What would you look for to judge differentiation?

A

Poorer differentiation = less controlled growth + poorer prognosis

Degrees:
Well differentiated
Moderately differentiated
Poorly differentiated
Anaplastic (can not tell what cell type)
  • Look for prickle cells and keratin: presence indicates well differentiated
  • Also look for discrete islands
131
Q

How can oral carcinoma spread?

A

Direct extension to adjacent tissue
Blood vessels
Lymphatics
Perineural infiltration

132
Q

How can spread of squamous cell carcinoma to lymph affect prognosis? What are the risk factors?

A

-Indication of poor prognosis

Risk factors:

  • Tumour site
  • Tumour size
  • Invasive front
  • Tumour thickness (if 5mm thick or more increased chance of lymph node involvement)
133
Q

What are the factors to consider in the clinical staging of oral cancer?

A

Based on
T= size
N= condition of lymph nodes
M= metastisis

134
Q

How is size staged?

A

T1 primary<2cm
T2: primary 2-4cm
T3 primary >4cm
T4 primary >4cm and invading local structures

135
Q

How is condition of regional lymph nodes staged?

A

N0=no clincal involvement
N1=Ipsilateral palpable
N2= Contralateral palpable
N3=fixed, palpable nodes

136
Q

How is metastisis staged?

A
  • M0 no metastisis

- M1=evidence of distant metastisis

137
Q

How is the spread of oral cancer staged?

A

Stage 1= T1, N0, M0
Stage 2= T2, N0, M0
Stage 3= T3, N0, M0 or any T with N1
Stage 4= Any T with N2 or N3 or any T any N M1

138
Q

How does staging influence survival rate?

A
1&amp;2 = >50% 5 year survival rate
3= 15-20% 5 year survival rate
4= <5% 5 year survival
139
Q

What are the treatment options for squamous cell carcinoma?

A
  • Surgery
  • Radiotherapy
  • Chemotherapy
  • Combination

Dentist has role in:

  • Detection
  • Management during treatment
  • Prevention of new lesions
140
Q

What are some possible surgical complications?

A

Defects
-Issue with function and aesthetics

Psychological
-Other issues may result in psychological consequences

Inadequate margins
-Can recur

May require rehab/reconstruction

141
Q

How does radiotherapy work? What are some complications/side effects?

A
  • Affects ability of rapidly dividing cells to replicate
  • Prevents tumour growth
Side effects:
-May also affect other rapidly dividing cells of body (e.g. salivary gland/mucosa)
Depending on location:
-Skin inflammation
-Skin burn (can be reversible)
-Mucositis
-Xerostomia
-Taste changes
-Osteoradionecrosis
142
Q

How can side effects of radiotherapy be managed?

A

Prevention:

  • Pre-treatment assessment
  • Extraction of teeth with poor prognosis
  • Restore any teeth that require them beforehand
  • Dosage and type of radiation
  • Field of treatment

Post-op

  • Fluoride
  • Salivary substitutes
  • Regular exam/monitoring
143
Q

What are some side effects of chemotherapy? How are they managed?

A
  • Affect oral epithelium, salivary glands, taste
  • Oral mucositis
  • increased susceptibility to infections (candidiasis, herpes simplex)
  • Prevention of oral infection
  • maintain oral hygiene
  • Supportive treatment
  • Fluoride
  • Saliva substitutes
144
Q

What are the main preventive regimes for squamous cell carcinoma?

A
Primary
-Tobacco control
-Healthy eating
-Sun protection
Secondary 
-Early detection
145
Q

What is an infiltrative squamous cell carcinoma?

A

-Spread by little islands of epithelium that break off from original mass (worse prognosis)

146
Q

What is a cohesive squamous cell carcinoma?

A

-Spread while remaining as one mass of tumour tissue (better prognosis)

147
Q

What are the main prognostic features for squamous cell carcinoma?

A
  • Degree of spread, if perivascular/bv/lymph involvement
  • Degree of differentiation
  • Invasive front: Cohesive or infiltrative invasion pattern
  • Tumour size
  • Tumour depth
  • Tumour site
148
Q

What are the suffixes for benign and malignant lesions?

A

Benign
“-oma” except melanoma and lymphoma which are malignant

Malignant
“-carcinoma” epithelial
“-sarcoma” mesenchymal

149
Q

What is a solitary fibrous tumour?

A
  • Benign fibrous tumour
  • Submucosal mass
  • Proliferation of spindle cells
  • Bands of collagen
  • Rare mitosis
150
Q

What is a myxoma?

A
  • Benign fibrous tumour
  • Submucosal mass
  • Slow growing
  • Not generally encapsulated
  • Spindle cell proliferation
  • Produce ground substance instead of collagen
151
Q

What is a fibrosarcoma?

A
  • Malignant fibrous tumour
  • Lobulated, sessile, painless mass
  • Variable growth rate, usually fast
  • Haemorrhagic

Histologically:

  • Presence of spindle cells
  • Lots of mitosis
  • Stains for vimentin
152
Q

What is a lipoma?

A
  • Benign adipose tumour
  • Usually appear as asymptomatic yellow mass with intact epithelium
  • Well circumscribed mass of fat
  • Well encaspulated
  • Regular shaped, organised adipose tissue
153
Q

What is a liposarcoma?

A

Malignant adipose tumour

  • May be slow growing
  • Cells appear irregular/disorganised
  • Not as well encaspulated
  • May have some hyperchromatic cells undergoing mitosis
154
Q

What is an angiosarcoma?

A
  • Neoplasm of endothelial cells
  • Unencapsulated, atypical/anaplastic endothelial cells
  • Stains for factor 8
  • Increased mitosis
  • Presence of spindle cells

-Can present as red vascular lesions

155
Q

What is a leiomyoma?

A
Benign smooth muscle neoplasm
Slow growing, painless submucosal mass
-Usually affects tongue, hard palate 
-Spindle cell lesion
-Stains for smooth muscle actin
156
Q

What is a leiomyosarcoma?

A

Malignant smooth muscle neoplasm

  • Spindle cell lesion
  • Atypical cells, mitotic figures
  • Stains for smooth muscle actin
157
Q

What is rhabdomyosarcoma?

A

Malignant skeletal muscle neoplasm

  • Show striated differentiation
  • Stain for desmin, actin, myogenin
  • Mass appears disorganised
158
Q

What is a schwannoma

A

Benign neoplasm of schwann cells

  • Submucosal mass
  • Asymptomatic
  • Have big pale areas of myelin protein, making for easy diagnosis
  • Large numbers of spindle cells
159
Q

What is a neurofibroma?

A
Benign proliferation of nerve fibres
Asymptomatic mucosal mass
Spindle cell lesion
Stains for S100
Malignant transformation can occur
160
Q

What is malignant peripheral nerve sheath tumour?

A
Malignant proliferation of schwann cells
Asymptomatic mass, radiolucency in bone
Spindle cell lesion
Atypical cells
Increased + abnormal mitosis
Stain for S100
161
Q

What is a granular cell tumour?

A
  • Present as painless smooth swellings
  • Occur on tongue
  • May get ulcerated
  • Pseudoepitheliolomatous hyperplasia: may appear similar to SCC, be sure to have sufficient biopsy depth
  • Big pink cells with foamy nuclei replace skeletal muscle
162
Q

What is granular cell epulis?

A
  • Occurs on gum
  • Benign tumour in newborns
  • Odontogenic epithelium
  • May involve alveolar ridge
  • Nests of cells with granular cytoplasm
  • No epithelial surface change
163
Q

What is non-hodgkin’s lymphoma?

A
  • Lymphoid cell neoplasm

- Present as ulcer, swelling, pain, paraesthesia, loose teeth

164
Q

What is a Hodgkin’s lymphoma?

A
  • Lymphoid cell neoplasm
  • Usually involves lymph nodes
  • Characteriesd by Reed-Sternberg cell histologically (bi-nuclear cell that appear like owl eyes)
165
Q

What is a malignant melanoma?

A
  • Neoplastic proliferation of melanocytes
  • Appear as diffuse dark colouring of mucosa with poorly defined margins
  • Can get ulcerations and swellings
166
Q

What do metastitic bone lesions normally present as? What is the exception/

A
  • Ill-defined radiolucency

- Exception is prostate cancer which is radiopaque