Oral Pathology Flashcards
What is incisional biopsy? And what does it allow for?
Where a small piece of a tissue is taken from a representative area of a lesion
It allows for diagnosis and future treatment planning.
After what type of biopsy is a specimen resection often carried out?
After incisional biopsy
In what two ways can a specimen be sent to pathology for investigation?
Fixed or fresh
In what way are most specimens sent to pathology for further investigation?
As fixed specimens
What is meant by a “fixed” specimen?
The specimen has been placed in a 10% neutral buffered formalin solution to stop the tissue from breaking down and to cross link the proteins to preserve the tissue histology.
What is meant by a “fresh” specimen? And in what situation is it likely used?
Where specimen comes as it is, patient may be in theatre and requires urgent diagnosis.
How are fixed specimens processed in the laboratory?
Tissue is placed within a cassette, which is placed into an automatic tissue processor, where further fixation then dehydration of tissue in ethanol takes place.
After processing of foxed specimen, what is the next step the pathology laboratory takes?
Embedding of tissue in hot paraffin wax to form tissue blocks
What instrument is used to precisely cut tissue blocks to a 4um thickness?
Microtome
What stains are most commonly used for tissue that is to be made into a slide and examined by pathologists?
Haematoxylin and Eosin stains (H&E stains)
Define, “the abnormal multiplication or increase in the number of normal cells in normal arrangement in a tissue.”
Hyperplasia
Define, “the enlargement or overgrowth of an organ or part due to an increase in size of its constituent cells.”
Hypertrophy
Define, “a decrease in cell size by loss of cell substance.”
Atrophy
Define, “a reversible change in which one adult cell type is replaced by another adult cell type.”
Metaplasia
Define, “a thickening of the stratum corneum”
Hyperkeratosis
What is the stratum corneum?
The outermost layer of the epidermis
Define, “the formation of an anuclear keratin layer, as in normal keratinised stratified squamous epithelium.”
Orthokeratosis
Define, “ the persistence of nuclei in the cells of a keratin layer”
Parakeratosis
Define, “premature keratinisation of epithelial cells that have not reached the keratinising surface layer.”
Dyskeratosis
Define, “ an increased thickness of the prickle cell layer”
Acanthosis
Define, “ the loss of intra cellular adhesion between keratinocytes.”
Acantholysis
Define, “alteration in differentiation, maturation and architecture of adult epithelial cells.”
Epithelial dysplasia
Define, “mucosal/skin defect with complete loss of surface epithelium”
Ulceration
Give an example of a developmental white lesion.
Fordyce granules
Give an example of a white lesion of normal variation.
Leukoedema
Give an example of a white lesion which is hereditary.
White sponge naevus
Give two examples of dermatological white lesions.
- Lichen planus
- Lupus erythematosus
Give an example of an infective white lesion.
Candidosis
Give an example of an idiopathic white lesion.
Leukoplakia
Give an example of a neoplastic white lesion.
Squamous cell carcinoma
What type of white lesion is described?:
-autosomal dominant
- may be apparent in infants or not until adolescence
- ill-defined
- shaggy surface
- often bilateral
- buccal mucosa most commonly affected
- mutations in keratins 4/13
White sponge naevus
What treatment is required for white sponge naevus?
None
What are the tow most characteristic histopathalogical signs of white sponge naevus?
- Thickened epithelium with marked hyperparakeratosis
- Basket weave appearance of upper prickle cells and parakeratinised cells
What white lesion is due to EBV infection? And string it associated with HIV infection in many cases?
Oral hairy leukoplakia
What are the clinical features of oral hairy leukoplakia?
- white, shaggy appearance on lateral tongue
- asymptomatic
What is the treatment for oral hairy leukoplakia?
None
What is the pathogenesis of lichen planus?
T cell-mediated immunological damage to the basal cells of epithelium.
Which sites in the oral cavity are more commonly affected by lichen planus?
- buccal mucosa
- tongue
- gingivae
- lips
Which sites in the oral cavity are LEAST commonly affected by lichen planus?
FOM and palate
Where on the body is the most common site for lichen planus skin lesions?
Flexor surface of the wrist
What are the 6 presentations of lichen planus?
- Reticular
- Atrophic
- Plaque-like
- Popular
- erosive
- Bullous
What can lead to the formation of subepithelial bullae (blisters) in bullous lichen planus?
Lack of cohesion between epithelium and lamina propria as a result of basal cell degeneration and oedema
What are “civatte” bodies? When are they present?
Degenerating cells appearing as hyaline, shrunken bodies, they are present when basal cells are undergoing apoptosis. Often seen histopathologically in patients with lichen planus.
What is the common treatmnet for lichen planus?
Steroids
Name 3 oral potentially malignant disorders dentists should be very aware of?
- Oral lichen planus
- Leukoplakia
- Proliferative verrucous leukoplakia
Define, “ a clinical term used to describe a white plaque of questionable risk after having excluded other known diseases.”
Leukoplakia
Define, “ a clinico-pathological variant of oral leukoplakia that is multi-focal, persistent and regressive with a high rate of recurrence, and a high risk of progression to SCC.”
*WHO 2024
Proliferative Verrucous leukoplakia
What are 3 examples of infective red patches?
- Periodontal disease
- Median rhomboid glossitis
- HIV gingivitis
What type of lichen planus is classified as a red patch?
Erosive lichen planus
Give two examples of idiopathic red patches.
- Geographic tongue
- Erythroplakia
What is median rhomboid glossitis?
“Rhomboid red patch on midline of posterior aspect of anterior 2/3rds of dorsal tongue”
What oral infection if medium rhomboid glossitis associated with in most cases?
Candida infection
Is median rhomboid glossitis symptomatic or asymptomatic?
Asymptomatic
What are the 4 key histopathlogical signs of median rhomboid glossitis?
- Loss of lingual papillae
- Parakeratosis and acanthosis of the squamous epithelium
- Candidal hyphae in parakeratin and associated neutrophils
- Chronic inflammatory infiltrate in connective tissue
What is the treatment for median rhomboid glossitis?
Anti-fungal medication
Which type of stain will highlight Candida on histopathlogical examination?
PAS (periodic acid-Schiff) stain
Denise, “ a red patch that cannot be characterised clinically or pathologically as another definable lesion.”
Erythroplakia
What are the typical clinical features of erythroplakia?
Red, “velvety” appearance
Smooth or nodular
On what three areas of the oral cavity is erythroplakia most frequently seen?
Palate, FOM and buccal mucosa
What two red patches are classified as oral potentially malignant disorders?
- Erythroplakia
- Erythroleukoplakia
What clinically characterises erythroleukoplakia?
It has both leukoplakia and erythroplakia components (both red and white).
Why might you worry if you spot an erythroplakia or erythroleukoplakia in the oral cavity?
They have a high likelihood of malignant transformation
(On biopsy, >90% are severe dysplasia or carcinoma)
What 5 exogenous factors can cause oral pigmentation?
- Superficial staining (e.g. foods/drinks, tobacco)
- Black hairy tongue
- Foreign bodies (e.g. amalgam tattoo)
- Heavy metal poisoning
- Drugs (e.g. NSAIDs, antimalarials, chlorohexidine)
Define, a condition characterised by papillary hyperplasia and overgrowth of pigment-producing bacteria.
Black hairy tongue
Define, a benign,well-defined small flat brown/black lesion that presents in the oral cavity due to an increased activity of melanocytes.
Melanotic Macule
What 2 histopathological changes would you expect to see in a Melanotic Macule?
- Increased melanin pigment in basal keratinocytes
- Melanin pigmentary incontinence in underlying connective tissue
Define, a malignant neoplasm of mucosal melanocytes which can vary in presentation from dark brown or black to non-pigmented or red. It is very invasive and metastasises early.
Mucosal melanoma
What is the treatment for mucosal melanoma?
Surgical resection, adjuvant radiotherapy and immunotherapy.
Describe the presentation of Melanotic neuroectodermal tumour of Infancy.
- very rare, most <1years old
- males> females
-locally aggressive, rapidly grows - most frequently affects the anterior maxillary alveolus
What causes Melanotic neuroectodermal tumour of infancy?
Might be neural crest cell origin, however pathogenesis is unknown.
What two cell populations comprise a Melanotic neuroectodermal tumour of infancy?
Neuroblastic cells and pigmented epithelial cells
What is the treatment for Melanotic neuroectodermal tumour of Infancy?
Complete local excision
What is an ulcer?
“Localised surface defect with loss of epithelium exposing underlying inflamed connective tissue”
Gave two examples of drugs/drug class that can often cause oral ulceration.
- Nicorandil
- NSAIDs
Define a vesicle.
Small blister
Define a bulla.
A blister >10mm
What is an immunobullous disorder?
“Autoimmune diseases in which autoantibodies against components of skin and mucosa produce blisters.”
How can disorders which result in vesicles/bullae be classified histologically?
Depending on the location of the bulla:
1. Intra epithelial
2. Subepithelial
What are the further classifications of intra epithelial vesicles/bullae?
- Non-acantholytic (death and rupture of cells)
- Acantholytic (desmosomal breakdown)
Give an example of intra-epithelial non-acantholytic vesicles/bullae?
Herpes simplex virus in primary herpetic stomatitis and herpes labialis
Describe in 4 steps, how herpes simplex viral infection leads to ulceration.
- Virus targets and replicates within epithelial cells
- Leads to cell lysis
- Groups of infected cells breakdown to form vesicles within the epithelium
- Infected cells infect nearby normal cells and an ulcer forms when the full thickness of the epithelium is involved and is destroyed.
Give an example of intra-epithelial acantholytic vesicles/bulla.
Pemphigus vulgaris
What sex and age group is most frequently affected by Pemphigus vulgaris?
Females, 40-6 years old.
What is the treatment for Pemphigus vulgaris?
Steroids
What are the 3 main histopathological features of Pemphigus vulgaris?
- Bullae just above basal cells forming base of lesion (tombstones)
- Acantholytic (Tzanck) cells lie free within bulla fluid
- Little inflammation until lesion ruptures
What type of specimen is mandatory for direct immunofluorescence studies?
Fresh specimen
What study is used in conjunction with routine histopathology to confirm diagnosis of vesiculobullous disorders?
Direct immunofluorescence (DIF) studies
Give 4 examples of subepithelial vesicles/bulla.
- Pemphigoid
- Erythema multiforme
- Dermatitis herpetiformis
- Epidermolysis bullosa acquisita
What sex and age range is mostly affected by the autoimmune condition, mucous membrane pemphigoid?
Females, 50-80 years old.
What clinical description is used for gingival lesions present in mucous membrane pemphigoid?
Desquamative gingivitis
What site is usually first affected by mucous membrane pemphigoid? And what other sites mat be involved?
Oral mucosa usually first affected.
Other sites:
1. Eyes
2. Nose
3. Larynx
4. Pharynx
5. Oesophagus
6. Genitalia
How does mucous membrane pemphigoid differ in bullae presentation to Pemphigus vulgaris?
Mucous membrane pemphigoid bullae tend to be relatively tough and involve full thickness of epithelium. Whereas, Pemphigus vulgaris bulla is much thinner.
What is the treatment for mucous membrane pemphigoid?
Steroids
What are the three histopathological features of mucous membrane pemphigoid?
- Separation of full thickness epithelium from connective tissue producing sub epithelial bulla with thick roof
- Infiltration of neutrophils and eosinophils around bulla
- Base of bulla comprised of inflamed connective tissue
Define, acquired autoimmune blistering dermatosis with subepithelial bullae.
Epidermolysis Bullosa Acquisita
What are the 3 variants of Epidermolysis bullosa?
- Simplex
- Junctional
- Dystrophic
Describe simplex Epidermolysis bullosa?
Intra-epithelial blistering, mutations in keratins 5/14.
Describe junctional Epidermolysis bullosa?
Subepithelial blistering, separation in lamina Lucinda, laminin mutations.
Describe dystrophic Epidermolysis bullosa?
Most severe form: Subepithelial blistering, separation beneath basal lamina, mutation in type VII collagen gene.
What is mean by angina bullosa Haemorrhagica?
Oral blood blistering , where blood-filled bullae burst to dorm ulcers and heal uneventfully.
Where does angina bullosa haemorrhagica most commonly occur in oral cavity?
On soft palate
Name a chronic, progressive, oral potentially malignant disorder associated with betel quid/areca nut chewing.
Oral submucous fibrosis
What are the clinical signs of oral submucous fibrosis?
- Clinically pale mucosa
- Firm to palpate
- Marked trismus
What are the three key histopathological features of oral submucous fibrosis?
- Dense collagenous tissue deposition in submucosa
- Loss of vascularity
- Marked epithelial atrophy
Define, atypical epithelial alterations limited to the surface squamous epithelium.
Epithelial dysplasia
What 4 sites in the mouth are associated with higher risk of malignant transformation if epithelial dysplasia is present?
- Lateral border of tongue
- Ventral tongue
- Retromolar area
- FOM
What grade of epithelial dysplasia is described:
Disorganisation, increased proliferation and atypia of basal cells.
Mild epithelial dysplasia
What grade of epithelial dysplasia is described:
More layers of disorganised basaloid cells, atypia, suprabasal mitoses.
Moderate epithelial dysplasia
What grade of epithelial dysplasia is described:
Very abnormal, affects full thickness of epithelium.
Severe epithelial dysplasia
According to WHO classifications, what are moderate and severe ED classified as?
High grade dysplastic lesions
What is the key histopathological difference between dysplasia and SCC?
In Dysplasia, atypical cells are confined to the surface epithelium.
In SCC, the atypical cells invade into the underlying connective tissue.
In the UK, what is the current incidence of mouth and oropharyngeal cancer?
8,500 cancers per year
Name the 11 variations in signs and symptoms for oral cancer.
- Lumps and bumps
- Ulcers
- White patches
- Red patched
- Speckled patches
- Non-healing socket
- Tooth mobility not associated with perio disease
- Induration/fixation of mucosa
- Dysphagia
- Pain/parasthesia
- Bleeding
Who should suspected oral cancer be referred to?
Oral and Maxillofacial surgery
When is a lesion/lump sent for referral as suspected oral cancer?
If it is persistent, unexplained and has been present for >3 weeks
What is the treatment for SCC?
Surgery, adjuvant therapy (chemotherapy or radiotherapy), monoclonal antibodies.
What is the importance of staging cancer?
Major determinant of appropriate treatment and prognosis
What staging is used for most cancers including external lip and oral cavity carcinomas?
TNM classification of malignant tumours staging
What do TNM staging components stand for?
T = extent of primary tumour
N = absence or presence and extent of regional lymph node metastasis
M = category described the absence or presence of distant metastasis
What would indicate a TNM staging suggests more extensive disease and poorer prognosis?
If the given numbers are high
Why is there usually no “M” stage in pathological staging using TNM classification?
Because we don’t receive tissue from distant sites so we cant test for distant metastases.
What are the 4 most significant prognostic factors for oral cancer?
- Tumour size
- Depth of invasion
- Nodal status
- Distant metastases
What is the most common cause of periradicular/periapical inflammation?
Due to bacterial infection following pulpal necrosis
What is the potential sequelae of acute periradicular periodontitis?
Acute abscess
Which can lead to:
Cellultis or chronic abscess
Periapical granuloma/radicular cyst
What is the potential sequelae of chronic periradicular periodontitis?
Periapical granuloma which can become:
A radicular cyst
An acute abscess, chronic abscess or lead to cellulitis.
What is a periapical granuloma?
Localised mass of inflamed granulation tissue at the apex of a non-vital tooth
A tooth has a history of trauma and pain, it is grossly carious into pulp/heavily restored, however not much is seen on the radiograph periapically. What is your diagnosis from these clinical features?
Acute periradicular periodontitis
What are the treatment options for acute periradicular periodontitis?
- extraction
- RCT
What are the clinical features of an acute periapical abscess?
Pain
Swelling/sinus
What are the treatment options for an acute periapical abscess?
- drainage and extraction
- RCT
A tooth has minimal symptoms, appears non-vital when tested but shows an apical radiolucency on radiograph. What is your diagnosis according to these clinical features?
Chronic periradicular periodontitis
What cells predominantly cause inflammation of granulation tissue?
Lymphocytes and plasma cells
