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CSP3 > Oral Medicine > Flashcards

Oral Medicine Flashcards

1
Q

How is Oral cancer classified?

A

International Classification of Disease for Oncology- ICD-O

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2
Q

What makes classification of cancer difficult?

A

Makes comparison difficult Makes epidemiology difficultMakes treatment planning difficult

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3
Q

Name the 2 distinct disease patterns for oral cancer?

A

Oral Cavity Cancer (OCC) Oro-Pharyngeal Cancer (OPC)

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4
Q

Describe the epidemiology of OCC?

A

2.5 per 100,000 pop (2012)Almost HALF (48.7%) in south central AsiaMale 2:1 Female Incidence not increasing worldwide- Decreasing in men, increasing in women- Linked to reduction in tobacco useScottish Cancer Registry- 10% increase 2001-2012

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5
Q

Name the 6 common sites for mouth cancer?

A

Floor of the mouthLateral border of the tongueRetromolar regionsSoft and hard palateGingivaeBuccal mucosa

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6
Q

Name the 3 higher sites for SSC in drinkers and smokers?

A

FoMLat. border of the tongueSoft palate

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7
Q

Name the 8 sites of oral cancer?

A

LipsPalateTonsilsFoMOther throatTongueOropharynxGums

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8
Q

Describe the epidemiology for OPC?

A

1.4 per 100,000 popMost in North America and south central AsiaMale 4.8:1 FemaleRates rapidly rising, especially in High Income areas (North America)- Linked to rising HPV epidemicScottish Cancer Registry- 85% increase 2001-2012 – highest increase for any cancer

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9
Q

Name the 5 main risk factors and their associations to Oral Cancer? - how much does each RF multiply the risk of OC?

A

Smokers who don’t drink x2 risk- Increases with quantity, duration and frequency of tobacco use- Fewer cigarettes for longer duration worse than high number, short term- Smoking risks were generally greater for larynx cancerDrinkers (3-4 drinks/day) x2 risk- Never smoked population- Frequency more important than duration – more drinks each day key- alcohol drinking for oral cavity and pharyngeal cancersSmoke and Drink x5 risk- Increases with frequency and duration of smoking and alcohol consumption- No safe lower limitBetel quid (paan) x3 risk- mixture of substances including areca nut with or without tobacco wrapped in a betel leaf and placed in the mouth Socioeconomic Status x2 risk- Even without other risk factors- Low educational attainment

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10
Q

Name the 3 risk factors that have not been confirmed as certain to increase the overall risk of Oral cancer?

A

Family History- 1st degree relative with H&N cancer may be importantOral Health- Early data suggests poor oral health may be associated with an increased cancer risk – small effectSexual Activity- a slight increased risk for oropharyngeal cancer with: - six or more lifetime sexual partners- four or more lifetime oral sex partners- early age (<18 years) of sexual debut (INHANCE)

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11
Q

What are the benefits of reducing smoking and alcohol intake?

A

Benefits seen between 1-4 yearsRisks reduced and reached a similar level to those who had never smoked after 20 years of quitting. In contrast, the risk effects associated with quitting heavy alcohol consumption take 20 years to begin to emerge.

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12
Q

What are the benefits of improving SE status?

A

Socioeconomic status- SE status is on a par with smoking and alcohol in terms of magnitude (two-fold increased risk)- specifically low educational attainment and low income. - These risks were not fully explained by smoking and alcohol consumption (‘the cause of the cause’)- have a more direct effect associated with socioeconomic circumstances

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13
Q

What are the benefits of reducing poor diet choices?

A
  • There is limited new evidence in relation to dietary factors beyond confirming that a high intake of fresh fruits and vegetables were associated with reducing by half the oral cancer risk- Obesity was not associated with an increased oral cancer risk- young people (aged 30-years or less) oral cancer was more likely in those who self-reported a low body mass index (BMI)
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14
Q

Name 4 potentially malignant lesions?

A

White lesions (leukoplakia)Red lesions (erythroplakia)Lichen planus- Candidal Leukoplakia- Chronic Hyperplastic CandidiasisOral Submucous Fibrosis

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15
Q

Describe the epidemiology of white lesions in OC?

A

incidence 0.2 - 4%- wide variation in different populations- Reliability of data not clearmalignant change- varied reports, most under 4%- period prevalence2.5% in 10 years, 4% in 20 yearsMost oral carcinomas in UK arise in initially clinically normal mucosaMost cancer in high incidence areas (e.g. India) from potentially malignant lesionWorldwide leukoplakia is 50 to 100 times more likely to progress to cancer than clinically normal mucosa

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16
Q

Name 3 types of descriptions of white lesions?

A

HomogenousErosiveNon-homogenous on atrophic background

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17
Q

How does erythroplakia compare to leukoplakia?

A

much less frequent than leukoplakiamuch higher risk of cancergreater dysplasia risk- Up to 50% already be carcinomano good follow-up studies available

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18
Q

What are the common characteristics of dysplasia and the new categorisation of severity?

A

Based on:- Cellular Atypia- Epithelial Architectural OrganisationNew categorisation- Low grade- high grade- carcinoma-in-situ

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19
Q

Describe the histological low grade of oral mucosal dysplasia?

A

Easy to identify that the tumour originates from squamous epitheliumArchitectural change into lower third Cytological atypia or dysplasia may not be prominent Shows a considerable amount of keratin productionEvidence of stratificationWell formed basal cell layer surrounding the tumour islands Tumour islands are usually well defined and are often continuous with the surface epithelium Invasion pattern with intact large branching rete pegs ‘pushing’ into underlying CT(Where there is architectural change into middle third, depending on the level of cytological atypia will be classified into low grade or high grade)

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20
Q

Describe the histological high grade of oral mucosal dysplasia?

A

Show little resemblance to a normal squamous epitheliumArchitectural change upper third Usually show considerable atypiaInvade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CTMitotic figures are prominent and many may be abnormal Degree of differentiation used to predict prognosis

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21
Q

Describe the histological carcinoma in situ of oral mucosal dysplasia?

A

Theoretical conceptCytologically malignant but not invadingAbnormal architecture- Full thickness (or almost full)- Severe cytological atypiaMitotic abnormalities frequent

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22
Q

Name the histoloigcal prognostic facors which give information on survivability?

A

Pattern of Invasion- Bulbous rete pegs infiltrating at same level is considered of a better prognosis than widely infiltrating small islands and single cells Depth of Invasion- Risk of metastases for a tumours greater than 4mm was 4x greater than for a tumour less than 4mmmPerineural Invasion- Is seen in up to 60% of OSCCs but is most significant when a tumour is seen within a large nerve at a site some distance from the main tumour massInvasion of Vessels- Widely thought to be associated with lymph node metastaes and a poor prognosis

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23
Q

Describe the Field Cancerisation concept?

A

Multiple primaries possible over time- up to 15 to 20 in some patientsConcept of “field cancerisation”- high cancer risk in 5cm radius of original primary - that’s most of the mouth/pharynxSynchronous or metachronous lesions- Can occur at the same time as the primary or at later times

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24
Q

Name the multiple variables for clinical cancer staging of OC?

A

site size (T)spread (N&M)

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25
Q

Describe the different varying change of cancer prognosis/survivability?

A

1/3 patients present at stage I/II- Stage I - 80% cure rate - Stage II – 65% cure rate- Later than this 5 year survival <50%, cure <30%- If untreated, with metastases, survival is about 4 monthsSurgery, Radiotherapy and Chemo/Immunotherapy all used- Choice will depend on patient choice and health/prognosis- Tumour location, size and nutitional status all important For resectable tumours, primary surgery offers the best outcome- Post surgical radiotherapy or chemotherapy

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26
Q

Describe the aetiology, behaviour and prognosis of Lip cancer?

A

Lower lip- non-healing ulcer or swellingAetiology- Sunlight UV-B- smokingBehaviour - slow growth - local invasion- rarely metastasise to nodesGood prognosis as early detection

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27
Q

How is OC detected?

A

Difficult to do – a judgement from experience- Use the ‘Oral Cancer Recognition Toolkit’ - Developed jointly by Cancer Research UK and the British Dental Association

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28
Q

What are the advantages and disadvantages of OC screening?

A

Benefits vs HarmUndetected lesions vs False positiveCost of Screening vs Cost of diseaseCost of Screening vs Disability from disease

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29
Q

Name the 5 OC screening tools?

A

HPV16 screeningToluidene blueVELscopePhotodynamic Diagnosis (PDD)Clinical judgement of experienced clinician

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30
Q

Describe what and how toluidine blue is and used?

A

false positive in inflammatory lesions ? 50 % false negatives good for invasive disease, but usually clinically evident

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31
Q

Describe what and how VELscope is and used?

A

Autofluorescence of tissues with blue light- Loss of fluorescence equates to ‘change’- Change may be cancer but can be other changesPublished work ‘thin’- May well work, but evidence not yet adequate

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32
Q

Explain the duty of Primary care dentistry in OC screening/detection?

A

Part of General CPD requirement nowDentist has opportunity for PRIMARY PREVENTION in patients attending for regular oral careDentist must be familiar with and competent in:- Smoking cessation advice - Alcohol reduction advice- Healthy diet promotionThere is a GDC expectation that a dentist will do this as part of ‘good patient care’ rather than any particular remunerationDentist has to make decision about their referral threshold for potentially malignant lesionsMonitor with photographs and education Remove local factors where ulcer may be due to trauma, then review2 WEEK RULE for referral to clinic for the hospitalPatient must be initially seen within this time62 day referral to treatment time for cancer patients

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33
Q

What is the definition of precancerous lesion?

A

An altered tissue in which cancer is more likely to form

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34
Q

What is the defintiion of precancerous condition?

A

A generalised state associated with an increased cancer risk

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35
Q

Name the 4 types that can’t be conisdered leukoplakia?

A

Tobacco related lesions Smokers keratosis Chronic hyperplastic candidosis Frictional keratosis

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36
Q

What is the definition of leukoplakia?

A

It is a clinical diagnosisIt has NO histological connotationEpithelial dysplasia may or may not be presentNon-homogeneous types are more likely to be dysplastic

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37
Q

Describe the epidemiology of leukoplakia?

A
  • Incidence ? 0.2 – 10% but wide variation in different parts of the world. 6 x commoner in tobacco users. Male > Female world wide but only marginally so in the west. More common in the “elderly.” - Malignant change in 3 -28%- Period prevalence - how many in what time? 2.5% in 10 years, 4% in 20 years (West) ? % in Far east and Africa
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38
Q

Name the clinical predictors of malignancy?

A

Clinical appearance - very variableNon-homogeneousVerrucous, speckled, Ulcerated, leuko-erythroplakia

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39
Q

Describe the molecular progression of oral cancer?

A

The development of oral cancer involves the progressive accumulation of 6 -10 genetic alterations in an epithelial cell leading to uncontrolled proliferation and clonal expansion.A genetic progression model based on chromosomes frequently identified as showing Loss of Heterozygosity (LOH) in oral carcinogenesis suggests:- Normal mucosa experiences a LOH at 9p: leads to predysplastic lesion.- Predysplastic lesion experiences an additional LOH at 3p, 17p :leads to dysplasia.- Dysplastic lesion experiences further LOH at 11q,13q and 14q leads to carcinoma-in-situ.- C-I-S lesion experiences a further LOH at 6p,8,4q which leads to invasion

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40
Q

What is the definition of hyperplasia?

A

Increased cell numbersArchitecture regular stratification altered compartment sizeNO cellular atypia

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41
Q

What is the definition of hyperplasia?

A

Increased cell numbersArchitecture regular stratification altered compartment sizeNO cellular atypia

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42
Q

What is the definition of hyperplasia of stratum spinosum (acanthosis)

A

Architecture -increased maturationcompartment

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43
Q

What is the definition of basal cell hyperplasia?

A

increased basal cells

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44
Q

What is the definition of low grade (mild hyperplasia)

A

Architecture -change in lower thirdMild -cytological atypia

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45
Q

What is the definition of high grade (mod/severe dysplasia)

A

Architecture -change into middle/upper third Marked cytological atypiaPossibility of numerous abnormal mitoses

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46
Q

What is the definition of oral candidosis?

A

Opportunistic fungal infection of the oral cavity.- Oral rarely in itself painful- Oesophageal may be in HIV

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47
Q

How do people aquire candida?

A

Majority of normal population are healthy carriersMost common isolate is C. albicans

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48
Q

Name 5 candidal virulence factors?

A

AdherenceSwitching mechanismsGerm tube formationExtracellular enzymesAcidic metabolites

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49
Q

Name the local predisposing factors for candidal infections?

A

SmokingDenturesLocal corticosteroidsXerostomiaTopical antimicrobials

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50
Q

Name the general predisposing factors for candidal infections?

A

Extremes of ageEndocrine disease- DiabetesImmunodeficiency- Steroid use, HIVNutritional deficiency- ironAntibiotics

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51
Q

Name the classification of oral candidosis?

A

Acute Pseudomembranous- Sudden local/systemic immunosuppressionChronic Erythematous- Longstanding & persisting issue- e.g. below poor fitting dentures, HIV, median rhomboid glossitis and antibioticChronic Hyperplastic

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52
Q

How to diagnose oral candidosis?

A

Laboratory tests- Differentiate from commensal- Only by QUANTIFIABLE assay- Culture and sensitivity to inform treatment- Multiple sites usually- Smear/microscopy occasionally

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53
Q

How to diagnose candidosis via lab?

A

Swab (mucosa or denture )Whole saliva/Oral rinse- Growth onto selective agarOral rinse- Patient rinses with 10ml of PBS. Inoculate onto selective agar on spiral plater. - Has the advantage of being a “Quantitative technique”

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54
Q

How to identify candidaosis in the lab?

A

Direct microscopyGerm Tube testPhysiological tests- Carbohydrate fermentation- Carbohydrate and nitrogen assimilationCommercial systems- API 20C systems

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55
Q

How to identify candidaosis in the lab?

A

Direct microscopyGerm Tube testPhysiological tests- Carbohydrate fermentation- Carbohydrate and nitrogen assimilationCommercial systems- API 20C systemsBiopsy- Essential for diagnosis of hyperplastic candidosis.- PAS stainDirect smear

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56
Q

Name the 5 candida species?

A

C. albicansC. glabrataC. tropicalisC. kruseiC. dubliniensis

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57
Q

Describe the principles of management for candidal infection?

A

Correction of predisposing factors OH, diet, trauma, steroid inhaler hygieneIdentify underlying illnessesAntifungal agentCo-infection with other microorganisms?

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58
Q

Name different categories of antifingal drugs?

A

Polyenes- Nystatin- AmphotericinImidazole- Miconazole- ClotrimazoleTriazoles- Fluconazole - Itraconazole

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59
Q

Explain the treatment regimes for oral candidosis?

A

Topical Therapy (lengthy courses required) - Nystatin (pastille, suspension, cream and ointment)- Amphotericin (not available in the UK)- MiconazoleSystemic treatment (often preferred)- Fluconazole- Itraconazole

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60
Q

What is the definition of miconazole?

A
  • Imidazole antifungal- Not absorbed systemically- Available as a cream, ointment, patch or a gel - Don’t use gel for skin lesions (orange!) - Cream/ointment available with hydrocortisone - Available without prescriptionSlow release adhesive preparation availableACTIVE AGAINST STAPHYLOCOCCI as well as Candida
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61
Q

Name the types of systemic antifungals and their treatment regimes?

A

Fluconazole - 50mg capsules taken once daily- 14 day courseItraconazole- 100mg capsule - 14 day course- 100mg twice in once daily for Pseudomembranous candidiasis

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62
Q

Name 3 antifungals that have resistance?

A

C. glabrataC. kruseiiC. dubliniensis

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63
Q

Name the disease that come from Human herpesvirus/

A

Herpes simplex virus (HSV) - Primary herpetic stomatitis - Herpes labialis (recurrence) Varicella-Zoster Virus (VZV) - Chickenpox - Zoster (recurrence) Epstein-Barr Virus - Infectious mononucleosis Cytomegalovirus (CMV) HHV8- Kaposi’s sarcoma

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64
Q

Explain the virion replication cycle?

A

Virus attachment and entryUncoating of virionMigration of acid to nucleusTranscriptionGenome replicationTranslation of virus mRNAsVirion assemblyRelease of new virus particles

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65
Q

Effect of viral infections on host cells?

A

Cell death (cytopathic effect)Latent infectionHyperplasia Transformation

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66
Q

Explain the lifecycle of HSV, VZV associated leison?

A

Intranuclear oedema (glass-appearance of nuclei) at basal cell layer“Ballooning degeneration” : Keratinocytes swelling and loss of attachment. Cells can be multinucleated with eosinophilic intranuclear inclusions and eosinophilic cytoplasmProgressive cell swelling (cells are large and clear)Rupture of infected cells and release of viral particles to non-infected cells

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67
Q

Explain how to diagnose human herpesvirus?

A

Laboratory investigations available:- Antigen-specific IgG or IgM serum titres- PCR- Immunofluorescence, immunocytochemistry on affected tissue- Virus isolation from lesion and cultivation

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68
Q

Describe the apperance of primary herpetic stomatosis?

A

HSV-1- Incubation period: 5-7 days- Intraoral vesicles- Vesicles on lips and crusting due to exudate coagulation- Generalized gingival inflammationExtra-oral involvement:- peri-oral- fingers (herpetic whitlow)- eyesSymptoms- Pain- Dysphagia- Dehydration - May be associated with fever, lymphadenopathy, - Pharyngitis in adolescentsRecurrent infection:- Occur in the same location, unilateral and recur 2-3 times a year on average- Most commonly on lips, but can involve other perioral tissues- Erythematous areas papules vesicles ulcers- Intraoral mucosal involvement is less common. - Chronic ulcers in immunocompromised individuals

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69
Q

Describe the apperance of chickenpox and recurrent zoster infection

A

VZV- Prodromes: fever, fatigue, pharyngitis- Small ulcers (rarely intact vesicles) mainly on soft palate and fauces- Intraoral lesions may precede skin lesions Recurrent infeection (Zoster)- Prodromes: pain and parasthesia- Unilateral vesicular eruption following distribution of sensory nerves, e.g. divisions of the trigeminal nerve, geniculate ganglion of facial nerve (Ramsay Hunt syndrome).- Intraoral vesicles rupture quickly- Cutaneous lesions clear within 3 weeks. Pain may persist (post-herpetic neuralgia)

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70
Q

Describe the managment for HSV-1 and VZV mild infections?

A

Symptomatic relief :- Hydration- Rest- Pain relief- Antimicrobial mouthwashes (chlorhexidine 0.2%, H2O2 6%)Mild infection of the lips in healthy individuals:- Aciclovir cream 5% every 4 h- Penciclovir cream 1% every 2 h

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71
Q

Describe the managment for HSV-1 and VZV severe and immunocompromised infections?

A

Severe infections in non-immunocompromised patients:- 200 mg Aciclovir tabs or oral suspension, 5 times daily, 5 days- Prophylaxis: aciclovir 400mg twice daily (in liaison with specialist)Immunocompromised patients:- 400mg Aciclovir tabs or oral suspension, 5 times daily, 5 days- Both adults and childrenImmunocompromised with severe infection:- Refer to specialist/GP for treatmentShingles:- 800mg Aciclovir tabs or oral suspension, 5 times daily, 5 days, within 72 h onset of rash- Not in children- Refer to specialist/GP

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72
Q

Describe the apperance of infectious mononucleosis?

A

EBV:- Long incubation period (4-6 weeks)- Prodromes: severe fatigue, malaise and anorexia (10-15 days)- Main symptoms: fever, pharyngitis and generalizedlymphoadenopathy (cervical nodes)Diagnostic features:- Paul-Brunell test +- Raised anti-EBV antibodies. - If above are negative consider CMV and toxoplasmosis.- Possible oral signs: tonsilar exudate, palatal petechiae

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73
Q

Describe the apperance of CMV?

A

Mostly subclinicalIf symptomatic, clinically similar to infectious mononucleosisLarge, shallow ulcers (Cytomegalovirus-associated ulceration) in immunocompromised individuals. Histopathology: Non-specific ulceration but CMV+ inclusion bodies present at ulcer floor.

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74
Q

Describe the apperance of hand-foot and mouth disease?

A

Coxsackie Virus (A):- Incubation period is 4-7 days. Highly infectious.- Small ulcers (rarely intact vesicles) causing little pain mainly on buccal, labial, lingual and palatal mucosae- Vesicles and ulcers on hands and feet (occasionally oral ulcers or skin rash in isolation)- No gingivitis, no lymphadenopathy, no systemic upset- Self-limiting (7 days)

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75
Q

Describe the apperance of herpangina?

A

Coxsackie A and B strains:- Prodromes: muscular pain, nausea, malaise.- Small ulcers mainly on palate, uvula, tonsils- Associated with fever, dysphagia and oropharyngitis- Self-limiting (8-10 days)

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76
Q

Describe the apperance of measles?

A

Koplik’s spots - Prodrome of measles (2-4 days before measles cutaneous rash).Appear mostly on buccal mucosa (opposite molars).White spots against an erythematous background.

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77
Q

Describe the apperance of warts?

A

HPV 2,4:- White or pinkish, raised but mostly sessile- Similar to squamous cell papilloma, but more rounded and sessile- Often multiple- Mainly children affected, secondary to self inoculation

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78
Q

Describe the apperance of squamous papilloma?

A

More common in individuals >20 of ageExophitic, peduncolatedDistinctive branched structure, finger-like processes, white or pinkishUp to 20 mm in diameter

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79
Q

Describe the apperance of condyloma acuminatum?

A

HPV 6, 11, 16:Venereal wartHIV infection manifestationTransmitted via oro-genital contactMultiple white/pink nodules.Fuse forming sessile or pedunculated papillary lesion.

80
Q

Describe the management of oral mucosal HPV-related lesions?

A

Diagnosis- Clinical- Biopsy (excisional if possible)Treatment- Reassurance and monitoring- Cryotherapy- Surgical excision

81
Q

Describe the histopathology of oral mucosal HPV-related lesions?

A

HPVs induce hyperplastic changes rather than “ballooning degeneration”Fibro-vascular core covered by stratified squamous epithelium with - hyperplastic basal cell layer- acanthosis - hyperortho/parakeratosisKoilocytes

82
Q

Name the 2 categories for diagnosis of infections? And their options?

A

Clinical features- history- examLaboratory tests- microscopy- culture- mass spec- nucleic acid amp- immuno tests

83
Q

Describe what sampling and testing involves?

A

Culture and sensitivity:- swab - mouth and related sitesWhole salivaAspirateSmearBiopsyBlood

84
Q

How to decide if infection need treatment?

A

Active symptoms:- directly related to the infectious agentConsequences of infection:- local- systemic

85
Q

How to decide appropriate treatment for infection?

A

Culture and sensitivity test - always preferredBest guessExperienceSide effect profile Cost

86
Q

What is the defintion of staphylococcal infection

A

Uncommon as an acute problem- immunocompromised Very common as chronic mixed infection (related angular cheilitis)Topical treatment sufficient If systemic indicated- consider narrow spectrum

87
Q

What is the defintion of scarlet fever?

A

Exotoxin mediated mucocutaneous manifestations

88
Q

Name the 4 clinical features of scarlet fever?

A

Incubation period of 2-4 daysProdromes: nausea, malaise, vomiting, pharyngitis and lymphoadenopathyMacular erythemaOral mucosa erythematous and oedematousDorsum tongue covered by white thick coating with enlarged fungiform papillae

89
Q

What are the clinical features of tuberculosis?

A

Chronic, painless and irregular ulcer Covered by yellowish exudateSurrounding tissue indurated with inflammLocalisation- tongue, palate gingivae, and lipsAssoc subman and services lymphoadenopathy

90
Q

What isnthe histopathology of tuberculosis ?

A

Granukomas containing muktinuc giant cells- mycobacteria not always identifiable

91
Q

What are the oral manifestations of syphilis?

A

Primary - chancre Secondary - mucosal patches and blisters LatentTertiary - gumma, CV and CNS complications

92
Q

What is the defintion of gonorrhea?

A

Second most common STIOral lesions result of progenitor contactNon-specific oral presentation:- multiple ulcers- erythema- white pseudomembranes- painful pharyngitis- lymphoadeno

93
Q

What are the clinical features of actinomycosis?

A

Cerviofacial most common form Painful and slow growing hard swelling Absfesses and draining sinusesDischarge yellow purulent material

94
Q

What are the histopathologucal features of actinomycosis?

A

Colony of actinomyces in centreDense collection of inflamm cellsSurround by wall of fibrous tissue

95
Q

What is the definition of sicca syndrome?

A

Partial Sjögrens findings

96
Q

What is the definition of primary and secondary sjogrens syndrome?

A

Primary- no connective tissue diseaseSecondary- connective tissue disease- SLE, Rheumatoid Arthritis, Scleroderma

97
Q

Describe the background of Sjogrens Syndrome - spread? gender? systemic? genetic? environemnt?

A

0.2-1.2% (0.5-3 million in the USA) people have this- Half ALSO have another connective tissue disease Mostly women – 10:1 - Diagnostic delay due to late presentations- Lifespan not affected- Risk of neonatal lupus in baby if pregnancySystemic involvement- Lungs, kidney, liver, pancreas, blood vessels, nervous system- Sometimes general fatigue and chronic painSpeculative Genetic- Genetic predisposition – runs in families, but no specific inheritance- Association with anti-Ro and anti-La seems genetic- low oestrogen risk gives a of getting CT disease – androgens protective?- Incomplete cell apoptosis leads to antigens being improperly exposed- Dysregulation of inflammatory process with dendritic AP cells recruiting Band T cell responses and pro-inflammatory cytokinesSpeculative Environment- EBV association – weak evidence – may be reactive rather than causative

98
Q

Name the 4 consequences of Sjogrens Syndrome?

A

Gradual loss of salivary/lacrimal gland tissue through inflammatory destructionEnlargement of major salivary glands – usually symmetrical- Usually painlessIncreased risk- Any lymphoma (5% quoted)- Salivary marginal B-cell (MALT) LymphomaOral and Ocular effects of loss of saliva and tears

99
Q

Describe how to diagnose Sjogrens Syndrome?

A

Complex – no single test yet gives ‘the answer’Balance of probabilities from multiple criteriaDifferent scoring systems in use:- American-European Consensus Group (2002)- ACR-EULAR joint criteria (2016)

100
Q

Describe the diagnosis crietria for AECG of Sjogrens syndrome?

A

Dry eyes/mouth- Subjective or objectiveAutoantibody findingsImaging findingsRadio nucleotide assessmentHistopathology findingsFOUR or more positive criteria for diagnosis

101
Q

Describe the diagnosis crietria for ACR-EULAR of Sjogrens syndrome?

A

Histopathology findings (Weight 3)focus score >1Autoantibody findings (Weight 3)anti-RoDry eyes/mouth (Weight 1)- objective salivary flow- Schirmer testUltrasound/sialogram now accepted as well (2020)Same exclusion criteria as AECG but also IgG4 disease

102
Q

Describe the oral and eye symptoms necessary to aid diagnosis? (Not tests) clinical symptoms

A

Oral Daily feeling of a dry mouth for >3 monthsRecurrent swelling of salivary glands as an adultFrequently drink liquid to aid swallowing dry foodsOcularPersistent troublesome dry eyes for >3 monthsRecurrent sensation of sand/gravel in the eyesTear substitutes used >3 times day

103
Q

Name the 2 eye tests for Sjogrens Syndrome?

A

Abnormal Schirmer test<5mm wetting in 5 minutesFluorescein Tear film assessment

104
Q

Name the oral test for Sjoregns Syndrome?

A

Abnormal UNSTIMULATED whole salivary flow (UWS)<1.5ml in 15 mins

105
Q

Explain to autoimmunity involved with Sjogrens Syndrome?

A

What do positive autoantibodies here mean?- NOT CAUSATIVE in the disease process- ASSOCIATED with the clinical pattern- Antibodies possible without disease – need clinical and lab findingsAnti-Ro and Anti-La antibodies- Collection of proteins found in the cell- Different ones found in different patients Ro52 (70%), Ro60 (40%) and La48 (50%)Other Autoantibodies?- Other Extractable Nuclear Antigens (ENA) not associated - ANA and RF not associated with Sjögrens

106
Q

Explain the typical findings in a positive labial gland biospy for Sjogrens Syndrome - AECG?

A

Collection of >50 lymphocytes around a duct = Lymphocytic Focus Generalised lymphocytic infiltrate is ‘non-specific sialadenitis’>1 Focus Score (FS) consistent with Sjogren’s SyndromeThought to be the MOST diagnostic feature on ACR-EULAR criteria

107
Q

Describe the procedure in which to start to process of Sjogrens Syndrome, if suspicious?

A

First, look in the patient’s mouth- Sjogren’s patients complaining of dryness will have a dry mouth- Early Sjogren’s patients will NOT have a dry mouth, nor complain of oneDo the least harmful tests first- UWS in 15 mins - <1.5ml- Anti-Ro antibody- Salivary USS- Baseline MRI of major salivary glands – for comparison for future lymphoma screenIf still equivocal do labial gland biopsy- Risk of area of skin numbness following procedure- Informed consent neededLGB and Anti-Ro may be the ONLY positive results in early Sjogren’s

108
Q

Describe the management for a patient suffering with Sjogrens Syndrome?

A

If patient presenting with a dry mouth and salivary deficit- Gland function is already very low- Oral Health needs paramount – diet, OHI, 5000ppm toothpaste- Symptomatic treatment of oral dryness- Salivary stimulants - pilocarpine?If patient presenting early – NO dry mouth yet – active gland disease- Liaise with rheumatologist – multisystem disease- Consider Immune modulating treatment – hydroxychloroquine, methotrexate

109
Q

Name the 3 categories of complications for patient living with Sjogrens Syndrome?

A

Effects of Oral Dryness- caries risk, denture retention, infections, functional issues –speech/swallowSalivary enlargement - Sialosis- can occur at any time – usually permanent- Reduction surgery possible but not advised – other health issuesLymphoma risk- Salivary lymphoma may present with unilateral gland swelling at any stage- Increased general lymphoma risk too- Screening? Who should review – generally the GDP with patient awareness

110
Q

Examination of the salivary gland locations?

A

Extra oral examination- Major salivary glandsIntraoral examination- Minor salivary glands- Duct orifices- Fluid expression

111
Q

What is the function of saliva?

A

Acid bufferingMucosal lubrication- Speech- SwallowingTaste facilitationAntibacterial

112
Q

Name the 5 main causes of a dry mouth?

A

Salivary Gland diseaseDrugs Medical Conditions & DehydrationRadiotherapy & cancer treatmentsAnxiety & Somatisation Disorders

113
Q

How does salivary gland changes with age between 17-90yrs old?

A

Acinar tissue loss37% Submandibular32% Parotid45% Minor glands

114
Q

Describe in/direct effect on salivation?

A

Indirect effect- External to the glandDirect Effect- Problems within the gland itself

115
Q

Name 6 drugs that cause indirect salivary problems?

A

Anti-muscarinic cholinergic drugs - Tricyclic antidepressant- Antipsychotics- Antihistamine- Atropine- Diuretics- Cytotoxics

116
Q

Name the 3 largest influencing drugs on dry mouth?

A

Antimuscarinic- Amitriptyline 26% reductionDiuretics- Bendrofluazide 10% reductionLithium- 70% have a significant reduction- Increased caries correlates with drug use

117
Q

Name other medical conditons that can have an indirect effect on salivation? - acute and chronic?

A

Chronic Medical Problems inducing dehydration- Diabetes – Mellitus & Insipidus- Renal disease?- Stroke- Addison’s Disease- Persisting VomitingAcute medical Problems- Acute oral mucosal diseases- Burns- Vesiculobullous diseases- Haemorrhage

118
Q

Name 5 direct salivary gland problems?

A

Aplasia - Ectodermal dysplasiaSarcoidosisHIV diseaseGland infiltration- Amyloidosis- HaemochromatosisCystic Fibrosis

119
Q

What is the defintion of ectodermal dysplasia?

A

Hair, Nails, Teeth, Salivary & Sweat glands- Hearing and vision may be affectedMay be limited in effect- Salivary aplasia aloneHypohidrotic – x-linked

120
Q

Haemachromatosis?

A

HFE gene mutation - 1:10 pop carry

121
Q

Describe radiotherapy effect on salivation?

A

Radiation effectsGraft versus host effectsAntineoplastic drugsRadioiodine

122
Q

What blood tests and other tests can be used to investiagte salivary disease?

A

Blood tests - FBC- U&Es, - Liver function tests- C-reactive Protein- Glucose- Anti Ro Antibody- Anti La Antibody- Antinuclear Antibody- Complement C3 and C4Functional Assay– Salivary FlowTissue Assay – Labial Gland BiopsyImaging - Plain radiographs – reduced dose – stones- Sialography – contrast to show ducts- MR Sialography – IV contrast- Ultrasound

123
Q

Describe how anxiety and somatisation disorders can cause dry mouth?

A

‘cephalic’ control of salivation- Inhibition of salivation – anxiety directly causes ‘real’ oral dryness‘cephalic’ control of perception- Altered perception of reality – normal information coming from the mouth is ‘misunderstood’ by small changes at synapses as it is processed- More often seen with anxiety disordersAnxiety can also inhibit swallowing and can lead to a complaint of ‘too much saliva’!

124
Q

Name 6 forms of somatoform disease that cause dry mouth?

A

Oral DysaesthesiaTMD painHeadacheneck/back painDyspepsiaIrritable Bowel Syndrome (IBS)

125
Q

Name 5 treatbale causes of dry mouth?

A

DehydrationMedicines with anti-muscarinic side effectsMedicines causing dehydrationPoor Diabetes control – type 1 or type 2 Somatoform Disorder – diagnosis of exclusionManagement of these should return the patient’s oral comfort

126
Q

Name th 3 treatment options for symptomatic dry mouth?

A

Sjögren’s SyndromeDry mouth from cancer treatmentDry mouth from salivary gland diseaseTreatment options for these cases- INTENSIVE DENTAL PREVENTION- Salivary substitutes- Salivary stimulants

127
Q

Name the 5 categroeis of dry mouth investigations?

A

Salivary Flow tests – less than 1.5ml unstimulated flow in 15minsBlood tests- Dehydration – U&Es, Glucose- Autoimmune disease – ANA, Anti-Ro, Anti-La (ENA Screen), CRP- Complement levels – c3 and c4Imaging- Salivary ultrasound – looking for ‘leopard spots’ or sialectasis- Sialography – useful where obstruction/ductal disease is suspectedDry eyes screen- Refer to optician for assessment of tear film (preferred)- Schirmer test – tear flow less than 5mm wetting of test paper in 15 minsTissue examination- Labial gland biopsy – lower lip – looking for lymphocytic infiltrate and focal acinar disease

128
Q

Describe the dental management of dry mouth?

A

Prevent oral disease- Caries risk assessment- Candida/staphylococci awareness and reduction – low sugar diet and OHI Angular chelitis Sore tongueMaximal preventative strategy- Diet!- Fluoride- Treatment Planning for a caries risk mouth

129
Q

Name 6 forms of saliva substitiues and their form?

A

Sprays- Glandosane- Saliva OrthanaLozenges- Saliva Orthana- SSTSalivary stimulants- Pilocarpine (Salagen)Oral Care Systems- Oral BalanceFrequent sips of water

130
Q

Name the causes of hypersalivation? - True and percieved?

A

TRUE (rare) – Actual increase in salivary flow- Drug causes- Dementia- CJD- StrokePERCEIVED (Common) – NO increase in saliva flowSwallowing Failure- Anxiety- Stroke- Motor Neurone Disease- Multiple SclerosisPostural Drooling- Being a baby- Cerebral Palsy

131
Q

Describe the dental management of excess salivation?

A

Treat the Cause- Anxiety disordersDrugs to reduce salivation- Anti-muscarinic agents- Botox to prevent gland stimulationBiofeedback training- Swallowing controlSurgery to salivary system- Gland removal- Duct repositioning

132
Q

Name the 3 forms of causes for changes in gland size?

A

Viral Inflammation - Mumps- HIVSecretion retention- Mucocele- Duct obstructionGland Hyperplasia- Sialosis- Sjögrens Syndrome

133
Q

Name the 7 symptoms of mumps?

A

HeadacheJoint painNauseaDry mouthMild abdominal painFeeling tiredloss of appetitePyrexia of 38C, or aboveParamyxovirusDroplet spreadIncubation 2-3 weeks1/3 have no symptomsSymptomatic treatment only

134
Q

What is the defintiion of HIV sailvary disease?

A

HIV can be a cause of salivary swellingCause of Unexplained salivary swellingMay have NO HIV symptoms when presentingGenerally does not improve with treatmentLympho-proliferative enlargement of the glands

135
Q

What is the definition of a mucocele?

A

Secretion retention- In the duct- Extravasated into the tissuesRECURRENT swelling – bursts in days- ‘salty taste’Common Sites Junction Hard/Soft Palate Lower lip

136
Q

What is the definition of subacute obstruction?

A

Swelling associated with meals- increases as salivary flow starts- reduces when salivary flow stopsUsually SUBMANDIBULARocc. ParotidCan be slowly progressive – over weeksEventually fixed & painfulCause – duct obstruction- Usually duct blockage in submandibular- Usually duct stricture in parotid

137
Q

Name the 3 main causes of subacute obstruction?

A

Sialolith (stones)‘mucous’ pluggingDuctal damage from chronic infection (scarring)(Salivary stones, Duct stricture, Duct dilation, chronic non-specific sialadenitis)

138
Q

Name the 5 investigations for subacute obstruction?

A

Low dose plain radiography lower true occlusalSIALOGRAPHY – when infection freeIsotope scan if gland function uncertainUltrasound assessment of duct system

139
Q

What is the definition of duct dilation?

A

Defect prevents normal emptyingMicro-organisms grow and lead to persisting and recurrent sialadenits Gland function gradually lost and persisting infection leads to gland removalMay follow Recurrent Parotitis of Childhood at age 20-30

140
Q

Describe the management of subacute obstruction?

A

Surgical sialolith removal if practicalSialography for ‘no stone’ cases – washing effectConsider gland removal if fixed swelling

141
Q

Describe the outcome for subacute obstruction?

A

Reformation of stone/obstructionDeformity of duct – stasis & infectionGland damage – low salivary flow, ascending infection

142
Q

What is the definition of silalosis?

A

Increase in Gland Tissue (Hyperplasia)- Sialosis- Sjögrens Syndrome Major gland enlargementNo identified cause - Alcohol abuse- Cirrhosis- Diabetes Mellitus- Drugs

143
Q

What investigations can be carried out to diagnose Sialosis?

A

Blood testsGlucoseFBC, U&Es, LFTs, bilirubinBBV screen – HIV, Hep B, Hep CAutoAntibody Screen - ANA, anti-Ro, anti-LaOther investigtionsMRI of major salivary glandsUSS for Sjögren’s changesLabial gland biopsyTear filmSialography – occasionallyPhotography

144
Q

What investigations can be carried out to diagnose Sialosis?

A

Blood testsGlucoseFBC, U&Es, LFTs, bilirubinBBV screen – HIV, Hep B, Hep CAutoAntibody Screen - ANA, anti-Ro, anti-LaOther investigtionsMRI of major salivary glandsUSS for Sjögren’s changesLabial gland biopsyTear filmSialography – occasionallyPhotography

145
Q

Name 2 types of dental manifestations of systemic disease?

A

Disruption to the tooth structure formationDisruption to the tooth structure content

146
Q

Name 3 forms of systemic diseases that exhibit dental mnifestations in children?

A

Congenital conditions/infections- Syphilis,TORCH- Ectodermal Dysplasia- perinatal illnessIllness/metabolic disorder- Severe childhood illness - Porphria- Cancer treatmentsPigmentation from substances in the blood- Bilirubin, tetracycline

147
Q

Name 6 oral mucosal effects from systemic disease?

A

Giant Cell GranulomaOrofacial GranulomatosisRecurrent Aphthous StomatitisDermatosesImmune Deficiency/Disease - Raised ACTH Addison’sDrug reactions

148
Q

What is the definition of a ginat cell lesion, in relation to oral medicine?

A

Peripheral’ and ‘Central’ lesionsCheck Parathyroid function – could be as a result of excess parathyroid stimulation of osteoclasts- renal failure- hypocalcaemia- parathyroid tumour

149
Q

What is the definition of hyperparathyroidism’s effect on the bones?

A

Causes thinking and finger-like projections of the bone

150
Q

Name 4 systemic illness that cause immunodeficiency throughout life, which show oral manifestations?

A

Orofacial GranuolomatosisSjogrens Autoimmune – AddisonsInfections – fungal/viral

151
Q

Name 2 forms of skin immune disease that show oral manifestations?

A

Lichen planus, VB disease

152
Q

What is the definition of immune disease orofacial granulomatosis?

A

Associated with Dietary Allergens?- Benzoate, Sorbate, Cinnamon, Chocolate (E210-219) Skin testing not reliable Use dietary exclusion to determine trigger (if any)enzoates found in tomato and tomato products- All things with tomato sauces must be avoidedClinical signs:- lip swelling, erythema and crustiness- gingivae erythematous and heavly inflammed

153
Q

What is included for Crohn’s screening?

A

Parental awareness of importance of altered bowel habit or abdominal painGrowth monitoring at each hospital visitFaecal Calprotectin assay- Unreliable in younger children- Screening test for endoscopy- Good predictor of Crohn’s disease activity

154
Q

Describe the management of orofacial granulamtosis?

A

Management- 3 month empirical dietary exclusion- Benzoate/cinnamon – unless clear other dietary triggersTopical treatment to angular chelitis/fissure- Miconazole/hydrocortisone creamTopical treatment to lip swelling or facial erythema- Tacrolimus ointment 0.03%- Intralesional steroids to lip- Systemic immune modulation?

155
Q

Name 4 forms of automimmune CT diseases, that show oral manifestations?

A

Systemic lupus erythematosis (SLE) - erytheamic gingiva and palateSystemic sclerosis (Scleroderma)Sjogrens syndromeMixed connective tissue disease (MCTD)

156
Q

Name 3 forms of vasculitic CT diseases, that show oral manifestations?

A

Large vessel Disease- Giant cell (temporal) arteritisMedium Vessel Disease- Polyarteritis nodosa- Kawasaki diseaseSmall vessel Disease- Wegener’s Granulomatosis

157
Q

Name 4 forms of acquired immune deficiency?

A

DiabetesDrug therapyCancer therapyHIV

158
Q

What is the definition of haematinic deficieinces - causes?

A

Poor intake – dietary analysis/reinforcementMalabsorbtion- GI diseases – Coeliac Disease, Crohn’s DiseaseBlood loss- Crohn’s Disease, Ulcerative Colitis, Peptic ulcer disease, Bowel Cancer, Liver DiseaseIncreased Demand- Childhood growth spurts

159
Q

What is the definition of the Parotid gland?

A

Largest of major glandsPositioned parotid bed anterior to ear overlying mandibular ramusLower pole extends into postauricular regionIntimately associated with facial nerve (VII)Serous gland. Produces thin watery secretion via parotid duct (Stensen’s duct)

160
Q

WHat is the definition of the submandibular gland?

A

Second largestSituated in submandibular triangle – associated with lower border of mandible, digastric and mylohyoid muscles and marginal mandibular branch of VIIMixed seromucous (80% serous)Expresses secretions via submandibular duct into floor of mouth (Wharton’s duct)

161
Q

What is the definition of the sublingual gland?

A

Smallest major glandLocated in submucosa of floor of mouthNearby structures: submandibular duct, lingual nerve and lingual arteryPredominantly mucousExpels secretions via Bartholin’s duct in floor of mouth

162
Q

Name the 2 categories and 5 types of cells?

A

Acini: - serous cells- mucous cells- mixedDucts- Luminal cells: cuboidal/columnar/squamous epithelium- Abluminal cells: myoepithelium and basal cells

163
Q

What is the definition of neoplasia?

A

A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change’BenignMalignant

164
Q

Describe the epidemiology of salivary gland neoplasms?

A

Rare - 3/100,000Commoner in women75% benign90% ParotidCommnest parotid and minor- plemorphic adenoma55% of palatal tumours - minor50% of minor neoplasms are maligantAll sublingual glands are malignant

165
Q

Name the 5 aetiologies of salivary gland neoplasms?

A

Radiation: nuclear bomb survivors, therapeutic radiation, dental x-rays, ?mobile phonesTobacco smoking: Warthin’s tumourViruses: EBV & lymphoepithelial carcinomaFamilial and geneticVarious industrial occupations

166
Q

Describe the differences between Benign and Malignant salivary gland tumours?

A

Benign - Encapsulated - Slow growing - ‘Rubbery’ consistency - Mobile - Overlying mucosa/skin appears normal - Not invasive Incapable of metastasis Local excision curativeMalignant - Unencapsulated - Rapid growth - Dense, firm mass - Fixed - Overlying skin/mucosa ulcerated Invades surrounding tissue including nerves Capable of metastasis Requires more aggressive therapy (surgery +/- radiotherapy)

167
Q

Name 3 investigations for susected salivary gland tumours?

A

Clinical history and examinationImaging: Radiography/Sialography, Ultrasound, CT, MRIPathology: Fine Needle Aspiration (FNA), core biopsy, open incisional biopsy, excisional biopsyIMAGING AND PATHOLOGY ARE NOT A SUBSTITUTE FOR ADEQUATE HISTORY AND EXAMINATION

168
Q

Name 5 types of benign epithelial tumoirs of the salivary gland?

A

Pleomorphic adenomaWarthin’s tumour Basal cell adenomaCanalicular adenomaOncocytoma

169
Q

Name 5 types of malignant salivary gland tumours?

A

Mucoepidermoid carcinomaAdenoid cystic carcinomaPolymorphous adenocarcinomaCarcinoma ex pleomorphic adenomaAcinic cell carcinoma

170
Q

What is the definition of a pleomorphic adenoma?

A

Pleomorphic adenoma is a tumour of variable capsulation characterized microscopically by architectural rather than cellular pleomorphism. Epithelial and modified myoepithelial elements intermingle most commonly with tissue of mucoid,myxoid or chondroid appearance.’

171
Q

Explain the management for a pleomorphic adenoma?

A

Wide surgical excision recommended due to high rate of recurrence in inadequately excised tumoursExcision complicated by lobulated structure, presence of satellite nodules and loose myxoid consistencyEnucleation usually results in incomplete excision and recurrencesParotid: optimum technique - superficial parotidectomy with preservation of facial nerve (extracapsular dissection technique developing)Submandibular: resection of glandMinor gland: wide local mucosal excision +/- bone

172
Q

What is the definition of Warthin’s Tumour?

A

A tumour composed of glandular andoften cystic structures, sometimes with apapillary cystic arrangement, lined bycharacteristic bilayered epithelium, comprisinginner columnar eosinophilic oroncocytic cells surrounded by smallerbasal cells. The stroma contains a variableamount of lymphoid tissue with germinalcentres.

173
Q

What is the aetiology of Warthin’s tumour?

A

Exclusively in the ParotidMale predominanceLink with smoking

174
Q

Explain the management of Warthin’s tumour?

A

Complete excision is curative (superficial parotidectomy)

175
Q

What is the definition of a Oncocytoma?

A

Benign tumour of salivary gland origincomposed exclusively of large epithelialcells with characteristic brighteosinophilic granular cytoplasm (oncocyticcells).

176
Q

What is the aetiology of a Oncocytoma?

A

Most in parotidComplete excision curative

177
Q

What is the definition of a canalicular adenoma?

A

The tumour is composed of columnarepithelial cells arranged in thin, anastomosingcords often with a beaded pattern.The stroma is characteristically paucicellularand highly vascular.

178
Q

What is the aetiology of a canalicular adenoma?

A

lip commonestconservatice excision curative

179
Q

What is the definition of a basal cell adenoma?

A

Basal cell adenoma (BCA) is a rarebenign neoplasm characterized by thebasaloid appearance of the tumour cellsand absence of the myxochondroid stromalcomponent present in pleomorphicadenoma.

180
Q

What is the aetiology of a basal cell adenoma?

A

Mostly Parotid glandComplete excision curative

181
Q

What is the definition of mucoepidermoid carcinoma?

A

Mucoepidermoid carcinoma is a malignantglandular epithelial neoplasm characterizedby mucous, intermediate andepidermoid cells, with columnar, clearcell and oncocytoid features.

182
Q

What is the aetiology of mucoepidermoid carcinoma?

A

most common saliary gland malignancyParotid most common, then palate, submand and other minors

183
Q

Exlain the management of mucoepidermoid carcinoma?

A

Low grade: cystic, lots of mucous cellsHigh grade: solid, few mucous cells, atypia, mitoses++, perineural invasion, infiltrative growth and necrosis.10 year overall survival rates: low grade 90% intermediate grade 70% high grade 25%

184
Q

What is the definition of an adenoid cystic carcinoma?

A

Adenoid cystic carcinoma is a basaloidtumour consisting of epithelial andmyoepithelial cells in variable morphologicconfigurations, including tubular,cribriform and solid patterns. It has arelentless clinical course and usually afatal outcome.

185
Q

What is the aetiology of an adenoid cystic carcinoma?

A

High grade malignnacyMore in femaleMajor glandsDistant metastases

186
Q

Explain the management of adenoid cystic carcinoma?

A

Surgery treatment of choiceWide resection. Extensive surgery often requiredClear margins difficult to achieve (mostly impossible)Radiotherapy with wide fieldsChemotherapy generally not effective

187
Q

What is the definition of a polymorphous adenocarcinoma?

A

A malignant epithelial tumour characterizedby cytologic uniformity, morphologicdiversity, an infiltrative growth pattern,and low metastatic potential.

188
Q

What is the aetiology of a polymorphous adenocarcinoma?

A

2nd most common intraoral malignant salivary glandPalate most commenMalig in minor

189
Q

Explain the management of polymorphous adenocarcinoma?

A

Surgical excision with clear margins usually curativeRole of radiotherapy not certain

190
Q

What is the definition of Carcinoma ex pleomorphic adenoma?

A

Carcinoma ex pleomorphic adenoma isdefined as a pleomorphic adenoma fromwhich an epithelial malignancy isderived.

191
Q

What is the aetiology of carcinoma ex pleomorphic adenoma?

A

Usually arises from an untreated benign pleomorphic adenoma present for several years; most arise in the parotid glandPresents as rapid swelling following an extremely long period of slow growth. Slightly more common in women

192
Q

Explain the management of carcinoma ex pleomorphic adenoma?

A

Extensive surgery with neck dissection is treatment of choicePost operative radiotherapy

193
Q

What is the definition of an acinic cell carcinoma?

A

Acinic cell carcinoma is a malignantepithelial neoplasm of salivary glands inwhich at least some of the neoplasticcells demonstrate serous acinar cell differentiation,which is characterized bycytoplasmic zymogen secretory granules.Salivary ductal cells are also a componentof this neoplasm

194
Q

What is the aetiology of an acinic cell carcinoma?

A

Second most common salivary gland malignancy in children

195
Q

Explain the management of an acinic cell carcinoma?

A

Complete excision requiredGenerally not aggressive but a proportion can metastasise to cervical lymph nodes and lungRecurrence rate as high as 35%

CSP3 (6 decks)

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