Oral Medicie YR4 Flashcards
(460 cards)
1
Q
Name the 4 categories of medcinies used in Oral Medicine (OM)?
A
Anti-microbial - virals, fungals and bioticsTopical Steroids - inhaled and mouthwashDry mouth medication - benzdamine washOthers - carbamazepine
2
Q
Name the 5 classification of medicines?
A
General SalesPharmacy MedicinesPrescription only MedicinesControlled DrugsMedical Devices
3
Q
What is the definition of a licensed medication?
A
A medicine that has been proven in evidence to the MHRA to have efficacy and safety at defined doses in a child and/or adult population when treating specified medical conditionsClinical trial data providedPost licence surveilence via MHRA
4
Q
What is the defintiion of an unlicensed medication?
A
Medicines that have not had evidence of efficacy submitted for the condition under treatmentWill be ‘licenced medicines’ – but for another conditionUse is at the discretion of the treating physicianPatient must be informed that medicine is being used ‘off-licence’Patient must be given PIL specific to the condition under treatment
5
Q
Name antimicrobials used for OM? and what they treat?
A
virals - primary herpetic gingivostomatosis, recurrent herpetic lesions and shingles- aciclovirfungals - Acute pseudomembranous candidiasis and acute erythematous candidiasis- miconazle- fluconazole- nystain
6
Q
Name topical steroids used for OM? and what they treat?
A
Betamethasone mouthwashBeclomethasone Metered Dose InhalerBoth used for - Treating aphthous ulcers- Treating Lichen planus
7
Q
What is the definition of a medical devices?
A
‘Medical device’ means any instrument, apparatus, implement, machine, appliance, implant, reagent for in vitro use, software, material or other similar or related article, intended by the manufacturer to be used, alone or in combination, forhuman beings, for one or more of the specific medical purpose- diagnosis, prevention, monitoring, treatment or alleviation of disease,• diagnosis, monitoring, treatment, alleviation of or compensation for an injury,• investigation, replacement, modification, or support of the anatomy or of a physiological process,• supporting or sustaining life,• control of conception,• disinfection of medical devices• providing information by means of in vitro examination of specimens derived from the human body
8
Q
Medical devices include dry mouth treatments - name 5 types of treatments?
A
Salivix pastillesSaliva orthanaBiotene Oral BalanceArtificial Saliva DPFGlandosane
9
Q
Name 6 other medicines used in OM?
A
Tricyclic AntidepressantsGabapentin/PregabalinAzathioprineMycophenolateHydroxycholoroquineColchicine
10
Q
What needs to be considered before any drug is prescribed or drug is reccomended?
A
Clinical indicationLicenced or unlicensed for this useDose and route of administrationImportant warnings for the patientDrug interactions and cautionsTreatment duration and monitoring
11
Q
What to include on a presciption?
A
Patient’s name, Address, Age (under 18)Patient identifier – DoB, CHI NumberNumber of Days treatmentDrug to be prescribedDrug formulation and DosageInstructions on quantity to be dispensedInstructions to be given to the patientSigned – identifier of Prescriber
12
Q
What are the rules and regulation on prescrption validity?
A
Six months from date issuedMore than one item on a scriptMore than one repeated dispensing occasion
13
Q
Tips for writing a prescription?
A
Key Patient information MUST be legibleAVOID abbreviations – write full instructions in INKOnly legal requirement is for dentist to SIGN prescription – this confirms all the other information is correct and has been checked.Essentially the SAME information for Private – GDC number usually added
14
Q
What are the advantages of written instruction for the patient?
A
Stressed patient may not remember instructionsLanguage issues may prevent proper understandingMultilingual options, large print optionsContact number for Patient Issues with the medicineLegal protection if post-treatment course questioned
15
Q
What advice should you give to your patient after prescribing the drug?
A
Take drugs at correct time and finish the courseUnexpected reactions: STOP! and contact prescriberKnown side-effects should be discussed e.g. Metronidazole and alcohol Keep medicines safe: especially from children
16
Q
Types of drugs for mucosal disease?
A
Non-steroid topical therapy - inconvientient lesions with discomfortSteroid topical therapy- disabling immunologically driven lesions
17
Q
Non-steroid topical therapy for mucosal diease? - Name 4?
A
Chlorhexidene mouthwash- dilute 50% with water if neededBenzdamine mouthwash or spray - green things help! Useful topical anaesthetic/pain reliefOTC remedies such as Igloo, Listerine, BonjelaAnything else the patient finds helpful!- check that it is not harmful though – bleach, aspirin!
18
Q
Steroid topical therapy for mucosal diease? - Name 3?
A
Hydrocortisone mucoadhesive pelletBetamethasone mouthwashBeclomethasone Metered Dose Inhaler (MDI/Puffer) - - CFC-free preparations, e.g. ‘Clenil Modulite’
19
Q
How does it work - hydrocortisone mucoadhesive tablet?
A
allow tablet to dissolve over the ulcer
20
Q
How to use betamethasone mouthwash?
A
Unlicenced product• Supply patient with a tailored information leafletUse Betnesol tabs 0.5mg - 1mg 2 tablets - 10mls water 2 teaspoons water - 2 mins rinsing - Twice dailyRefrain from eating/drinking for 30 min after useDO NOT SWALLOWDo not rinse after use
21
Q
What must be included on betamethasone mouthwash PIL?
A
Licenced for other medical conditionsExplain dose range and frequency of useExplain hazards of exceeding the standard doseAdd any known side effects – small oral candida riskAdd special instructions
22
Q
How to use beclomethasone medical device?
A
Unlicenced product - Supply patient with a tailored information leafletDental Prescribing 50mcg/puff device - Position device correctly – exit vent directly over ulcer area - 2 puffs - 2-4 times daily - Don’t rinse after useMust be a pressurised device
23
Q
What must be included on beclomethasone medical device PIL?
A
This is an accepted and proven effective treatment for the oral conditionLicensed for other medical conditions – asthma and COPDInstruct to discard the manufacturer’s PiLExplain dose range and frequency of useExplain technique used for oral lesions – different from use for lung conditionsAdd any known side effects – small oral candida riskAdd special instructions
24
Q
Systemic drugs used in OM, only for specialists?
A
Disease modulator- colchineSteroid- prednisilone (ulcers) 30mg for 5 daysImmune suppressants:- hydroxychloroquine - lichen planus- azathioprine- mycophenolateImmunotherapy:- adalimumab- enterecept
25
Systemic use of steroid risk - side effects?
If prolonged course – or repeated short courses over many months• 3 months continuous • Gaps of 2 weeks or less between ‘pulses’ of prednisolone.Adrenal suppression – steroid dependency – don’t stop suddenly – taper doseCushingoid featuresOsteoporosis risk – bone prophylaxis – Calcium supps and bisphosphonates- DEXA bone density scan may be needed from time to timePeptic ulcer risk – Proton Pump Inhibitor prophylaxisMood/Sleep alteration and mania/depression risk – can be very quick onset
26
What preparation do patients need for systemic immunomodulatory treatmets?
Must ensure that immunosuppression will not harm the patientPre-existing medical condition not yet detectedScreening for:Blood borne virus screen- Hep B, Hep C, HIV• FBC• Electrolytes• Liver Function tests• Thiopurine Methyltransferase (TPMT)- Only for Azathioprine use• Zoster antibody screen• EBV• Chest X-Ray- Evidence of previous/active TB• Cervical Smear up to date• Pregnancy test
27
What must be included when planning immunomodulatory treatment?
Needs full consent from patient - Alternative treatments tried or discussedPatient information given and patient reviewed to discuss this - Short term risk – acute drug reaction - Long term risk – cancer risk increased – Azathioprine and skin cancer especially - Effective Contraception to be used and any pregnancy planned with clinical care teamTreatment outcome understood by patient and clinician - Complete remission, acceptable level of symptoms - Trial treatment – perhaps 6 months then reassess benefit/need for treatment
28
What are the differential diagnoses of oral white lesions? 5 examples?
HereditarySmoking/frictionalLichen planus- lupus erythematosus- gvhdCandidal leukoplakiaCarcinoma
29
What does a typical white spot lesion look like?
Thickening of the mucosa or keratin- Less visibility of bloodLess blood in the tissues- vasoconstrictor
30
What is the definition of Leukoplakia?
A white patch which cannot be scraped off or attributed to any other causeNo histopathological connotation- it is a clinical descriptionDiagnosis of exclusion1 - 5% become malignant
31
Name 4 types of leukoplakia?
Fordyce's spotsSmoker's KeratosisFrictional KeratosisHereditary Keratosis
32
What is the link between smoking and leukoplakia?
Smokers are six times more likely to have “leukoplakia"Low malignant potential of the lesion- But higher oral cancer risk overall!
33
Name 3 types of infective leukoplakia?
Candidosis- pseudomembranous acute (thrush)- denture associated (chronic)Herpes Simplex
34
When should you refer a white spot lesion?
Most are benignIf RED and WHITE concentrate on the RED partIf the lesion is becoming more raised and thickenedIf the lesion is ‘without cause’- lateral tongue- anterior floor of mouth- soft palate area
35
Why are red spot lesions red?
Blood flow increases- inflammation- dysplasiaReduced thickness of the epithelium
36
What is the definition of Erythroplakia?
Atrophic or non-keratotic end of the spectrumA red patch which cannot be attributed to any other causeMore of a concern for malignancy than leukoplakia
37
Why does a red/blue lesion look like it does? explain why?
Fluid in the connective tissue- Dark – slow moving blood – varicosities - veins or cavernous haemangiomaLight Blue – clear fluid- saliva (mucocele), Lymph (Lymphangioma)
38
Name 2 types of vascular hamartomas?
Haemangioma- capillary- cavernous
39
What is thw defintion of a lymphangioma?
Lymphangioma- most are cavernousTongue- cystic hygroma
40
Name 3 types of connective tissue diseases?
Large vessel Disease- giant cell (temporal) arteritisMedium Vessel Disease- polyarteritis nodosa- kawasaki diseaseSmall vessel Disease- granulomatosis with Polyangiitis
41
What are the 3 types of mucosal pigmentations?
Exogenous stainIntrinsic PigmentationIntrinsic foreign body
42
Name the 4 examples of exogenous stains for mucosal pigmentation?
TeacoffeechlorhexidineBacterial overgrowth
43
Name the 4 examples of intrinsic pigmentation for mucosal pigmentation?
Reactive Melanosis/melanotic maculeMelanocytic naevusMelanomaEffect of systemic disease - paraneoplastic phenomenon
44
Name the 1 examples of intrinsic foriegn body for mucosal pigmentation?
Metals
45
Name the differential diagnoses for brown/black lesions - localised and generalsied?
Localised:- Amalgam- Melanotic Macule- Melanotic naevus -Malignant Melanoma- Peutz-Jehger’s syndrome- Pigmentary incontinence- Kaposi’s sarcomaGeneralised:- Racial/familial- Smoking- Drugs- Addison’s disease (Raised ACTH conditions)
46
Name 2 types of melanin pigmentation?
Racial pigmentationMelanotic macule
47
What questions to think about when deciding whether to refer for mucosal pigmentations?
Is it easily explained?- Racial- Smoking- MedicinesIs it increasing in size, colour or quantity?Any NEW systemic problem?Do I have an EXISTING radiograph showing it to be amalgam?
48
What is the ateiolog of mucosal inflammation?
trauma - physical or chemicalinfection - viral, bacterial or fungalimmunologicalcan be remalignant or melignant
49
How to decide whether something is a melanoma? questions?
Variable pigmentationIrregular outlineRaised surfaceSymptomatic- Itch- bleed
50
What is the purpose of a biopsy?
identifies or excludes malignancyidentifies dysplasiaidentifies other disease, e.g. lichen planus
51
When must you biopsy?
if unexplained
52
When should a patient be referred to oral medicine?
Patients with abnormal and/or unexplained changes to the oral mucosa- Practitioner threshold will vary with experience If there is concern about dysplasia risk- Appearance of lesion- Risk site- Risk behavior- Family history
53
When should you NOT refer a patient to Oral Medicine?
Asymptomatic VARIATIONS of NORMAL mucosaBenign conditions the practitioner has diagnosed that:- Are asymptomatic- Do not have potentially malignant risk- For which there is no treatmentIf unsure – consider clinical photography to- Monitor area until next check up- Send to specialist for an opinion
54
When should a mucsoal lesion be refered to oral medicine for an opinion?
ANYTHING the dentist thinks is might be cancer or dysplasia- 2 week Cancer referral pathway for actual malignancies- NICE and SIGN Head & Neck cancers guidelinesAny SYMPTOMATIC lesion that has not responded to standard treatment- Hospital referral criteria- SDCEP guidanceAny BENIGN lesion that the patient can’t be persuaded is not cancer…..
55
What is the oral mucosa made up of?
stratified squamous epitheliumlamina propriagross types - lining, masticatory, gustatorymicroscopic - non-keratinised - keratinised - orthokeratosis or parakeratosis
56
Different parts of the mouth which are keratinised and non-keratinised?
Keratinised - palateNon-keratinised - cheek
57
What are the compartments of the oral mucosa?
STratumCorneumGranulosumSpinosumBasalLamina ProperiaCornified, Maturation, Progenitor
58
Name the 3 reactive chnages of the oral epithelium?
Keratosis - nonkeratinised site (parakeratosis) Acanthosis - hyperplasia of stratum spinosum Elongated rete ridges - hyperplasia of basal cells
59
Name the 5 mucosal reactions of the oral mucosa?
Atrophy - reduction in viable layersErosion - partial thickness lossUlceration - fibrin on surfaceOedema - intracellular - intercellular (spongiosis)Blister - vesicle or bulla
60
How do age and nutritiona ffect the oral mucosa?
Age - progressive mucosal atrophyNutritional deficiency - iron or B group vitamins - atrophy - predisposes to infection
61
Name 3 types of benign tongue conditions? Dorsal surface
Geographic tongue - 1-2% of population - less in children - desquamation - varied pattern and timingBlack hairy tongue - hyperplasia of papillae - bacterial pigmentFissured tongue (scrotal tongue)
62
What are the symptoms of geographic tongue?
Sensitive with acidic/spicy foodsIntermittentMuch worse in young children
63
What is the aetiology of geographic tongue?
None!Something else is causing the trouble- Haematinic deficiency (B12, Folate, Ferritin)- Parafunctional trauma - Dysaesthesia
64
How to manage a black hairy tongue?
Sucking on a peach stone
65
What is the definition of a fissued tongue?
Fissured tongue is a benign condition characterized by deep grooves (fissures) in the dorsum of the tongue. Although these grooves may look unsettling, the condition is usually painless. Some individuals may complain of an associated burning sensationThe cause is unknown, but it may be partly a genetic trait. Aging and environmental factors may also contribute to the appearanceIs there another disease process there?- Candida- Lichen planus
66
What is the defintion of glossitis? And possible investigations?
What is Glossitis?- Glossitis can mean soreness of the tongue, or more usually inflammation with depapillation of the dorsal surface of the tongue (loss of the lingual papillae), leaving a smooth and erythematous (reddened) surfaceWhat investigations are needed?- Haematinics- Fungal cultures
67
What is the definition of black hairy tongue?
is a condition of the tongue in which the small bumps on the tongue elongate with black or brown discoloration, giving a black and hairy appearance.
68
What is the aetiology of black hairy tongue?
smoking, xerostomia (dry mouth), soft diet, poor oral hygienecertain medications
69
What is the aetiology of glossitis?
Often caused by nutritional deficiencies- Fe- B- Infection- others
70
When should you refer a swelling to Oral Medicine?
Symptomatic (pain is a feature of salivary gland malignancy!)Abnormal overlying and surrounding mucosaIncreasing in size'rubbery' consistencyTrauma from teethUnsightly
71
What is the definition of a pyogenic granuloma?
granulation tissue – mixed inflammatory infiltrate on fibro-vascular backgroundany mucosal site response to traumaNot a granuloma, not pyogenicother names- gingiva – aka vascular epulismost frequent site- gingiva, during pregnancypregnancy epulis
72
Name the 5 causes of mucosal ulcerative reactions?
TraumaImmunologicalInfectionsGICarcinoma
73
Name the differential diagnoses for immunological and GI mucosal ulcerative reactions?
Immunological:- aphthous ulcers- lichen planus- Lupus- vesiculo-bullous- Erythema multiformeGI:- Crohn's- UC
74
What are the differential diagnoses for single episode oral ulceration?
Trauma1st episode of Recurrent Oral UlcerationPrimary Viral infectionsOral Squamous Cell Carcinoma
75
What are the differential diagnoses for Recurrent Oral Ulceration?
Aphthous ulceration- minor, major, herpetiformLichen PlanusVesiculobullous lesions- pemphigoid, pemphigus- angina bullosa haemorrhagica- erythema multiformeRecurrent viral lesion – HSV, VZVTraumaSystemic disease – Crohn’s Disease ulceration
76
Describe the difference between Crohn's ulcers and aphthous ulcers?
Aphthous-type ulcers:- haematinic deficiency associated- behave like aphthous ulcersCrohn's specific ulcers:- linear at the depth of the sulcus- full of Crohn’s associated granulomas- persist for months – intralesional steroids help
77
Explain what to include for an Oral Ulceration History?
Where?Size & Shape?Blister or ulcer?How long for?- more than 2 weeks?Recurrent?- same site? different Sites?Painful?
78
Explain how to describe/examine an ulcer?
Margins?- flat? raised? rolled?Base?- soft? firm? hard? Surrounding tissue- inflamed? normal?Systemic Illness?
79
What is the definition of traumatic ulceration?
CommonUsually single episode - can be recurrent if cause not removedNormal or abnormal epitheliumHealing - remove cause - heal in about 2 weeks
80
Describe a recurrent herpetic lesion? - location and treatment
Ulceration limited to one nerve group/branchOften Hard palate- lesion recurs in the same place- patient often aware of prodrome and vesiculation which bursts- PAIN suggests Herpes ZOSTER rather than simplexTreat with systemic ACICLOVIR - prophylactic if a severe problem
81
Describe recurrent aphthous stomatitis (RAS)? severity? diagnosis?
Severity:- minor- major- herpetiform- Behçet’s syndromeDiagnosis by :- history- examination
82
What is the general rule for recurrent self-healing ulcers?
Those affecting exclusively the non-keratinized mucosa are inevitably aphthae.
83
The overall summary of Oral Ulceration?
Not all ulcers are aphthous!Is the lesion on keratinized or non-keratinized mucosaAre there systemic symptoms? - consider infection – herpes group, coxsackie groupAlways look for a traumatic cause - primary – sharp edge on a tooth/appliance - secondary – parafunction rubbing mucosa against the teeth
84
What is the definition of an Aphthous Ulcer?
- Immunologically generated RECURRING oral ulcers- Follow a set pattern depending upon the ulcer type- Genetically driven with environmental modification- Multifactorial environmental triggers and variable expression - Ulcer experience may change as ‘risk factors’ change over life
85
Describe the characteristics of a minor aphthous ulcers?
- Less than 10mm diameter- Last up to 2 weeks- ONLY affect NON-Keratinised mucosa- Heal without scarring- Usually a good response to topical steroidsThis is the commonest type of recurrent oral ulceration- One is a nuisance, many more at once can be disablingThe ULCER FREE PERIOD is a good guide to morbitity – longer ulcer free + less morbidity
86
Describe the characteristics of a major aphthous ulcers?
- Can last for months- Can affect ANY part of the oral mucosa - keratinised OR non keratinised or both- MAY scar when healing- Poorly responsive to topical steroids - intralesional steroids often more usefulUsually LARGER than 10mm - may get smaller ulcers too – diagnose from the worst ulcer
87
Describe the characteristics of a herpetiform aphthae ulcer?
- Rarest form of Aphthous ulcers- Multiple small ulcers on non-keratinized mucosa- Heal within 2 weeksCan coalesce into larger areas of ulcerationNOTHING to do with herpes viruses - in the early stages looks like primary herpetic gingivostomatitis - in HSV get KERATINISED epithelium involved – not in herpetiform aphthae
88
What cause Oral and Genital Ulceration?
Behçet’s Disease (mainly)Vesiculobullous diseasesLichen Planus
89
How to diagnose Behcet's disease?
Many who don’t meet the criteriaDiagnosis - three episodes of mouth ulcers in a year - at least two of the following: genital sores, eye inflammation, skin ulcers, pathergy
90
What is the definition of Behcet's Disease? and where can it effect?
PRIMARILY a Vasculitis – inflammation of blood vessels- Oral & genital ulceration- Eye disease - snterior or posterior uveitis – can lead to loss of vision in 20%- Bowel ulceration – iliocaecal area – pain and cramping- Heart and lungs- Brain- Joints
91
How to manage a patient with Behcet's Disease?
Treat local oral disease or RASSystemic immunomodulation where multisystem involvement: - Colchicine used ‘off label’ often a first treatment - Azathioprine/Mycophenolate - Biologics – infliximab and othersManaged with help of Rheumatology - also National specialist treatment centres
92
Name the 7 predisposing factors for Recurrent Aphthous Stomatitis (RAS)?
Viral and bacterial infectionsGenetic predispositionSystemic diseasesStressMechanical injuriesHormonal level fluctuationsMicroelement deficiences
93
What to remember for Aphthous ulcers?
Damage happen before the ulcer appears - treatment is most effective in ulcer rpodrome period
94
What tests to carry out when investigating aphthous ulcers?
Blood test:- haematinic deficiencies Iron B12 or folic acid- coeliac disease - TTG (tissue transgutaminase) - if TTg +ve anti-glidain and anti-endomysial absAllergy tests - contact or immediate hypersensitivty- food additives E210-E219- benzoate- sorbate- cinnamon- chocolate
95
Explain the treatment of a recurrent Aphthae?
Management:Correct blood deficiencies - ferritin (iron), folic Acid, vit B12Refer for investigation if Coeliac positive - endoscopy and jejunal biopsyAvoid dietary triggers - SLS containing toothpaste – (Sensodyne Pronamel and Kingfisher are SLS free)Dietary triggers - identified from testing - empirical dietary avoidance – use FOOD MAESTRO app to help with identifying foods
96
Explain the treatment of a recurrent Aphthae?
Management:Correct blood deficiencies - ferritin (iron), folic Acid, vit B12Refer for investigation if Coeliac positive - endoscopy and jejunal biopsyAvoid dietary triggers - SLS containing toothpaste – (Sensodyne Pronamel and Kingfisher are SLS free)Dietary triggers - identified from testing - empirical dietary avoidance – use FOOD MAESTRO app to help with identifying foods
97
What drugs can be prescribed for aphthous ulcers?
In dental practice follow SDCEP ’Drugs in Dentistry’ GuidanceNon-Steroid Topical Therapy - for inconvenient lesionsSteroid Topical Therapy - for disabling lesions
98
Why do chuildren get aphthous ulcers?
Periods of rapid growth – very few before this- 8-11 years and 13-16 years- feet usually grow first so look for ‘new shoe sign’Treatment- usually respond to 3/12 iron supplements – always check the diet for peculiaritiesNOT related to growth (present since birth) then largely a genetic component:- consider allergy testing as well as bloodsTreatment:- issues with Betnesol under age 12 - licence- issues with Betnesol if child unable to spit mouthrinse out reliably
99
When should you refer an Aphthous ulcer case?
After simple investigationsAfter topical trreatmentIf no good result has been achievedIf patient under 12 YO
100
What is the defintion of oral thrush?
Caused by candidaCan be associated with dentures causing denture stomatitis
101
What species of candida causes oral thrush?
Candida albicans
102
Name the 10 host factors that predispose you to developing oral thrush?
ImmunosuppressionEndocrine disordersNutritional deficiencyAntibioticsSteroidsFemaleExtremes of ageHospitalisationSmokingHigh carb diet
103
Name the 5 intraoral factors that predispose you to oral thrush?
Poor oral hygiene Salivary gland dysfunction Oral mucosal damageDental prosthesisChanges to commensal flora
104
Name the topical and systemic treatment of oral thrush?
Topical:- nystatin - miconazoleSystemic:- fluconazole- targeted therapy
105
Explain how to use nystatin suspension?
1ml QDSKeep in mouth for as long as possibleContinue for 48 hours after resolvedLow risk for inters
106
Explain how tonuse miconazole oral gel?
2.5 ml QDS - gold in mouth after foodContinue for 7 days after resolvedUse gel to brush dentures
107
What treatment is advised for angular cheilitis?
Miconazole- antifungal- bacteriostatic vs gram positive- topical- with mild steroid
108
Name the drug interactions of Miconazole?
Inhjbits the metabolism of drugs metabolised by the CYP3A4 and CYP 2C9 enzyme systemsCYP3A4:- statins - Ca ch blocker- tacrolimus- carbamazepine- midazolam CYP2C9- warfarin- sulphonylureas - phenytoin
109
Name the contraindications of miconazole?
Liver dysfunctionCoadministration with drugs that are metabolised by CYP3A4Substrates known to prolong QT interval - astemizole, cisapride, dofetilide, mizolastine, pimozide, quinidine, sertindole and terfenadineErgot alkaloidsHMG-CoA reductase inhibitors - simvastatinTriazolam and oral midazolam
110
Explain how to take fluconazole?
50-200mg capsules50-5ml oral suspensionIV avaliable 50mg once a day for 7-14 days100mg if immunocompromised
111
Name the 6 contraindications of fluconazole?
Mod inhib of P3A4 and 2C9Strong inhib of 2C19AlfentanilAmitriptylineBenzodiazepinesCitalopramClopidogrelWarfarin
112
How importance is drug resistance to antifungal?
A growing problemsMost common in azoles
113
Explain a dentists role in antimicrobial stewardship?
Don't start antibiotics without bacterial infectionUse local guidelinesDocument everything such as indication, duration, dose and routeReview clinical diagnosis and the need for the pt to continue the dose 48 hours after symptoms go
114
Name 7 types of oral symptoms?
Dry mouthOral discomfortTaste disturbanceDifficulty chewingDifficulty swallowingDifficuly speakingHalitosis
115
Advice for toothbrushing?
At least twice a daySmall headed brushMedium texture filamentSoft brush if very soreToothpaste between 1350-1550 ppm FlWater if toothpaste is unworkable
116
How can a nurse care for a patients teeth if they can't?
Twice daily brushingGloves with toothpaste Small circular motionsStart on outer surfaces then move to inner surfacesSpit out toothpaste after brushingAvoid rinsing
117
How can a nurse care for a patients denture?
Cleanse denture after mealsCleaned and removed overnight Ensure denture fits wellAdhesive if necessary
118
How can a nurse care for a patients soft tissue?
Glove and run finger over tissuesRenew gause on cleansingCan use cleaning stock if gause not goodRecord mouth condition
119
How can a nurse care for a patients lips?
Moisten with waterApply saliva replacementOr apply aqueous cream BP
120
What to implement for a dry or coated mouth patient?
At least 4 x a dayReview medicinesGently remove coating, debris and plaque Maintain hydrationStimulate saliva
121
Which 5drug types cause dry mouth?
OpoidsAnticholinergics AntidepressantsDiureticsOxygen
122
Explain how to manage dry mouth?
Treat underlying causeReview medicationGood oral hygieneDietary adviceRegular dental checksRegular sips of waterLubricate cracked lipsSaliva substitutesSaliva stimulants
123
What does saliva consist of?
6.8-7.4 pHWaterMucin-principal active componentElectrolytesEnzymesProteins
124
Name saliva stimulants?
Sugar free chewing gum or sweetsFrozen fruit juices or lolliesOrganic acids such as salivix pastilles
125
Describe and name artificial replacement saliva?
Mucon or carboxymethylcellulose based Short duration of actionAvoid acidic products - glandosaneNeutral pH- AS saliva Orthana- Biothene Oralbalance gel- BioXtra gel- Saliveze
126
Which saliva replacements can a dentist prescribed on the NHS?
GlandosaneSalivezeSalivix pastillesSalivox Plus pastilles
127
At what age does lichen planus usually affect?
30-50 years old
128
What percentage of skin and oral cases are there.
50% oral lesions10-30% skin lesions
129
Name the 3 different types of Lichen Planus
ReticularErosive/atrophicUlcerative
130
What is the histopathological findings of lichenoid reaction?
Chronic inflammatory cell infiltrate Saw tooth rete ridgesBadal cell damagePatchy acanthosis Parakeratosis
131
What is the histopathological findings of licehn planus?
OrthokerstosisWedge shaped hypergrabulosisDermal epidermal Junction obscured lymphocytesVacuoles at basal laterLuck band of lymphocytes under epidermisCivatte bodies - dead keratinocytes
132
What does the histopathological findings tell us?
Lymphocyte activationOverreaction to normal triggerVirus umplicated in immune upregulation but NOT as a cause of LP - hep C or herpesSometimes has external triggers - medicines or amalgam
133
What are the 8 aetiologices of lichen planus
AutoimmuneViralGenetic predispositionPhysical and emotional stressTrauma - scraped or after surgery an isomorphic response (koebnerisation)Localised skin disease - herpes zoster - isotopic responseContact allergy - amalgamDrugs - gold, quinine, beta blockers and ACE inhibitors
134
What are the symptoms of lichen planus?
Often noneMay relate to thinning of epithelium - sensitive to hot and spicy food- burning sensation in the mucosa
135
What other body parts can LP affect?
SkinScalpGenitalsHairNails
136
What are the 5 main sites for oral LP?
Biccal mucosaGingiva - desquamative gingivitisTongue- lateral or dorsumLipsPalate
137
Describe buccal lichen planus?
CommonestCan be found anywhere - ant at commisure- mid- post around 3rd molarMainly an incidental findingEasy to biopsy
138
Describe gingival lichen planus?
Found in isolationTermed desquamative gingivitis- similar to gingival pemphigoid and to plasma cell gingivitis - clear histologicalVery erythematous appearance to the gingivaPatchyReticular pattern more commonOral hygiene is essential to settle the lesion - plaque driven- especially interdentally Biopsy can be difficult - risk of damage to attachment area- adherent attached mucosa damaged lifting from bone
139
Describe tongue lichen planus?
Dorsum usually idiopathic- loss of papillary becoming smoothLateral may be drug/amalgam trigger- amalgam most likely in isolated lesion- look at tongue rest position - contact amalgam?Easy biopsy but painful
140
Describe lip lichen planus?
On the lipBiopsy hard?Looks soreErythema
141
What is it called if the cause is known for oral lesion?
Lichenoid reaction to...
142
Medications which can cause LP?
ACE inhibBeta blockersDiuretics - bendroflu and frusemideNSAIDs DMARDsRare - phenothiazines
143
Name 3 types of DMARDs?
PenicillamineGoldSulphasalazine
144
What are the discriminative characteristics of a lichenoid drug reaction?
Widespread lesionBilateral and mirrorsPoorly response to standard steroid treatment
145
How to manage lichenoid drug reactions?
Benefit of the drug vs the risk of stopping the drugHow bad is the discomfort from the symptoms If significant symptoms - may need to find alternative medicationDiscuss with GP
146
What is the defintion of amalgam contact sensitivity LP?
Is it the amalgam, Mercury or something else as the triggerPatch test to the allergen
147
How to manage an amalgam related lichen planus lesion?
If asymptomatic do nothing Any replacement will lose tooth tissue
148
Which materials to replace amalgam with?
CompositeGlassGold - low palladium alloyBonded crown
149
Srmamentarium for amalgam removal?
DamHigh vol suctionPPIAvoid during preg
150
Explain the overall lichen planus management for the patient?
Remove any cause- medicines- dental restorationsBiospy- unless a good reason not toBlood test- haematinics- fbc- if lulus suspected autoantibody screen for ANA, Ro and dsDNA
151
What treatment would be recommended for mild intermittent lichen planus lessons?
Topical OTC remedies- chlorhexidine - benzdamineAvoid SLS containing toothpaste
152
What treatment would be recommended for a persisting synthetic lichen planus lesion?
Topical steroids- beclomethasone inhaler - betamethasone rinse Higher strength steroid- skin steroid cream - ClobetasolTopical tacrolimus mwHydroxycholorquineSystemtic immumodilators - azathioprine and mycophenolate
153
What are the histological findings of lupus erythematosis?
Basal vacuolar damageAtrophic epitheliumMelanophageIntense lymphocytic infiltrate
154
Describe lichen like lesions?
Underlying disease needs considerationGVHD common after stem cell transplantLupus lesion can be- only in mouth - discoid lupus no auto abs- mouth and elsewhere (systemic ANA/Ro/dsDNAIf oral symptoms only treat like lichen llanjs
155
Name 5 vesiculobulloua conditions?
Erythema multiformPemphigusPemphigoidAngina Bullish HaemorrhagiaBullous lichen planus
156
What is the defintion of Pemphigoid?
A subepithelial antibody attackThick walled blisters- persist to be seen- clear or blood filled
157
Name 3 different forms and presentations of Pemphigoid?
Bullous pemphigoid - skinMucous membrane pemphigoid - all mucous membranes Cicatritial pemphigoid - mucosal with scarring
158
Describe the histopathogy of pemphigoid?
Sub epithelial split - epithelial/CT tissue junctionHemi-desmosomes involved at basement membrane
159
Describe how Pemphigoid is seen with immunofluorescence?
Linear staining along the basement membrane C3 and IgG detected in this area in 'standard' pemphigoid IgA occasionally found - linear staining with C3 is 'Linear IgA disease'- granular IgA and C3 deposits is seen in 'dermatitis herpetiformis'
160
What is a symblepharon?
Pemphigoid that is present on the eye
161
Non-oral locations of Pemphigoid?
Oral and skin lesions- bullous on skin- mucous mem usually mouth, eye or genitals (needs specialist)Scarring is a feature in some cases - cicatritial pemphigoid
162
How to manage Pemphigoid?
SteroidsImmune modulating drugs- azathioprine- mycophenolate
163
What is the defintion of Pemphigus?
Commonest form is vulgarisIntraepithelial bullaeClinically:- more common in females and over 50s- genetic with ashkenazi JewsSites:- skin- mucosaThey blister, then burst and then it spreads
164
Describe Pemphigus histopathologically?
Supra-basal split with tzank cells
165
Describe Pemphigus using immunofluorescence?
Very greenBasket weave pattern - around each epithelial cellC3 and IgG in Pemphigus vulgaris
166
How to treat Pemphigus?
It affects the mucosa and skin Rarely see intact bullae- intra epithelial blistersCan be fatal without disease- complications of treatment are major cause of death
167
Explain 2 different types of immune mediated disease?
HypersensitivityImmunogenic
168
How many types of hypersentivitiy?
5
169
Name the 2 types of immunogenic immune mediated disease?
Cell mediatedAntibody mediated
170
Name 3 types of local immunological oral disease?
Aphthous ulcersLichen planusOrofaxial granulomatosis
171
Name 6 systemic diseases with local oral effects?
Eythema multiformPemphigusPemphigoidLupusSystemic sclerosisSjogren's syndrome
172
Type 3 Hypersensitivity example?
Erythema multiform
173
Name 3 examples of cell mediated immunity?
Aphtous ulcersLichen PlanusOrofaxial Granulomatosis
174
Name 2 examples of antibody mediated immunity?
PemphigusPemphigoid
175
Immunological skin diseases?
Skin and oral.mucosa.share many antigens and epitopes - blistering skin conditions can also affect the mouth
176
Explain the mechanism of immunological skin disease?
Auto-antibody attack on skin compartments causing loss of cell to cell adhesion- causing splits in the skin- fill with inflammatory exudate- form vesicles or blisters
177
How do cells of the epidermis adhere to eachother?
Via desmosomes and hemidesmosomes 2 proteins - desmoglein (VIP) and desmocollin
178
Explain the mechanism of action for immunofluorescence?
A fluorescein molecule is attached to an engineered antibody, that when binds fluorescence and becomes active
179
Explain the difference between direct and indirect immunofluorescence?
Direct:- antibody mediated tissue disease- antibody bound to tissues - targeted in DIFIndirect:- circulating antibody not yet bound to the tissue- detected by immunofluorescence from a plasma sample- not always useful for diagnosis - often good for monitoring disease activity
180
What is the defintion of erythema multiforme?
Acute onset - more menSkin - show target lesionsMucosa - show ulcersFor young males it is recurrent within a short period
181
What is the aetiology of erythema multiforme?
Immune complex?- drugs- herpes simplex- mycoplasma
182
What specific sites do erythema multiforme target?
Lips and anterior part of the mouthHeals in 2 weeksVery painful - unable to eat or drink
183
What os erythema multiforme relation to Stevens Johnson syndrome?
Can be involved with Stevens-Johnson syndrome- sevre multisystem involvement- skin, conjunctivae, nose, pharynx, mouth and genitals
184
What is the treatment for erythema multiforme?
Oral lesions:Urgent medical therapy:- systemic steroids of up to 60mg per day- systemic aciclovirEncourage fluid - possible I Encourage analgesia If recurrent:- prophylactic acyclovir daily- allergen test for triggersMycoplasma infective agent
185
What is the defintion of angina bullous haemorrhagica?
Commonest oral blistering condition Blood blisters in mouth:- buccal mucosa and soft palate- rapid onset- 1 hr then burstPainlessIniated by minor trauma or eatingHeal with no scar within days
186
Give a brief overview of how to treat and what tests for angina bullish haemorrhagica?
Non specific ulcerationDIF and IFF negativeNo defectsChlorhex MWMay recur
187
How to manage angina bullish haemorrhagica?
No treatmentReassure patient that is benignExplain known triggers
188
Why are mucosal lesions more frequent in children?
Clinical issues traditionally related to immunologicalimmaturity
189
Name the 2 types of congenital oral mucosal lesions?
HereditaryDevelopmental defects
190
Name the 6 types of acquired oral mucosal lesions?
TraumaticDrug-relatedChronic inflammatoryHyperplasticNeoplasticInfective
191
What is the defintion of white sponge naevus?
HereditaryInherited as autosomal dominant condition . Defect in keratin gene 4 and 13.Uncommon
192
Name the clinical features of white sponge naevus?
•White, soft, irregularly thickened, nodefined borders•Bilateral•Genital tissues can also be affected•Often misdiagnosed with candidosis
193
Name the histopathology of white sponge naevus?
•Uniform acanthosis•Hyperparakeratosis• Intracellular oedema•No dysplasia, no inflammation
194
How to manage white sponge naevus?
Reassurance
195
Name 3 developmental defect oral mucosal lesions?
Fordyxe's granulesFoliate papillaeGeographic tongue
196
Describe the clinical features of fordyce's granules?
▪Ectopic sebaceous glands▪Association with hormonal changes in puberty?▪Bilateral, most commonly on buccal mucosa
197
Describe the clinical feattures of folaite papillae?
▪Pinkish soft nodules▪Bilateral, ventral tongue▪Lymphoid tissue, sometimesinflamed/hyperplastic
198
Describe the clinical features of geographic tongue?
▪Dorsum of tongue▪Irregular, smooth, red areas (depapillated)with sharply-defined edge▪Recurrent, migrates
199
Describe the histology of geographic tongue?
▪Thinning of epithelium at centre, mildhyperplasia at periphery▪Epithelium infiltrated by neutrophils
200
Explain how to manage geographic tongue?
reassurance. If symptomatic exclude heamatological deficiencies.Median rhomboid glossitis generally not seen in children
201
Name 3 traumatic oral mucosal lesions?
mucoceletraumatic ulcerfrictional keratosis
202
Describe the clinical fearues of frictional keratosis?
▪Pale and translucent or white/dense withrough surface
203
Describe the histology of frictional keratosis?
Epithelial hyperplasia, with thick granularcell layer and hyperorthokeratosis▪Scattered subepithelial lymphocytes
204
Describe the clinical features of traumatic ulcer?
Mechanical, thermal or chemical trauma▪Inflammation levels and clinical features vary▪Yellowish floor of fibrin slough often present
205
Describe the histology of traumatic ulcers?
Non-specific ulceration. See RAS▪Destruction of epithelium▪Tissue infiltration by neutrophils
206
Describe the clinical features of a mucocele?
▪Most commonly on lower labial mucosa▪Overlying mucosa is intact and healthytypically circular▪Firm or fluctuant and bluish
207
Describe the histology of a mucocele?
▪Damage to duct of salivary gland▪Mucin and macrophages surrounded bycompressed connective tissues▪No epithelial lining
208
Name a drug-induced oral mucsoal lesion?
Chemo-induced stomatitisAspirin burns
209
Name 3 types of inflammaotry oral mucosal lesions?
Orofacial granulomatosiserythema multiformerecurrent apthous stomatitis
210
Describe the clinical features for recurrent aphthous stomatitis?
▪Idiopathic, but systemic factors known to modulate the severity of disease▪Onset in childhood, but peak in adolescenceMinorMajorHerptiform
211
Describe the histology of recurrent aphthous stomatitis?
▪Initial lymphocitic infiltration?▪Destruction of epithelium▪Tissue infiltration by neutrophils▪Dilated vessels
212
Explain the management for a mucocele?
Reassurance/excision if symptomatic or interferes with oral functions
213
What should be excluded when dealing with recurrent aphthous stomatitis?
Extraoral involvement should be excluded, e.g. GI (coeliac disease, Crohn’s), genital/ocular(Behcet’s).
214
Describe the clinical features for erythema multiforme?
▪Mostly HSV-related, drug-induced▪Cutaneous erythema or “target” lesions▪Ulceration of outer lip with bleeding,crusting.▪Intraorally irregular fibrin- covered erosionand erythema▪Ddx with HSV-1 infection
215
Describe the histology of erythema multiforme?
▪Necrosis of keratonocytes▪Epithelial infiltration by inflammatory cells▪Intraepithelial or subepithelial vesiculation
216
Describe the clinical features for orofacial granulomatosis?
▪Swelling of the lips▪Mucosal nodularity (cobblestoning)▪Mucosal tags▪Gingival hyperplasia▪Aphthous oral ulcers▪Children more likely to develop Crohn’s disease
217
Describe the histology for orofacial granulomatosis?
Granulomas containingmultinucleated giant cells▪Lymphoedema
218
What are possible differential for orofacial granulomatosis?
DDx with sarcoidosis and tubercolosis. Primary TB of the oral cavity is rare,?morecommon in children than adults
219
Name 3 inflammaotry oro mucosal diseases rarely seen in children?
Oral Lichen Planus• Mucous Membrane Pemphigoid• Pemphigus vulgaris
220
Describe the clinical features for oral lichen planus?
▪White striae and/or mucosal atrophy, and/orerosions, and/or plaques▪Desquamative gingivitis in isolation or incombination with above▪Bilateral lesions
221
Describe the histology for oral lichen planus?
Basal membrane thickening Band-like lymphocitic infiltrate Colloid bodies,apoptotic basal cells
222
Describe the clinical features for mucous membrane pemphigoid?
▪Bullae, sometimes intact, can appear as bloodblisters. If ruptured raw ulcer▪Desquamative gingivitis▪Conjuctival involvement▪Cutaneous involvement less prominent thanbullous pemphigoid
223
Describe the histology for mucous membrane pemphigoid?
•Separation of full thickness of epithelium from CT•Linear deposition of IgG and C3/C4 along basalmembrane.•Auto-antibodies bind along basal membrane indirect immunofluorescence assay•CT infiltrated with inflammatory cells
224
Describe the clinical features of pemphigus?
▪Fragile vesicles/bullae▪Ruptured vesicles▪Nikolsky’s sign positive▪Widespread cutaneous involvement
225
Describe the histology for pemphigus?
•Acantholysis•Intraepithelial vesicles.•‘Chickenwire’ deposition of IgG and C3/C4within the epithelium.•Anti-desmoglein3 antibodies bindintercellular substance in directimmunofluorescence assay
226
Deswcribe the clinical features for epydermolysis bullosa?
▪Subepithelial bullae leading to severe scarring after minimal trauma.▪Type VII collagen defect.▪Autosomal recessive
227
Name 3 hyperplastic forms of oral mucosal lesions?
Vascular malformationGiant cell epulisPyognic granuloma
228
Describe the clinical features for a pyogenic granuloma?
▪Soft, red polypoidswelling▪Most commonly gingivalbut not exclusively
229
Describe the histology for a pyogenic granuloma?
•Granulation tissue•Dilated blood vessels inoedematous CT•Dense infiltration byneutrophilsNO GRANULOMAS, NOPYOGENIC BACTERIA
230
Describe the clinical features of a giant cell epulis?
▪Soft, violaceus swelling▪Central gingival segmentsRelated to resorption of deciduous teeth?
231
Describe the histology for giant cell epulis?
•Subepithelial clusters of giant cells in fibro-vascular tissue
232
What to exclude when dealing with a giant cell epulis?
Need to exclude central GCG andunderlying hyperparathyroidism
233
Describe the clinical features of vascular malformation?
Purple nodular lesion▪Blanches upon pressure
234
Describe the histology for a vascular malformation?
•Capillary: small vessels and vasoformative tissue•Cavernous: large blood filled sinusoids
235
Name 2 pigmentary chnages ivolved with oral mucosal lesions?
Puetz-Jeghers syndromeAddison's Disease
236
Name the clinical features of Peutz-Jegher's syndrome?
Clinical features▪Intestinal polyposis▪Mucocutaneous pigmented lesionsappearing during childhood
237
Describe the histology for Addison's disease?
•Mild acanthosis•Melanin in basal layer
238
Describe the clinical features for warts?
HPV 2, 4•White or pinkish, raised•Sessile or pedunculated•Often multiple•Mainly secondary to self inoculation
239
Describe the histopathology of warts?
•Papillary processes of hyperplastic epithelium with acanthosis, hyperkeratosis,hyperplastic basal cell layer•Connective tissue core•Koilocytes often present
240
Describe the clinical features for pseudomembranous candidosis?
•Acute•Thick white pseudomembranes of various sizes•Erythematous background•Often idespread
241
Diseases that cause immunocompromisation and lead to oral mucosal lesions?
HIV/AIDS
242
How are viruses transmitted?
Exchange of blood productsSexual transmissionPerinatal infection
243
MoA of HIV?
Retrovirus - group VI (baltimore)Infects activated T cells and macrophages vis the envelope glycoproteinTransferred by dendritic cells via DC-SIGN, then migrate to lymph nodes to transfer the CD4 T cells
244
How does HIV infect T cells?
HIV gp120 binds T cells through CCR5/CXCR4 and CD4
245
How does HIV infect macrophages?
HIV gp120 binds macrophages through CCR5 and CD4
246
What infections are diagnostic for acute HIV infection?
PyrexiaSkin rashHaedacheDiarrhoea OropharyngitisOral mucosal erythema
247
What infections are diagnostic fir ARC asymptomatic seropostive HIV?
LymphoadenopathyPersistent pyrexiaDiahorreaWeight losFatigue and malaise
248
What infections are diagnostic for AIDS?
Kaposi's sarcomaNH lymphomaThrombocytopeniaNeurologival diseases
249
What drug is Pre-exposure prophylaxis of HIV?
Trivada - emtricitabine
250
When will HIV/AIDS related oral lesions occur?
May occur during mild immunodeficiency and prior to severe opportunistic infectionsEvidence suggests that patient s with oral.lesikns may progress to AIDS more rapidly compared to patients without
251
Why can oral lesions occur?
Immunodeficiency
252
Name 5 oral mucosal lesions strongly associated with HIV?
Candidiasis: - erythematous, pseudo and angular cheilitisHairy leukoplakiaKaposi sarcomaNH lymphomaPerio disease: linear gingival erythema, necrotising gingivitis and periodontitis - more commonly seen due to immunosuppressant therapy
253
Describe candidiasis in HIV patients?
Mild immunodeficiency If psuedomem, indicative of acture immunosuppression - widespread oropharyn and oesoph Can persist for monthErythamtousHyperplastic
254
Describe linear gingival erythema in HIV patients?
Red band involving the free gingival margin - not plaque induced - hypermedia due to vasoactive cytokines
255
Describe hairy leukoplakia in HIV?
Not pre malignant White patches that can't be removed Lateral border of the tongueVertical white folds with hair like surfaceSmooth
256
Describe the histopathology of hairy leukoplakia?
Acabthotic parakerarinsed epithelium Finger like keratin projections on the surfaceBand of ballon cells in prickle cell layerSecondary candidal infections Swollen cells are EBV+ (koliocytes), EBV demonstration essential for diagnosis
257
Describe Kaposi sarcoma in HIV patients?
Most commonly associated with HIVHHV8Involves skin and mucosal surfacesRed purple patch - becomes nodular
258
Describe the histopathology of Kaposi sarcoma?
Early lesions consit of proliferating endothelial cells, extravasated blood cells, haemosiderin and inflamm cellsLate lesions have a more predominant vascular component and atypical spindle cells
259
Describe non-hodgkins lymphoma in HIV patients?
AIDA and severely immunocompromised patientsAssociated with EBV
260
Name 4 less commonly oral mucosal lesions with HIV?
Bacterial infectionsSalivary glabd diseaseOral ulceration Viral infections
261
Describe HSV and VZV infections in HIV?
More severe and higher recurrence
262
Describe the HPV infection in HIV patients?
6,11 and 16Venereal warTransmitted via oro genital contact Multiple white/pink nodulesFuse forming sessile or pedunculated papillary lesions
263
Describe the histopathology of HPV in HIV patients?
Induce hyperplastic changes rather than ballooning degenerationFibrovascular core covered by stratified squamous epithelium with- hyperpladtiv basal cell layer - acanthosis- parakeratosisKoilocytes
264
Describe atylical ulceration in HIV patients?
Oropharyns most commonly affectedAssociated with CMV infection- can also be aphthous stomatitis
265
Describe salivary gland disease in HIV patients?
Salivary gland enlargement - mainly parotidXerostomuaLymphocyte infiltration Lympho-epothelial cystsEnlargement of intraparotid nodes as part of P
266
How is Oral cancer classified?
International Classification of Disease for Oncology- ICD-O
267
What makes classification of cancer difficult?
Makes comparison difficult Makes epidemiology difficultMakes treatment planning difficult
268
Name the 2 distinct disease patterns for oral cancer?
Oral Cavity Cancer (OCC) Oro-Pharyngeal Cancer (OPC)
269
Describe the epidemiology of OCC?
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
270
Name the 6 common sites for mouth cancer?
Floor of the mouthLateral border of the tongueRetromolar regionsSoft and hard palateGingivaeBuccal mucosa
271
Name the 3 higher sites for SSC in drinkers and smokers?
FoMLat. border of the tongueSoft palate
272
Name the 8 sites of oral cancer?
LipsPalateTonsilsFoMOther throatTongueOropharynxGums
273
Describe the epidemiology for OPC?
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
274
Name the 5 main risk factors and their associations to Oral Cancer? - how much does each RF multiply the risk of OC?
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
275
Name the 3 risk factors that have not been confirmed as certain to increase the overall risk of Oral cancer?
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)
276
What are the benefits of reducing smoking and alcohol intake?
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.
277
What are the benefits of improving SE status?
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
278
What are the benefits of reducing poor diet choices?
- 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)
279
Name 4 potentially malignant lesions?
White lesions (leukoplakia)Red lesions (erythroplakia)Lichen planus- Candidal Leukoplakia- Chronic Hyperplastic CandidiasisOral Submucous Fibrosis
280
Describe the epidemiology of white lesions in OC?
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
281
Name 3 types of descriptions of white lesions?
HomogenousErosiveNon-homogenous on atrophic background
282
How does erythroplakia compare to leukoplakia?
much less frequent than leukoplakiamuch higher risk of cancergreater dysplasia risk- Up to 50% already be carcinomano good follow-up studies available
283
What are the common characteristics of dysplasia and the new categorisation of severity?
Based on:- Cellular Atypia- Epithelial Architectural OrganisationNew categorisation- Low grade- high grade- carcinoma-in-situ
284
Describe the histological low grade of oral mucosal dysplasia?
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)
285
Describe the histological high grade of oral mucosal dysplasia?
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
286
Describe the histological carcinoma in situ of oral mucosal dysplasia?
Theoretical conceptCytologically malignant but not invadingAbnormal architecture- Full thickness (or almost full)- Severe cytological atypiaMitotic abnormalities frequent
287
Name the histoloigcal prognostic facors which give information on survivability?
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
288
Describe the Field Cancerisation concept?
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
289
Name the multiple variables for clinical cancer staging of OC?
site size (T)spread (N&M)
290
Describe the different varying change of cancer prognosis/survivability?
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
291
Describe the aetiology, behaviour and prognosis of Lip cancer?
Lower lip- non-healing ulcer or swellingAetiology- Sunlight UV-B- smokingBehaviour - slow growth - local invasion- rarely metastasise to nodesGood prognosis as early detection
292
How is OC detected?
Difficult to do – a judgement from experience- Use the 'Oral Cancer Recognition Toolkit’ - Developed jointly by Cancer Research UK and the British Dental Association
293
What are the advantages and disadvantages of OC screening?
Benefits vs HarmUndetected lesions vs False positiveCost of Screening vs Cost of diseaseCost of Screening vs Disability from disease
294
Name the 5 OC screening tools?
HPV16 screeningToluidene blueVELscopePhotodynamic Diagnosis (PDD)Clinical judgement of experienced clinician
295
Describe what and how toluidine blue is and used?
false positive in inflammatory lesions ? 50 % false negatives good for invasive disease, but usually clinically evident
296
Describe what and how VELscope is and used?
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
297
Explain the duty of Primary care dentistry in OC screening/detection?
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
298
What is the definition of precancerous lesion?
An altered tissue in which cancer is more likely to form
299
What is the defintiion of precancerous condition?
A generalised state associated with an increased cancer risk
300
Name the 4 types that can't be conisdered leukoplakia?
Tobacco related lesions Smokers keratosis Chronic hyperplastic candidosis Frictional keratosis
301
What is the definition of leukoplakia?
It is a clinical diagnosisIt has NO histological connotationEpithelial dysplasia may or may not be presentNon-homogeneous types are more likely to be dysplastic
302
Describe the epidemiology of leukoplakia?
- 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
303
Name the clinical predictors of malignancy?
Clinical appearance - very variableNon-homogeneousVerrucous, speckled, Ulcerated, leuko-erythroplakia
304
Describe the molecular progression of oral cancer?
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
305
What is the definition of hyperplasia?
Increased cell numbersArchitecture regular stratification altered compartment sizeNO cellular atypia
306
What is the definition of hyperplasia?
Increased cell numbersArchitecture regular stratification altered compartment sizeNO cellular atypia
307
What is the definition of hyperplasia of stratum spinosum (acanthosis)
Architecture -increased maturationcompartment
308
What is the definition of basal cell hyperplasia?
increased basal cells
309
What is the definition of low grade (mild hyperplasia)
Architecture -change in lower thirdMild -cytological atypia
310
What is the definition of high grade (mod/severe dysplasia)
Architecture -change into middle/upper third Marked cytological atypiaPossibility of numerous abnormal mitoses
311
What is the definition of oral candidosis?
Opportunistic fungal infection of the oral cavity.- Oral rarely in itself painful- Oesophageal may be in HIV
312
How do people aquire candida?
Majority of normal population are healthy carriersMost common isolate is C. albicans
313
Name 5 candidal virulence factors?
AdherenceSwitching mechanismsGerm tube formationExtracellular enzymesAcidic metabolites
314
Name the local predisposing factors for candidal infections?
SmokingDenturesLocal corticosteroidsXerostomiaTopical antimicrobials
315
Name the general predisposing factors for candidal infections?
Extremes of ageEndocrine disease- DiabetesImmunodeficiency- Steroid use, HIVNutritional deficiency- ironAntibiotics
316
Name the classification of oral candidosis?
Acute Pseudomembranous- Sudden local/systemic immunosuppressionChronic Erythematous- Longstanding & persisting issue- e.g. below poor fitting dentures, HIV, median rhomboid glossitis and antibioticChronic Hyperplastic
317
How to diagnose oral candidosis?
Laboratory tests- Differentiate from commensal- Only by QUANTIFIABLE assay- Culture and sensitivity to inform treatment- Multiple sites usually- Smear/microscopy occasionally
318
How to diagnose candidosis via lab?
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”
319
How to identify candidaosis in the lab?
Direct microscopyGerm Tube testPhysiological tests- Carbohydrate fermentation- Carbohydrate and nitrogen assimilationCommercial systems- API 20C systems
320
How to identify candidaosis in the lab?
Direct microscopyGerm Tube testPhysiological tests- Carbohydrate fermentation- Carbohydrate and nitrogen assimilationCommercial systems- API 20C systemsBiopsy- Essential for diagnosis of hyperplastic candidosis.- PAS stainDirect smear
321
Name the 5 candida species?
C. albicansC. glabrataC. tropicalisC. kruseiC. dubliniensis
322
Describe the principles of management for candidal infection?
Correction of predisposing factors OH, diet, trauma, steroid inhaler hygieneIdentify underlying illnessesAntifungal agentCo-infection with other microorganisms?
323
Name different categories of antifingal drugs?
Polyenes- Nystatin- AmphotericinImidazole- Miconazole- ClotrimazoleTriazoles- Fluconazole - Itraconazole
324
Explain the treatment regimes for oral candidosis?
Topical Therapy (lengthy courses required) - Nystatin (pastille, suspension, cream and ointment)- Amphotericin (not available in the UK)- MiconazoleSystemic treatment (often preferred)- Fluconazole- Itraconazole
325
What is the definition of miconazole?
- 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
326
Name the types of systemic antifungals and their treatment regimes?
Fluconazole - 50mg capsules taken once daily- 14 day courseItraconazole- 100mg capsule - 14 day course- 100mg twice in once daily for Pseudomembranous candidiasis
327
Name 3 antifungals that have resistance?
C. glabrataC. kruseiiC. dubliniensis
328
Name the disease that come from Human herpesvirus/
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
329
Explain the virion replication cycle?
Virus attachment and entryUncoating of virionMigration of acid to nucleusTranscriptionGenome replicationTranslation of virus mRNAsVirion assemblyRelease of new virus particles
330
Effect of viral infections on host cells?
Cell death (cytopathic effect)Latent infectionHyperplasia Transformation
331
Explain the lifecycle of HSV, VZV associated leison?
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
332
Explain how to diagnose human herpesvirus?
Laboratory investigations available:- Antigen-specific IgG or IgM serum titres- PCR- Immunofluorescence, immunocytochemistry on affected tissue- Virus isolation from lesion and cultivation
333
Describe the apperance of primary herpetic stomatosis?
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
334
Describe the apperance of chickenpox and recurrent zoster infection
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)
335
Describe the managment for HSV-1 and VZV mild infections?
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
336
Describe the managment for HSV-1 and VZV severe and immunocompromised infections?
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
337
Describe the apperance of infectious mononucleosis?
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
338
Describe the apperance of CMV?
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.
339
Describe the apperance of hand-foot and mouth disease?
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)
340
Describe the apperance of herpangina?
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)
341
Describe the apperance of measles?
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.
342
Describe the apperance of warts?
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
343
Describe the apperance of squamous papilloma?
More common in individuals >20 of ageExophitic, peduncolatedDistinctive branched structure, finger-like processes, white or pinkishUp to 20 mm in diameter
344
Describe the apperance of condyloma acuminatum?
HPV 6, 11, 16:Venereal wartHIV infection manifestationTransmitted via oro-genital contactMultiple white/pink nodules.Fuse forming sessile or pedunculated papillary lesion.
345
Describe the management of oral mucosal HPV-related lesions?
Diagnosis- Clinical- Biopsy (excisional if possible)Treatment- Reassurance and monitoring- Cryotherapy- Surgical excision
346
Describe the histopathology of oral mucosal HPV-related lesions?
HPVs induce hyperplastic changes rather than “ballooning degeneration”Fibro-vascular core covered by stratified squamous epithelium with - hyperplastic basal cell layer- acanthosis - hyperortho/parakeratosisKoilocytes
347
Name the 2 categories for diagnosis of infections? And their options?
Clinical features- history- examLaboratory tests- microscopy- culture- mass spec- nucleic acid amp- immuno tests
348
Describe what sampling and testing involves?
Culture and sensitivity:- swab - mouth and related sitesWhole salivaAspirateSmearBiopsyBlood
349
How to decide if infection need treatment?
Active symptoms:- directly related to the infectious agentConsequences of infection:- local- systemic
350
How to decide appropriate treatment for infection?
Culture and sensitivity test - always preferredBest guessExperienceSide effect profile Cost
351
What is the defintion of staphylococcal infection
Uncommon as an acute problem- immunocompromised Very common as chronic mixed infection (related angular cheilitis)Topical treatment sufficient If systemic indicated- consider narrow spectrum
352
What is the defintion of scarlet fever?
Exotoxin mediated mucocutaneous manifestations
353
Name the 4 clinical features of scarlet fever?
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
354
What are the clinical features of tuberculosis?
Chronic, painless and irregular ulcer Covered by yellowish exudateSurrounding tissue indurated with inflammLocalisation- tongue, palate gingivae, and lipsAssoc subman and services lymphoadenopathy
355
What isnthe histopathology of tuberculosis ?
Granukomas containing muktinuc giant cells- mycobacteria not always identifiable
356
What are the oral manifestations of syphilis?
Primary - chancre Secondary - mucosal patches and blisters LatentTertiary - gumma, CV and CNS complications
357
What is the defintion of gonorrhea?
Second most common STIOral lesions result of progenitor contactNon-specific oral presentation:- multiple ulcers- erythema- white pseudomembranes- painful pharyngitis- lymphoadeno
358
What are the clinical features of actinomycosis?
Cerviofacial most common form Painful and slow growing hard swelling Absfesses and draining sinusesDischarge yellow purulent material
359
What are the histopathologucal features of actinomycosis?
Colony of actinomyces in centreDense collection of inflamm cellsSurround by wall of fibrous tissue
360
What is the definition of sicca syndrome?
Partial Sjögrens findings
361
What is the definition of primary and secondary sjogrens syndrome?
Primary- no connective tissue diseaseSecondary- connective tissue disease- SLE, Rheumatoid Arthritis, Scleroderma
362
Describe the background of Sjogrens Syndrome - spread? gender? systemic? genetic? environemnt?
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
363
Name the 4 consequences of Sjogrens Syndrome?
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
364
Describe how to diagnose Sjogrens Syndrome?
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)
365
Describe the diagnosis crietria for AECG of Sjogrens syndrome?
Dry eyes/mouth- Subjective or objectiveAutoantibody findingsImaging findingsRadio nucleotide assessmentHistopathology findingsFOUR or more positive criteria for diagnosis
366
Describe the diagnosis crietria for ACR-EULAR of Sjogrens syndrome?
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
367
Describe the oral and eye symptoms necessary to aid diagnosis?
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
368
Name the 2 eye tests for Sjogrens Syndrome?
Abnormal Schirmer test<5mm wetting in 5 minutesFluorescein Tear film assessment
369
Name the oral test for Sjoregns Syndrome?
Abnormal UNSTIMULATED whole salivary flow (UWS)<1.5ml in 15 mins
370
Explain to autoimmunity involved with Sjogrens Syndrome?
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
371
Explain the typical findings in a positive labial gland biospy for Sjogrens Syndrome - AECG?
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
372
Describe the procedure in which to start to process of Sjogrens Syndrome, if suspicious?
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
373
Describe the management for a patient suffering with Sjogrens Syndrome?
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
374
Name the 3 categories of complications for patient living with Sjogrens Syndrome?
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
375
Examination of the salivary gland locations?
Extra oral examination- Major salivary glandsIntraoral examination- Minor salivary glands- Duct orifices- Fluid expression
376
What is the function of saliva?
Acid bufferingMucosal lubrication- Speech- SwallowingTaste facilitationAntibacterial
377
Name the 5 main causes of a dry mouth?
Salivary Gland diseaseDrugs Medical Conditions & DehydrationRadiotherapy & cancer treatmentsAnxiety & Somatisation Disorders
378
How does salivary gland changes with age between 17-90yrs old?
Acinar tissue loss37% Submandibular32% Parotid45% Minor glands
379
Describe in/direct effect on salivation?
Indirect effect- External to the glandDirect Effect- Problems within the gland itself
380
Name 6 drugs that cause indirect salivary problems?
Anti-muscarinic cholinergic drugs - Tricyclic antidepressant- Antipsychotics- Antihistamine- Atropine- Diuretics- Cytotoxics
381
Name the 3 largest influencing drugs on dry mouth?
Antimuscarinic- Amitriptyline 26% reductionDiuretics- Bendrofluazide 10% reductionLithium- 70% have a significant reduction- Increased caries correlates with drug use
382
Name other medical conditons that can have an indirect effect on salivation? - acute and chronic?
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
383
Name 5 direct salivary gland problems?
Aplasia - Ectodermal dysplasiaSarcoidosisHIV diseaseGland infiltration- Amyloidosis- HaemochromatosisCystic Fibrosis
384
What is the defintion of ectodermal dysplasia?
Hair, Nails, Teeth, Salivary & Sweat glands- Hearing and vision may be affectedMay be limited in effect- Salivary aplasia aloneHypohidrotic – x-linked
385
Haemachromatosis?
HFE gene mutation - 1:10 pop carry
386
Describe radiotherapy effect on salivation?
Radiation effectsGraft versus host effectsAntineoplastic drugsRadioiodine
387
What blood tests and other tests can be used to investiagte salivary disease?
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
388
Describe how anxiety and somatisation disorders can cause dry mouth?
‘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’!
389
Name 6 forms of somatoform disease that cause dry mouth?
Oral DysaesthesiaTMD painHeadacheneck/back painDyspepsiaIrritable Bowel Syndrome (IBS)
390
Name 5 treatbale causes of dry mouth?
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
391
Name th 3 treatment options for symptomatic dry mouth?
Sjögren’s SyndromeDry mouth from cancer treatmentDry mouth from salivary gland diseaseTreatment options for these cases- INTENSIVE DENTAL PREVENTION- Salivary substitutes- Salivary stimulants
392
Name the 5 categroeis of dry mouth investigations?
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
393
Describe the dental management of dry mouth?
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
394
Name 6 forms of saliva substitiues and their form?
Sprays- Glandosane- Saliva OrthanaLozenges- Saliva Orthana- SSTSalivary stimulants- Pilocarpine (Salagen)Oral Care Systems- Oral BalanceFrequent sips of water
395
Name the causes of hypersalivation? - True and percieved?
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
396
Describe the dental management of excess salivation?
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
397
Name the 3 forms of causes for changes in gland size?
Viral Inflammation - Mumps- HIVSecretion retention- Mucocele- Duct obstructionGland Hyperplasia- Sialosis- Sjögrens Syndrome
398
Name the 7 symptoms of mumps?
HeadacheJoint painNauseaDry mouthMild abdominal painFeeling tiredloss of appetitePyrexia of 38C, or aboveParamyxovirusDroplet spreadIncubation 2-3 weeks1/3 have no symptomsSymptomatic treatment only
399
What is the defintiion of HIV sailvary disease?
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
400
What is the definition of a mucocele?
Secretion retention- In the duct- Extravasated into the tissuesRECURRENT swelling – bursts in days- ‘salty taste’Common Sites Junction Hard/Soft Palate Lower lip
401
What is the definition of subacute obstruction?
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
402
Name the 3 main causes of subacute obstruction?
Sialolith (stones)‘mucous’ pluggingDuctal damage from chronic infection (scarring)(Salivary stones, Duct stricture, Duct dilation, chronic non-specific sialadenitis)
403
Name the 5 investigations for subacute obstruction?
Low dose plain radiography lower true occlusalSIALOGRAPHY – when infection freeIsotope scan if gland function uncertainUltrasound assessment of duct system
404
What is the definition of duct dilation?
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
405
Describe the management of subacute obstruction?
Surgical sialolith removal if practicalSialography for ‘no stone’ cases – washing effectConsider gland removal if fixed swelling
406
Describe the outcome for subacute obstruction?
Reformation of stone/obstructionDeformity of duct – stasis & infectionGland damage – low salivary flow, ascending infection
407
What is the definition of silalosis?
Increase in Gland Tissue (Hyperplasia)- Sialosis- Sjögrens Syndrome Major gland enlargementNo identified cause - Alcohol abuse- Cirrhosis- Diabetes Mellitus- Drugs
408
What investigations can be carried out to diagnose Sialosis?
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
409
What investigations can be carried out to diagnose Sialosis?
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
410
Name 2 types of dental manifestations of systemic disease?
Disruption to the tooth structure formationDisruption to the tooth structure content
411
Name 3 forms of systemic diseases that exhibit dental mnifestations in children?
Congenital conditions/infections- Syphilis,TORCH- Ectodermal Dysplasia- perinatal illnessIllness/metabolic disorder- Severe childhood illness - Porphria- Cancer treatmentsPigmentation from substances in the blood- Bilirubin, tetracycline
412
Name 6 oral mucosal effects from systemic disease?
Giant Cell GranulomaOrofacial GranulomatosisRecurrent Aphthous StomatitisDermatosesImmune Deficiency/Disease - Raised ACTH Addison'sDrug reactions
413
What is the definition of a ginat cell lesion, in relation to oral medicine?
Peripheral’ and ‘Central’ lesionsCheck Parathyroid function – could be as a result of excess parathyroid stimulation of osteoclasts- renal failure- hypocalcaemia- parathyroid tumour
414
What is the definition of hyperparathyroidism's effect on the bones?
Causes thinking and finger-like projections of the bone
415
Name 4 systemic illness that cause immunodeficiency throughout life, which show oral manifestations?
Orofacial GranuolomatosisSjogrens Autoimmune – AddisonsInfections – fungal/viral
416
Name 2 forms of skin immune disease that show oral manifestations?
Lichen planus, VB disease
417
What is the definition of immune disease orofacial granulomatosis?
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
418
What is included for Crohn's screening?
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
419
Describe the management of orofacial granulamtosis?
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?
420
Name 4 forms of automimmune CT diseases, that show oral manifestations?
Systemic lupus erythematosis (SLE) - erytheamic gingiva and palateSystemic sclerosis (Scleroderma)Sjogrens syndromeMixed connective tissue disease (MCTD)
421
Name 3 forms of vasculitic CT diseases, that show oral manifestations?
Large vessel Disease- Giant cell (temporal) arteritisMedium Vessel Disease- Polyarteritis nodosa- Kawasaki diseaseSmall vessel Disease- Wegener’s Granulomatosis
422
Name 4 forms of acquired immune deficiency?
DiabetesDrug therapyCancer therapyHIV
423
What is the definition of haematinic deficieinces - causes?
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
424
What is the definition of the Parotid gland?
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)
425
WHat is the definition of the submandibular gland?
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)
426
What is the definition of the sublingual gland?
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
427
Name the 2 categories and 5 types of cells?
Acini: - serous cells- mucous cells- mixedDucts- Luminal cells: cuboidal/columnar/squamous epithelium- Abluminal cells: myoepithelium and basal cells
428
What is the definition of neoplasia?
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
429
Describe the epidemiology of salivary gland neoplasms?
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
430
Name the 5 aetiologies of salivary gland neoplasms?
Radiation: nuclear bomb survivors, therapeutic radiation, dental x-rays, ?mobile phonesTobacco smoking: Warthin’s tumourViruses: EBV & lymphoepithelial carcinomaFamilial and geneticVarious industrial occupations
431
Describe the differences between Benign and Malignant salivary gland tumours?
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)
432
Name 3 investigations for susected salivary gland tumours?
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
433
Name 5 types of benign epithelial tumoirs of the salivary gland?
Pleomorphic adenomaWarthin’s tumour Basal cell adenomaCanalicular adenomaOncocytoma
434
Name 5 types of malignant salivary gland tumours?
Mucoepidermoid carcinomaAdenoid cystic carcinomaPolymorphous adenocarcinomaCarcinoma ex pleomorphic adenomaAcinic cell carcinoma
435
What is the definition of a pleomorphic adenoma?
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.’
436
Explain the management for a pleomorphic adenoma?
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
437
What is the definition of Warthin's Tumour?
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.
438
What is the aetiology of Warthin's tumour?
Exclusively in the ParotidMale predominanceLink with smoking
439
Explain the management of Warthin's tumour?
Complete excision is curative (superficial parotidectomy)
440
What is the definition of a Oncocytoma?
Benign tumour of salivary gland origincomposed exclusively of large epithelialcells with characteristic brighteosinophilic granular cytoplasm (oncocyticcells).
441
What is the aetiology of a Oncocytoma?
Most in parotidComplete excision curative
442
What is the definition of a canalicular adenoma?
The tumour is composed of columnarepithelial cells arranged in thin, anastomosingcords often with a beaded pattern.The stroma is characteristically paucicellularand highly vascular.
443
What is the aetiology of a canalicular adenoma?
lip commonestconservatice excision curative
444
What is the definition of a basal cell adenoma?
Basal cell adenoma (BCA) is a rarebenign neoplasm characterized by thebasaloid appearance of the tumour cellsand absence of the myxochondroid stromalcomponent present in pleomorphicadenoma.
445
What is the aetiology of a basal cell adenoma?
Mostly Parotid glandComplete excision curative
446
What is the definition of mucoepidermoid carcinoma?
Mucoepidermoid carcinoma is a malignantglandular epithelial neoplasm characterizedby mucous, intermediate andepidermoid cells, with columnar, clearcell and oncocytoid features.
447
What is the aetiology of mucoepidermoid carcinoma?
most common saliary gland malignancyParotid most common, then palate, submand and other minors
448
Exlain the management of mucoepidermoid carcinoma?
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%
449
What is the definition of an adenoid cystic carcinoma?
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.
450
What is the aetiology of an adenoid cystic carcinoma?
High grade malignnacyMore in femaleMajor glandsDistant metastases
451
Explain the management of adenoid cystic carcinoma?
Surgery treatment of choiceWide resection. Extensive surgery often requiredClear margins difficult to achieve (mostly impossible)Radiotherapy with wide fieldsChemotherapy generally not effective
452
What is the definition of a polymorphous adenocarcinoma?
A malignant epithelial tumour characterizedby cytologic uniformity, morphologicdiversity, an infiltrative growth pattern,and low metastatic potential.
453
What is the aetiology of a polymorphous adenocarcinoma?
2nd most common intraoral malignant salivary glandPalate most commenMalig in minor
454
Explain the management of polymorphous adenocarcinoma?
Surgical excision with clear margins usually curativeRole of radiotherapy not certain
455
What is the definition of Carcinoma ex pleomorphic adenoma?
Carcinoma ex pleomorphic adenoma isdefined as a pleomorphic adenoma fromwhich an epithelial malignancy isderived.
456
What is the aetiology of carcinoma ex pleomorphic adenoma?
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
457
Explain the management of carcinoma ex pleomorphic adenoma?
Extensive surgery with neck dissection is treatment of choicePost operative radiotherapy
458
What is the definition of an acinic cell carcinoma?
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
459
What is the aetiology of an acinic cell carcinoma?
Second most common salivary gland malignancy in children
460
Explain the management of an acinic cell carcinoma?
Complete excision requiredGenerally not aggressive but a proportion can metastasise to cervical lymph nodes and lungRecurrence rate as high as 35%
