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4th Year Adapted > 4th Year #2 > Flashcards

4th Year #2 Flashcards

1
Q

Advantages of the coronal seal? vital and nonvital?

A

Vital:➢Provides increased pulpal protection➢Prevents caries at and beneath restoration marginNon-vital:➢Provides additional line of defence to endodontic seal➢Prevents caries at and beneath restoration margin

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2
Q

Describe amalgam as a core material? Adv and Dis?

A

Advantages - Not especially technique sensitive - Strong in bulk section - Sealed by corrosion products - Can be bonded into place withcements and resinsDisadvantages- Best left to set for 24 hours before tooth preparation- Weak in thin section- Potential electrolytic action betweencore and metal crown- Not intrinsically adhesive- Poor aesthetics under ceramicrestorations

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3
Q

Indications for amalgam as a core material?

A

 Excellent core build-up material for posterior teeth Excellent interim restoration for posterior teeth Adhesives and preparation features can often substitute for pinretention

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4
Q

Describe composite as a core material? Adv and Dis?

A

Advantages - Strong- Can be used in a thinner section thanamalgam- Fast setting (either light or chemicallycured)- Does not always need a matrixduring placementDisadvantages- Highly technique sensitive- Relies on multi-stage dentinebonding requiring effective isolation- Dentine bond can be ruptured bypolymerisation contraction- Can be difficult to distinguishbetween tooth and core duringpreparation

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5
Q

Indications of composite for core build up?

A

Excellent build-up material for posterior and anterior teeth if isolationassuredAesthetic interim restoration, but takes far longer to place than amalgam

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6
Q

Should we remove the exisiting restoration?

A

Removal of existingrestorations allows properassessment of:➢The tooth’s structural integrity➢Pulpal exposure➢Underlying caries

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7
Q

Describe the Nayyar core?

A

“Postless” preparationRetention from coronal and radicular toothtissueUses pulp chamber as retention and resistance form

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8
Q

Advantages of the Nayyar core?

A

 Can be placed immediately after endo –reducing risk of coronal leakage Utilises coronal tooth structure to increaseretention Reduces stresses created by post placement Usually easily retrievable

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9
Q

How to diagnose post-treatment disease?

A

may not be straight forward as you may be dealing with partially treated pulp canals, missed canals or procedural mishaps. These should be included in the diagnostic description.

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10
Q

Name the 3 advantages of fixed options?

A

PsychologicalBiologicalFunctional

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11
Q

What are the the psychological advantages of fixed options?

A

If own tooth used, reduces the impact of “loss”Looks and feels the same as before- no adaptation to new “body image”No need to remove – is part of the patient, no embarrassment

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12
Q

What are the the biological advantages of fixed options?

A

No additional soft tissue coverageNo increase in plaque retentionMaintains interdental space effectively - worn constantly unable to remove

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13
Q

What are the the functional advantages of fixed options?

A

Speech is unaffectedCannot be easily lostLess susceptible to breakageMinimal need for patient adaptation

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14
Q

Explain the process to prepare a recently extracted tooth for fixed immediate replacement?

A

Extraction + cleaningTooth decoronatedRC sealed with GICOrtho wires attachedTooth carefully positioned and attached to adj teeth using composite resinOcclusion was carefully checked and adjusted

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15
Q

Explain the process to prepare an acrylic tooth for fixed immediate replacement?

A

Model made prior to extractionLab cuts tooth from modelTrims acrylic denture tooth to fit space and occlusal schemeAdds orthodontic wire for bonding to adjacent teethAcrylic denture tooth to fit space and occlusal schemeOrthodontic wire for bonding to adjacent teeth

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16
Q

Explain the process to prepare asemi-permanent solution for fixed immediate replacement?

A

Prepare palatal surfaces of both the pontic and abutment teethMake working casts of upper and lower archesCut tooth to be replaced from the modelReposition the “extracted” toothConstruct metal framework for retentive elementsExtraction of the affected toothPartially decoronate toothWiden canal access and irrigate with sodium hypochlorite solutionComplete trimming of the tooth to the correct gingival length and contour.Seal the opening to the pulp chamber with glass ionomer cement.Position tooth on metal retainer and bond with bonding agent.Position the bridge retainer accurately against the abutment tooth and check fit and asestetics.Carefully isolate the abutment tooth. Wash and dry the retainer.Bond the bridge into position using appropriate bonding agent.

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17
Q

What are the risks and benefits of orthodontic treatment?

A

Benefit:- improved function- improved aestehticsRisks:- reduced dental health- failre to achieve aims

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18
Q

Name the 7 suggested health benefits of orthodontic treatment?

A

Reducing caries susceptibility - however caries progression is multifactoralReduces Gingivitis and Periodontal disease - other factors can be importantReducing trauma risk (Correcting Increased overjet) - >6mm overjet 3 x riskMasticatory Function - overjet/AOB eating difficultiesSpeech - malocclusion little impactTooth impactionPsychological well being (Aesthetic impact) - impact on self-esteemand quality of life

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19
Q

Name the 4 risks of orthodontic treatment?

A
  • Dental caries (Decalcification) : - ↑poor oral hygiene, cariogenic diet * Root Resorption (Root shortening)* Ginigivitis / loss of attachment ↑ patients with unstable periodontal disease* Soft tissue trauma (Ulcers
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20
Q

What is the purpose of the index of orthodontic treatment need?

A

developed to help determine likely impact of malocclusion on dental health and psychological well being.

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21
Q

Name 3 types of treatment startegies for orthodontic treatment?

A

Orthodontic treatment onlyOrthodontic / Surgical TreatmentOrthodontic / Restorative Treatment

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22
Q

What are the 6 indications for orthodontic treatment?

A
  • Motivated Patient * Stable dental health * Caries free minimum of 12 months* Healthy periodontium* Low plaque scores (adequate Oral hygiene)* Benefits of orthodontic treatment outweigh risks (IOTN)
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23
Q

Name the 4 contraindicators for orthodontic treatment?

A
  • Poor Dental Health (active caries/periodontal health issues)* Oral Hygiene Issues * Poor Co-operation / Tolerance issues* Low treatment need (Risks vs Benefits-IOTN)
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24
Q

Name the 3 types of orthodontic appliances?

A
  • Removable* Functional * Fixed
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25
Q

What is the definition of a removable appliance?

A

An orthodontic appliance that can be removed by the patient

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26
Q

Name the 3 main components of an orthodontic appliance?

A
  • Active Components* Retentive Components* Anchorage (Newtons 3rd Law of motion)* Baseplate/ Bite planes
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27
Q

Name a form of retentive components?

A

Adams clasps

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28
Q

Name a form of active component?

A

Palatal finger spring

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29
Q

What is the definition of anchorage?

A
  • Newtons ‘third law of motion’* For every force applied there is an equal and opposite reactionary force* Anchorage relates to control of these reactionary forces
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30
Q

Name the 3 planes of space for anchorage?

A
  • A-P * Transverse* Vertical
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31
Q

What are the advantages and disadvantages of removable appliances?

A

Advantages* Can be removed for cleaning (after meals)* Cheap (cf fixed appliances)* Less chair-side time * Palatal Coverage / Good AnchorageDisadvantages* Appliance is removable!* Limited tooth movements possible (tipping)* Lower appliance poorly-tolerated

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32
Q

What are 12 clinical tips for the use of a removable appliance?

A
  • Fit appliance passively initially * Demo fit and removal carefully* Stress F/T wear except cleaning* Warn re: speech* No extractions until compliance confirmed* Review every 4 weeks* First return appointment* Assess progress- is patient wearing it (not in a box or their pocket !) * Appliance fit* Wear signs – on mucosa* Speech returned to normal* Gentle activation of active components
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33
Q

Name the 8 indications for the use of a removable orthodontic appliance?

A
  1. Alignment of mesially-inclined canines2. Crossbite correction3. Overjet reduction4. Overbite reduction5. Eliminate occlusal interferences6. Adjunct to fixed appliances7. Space maintenance8. Retention
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34
Q

Name the 2 contraindications for removable orthodontic appliances?

A

Multiple tooth movements* Complex tooth movements required1. Intrusion/extrusion2. Bodily movement3. De-rotation

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35
Q

What is the definition of a functional orthodontic appliance?

A

‘Removable or fixed orthodontic appliances which use forces generated by the stretching of muscles, fascia and/or periodontium to alter skeletal and dental relationships

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36
Q

What are the benefits of using a functional orthodontic appliance?

A
  • Growing Patients* Correct Malocclusions of Skeletal Origin* May modify growth ? ?* Commonly used in Class 2 patients with mandibular retrognathia.* Hoping to enhance mandibular growth/restrain maxillary growth * Treatment approach often referred to as ‘Growth Modification’
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37
Q

What situation is best for a functional orthodontic appliance?

A
  • Class 2 malocclusions-* Class 3 malocclusions (Less common)
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38
Q

Describe an ideal functional orthodontic appliance patient?

A
  • Growing patient* Class 2 div 1 malocclusion (or Class 2 Div 2 )* Mandibular Retrognathia* Average or reduced vertical proportions* Increased OJ/OB* (Well aligned arches) also crowded cases as first stage treatment
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39
Q

Explain how to construct a functional appliance?

A
  • U + L Alginate impressions* Working bite* Teeth out of occlusion* Postured forward (the facial musculature is stretched and forces are generated)
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40
Q

Explain how to take a working bite for a functional appliance?

A
  • Patient postures to Class 1 or edge to edge* Record the postured occlusion with wax or silicone registration paste
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41
Q

Name 3 types of mode of action for rothodontic appliances?

A
  • Dentoalveolar (Dental Effects)- Tipping movements - Eruption guidance* Skeletal (Orthopaedic or Growth Effects)- Restriction of maxillary growth- Increased rate of mandibular growth- Remodelling changes in the TMJ* Modification of soft tissue activity
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42
Q

What is the definition of dental tipping?

A
  • Typical Class 2 div 1- Upper incisor retroclination- Lower incisor proclination
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43
Q

What is the definition of eruption guidance?

A
  • Achieved with bite planes/capping- Anterior - PosteriorProduce - Differential eruption - Inhibits eruption of upper posteriors- Encourages mesial eruption of lower posteriors (Class 2 correction)
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44
Q

What is the defintion of skeletal mode of action?

A
  • Enhanced Mandibular Growth ?* Elongation is brought about by deposition at the condyle and the posterior border of the ramus.
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45
Q

What is the definition of modifying soft tissues?

A
  • Lip competency * Changing the linguo-facial muscle balance - Shields - Screens* Teeth erupt into a position of balance
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46
Q

WHich modes of action do functional appliances use?

A
  • Eruption guidance - Bite planes* Mandibular repositioning - Working bites* Altering soft tissue balance - Shields and modifying lip activity
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47
Q

Name the 3 classifications for functional appliances?

A
  • Tooth borne (‘Twin block’)- Mostly dental tipping- Good retention- generally well tolerated* Soft tissue borne- Less retention - Difficult to achieve 24 hr wear* Fixed functionals
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48
Q

Name 3 examples of tooth borne functional appliances?

A
  • Twin Block* Frankel* Bionator* Herbst
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49
Q

Describe a twin block functional appliance? - retention?

A
  • Tooth borne via Clasps* Most commonly used* Well tolerated* F/T wear possible* In 2 parts, one upper, one lower* Bite blocks posture the mandible forward
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50
Q

Describe a frankel functional appliance? - dentition type? soft tissue? probelms?

A
  • Soft tissue borne appliance (‘Monobloc’)* Good in mixed dentition - Tooth loss does not affect retention* Good when soft tissues significantly contribute to the malocclusion- Expressive lower lip, lip trap* Problems : bulky, P/T wear only and breakages+
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51
Q

How to maximise the success of a functional appliance?

A
  • Keen patient and family support* Mild / moderate skeletal problem* Patient actively growing * Coordinate treatment with pubertal growth spurt- Boys age 12-14- Girls age 11-13
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52
Q

Do functional appliances grow mandibles?

A
  • Controversial* Early studies (Animal) suggested significant skeletal effects * Recent RCTs suggest mainly dental effects 90% and 10 % skeletal* Large individual variation in response* Difficult to predict
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53
Q

Explain why to use a functional appliance to correct an increased overjet?

A
  • Reduce risk of trauma * Improve profile* Help to allow lips to become competent* Improve smile aesthetics* Makes subsequent fixed orthodontics easier or can even be the only treatment required
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54
Q

What is the definition of a fixed appliance?

A
  • ‘Orthodontic appliance that is ‘fixed’/attached to teeth’. * Many different systems /lots of manufacturers
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55
Q

Describe the differences in force betweeen fixed and removable appliances?

A

Bodily movement: - 1 area of tension- Heavier forces 100-150 gmsTipping: - different areas of tension (2)- Lighter forces 25-30 gms

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56
Q

Name the 7 indications for the use of fixed appliances?

A
  • Multiple tooth movements* Space closure with bodily movement * Intrusion/extrusion of teeth * Rotation correction * OB control with incisor intrusion* Mild to moderate skeletal discrepancies (camouflage treatment)* Severe Skeletal Discrepancies (+ Surgery)
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57
Q

Name the advantages and disadvantages of using a fixed appliance?

A

Advantages:* Treating complex cases* High standards of finishing* Wear co-operation is not as essential as with removable appliances but still OH and diet care !* Less bulkier than removable appliances* Do not affect speechDisadvantages* Diet restriction and meticulous OH * Can cause iatrogenic effects (decalcification)* Cause Orthodontic root resorption (shortening)* Require special skill and training* Require close monitoring

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58
Q

Describe the differences between Fixed and Removable?

A

Fixed:- Bodily Movement- Multiple tooth movements- Rotations corrected- OH more difficult- Less Co-op ??Removable:- Tipping movements only- Simple tooth movements- Rotations not corrected- OH easier (Removable)- More Co-op (Wear compliance)

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59
Q

Name the components of fixed appliances?

A

BracketsArchwireElastic ligature

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60
Q

What is the defintion of a bracket?

A

‘Handles on the teeth’ – control tooth position in combination with archwire.* 0.022’’ (inch) slot width size commonest * 0.018’’ (inch) more common in past* Slot design specific for each tooth (prescription)

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61
Q

Describe the material of a bracket?

A
  • Base of bracket* Curved to fit each tooth* Mesh base / retains composite resin* Pre –coated (APC) with composite .* Non pre-coated
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62
Q

Name the 7 bracket types?

A
  • Metal – standard SWA brackets ↑ * Metal – Self ligating* Metal- ‘tip-edge’* Aesthetic Systems* Ceramic* Lingual * (Aligners)
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63
Q

What are the benefits of self ligating brackets?

A
  • Claims by manufacturers* Quicker treatment * Allows expansion/favours non-extraction tx* Controversial as no evidence to support * Studies / RCTs* No difference Tx time* ? Longer appt intervals
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64
Q

Describe a self ligating bracket type?

A
  • Self Ligating* eg‘Damon’, Speed, Innovation, Smartclip* Active or Passive clip or gate* Less friction cf normal ligation
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65
Q

What is the definition of tip edge brckets?

A
  • Different tx philosophy* 2 stage tooth movement* Easy tipping – bracket ‘cut away’ design * Tip crowns and then upright roots* Lighter on anchorage
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66
Q

What is the defintion of a lingual bracket type?

A
  • Lingual* ‘Incognito’ 3M system* Expensive* Cast Gold* Customised for each tooth* Bonded – indirectly with preformed trays* Different instruments* Archform shape -‘mushroom’
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67
Q

Explain the process to bond brackets to the teeth?

A
  • Isolate* Pumice/Prophylaxis* Acid Etch (Phosphoric acid)* Irrigate/Dry* Apply Bonding agent* Place bracket with composite resin on bracket base* Remove excess composite* Light Cure
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68
Q

What is the definition of an orthodontic band?

A
  • Now – used on molars * Different sizes* Cemented with G.I.C* Separators / 1 week before placement* Can pre-select on model* Cemented with glass ionomer cement or light cured compomer* Glass ionomer / fluoride release
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69
Q

What is the definition of an archwire?

A
  • Interaction archwire/bracket slot → tooth movement* Archwire Variations* Shape * Size* Alloy type
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70
Q

Describe the different types of archwire shapres?

A
  • Round eg .014 Niti* Square eg .020 x .020 NiTi* Rectangular eg .019 x .025 NiTi
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71
Q

Name the 3 alloy types of archwire?

A
  • Nickel Titanium* Stainless Steel* B-Titanium (TMA)
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72
Q

What is the definiion of NiTi archwire alloy?

A
  • Thermally active / non thermally active* Super-elastic* increased Flexible* Shape memory * Initial alignment stages of treatment
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73
Q

What is the defintiion of stainless steel archwire?

A
  • increased Stiffness* increased Rigidity* decreased Flexibility* - if multistrated it increases* Working archwires* Levelling* Space closure* Finishing (add bends)
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74
Q

What is the definition of Beta - Titanium archwire?

A
  • Beta – Titanium (TMA)* Half way between NiTi and SS* Some flexibilty but more rigid than NiTi* Useful finishing stages of treatment eg adding torque or bends to archwire
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75
Q

What is the definition of a elastic modules ligature?

A
  • Used to retain archwire* Varied colours
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76
Q

What is the definition of a elastic chain ligature?

A
  • ‘Linked’ elastic modules* Used to space close
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77
Q

What is the definition of a transpalatal arch?

A
  • Across upper arch between molars* Soldered or removable attached to molar bands* Increases posterior anchorage* Maintains molar widths
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78
Q

What is the definition of a Nance appliance?

A
  • Similar to TPA* Anchors upper molar position* Acrylic button for additional anchorage from palate
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79
Q

What is the definition of a coil spring?

A
  • Orthodontic Coil Springs * Open/closed* Used space closure and openig
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80
Q

What is the definition of a Zing String (Power thread)

A
  • Elastic thread or tubing* Used to apply traction forces to teeth during fixed appliance treatment
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81
Q

What is the definition of an expanders-RME?

A
  • Rapid maxillary expander (RME)* Commonly cemented with bands on 1st permanent molars and 1st premolars* Midline screw* Activated to expand upper arch (1/2 mm per day hence ‘rapid’)
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82
Q

What is the defintion of an expanders-Quad helix?

A
  • Fixed expansion appliance* Bands on 1st permanent molars* Has 4 circle loops (helices) to give flexibility and good range of action
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83
Q

What is the definition of temporary anchorage device?

A
  • ‘TADS’* Titanium screws* Inserted intra-radicular alveolar bone* Topical/LA* Common sites- between upper 5 and 6.
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84
Q

Describe the 4 general categories of elastics?

A
  • Class I – Intra-arch* Class II – Inter –arch :To correct Class II malocclusion* Class III – Inter –arch :To correct Class III malocclusion* Vertical – To correct open bitesOthers* Anterior cross elastics - correct dental centreline discrepancies* Posterior cross elastics
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85
Q

Summary of the management of patients with mandibular third molars?

A

Asymptomstic high risk - caries, perio, resorption and cysts/tumoursSymptomatic high risk - acute pericorontis, unrestorable caries, perio disease, resorption, fracture, abscess or surrounding pathology Asymptomatic low risk - bisphosphonates, antiangiogenics and chemo, radiotherapy H/N, immunosuppression, mandibular fracture and cancerSymptomatic low risk - TMJ disorder, parotid disease, skin lesion, migraines, referred pain or oropharyngeal cancer

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86
Q

Name the 7 ways in which the root can be affected by the nerve?

A

Darkening of rootDeflection of rootNarrowing of rootDark and bifid rootInterruption of white line of canal Diversion of canalNarrowing of canal

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87
Q

What to do for a horizontally impacted tooth?

A

Decoronation

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88
Q

What to do for a vertically impacted tooth..

A

Root separation

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89
Q

Complication with sectioning teeth?

A

Failure to split roots Drill to far through the bone - lingual nerve damage or causing an OAC

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90
Q

Name other techniques for tooth sectioning.

A

Hemisection- surgical separation of a multi rooted tooth and extraction of one or more rootsRoot resection- sectioning and removal of a diseased rootPremolarisation- sectioning of lower molar crown between roots to leave 2 single teeth to allow maintainer of oral hygiene Coronectomy- removal of crown but leaving the roots in situ

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91
Q

Contraindications to coronectomy?

A

Too close to IAN canalActive infectionPreexisitng numbnessPreexisiting mobilityHorizontally impacted tooth along IANMedical conditions

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92
Q

Name 7 indications for removal of 8s according the the NICE guidelines?

A

Unrestorable cariesNon-treatable pupal and/or periapical pathologyCellulitis, abscess and osteomyelitisFracture of toothResorption of tooth or adjacent teethDisease of the following such as cyst/tumourTooth impeding surgery or reconstructive jaw surgery

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93
Q

When should you leave 8s in place?

A

Symptom freeNo evidence of diseaseRemoving the tooth may cause more harm

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94
Q

Name 5 non-NICE guidelines for removal?

A

To exclude atypical facial painTo prevent late lower incisor crowding or relapse of orthoPrior to travel Financial - >25Known later complications

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95
Q

When does pericoronitis become a valid indication for wisdom tooth removal?

A

Severe first case of pericoronitis Second or subsequent episodes should be considered

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96
Q

NICE consultation 2017-2019 findings?

A

Removal of non-pathological 8s is not indicated, however down the line the 8s will become a problem and be extracted

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97
Q

What is the overall risk of nerve damage of lower wisdom tooth extractions?

A

Up to 5%

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98
Q

Neurapraxia definition?

A

Contusion of the nerve in which the continuity of the nerve is maintained - blunt trauma, traction or local ischaemia

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99
Q

Axonotomesis defintion?

A

Discontinuity of the axons but the shealth is intact - severe blunt trauma, nerve crushing and extreme traction

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100
Q

Neurotmesis defintion?

A

Complete loss of nerve continuity - mandibular fracture

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101
Q

Anaesthesia definition?

A

Lack of sensation

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102
Q

Paraesthesia definition?

A

Spontaneous and subjective altered sensation that a patient does not find painful

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103
Q

Dysaesthesia definition?

A

Spontaneous and subjective altered sensation that a patient does find painful

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104
Q

Hypoaesthesia definition?

A

Decreased sensitivity of a nerve to stimulation

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105
Q

Hypoalgesia definition.

A

Decreased sensitivity to noxious stimulation

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106
Q

Hyperaesthesia definition?

A

Increased sensitivity if annerve to stimulation

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107
Q

Hyperalgesia definition?

A

Increased sensitivity to noxious stimulation

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108
Q

Allodynia definition?

A

Pain caused by a stimulus that does not normally cause pain

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109
Q

What are Winter’s classification of impacted wisdom teeth?

A

VerticalMesioangularHorizontalDistoangular

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110
Q

When is 4/0 Coated vicryl used?

A

delicate or maceratedmucosa. Easy to pull toohard and break the suturewhen suturing.

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111
Q

When is 3/0 vicryl rapide used?

A

across sockets andapplying pressure to achievehaemostasis

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112
Q

Name 2 types of peri-raduclar surgery?

A

Root end resection (apicectomy)Retrograde root filling (RRF)

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113
Q

What is the flap design for peri-radicular surgery?

A

3 sided full thickness BMPF- Risk of gingival recession in thevisible anterior region especiallynoticeable with crowned teeth

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114
Q

What flap design can be used for peri-raducular surgery to minimise the risk of gingival recession?

A

Luebke –Oschenbein sub-marginal flap:- Minimises risk of gingival recession- Difficult to suture as the horizontal incision is inattached gingivae- Requires at least 4mm of attached gingivaeSemi-lunar flap:- poor healing (flap margin not on solid bone)- minimised gingival recession

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115
Q

How to promote healing for flap design?

A

by preserving blood supply – wide base

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116
Q

When suturing over the bone, what must you do?

A

Place the mesial relieving incisionaway from the area of bone removal/lossto provide support for the incision margin when closed

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117
Q

Describe the process to remove a mesio-angulary impacted partially eruped LL8?

A
  1. Mucoperiosteal flap marginsincised – 3 sided BMPF2. Flap retracted from buccal side3. Collar of bone guttered frombuccal side of LL84. Sectioning of toothThe groove has been drilled only half way through thetooth bucco-lingually to protect the lingual nerve5. Elevator used to separate the 2 roots6. Distal root delivered with forceps7. Mesial root elevated into the space created by removal of the distal root – disimpacted – thendelivered8. Socket debrided and washed withcopious sterile saline9. Wound closure with sutures
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118
Q

Describe the palatal flap for buried canines?

A
  1. Sacrifice the incisive bundle – no clinicalsignificance to the resulting area of anaesthesia2. Extensive crevicular incision extending from UR6 to UL4 on the palatal aspect as no relieving incisions possible3. Buried canine located and exposedby drilling overlying bone
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119
Q

Name 2 types of flap design is for oro-antral communiction?

A

Buccal Advancement Flap:- based on a 3 sided BMPF with the periosteal layerscored to permit extension of the flap to the palatal side- pull flap across defect and suturePalatal Rotational Flap:- based arounnd the greater palantine vascular bundle

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120
Q

What is the main side effect of a buccal advancement flap?

A

Results in loss of buccal sulcus depth makingsubsequent denture fit difficult without further sulcus deepening surgery.

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121
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

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122
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

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123
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

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124
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

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125
Q

Types of drugs for mucosal disease?

A

Non-steroid topical therapy - inconvientient lesions with discomfortSteroid topical therapy- disabling immunologically driven lesions

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126
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!

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127
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’

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128
Q

How does it work - hydrocortisone mucoadhesive tablet?

A

allow tablet to dissolve over the ulcer

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129
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

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130
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

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131
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

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132
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

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133
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

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134
Q

Systemic use of steroid risk - side effects?

A

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

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135
Q

What are the differential diagnoses of oral white lesions? 5 examples?

A

HereditarySmoking/frictionalLichen planus- lupus erythematosus- gvhdCandidal leukoplakiaCarcinoma

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136
Q

What does a typical white spot lesion look like?

A

Thickening of the mucosa or keratin- Less visibility of bloodLess blood in the tissues- vasoconstrictor

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137
Q

What is the definition of Leukoplakia?

A

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

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138
Q

Name 4 types of leukoplakia?

A

Fordyce’s spotsSmoker’s KeratosisFrictional KeratosisHereditary Keratosis

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139
Q

What is the link between smoking and leukoplakia?

A

Smokers are six times more likely to have “leukoplakia”Low malignant potential of the lesion- But higher oral cancer risk overall!

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140
Q

Name 3 types of infective leukoplakia?

A

Candidosis- pseudomembranous acute (thrush)- denture associated (chronic)Herpes Simplex

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141
Q

When should you refer a white spot lesion?

A

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

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142
Q

Why are red spot lesions red?

A

Blood flow increases- inflammation- dysplasiaReduced thickness of the epithelium

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143
Q

What is the definition of Erythroplakia?

A

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

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144
Q

What are the 3 types of mucosal pigmentations?

A

Exogenous stainIntrinsic PigmentationIntrinsic foreign body

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145
Q

Name the 4 examples of exogenous stains for mucosal pigmentation?

A

TeacoffeechlorhexidineBacterial overgrowth

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146
Q

Name the 4 examples of intrinsic pigmentation for mucosal pigmentation?

A

Reactive Melanosis/melanotic maculeMelanocytic naevusMelanomaEffect of systemic disease - paraneoplastic phenomenon

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147
Q

Name the 1 examples of intrinsic foriegn body for mucosal pigmentation?

A

Metals

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148
Q

Name the differential diagnoses for brown/black lesions - localised and generalsied?

A

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)

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149
Q

Name 2 types of melanin pigmentation?

A

Racial pigmentationMelanotic macule

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150
Q

How to decide whether something is a melanoma? questions?

A

Variable pigmentationIrregular outlineRaised surfaceSymptomatic- Itch- bleed

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151
Q

When should a patient be referred to oral medicine?

A

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

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152
Q

When should you NOT refer a patient to Oral Medicine?

A

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

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153
Q

When should a mucsoal lesion be refered to oral medicine for an opinion?

A

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 hasÂnot responded to standard treatment- Hospital referral criteria- SDCEP guidanceAny BENIGN lesion that the patient can’t be persuaded is not cancer…..

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154
Q

Name the 3 reactive chnages of the oral epithelium?

A

Keratosis - nonkeratinised site (parakeratosis) Acanthosis - hyperplasia of stratum spinosum Elongated rete ridges - hyperplasia of basal cells

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155
Q

Name the 5 mucosal reactions of the oral mucosa?

A

Atrophy - reduction in viable layersErosion - partial thickness lossUlceration - fibrin on surfaceOedema - intracellular - intercellular (spongiosis)Blister - vesicle or bulla

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156
Q

What are the symptoms of geographic tongue?

A

Sensitive with acidic/spicy foodsIntermittentMuch worse in young children

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157
Q

What is the aetiology of geographic tongue?

A

None!Something else is causing the trouble- Haematinic deficiency (B12, Folate, Ferritin)- Parafunctional trauma - Dysaesthesia

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158
Q

What is the definition of a fissued tongue?

A

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

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159
Q

What is the defintion of glossitis? And possible investigations?

A

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

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160
Q

What is the definition of black hairy tongue?

A

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.

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161
Q

What is the aetiology of black hairy tongue?

A

smoking, xerostomia (dry mouth), soft diet, poor oral hygienecertain medications

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162
Q

What is the aetiology of glossitis?

A

Often caused by nutritional deficiencies- Fe- B- Infection- others

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163
Q

What is the definition of a pyogenic granuloma?

A

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

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164
Q

What are the differential diagnoses for single episode oral ulceration?

A

Trauma1st episode of Recurrent Oral UlcerationPrimary Viral infectionsOral Squamous Cell Carcinoma

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165
Q

What are the differential diagnoses for Recurrent Oral Ulceration?

A

Aphthous ulceration- minor, major, herpetiformLichen PlanusVesiculobullous lesions- pemphigoid, pemphigus- angina bullosa haemorrhagica- erythema multiformeRecurrent viral lesion – HSV, VZVTraumaSystemic disease – Crohn’s Disease ulceration

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166
Q

Describe the difference between Crohn’s ulcers and aphthous ulcers?

A

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

167
Q

Explain what to include for an Oral Ulceration History?

A

Where?Size & Shape?Blister or ulcer?How long for?- more than 2 weeks?Recurrent?- same site? different Sites?Painful?

168
Q

Explain how to examine an ulcer?

A

Margins?- flat? raised? rolled?Base?- soft? firm? hard? Surrounding tissue- inflamed? normal?Systemic Illness?

169
Q

What is the definition of traumatic ulceration?

A

CommonUsually single episode - can be recurrent if cause not removedNormal or abnormal epitheliumHealing - remove cause - heal in about 2 weeks

170
Q

Describe a recurrent herpetic lesion? - location and treatment

A

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

171
Q

Describe recurrent aphthous stomatitis (RAS)? severity? diagnosis?

A

Severity:- minor- major- herpetiform- Behçet’s syndromeDiagnosis by :- history- examination

172
Q

The overall summary of Oral Ulceration?

A

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

173
Q

What is the definition of an Aphthous Ulcer?

A

NAME?

174
Q

Describe the characteristics of a minor aphthous ulcers?

A
  • 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
175
Q

Describe the characteristics of a major aphthous ulcers?

A
  • 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
176
Q

Describe the characteristics of a herpetiform aphthae ulcer?

A
  • 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
177
Q

What cause Oral and Genital Ulceration?

A

Behçet’s Disease (mainly)Vesiculobullous diseasesLichen Planus

178
Q

How to diagnose Behcet’s disease?

A

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

179
Q

What is the definition of Behcet’s Disease? and where can it effect?

A

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

180
Q

How to manage a patient with Behcet’s Disease?

A

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

181
Q

Name the 7 predisposing factors for Recurrent Aphthous Stomatitis (RAS)?

A

Viral and bacterial infectionsGenetic predispositionSystemic diseasesStressMechanical injuriesHormonal level fluctuationsMicroelement deficiences

182
Q

What tests to carry out when investigating aphthous ulcers?

A

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

183
Q

Explain the treatment of a recurrent Aphthae?

A

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

184
Q

What drugs can be prescribed for aphthous ulcers?

A

In dental practice follow SDCEP ’Drugs in Dentistry’ GuidanceNon-Steroid Topical Therapy - for inconvenient lesionsSteroid Topical Therapy - for disabling lesions

185
Q

Why do chuildren get aphthous ulcers?

A

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

186
Q

When should you refer an Aphthous ulcer case?

A

After simple investigationsAfter topical trreatmentIf no good result has been achievedIf patient under 12 YO

187
Q

What is the defintion of oral thrush?

A

Caused by candidaCan be associated with dentures causing denture stomatitis

188
Q

What species of candida causes oral thrush?

A

Candida albicans

189
Q

Name the topical and systemic treatment of oral thrush?

A

Topical:- nystatin - miconazoleSystemic:- fluconazole- targeted therapy

190
Q

Explain how to use nystatin suspension?

A

1ml QDSKeep in mouth for as long as possibleContinue for 48 hours after resolvedLow risk for inters

191
Q

Explain how tonuse miconazole oral gel?

A

2.5 ml QDS - gold in mouth after foodContinue for 7 days after resolvedUse gel to brush dentures

192
Q

What treatment is advised for angular cheilitis?

A

Miconazole- antifungal- bacteriostatic vs gram positive- topical- with mild steroid

193
Q

Name the drug interactions of Miconazole?

A

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

194
Q

Name the contraindications of miconazole?

A

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

195
Q

Explain how to take fluconazole?

A

50-200mg capsules50-5ml oral suspensionIV avaliable 50mg once a day for 7-14 days100mg if immunocompromised

196
Q

Name the 6 contraindications of fluconazole?

A

Mod inhib of P3A4 and 2C9Strong inhib of 2C19AlfentanilAmitriptylineBenzodiazepinesCitalopramClopidogrelWarfarin

197
Q

Which 5drug types cause dry mouth?

A

OpoidsAnticholinergics AntidepressantsDiureticsOxygen

198
Q

Explain how to manage dry mouth?

A

Treat underlying causeReview medicationGood oral hygieneDietary adviceRegular dental checksRegular sips of waterLubricate cracked lipsSaliva substitutesSaliva stimulants

199
Q

At what age does lichen planus usually affect?

A

30-50 years old

200
Q

What is the histopathological findings of lichenoid reaction?

A

Chronic inflammatory cell infiltrate Saw tooth rete ridgesBadal cell damagePatchy acanthosis Parakeratosis

201
Q

What is the histopathological findings of licehn planus?

A

OrthokerstosisWedge shaped hypergrabulosisDermal epidermal Junction obscured lymphocytesVacuoles at basal laterLuck band of lymphocytes under epidermisCivatte bodies - dead keratinocytes

202
Q

What are the 8 aetiologices of lichen planus

A

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

203
Q

What are the symptoms of lichen planus?

A

Often noneMay relate to thinning of epithelium - sensitive to hot and spicy food- burning sensation in the mucosa

204
Q

What other body parts can LP affect?

A

SkinScalpGenitalsHairNails

205
Q

What are the 5 main sites for oral LP?

A

Biccal mucosaGingiva - desquamative gingivitisTongue- lateral or dorsumLipsPalate

206
Q

Describe buccal lichen planus?

A

CommonestCan be found anywhere - ant at commisure- mid- post around 3rd molarMainly an incidental findingEasy to biopsy

207
Q

Describe gingival lichen planus?

A

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

208
Q

Describe tongue lichen planus?

A

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

209
Q

Describe lip lichen planus?

A

On the lipBiopsy hard?Looks soreErythema

210
Q

What is it called if the cause is known for oral lesion?

A

Lichenoid reaction to…

211
Q

Medications which can cause LP?

A

ACE inhibBeta blockersDiuretics - bendroflu and frusemideNSAIDs DMARDsRare - phenothiazines

212
Q

What are the discriminative characteristics of a lichenoid drug reaction?

A

Widespread lesionBilateral and mirrorsPoorly response to standard steroid treatment

213
Q

How to manage lichenoid drug reactions?

A

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

214
Q

Explain the overall lichen planus management for the patient?

A

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

215
Q

What treatment would be recommended for mild intermittent lichen planus lessons?

A

Topical OTC remedies- chlorhexidine - benzdamineAvoid SLS containing toothpaste

216
Q

What treatment would be recommended for a persisting synthetic lichen planus lesion?

A

Topical steroids- beclomethasone inhaler - betamethasone rinse Higher strength steroid- skin steroid cream - ClobetasolTopical tacrolimus mwHydroxycholorquineSystemtic immumodilators - azathioprine and mycophenolate

217
Q

What are the histological findings of lupus erythematosis?

A

Basal vacuolar damageAtrophic epitheliumMelanophageIntense lymphocytic infiltrate

218
Q

Describe lichen like lesions?

A

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

219
Q

Name 5 vesiculobulloua conditions?

A

Erythema multiformPemphigusPemphigoidAngina Bullish HaemorrhagiaBullous lichen planus

220
Q

What is the defintion of Pemphigoid?

A

A subepithelial antibody attackThick walled blisters- persist to be seen- clear or blood filled

221
Q

Name 3 different forms and presentations of Pemphigoid?

A

Bullous pemphigoid - skinMucous membrane pemphigoid - all mucous membranes Cicatritial pemphigoid - mucosal with scarring

222
Q

Describe the histopathogy of pemphigoid?

A

Sub epithelial split - epithelial/CT tissue junctionHemi-desmosomes involved at basement membrane

223
Q

Describe how Pemphigoid is seen with immunofluorescence?

A

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’

224
Q

What is a symblepharon?

A

Pemphigoid that is present on the eye

225
Q

Non-oral locations of Pemphigoid?

A

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

226
Q

How to manage Pemphigoid?

A

SteroidsImmune modulating drugs- azathioprine- mycophenolate

227
Q

What is the defintion of Pemphigus?

A

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

228
Q

Describe Pemphigus histopathologically?

A

Supra-basal split with tzank cells

229
Q

Describe Pemphigus using immunofluorescence?

A

Very greenBasket weave pattern - around each epithelial cellC3 and IgG in Pemphigus vulgaris

230
Q

How to treat Pemphigus?

A

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

231
Q

Name the 2 types of immunogenic immune mediated disease?

A

Cell mediatedAntibody mediated

232
Q

Name 3 types of local immunological oral disease?

A

Aphthous ulcersLichen planusOrofaxial granulomatosis

233
Q

Name 6 systemic diseases with local oral effects?

A

Eythema multiformPemphigusPemphigoidLupusSystemic sclerosisSjogren’s syndrome

234
Q

Type 3 Hypersensitivity example?

A

Erythema multiform

235
Q

Name 3 examples of cell mediated immunity?

A

Aphtous ulcersLichen PlanusOrofaxial Granulomatosis

236
Q

Name 2 examples of antibody mediated immunity?

A

PemphigusPemphigoid

237
Q

How do cells of the epidermis adhere to eachother?

A

Via desmosomes and hemidesmosomes 2 proteins - desmoglein (VIP) and desmocollin

238
Q

Explain the mechanism of action for immunofluorescence?

A

A fluorescein molecule is attached to an engineered antibody, that when binds fluorescence and becomes active

239
Q

Explain the difference between direct and indirect immunofluorescence?

A

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

240
Q

What is the defintion of erythema multiforme?

A

Acute onset - more menSkin - show target lesionsMucosa - show ulcersFor young males it is recurrent within a short period

241
Q

What specific sites do erythema multiforme target?

A

Lips and anterior part of the mouthHeals in 2 weeksVery painful - unable to eat or drink

242
Q

What os erythema multiforme relation to Stevens Johnson syndrome?

A

Can be involved with Stevens-Johnson syndrome- sevre multisystem involvement- skin, conjunctivae, nose, pharynx, mouth and genitals

243
Q

What is the treatment for erythema multiforme?

A

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

244
Q

What is the defintion of angina bullous haemorrhagica?

A

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

245
Q

Give a brief overview of how to treat and what tests for angina bullish haemorrhagica?

A

Non specific ulcerationDIF and IFF negativeNo defectsChlorhex MWMay recur

246
Q

How to manage angina bullish haemorrhagica?

A

No treatmentReassure patient that is benignExplain known triggers

247
Q

Why are mucosal lesions more frequent in children?

A

Clinical issues traditionally related to immunologicalimmaturity

248
Q

Name the 2 types of congenital oral mucosal lesions?

A

HereditaryDevelopmental defects

249
Q

Name the 6 types of acquired oral mucosal lesions?

A

TraumaticDrug-relatedChronic inflammatoryHyperplasticNeoplasticInfective

250
Q

What is the defintion of white sponge naevus?

A

HereditaryInherited as autosomal dominant condition . Defect in keratin gene 4 and 13.Uncommon

251
Q

Name the clinical features of white sponge naevus?

A

•White, soft, irregularly thickened, nodefined borders•Bilateral•Genital tissues can also be affected•Often misdiagnosed with candidosis

252
Q

Name the histopathology of white sponge naevus?

A

•Uniform acanthosis•Hyperparakeratosis• Intracellular oedema•No dysplasia, no inflammation

253
Q

How to manage white sponge naevus?

A

Reassurance

254
Q

Describe the clinical features of fordyce’s granules?

A

â–ªEctopic sebaceous glandsâ–ªAssociation with hormonal changes in puberty?â–ªBilateral, most commonly on buccal mucosa

255
Q

Describe the clinical feattures of folaite papillae?

A

â–ªPinkish soft nodulesâ–ªBilateral, ventral tongueâ–ªLymphoid tissue, sometimesinflamed/hyperplastic

256
Q

Describe the clinical features of geographic tongue?

A

â–ªDorsum of tongueâ–ªIrregular, smooth, red areas (depapillated)with sharply-defined edgeâ–ªRecurrent, migrates

257
Q

Describe the histology of geographic tongue?

A

â–ªThinning of epithelium at centre, mildhyperplasia at peripheryâ–ªEpithelium infiltrated by neutrophils

258
Q

Explain how to manage geographic tongue?

A

reassurance. If symptomatic exclude heamatological deficiencies.Median rhomboid glossitis generally not seen in children

259
Q

Describe the clinical fearues of frictional keratosis?

A

â–ªPale and translucent or white/dense withrough surface

260
Q

Describe the histology of frictional keratosis?

A

Epithelial hyperplasia, with thick granularcell layer and hyperorthokeratosisâ–ªScattered subepithelial lymphocytes

261
Q

Describe the clinical features of traumatic ulcer?

A

Mechanical, thermal or chemical traumaâ–ªInflammation levels and clinical features varyâ–ªYellowish floor of fibrin slough often present

262
Q

Describe the histology of traumatic ulcers?

A

Non-specific ulceration. See RASâ–ªDestruction of epitheliumâ–ªTissue infiltration by neutrophils

263
Q

Describe the clinical features of a mucocele?

A

â–ªMost commonly on lower labial mucosaâ–ªOverlying mucosa is intact and healthytypically circularâ–ªFirm or fluctuant and bluish

264
Q

Describe the histology of a mucocele?

A

â–ªDamage to duct of salivary glandâ–ªMucin and macrophages surrounded bycompressed connective tissuesâ–ªNo epithelial lining

265
Q

Name a drug-induced oral mucsoal lesion?

A

Chemo-induced stomatitisAspirin burns

266
Q

Describe the clinical features for recurrent aphthous stomatitis?

A

â–ªIdiopathic, but systemic factors known to modulate the severity of diseaseâ–ªOnset in childhood, but peak in adolescenceMinorMajorHerptiform

267
Q

Describe the histology of recurrent aphthous stomatitis?

A

â–ªInitial lymphocitic infiltration?â–ªDestruction of epitheliumâ–ªTissue infiltration by neutrophilsâ–ªDilated vessels

268
Q

What should be excluded when dealing with recurrent aphthous stomatitis?

A

Extraoral involvement should be excluded, e.g. GI (coeliac disease, Crohn’s), genital/ocular(Behcet’s).

269
Q

Describe the clinical features for erythema multiforme?

A

▪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

270
Q

Describe the histology of erythema multiforme?

A

â–ªNecrosis of keratonocytesâ–ªEpithelial infiltration by inflammatory cellsâ–ªIntraepithelial or subepithelial vesiculation

271
Q

Describe the clinical features for orofacial granulomatosis?

A

▪Swelling of the lips▪Mucosal nodularity (cobblestoning)▪Mucosal tags▪Gingival hyperplasia▪Aphthous oral ulcers▪Children more likely to develop Crohn’s disease

272
Q

Describe the histology for orofacial granulomatosis?

A

Granulomas containingmultinucleated giant cellsâ–ªLymphoedema

273
Q

What are possible differential for orofacial granulomatosis?

A

DDx with sarcoidosis and tubercolosis. Primary TB of the oral cavity is rare,?morecommon in children than adults

274
Q

Describe the clinical features for oral lichen planus?

A

â–ªWhite striae and/or mucosal atrophy, and/orerosions, and/or plaquesâ–ªDesquamative gingivitis in isolation or incombination with aboveâ–ªBilateral lesions

275
Q

Describe the histology for oral lichen planus?

A

Basal membrane thickening Band-like lymphocitic infiltrate Colloid bodies,apoptotic basal cells

276
Q

Describe the clinical features for mucous membrane pemphigoid?

A

â–ªBullae, sometimes intact, can appear as bloodblisters. If ruptured raw ulcerâ–ªDesquamative gingivitisâ–ªConjuctival involvementâ–ªCutaneous involvement less prominent thanbullous pemphigoid

277
Q

Describe the histology for mucous membrane pemphigoid?

A

•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

278
Q

Describe the clinical features of pemphigus?

A

▪Fragile vesicles/bullae▪Ruptured vesicles▪Nikolsky’s sign positive▪Widespread cutaneous involvement

279
Q

Describe the histology for pemphigus?

A

•Acantholysis•Intraepithelial vesicles.•‘Chickenwire’ deposition of IgG and C3/C4within the epithelium.•Anti-desmoglein3 antibodies bindintercellular substance in directimmunofluorescence assay

280
Q

Deswcribe the clinical features for epydermolysis bullosa?

A

â–ªSubepithelial bullae leading to severe scarring after minimal trauma.â–ªType VII collagen defect.â–ªAutosomal recessive

281
Q

Describe the clinical features for a pyogenic granuloma?

A

â–ªSoft, red polypoidswellingâ–ªMost commonly gingivalbut not exclusively

282
Q

Describe the histology for a pyogenic granuloma?

A

•Granulation tissue•Dilated blood vessels inoedematous CT•Dense infiltration byneutrophilsNO GRANULOMAS, NOPYOGENIC BACTERIA

283
Q

Describe the clinical features of a giant cell epulis?

A

â–ªSoft, violaceus swellingâ–ªCentral gingival segmentsRelated to resorption of deciduous teeth?

284
Q

Describe the histology for giant cell epulis?

A

•Subepithelial clusters of giant cells in fibro-vascular tissue

285
Q

What to exclude when dealing with a giant cell epulis?

A

Need to exclude central GCG andunderlying hyperparathyroidism

286
Q

Describe the clinical features of vascular malformation?

A

Purple nodular lesionâ–ªBlanches upon pressure

287
Q

Describe the histology for a vascular malformation?

A

•Capillary: small vessels and vasoformative tissue•Cavernous: large blood filled sinusoids

288
Q

Name 2 pigmentary chnages ivolved with oral mucosal lesions?

A

Puetz-Jeghers syndromeAddison’s Disease

289
Q

Name the clinical features of Peutz-Jegher’s syndrome?

A

Clinical featuresâ–ªIntestinal polyposisâ–ªMucocutaneous pigmented lesionsappearing during childhood

290
Q

Describe the histology for Addison’s disease?

A

•Mild acanthosis•Melanin in basal layer

291
Q

Describe the clinical features for warts?

A

HPV 2, 4•White or pinkish, raised•Sessile or pedunculated•Often multiple•Mainly secondary to self inoculation

292
Q

Describe the histopathology of warts?

A

•Papillary processes of hyperplastic epithelium with acanthosis, hyperkeratosis,hyperplastic basal cell layer•Connective tissue core•Koilocytes often present

293
Q

Describe the clinical features for pseudomembranous candidosis?

A

•Acute•Thick white pseudomembranes of various sizes•Erythematous background•Often idespread

294
Q

Diseases that cause immunocompromisation and lead to oral mucosal lesions?

A

HIV/AIDS

295
Q

What infections are diagnostic for acute HIV infection?

A

PyrexiaSkin rashHaedacheDiarrhoea OropharyngitisOral mucosal erythema

296
Q

What infections are diagnostic fir ARC asymptomatic seropostive HIV?

A

LymphoadenopathyPersistent pyrexiaDiahorreaWeight losFatigue and malaise

297
Q

What infections are diagnostic for AIDS?

A

Kaposi’s sarcomaNH lymphomaThrombocytopeniaNeurologival diseases

298
Q

What drug is Pre-exposure prophylaxis of HIV?

A

Trivada - emtricitabine

299
Q

When will HIV/AIDS related oral lesions occur?

A

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

300
Q

Why can oral lesions occur?

A

Immunodeficiency

301
Q

Name 5 oral mucosal lesions strongly associated with HIV?

A

Candidiasis: - erythematous, pseudo and angular cheilitisHairy leukoplakiaKaposi sarcomaNH lymphomaPerio disease: linear gingival erythema, necrotising gingivitis and periodontitis - more commonly seen due to immunosuppressant therapy

302
Q

Describe candidiasis in HIV patients?

A

Mild immunodeficiency If psuedomem, indicative of acture immunosuppression - widespread oropharyn and oesoph Can persist for monthErythamtousHyperplastic

303
Q

Describe linear gingival erythema in HIV patients?

A

Red band involving the free gingival margin - not plaque induced - hypermedia due to vasoactive cytokines

304
Q

Describe hairy leukoplakia in HIV?

A

Not pre malignant White patches that can’t be removed Lateral border of the tongueVertical white folds with hair like surfaceSmooth

305
Q

Describe the histopathology of hairy leukoplakia?

A

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

306
Q

Describe Kaposi sarcoma in HIV patients?

A

Most commonly associated with HIVHHV8Involves skin and mucosal surfacesRed purple patch - becomes nodular

307
Q

Describe the histopathology of Kaposi sarcoma?

A

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

308
Q

Describe non-hodgkins lymphoma in HIV patients?

A

AIDA and severely immunocompromised patientsAssociated with EBV

309
Q

Name 4 less commonly oral mucosal lesions with HIV?

A

Bacterial infectionsSalivary glabd diseaseOral ulceration Viral infections

310
Q

Describe HSV and VZV infections in HIV?

A

More severe and higher recurrence

311
Q

Describe the HPV infection in HIV patients?

A

6,11 and 16Venereal warTransmitted via oro genital contact Multiple white/pink nodulesFuse forming sessile or pedunculated papillary lesions

312
Q

Describe the histopathology of HPV in HIV patients?

A

Induce hyperplastic changes rather than ballooning degenerationFibrovascular core covered by stratified squamous epithelium with- hyperpladtiv basal cell layer - acanthosis- parakeratosisKoilocytes

313
Q

Describe atypical ulceration in HIV patients?

A

Oropharyns most commonly affectedAssociated with CMV infection- can also be aphthous stomatitis

314
Q

Describe salivary gland disease in HIV patients?

A

Salivary gland enlargement - mainly parotidXerostomuaLymphocyte infiltration Lympho-epothelial cystsEnlargement of intraparotid nodes as part of P

315
Q

How is Oral cancer classified?

A

International Classification of Disease for Oncology- ICD-O

316
Q

What makes classification of cancer difficult?

A

Makes comparison difficult Makes epidemiology difficultMakes treatment planning difficult

317
Q

Name the 2 distinct disease patterns for oral cancer?

A

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

318
Q

Describe the epidemiology of OCC?

A

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

319
Q

Name the 6 common sites for mouth cancer?

A

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

320
Q

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

A

FoMLat. border of the tongueSoft palate

321
Q

Name the 8 sites of oral cancer?

A

LipsPalateTonsilsFoMOther throatTongueOropharynxGums

322
Q

Describe the epidemiology for OPC?

A

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

323
Q

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

A

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

324
Q

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

A

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

325
Q

What are the benefits of reducing smoking and alcohol intake?

A

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

326
Q

What are the benefits of improving SE status?

A

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

327
Q

What are the benefits of reducing poor diet choices?

A
  • There is limited new evidence in relation to dietary factors beyond confirming that a high intake of fresh fruits and vegetables were associated with reducing by half the oral cancer risk- Obesity was not associated with an increased oral cancer risk- young people (aged 30-years or less) oral cancer was more likely in those who self-reported a low body mass index (BMI)
328
Q

Name 4 potentially malignant lesions?

A

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

329
Q

Describe the epidemiology of white lesions in OC?

A

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

330
Q

Name 3 types of descriptions of white lesions?

A

HomogenousErosiveNon-homogenous on atrophic background

331
Q

How does erythroplakia compare to leukoplakia?

A

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

332
Q

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

A

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

333
Q

Describe the histological low grade of oral mucosal dysplasia?

A

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

334
Q

Describe the histological high grade of oral mucosal dysplasia?

A

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

335
Q

Describe the histological carcinoma in situ of oral mucosal dysplasia?

A

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

336
Q

Name the histoloigcal prognostic facors which give information on survivability?

A

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

337
Q

Describe the Field Cancerisation concept?

A

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

338
Q

Name the multiple variables for clinical cancer staging of OC?

A

site size (T)spread (N&M)

339
Q

Describe the different varying change of cancer prognosis/survivability?

A

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

340
Q

Describe the aetiology, behaviour and prognosis of Lip cancer?

A

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

341
Q

How is OC detected?

A

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

342
Q

What are the advantages and disadvantages of OC screening?

A

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

343
Q

Name the 5 OC screening tools?

A

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

344
Q

Describe what and how toluidine blue is and used?

A

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

345
Q

Describe what and how VELscope is and used?

A

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

346
Q

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

A

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

347
Q

What is the definition of precancerous lesion?

A

An altered tissue in which cancer is more likely to form

348
Q

What is the defintiion of precancerous condition?

A

A generalised state associated with an increased cancer risk

349
Q

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

A

Tobacco related lesions Smokers keratosis Chronic hyperplastic candidosis Frictional keratosis

350
Q

What is the definition of leukoplakia?

A

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

351
Q

Describe the epidemiology of leukoplakia?

A
  • Incidence ? 0.2 – 10% but wide variation in different parts of the world. 6 x commoner in tobacco users. Male > Female world wide but only marginally so in the west. More common in the “elderly.” - Malignant change in 3 -28%- Period prevalence - how many in what time? 2.5% in 10 years, 4% in 20 years (West) ? % in Far east and Africa
352
Q

Name the clinical predictors of malignancy?

A

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

353
Q

Describe the molecular progression of oral cancer?

A

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

354
Q

What is the definition of hyperplasia?

A

Increased cell numbersArchitecture regular stratification altered compartment sizeNO cellular atypia

355
Q

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

A

Architecture -increased maturationcompartment

356
Q

What is the definition of basal cell hyperplasia?

A

increased basal cells

357
Q

What is the definition of low grade (mild hyperplasia)

A

Architecture -change in lower thirdMild -cytological atypia

358
Q

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

A

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

359
Q

What is the definition of oral candidosis?

A

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

360
Q

How do people aquire candida?

A

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

361
Q

Name 5 candidal virulence factors?

A

AdherenceSwitching mechanismsGerm tube formationExtracellular enzymesAcidic metabolites

362
Q

Name the local predisposing factors for candidal infections?

A

SmokingDenturesLocal corticosteroidsXerostomiaTopical antimicrobials

363
Q

Name the general predisposing factors for candidal infections?

A

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

364
Q

Name the classification of oral candidosis?

A

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

365
Q

How to diagnose oral candidosis?

A

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

366
Q

How to diagnose candidosis via lab?

A

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

367
Q

How to identify candidaosis in the lab?

A

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

368
Q

Name the 5 candida species?

A

C. albicansC. glabrataC. tropicalisC. kruseiC. dubliniensis

369
Q

Describe the principles of management for candidal infection?

A

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

370
Q

Name different categories of antifingal drugs?

A

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

371
Q

Explain the treatment regimes for oral candidosis?

A

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

372
Q

What is the definition of miconazole?

A
  • Imidazole antifungal- Not absorbed systemically- Available as a cream, ointment, patch or a gel - Don’t use gel for skin lesions (orange!) - Cream/ointment available with hydrocortisone - Available without prescriptionSlow release adhesive preparation availableACTIVE AGAINST STAPHYLOCOCCI as well as Candida
373
Q

Name the types of systemic antifungals and their treatment regimes?

A

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

374
Q

Name 3 antifungals that have resistance?

A

C. glabrataC. kruseiiC. dubliniensis

375
Q

Name the disease that come from Human herpesvirus/

A

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

376
Q

Explain the virion replication cycle?

A

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

377
Q

Effect of viral infections on host cells?

A

Cell death (cytopathic effect)Latent infectionHyperplasia Transformation

378
Q

Explain the lifecycle of HSV, VZV associated leison?

A

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

379
Q

Explain how to diagnose human herpesvirus?

A

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

380
Q

Describe the apperance of primary herpetic stomatosis?

A

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

381
Q

Describe the apperance of chickenpox?

A

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

382
Q

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

A

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

383
Q

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

A

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

384
Q

Describe the apperance of infectious mononucleosis?

A

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

385
Q

Describe the apperance of CMV?

A

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

386
Q

Describe the apperance of hand-foot and mouth disease?

A

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

387
Q

Describe the apperance of herpangina?

A

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

388
Q

Describe the apperance of measles?

A

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

389
Q

Describe the apperance of warts?

A

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

390
Q

Describe the apperance of squamous papilloma?

A

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

391
Q

Describe the apperance of condyloma acuminatum?

A

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

392
Q

Describe the management of oral mucosal HPV-related lesions?

A

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

393
Q

Describe the histopathology of oral mucosal HPV-related lesions?

A

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

394
Q

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

A

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

395
Q

Describe what sampling and testing involves?

A

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

396
Q

How to decide if infection need treatment?

A

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

397
Q

How to decide appropriate treatment for infection?

A

Culture and sensitivity test - always preferredBest guessExperienceSide effect profile Cost

398
Q

What is the defintion of staphylococcal infection

A

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

399
Q

What is the defintion of scarlet fever?

A

Exotoxin mediated mucocutaneous manifestations

400
Q

Name the 4 clinical features of scarlet fever?

A

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

401
Q

What are the clinical features of tuberculosis?

A

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

402
Q

What isnthe histopathology of tuberculosis ?

A

Granukomas containing muktinuc giant cells- mycobacteria not always identifiable

403
Q

What are the oral manifestations of syphilis?

A

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

404
Q

What is the defintion of gonorrhea?

A

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

405
Q

What are the clinical features of actinomycosis?

A

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

406
Q

What are the histopathologucal features of actinomycosis?

A

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

407
Q

Court ordered mandate for release of dental records?

A

Must be sent to the lawyer

408
Q

What if a patient doesn’t attend their referral appointment?

A

If it is possibly harmful such as a biopsy - you should try and persuade them to goIf they still refuse to go to their referral and explain that they don’t want to be referred anymore - you still MUST refer them, protected under the data protection act. If they still don’t attend it is essential to try and persuade them to go

409
Q

What is the period of time for a complaint to be dealt informally?

A

5 days

410
Q

If a formal complaint has been made, when must the dentist acknowledge it?

A

Within 3 working days

411
Q

How many days must the complaint be responded to?

A

20 days

412
Q

Complaints procedure - how long to reply?

A

Acknowledge receiving complaint within 3 daysRespond informally in 5 days And respond formally in 20 days5 days response to decide formally or informally3 days after formal 20 days in total

413
Q

How can the patient take their complaint to the next step?

A

Complaint NHS Ombudsman, within 28 day reply

4th Year Adapted (2 decks)

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