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BODC > BCS/Pulpal Disease > Flashcards

BCS/Pulpal Disease Flashcards

1
Q

Role of cementum in the spread of bacteria from pulp

A

Stops the bacteria and toxins spreading from pulp into dentine tubules and surrounding PDL.

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2
Q

Pulpal 1st/2nd line of defense

A 
1 = odontoblasts make tertiary dentine
2 = inflammation and immune response at the apex/periapical area to stop bacteria going into the surrounding tissues.
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3
Q

What to check for in a pre-op assessment before RCT

A 
Reference point
Radiographic apex
Number and shape of canals and roots
Size of canals space e.g. is it patent
Periapical pathology
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4
Q

Steps to a RCT

A 
Access cavity - straight-line access
Coronal 2/3 of pulp prep
Full glide path
Working length and master apical file
Step back to shape the file.
Apical guaging
Obturate
Cut back
Restore
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5
Q

Chemical prep of the RCT aims

A

Lubricant for the instruments
Kill and remove bacteria and the smear layer.
Remove debris to stop the apex getting blocked
Dissolution of the pulp material and necrotic tissue so it can then be flushed away.
Disinfectant.

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6
Q

Aims of a RCT

A

Remove all the dead tissue and seal all the entry and exits, create a full glide path.

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7
Q

Why is rubber dam important for RCT

A

Protect surrounding tissues and teeth from the irrigant and bacteria. Can use oroseal too.

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8
Q

How to do a good access cavity for RCT

A

Check long axis of the tooth before rubber dam and follow the long axis. Remove all of the pulp roof and chamber so u can see all the way to the apex and it is straight-line access.
No ledges or overhangs and smooth axial walls and tapered shape. Can see all the orifices.

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9
Q

Instrument used for access cavity and coronal 2/3 of root prep

A

Diamond burs - pear and round
Rosehead burs - long shaft
Gates Glidden burs in different sizes, smaller as u get closer to coronal 2/3 of the canal.
Endo Z file - has a rounded blunt end so just used for shaping the access cavity e.g. doesn’t enter the pulp canal.

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10
Q

Benefits of a straight-line access and full glide path.

A

No ledges or perforations or transported axis. Easy instrumentation/less stress e.g. less chance of them breaking.

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11
Q

What is the working length

A

0.5-1mm short of the radiographic apex, at the apical constriction. Delta shape of apex means that you can’t see it radiographically but can feel it (tactile sensation)

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12
Q

Importance of getting the correct working length

A

Too long = bacteria and debris and irrigant pushed out of apex into the surrounding tissue, and the canal will end up being over-filled and the material will be recognised as foreign and cause an immune response.

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13
Q

How to determine the working length

A
  • Paper points to working length - if they are wet or have blood on them then they’re too long.
  • Radiographically by measuring the length.
  • Place GP point or file (min 15mm to be seen radiographically) and check where it ends on the radiograph.
  • Tactile sensation
  • Electronic apex detector
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14
Q

How to find the master apical file size.

A

The biggest file that goes to the working length + 2 file sizes. Minimum will be 25mm because you need at least 15mm file size to see it on a radiograph.

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15
Q

Recapitulating

A

While prepping the canal. Each time u go up a file size, go back with a smaller file size to the working length to stir up the debris and stop it blocking the apex, and irrigate.

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16
Q

Apical guaging

A

To check if the master apical file fills the apical constriction:

  1. If u apply pressure, the master apical file doesn’t get pushed further down past the working length and should fit snuggle.
  2. A size larger file stops 1mm short of the working length.
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17
Q

Ideal properties of the irrigant

A 
Non-corrosive to the instruments
Non-toxic
Removes organic and inorganic e.g. smear layer
Kills microbes
Antiseptic
Antisepsis properties to stop bleeding for better visualisation
Lubricant
Dissolve pulp tissue
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18
Q

What is the irrigant normally used in RCT

A

1 to 5% sodium hypochloride - antibacterial and dissolves organic
17% EDTA removes inorganic material

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19
Q

What is the alternative irrigant used in RCT

A

Chlorhexidine 2%, if you are allergic to the other. Antibacterial but doesn’t dissolve organic or inorganic. Can’t be combined with sodium hypochloride bc it forms a toxic ppt.

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20
Q

Why is it important to remove the smear layer in a RCT

A

Bacteria and nutrients in the smear layer and it blocks the dentine tubules and reduced the quality of the bond when it is filled and if it breaks down later it leaves voids.
Can act as a barrier to irrigants.

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21
Q

The importance of inter-visit medication in RCT

A

Stops the bacteria proliferating and reduced the number of bacteria in the canal. Seals the canal so stops more bacteria or nutrients getting in.

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22
Q

Types of inter-visit medication

A

Non-setting calcium hydroxide and odontopaste

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23
Q

Non-setting calcium hydroxide as a inter-visit medication

A

Easy to apply and remove. Is temporary and begins to break down after 2 weeks. Very alkaline so denatures bacteria and proteins. Barium sulphate added so that it is radioopaque.

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24
Q

How to apply and remove inter-visit medication

A

Apply with paper points or k files. Remove by breaking it up using k-files or ultrasonic scaler with water and irrigate.

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25
Q

Odontopaste as an inter-visit medication

A

anti-inflammatory (steroids) so reduced post-op pain and antibacterial (antibiotics) so good for patients in pain.

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26
Q

What covers the inter-visit medication

A

Cavit or coltosol or sponge and then a temporary restoration (all easy to remove). Don’t use wool or cotton bc fibres track bacterial in and get stuck in the cavity.

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27
Q

Post-operative instructions after inter-visit medication applied.

A

Take NSAIDs and analgesics

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28
Q

The importance of obturating

A

Blocks all entries and exits from the pulp and fills the canal so bacteria and fluids can’t enter or proliferate. Prevent reinfection and seals everything in.

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29
Q

Obturation techniques

A

Cold-lateral condensation

Thermalplastic condensation - warm verticle or lateral.

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30
Q

Ideal properties of root canal filing material and an example

A

E.g. gutta percha

  • Easy to place and remove
  • Inexpensive
  • Radioopaque
  • Inert non-toxic etc
  • Doesn’t change dimension on setting
  • Insoluble in tissue fluid
  • Can follow canal’s shape
  • Stops leakages
  • Compatable with other materials
  • Long shelf life/stable
  • Bactericidal
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31
Q

Root canal sealer uses

A

To fill voids, stick the GP points together and fill lateral canals. Lubricates and help the GP points move.

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32
Q

Cold lateral condensation

A
  1. GP point to working length and the same size as the master apical file. Tug back to check that it fits snuggly.
  2. Radiograph to check that it goes to working length.
  3. Sealer applied to walls of canal and tip of GP point.
  4. Finger spreaders used to push GP to the side of the canal and then a GP accessory point of the same size is inserted (+sealer at the tip).
  5. Repeat until can’t fit anymore accessory point.
  6. Take a radiograph to check for voids.
  7. Cut back the GP at the canal orifice
  8. Restore
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33
Q

When to take a radiograph during obturation and why

A

To check master GP file length
To check for voids
To review

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34
Q

Properties of an ideal RCT filling

A

3D and dense filling (no voids)
To full working length and no longer e.g. 1mm short of radiographic apex.
Smooth tapered shape

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35
Q

What form does GIC come in/what is it made of

A

Powder + liquid.
Liquid = soluble acid polymer
Solid = glass powder

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36
Q

How does GIC set

A

Acid/base reaction
Polymer dissolves in water and H+ ions released which attack the glass surface and release calcium and phosphate ions. These bind to the COO- on the acid chain and form cross-links and harden the mixture.
Dissolution -> gelation -> hardening

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37
Q

Properties of GIC

A

Strong bond to the tooth, doesn’t need moisture control, safe and biocompatible, F- releasing, antibacterial properties, doesn’t shrink when setting.
Poor aesthetics and poor wear resistance bc larger particles. Not good for incisal edges bc not durable/is brittle. Not command set so is technique sensitive.

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38
Q

Clinical uses of GIC

A

Class V or where moisture control is difficult.
Temporary restorations
Primary teeth
When aesthetics aren’t important

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39
Q

RM-GIC

A

HEMA monomers added

and photoinitiator. Sets by acid-base reaction and photo-polymerisation of HEMA monomers.

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40
Q

Polyacid modified resin composite

A

Normal resin composite but F- releasing glass particles added - need water to release F- so don’t act until much later and v slowly.

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41
Q

Advantages of resin composite

A 
Bonds to tooth material = more conservative
Better for environment and health
Better aesthetics
Strong and durable
Chemically stable
Safe to use
Easy to place
Command set
Minimal tooth prep.
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42
Q

Disadvantages of resin composite

A 
Less wear resistant
Polymerisation shrinkage = leakages
Need moisture control.
Technique sensitive.
Needs bonding system.
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43
Q

2 phases of composite resin and what they contain

A

Organic phase = methacrylate monomers, accelerators (faster reaction), stabilizers (for when not being used), inhibitors (stop normal light polymerising it).
Filler phase = filler particles (quartz or silica), photoinitiator.

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44
Q

Large filler size composite properties

A

Less wear resistance, poorer aesthetics, weaker bond to enamel surface and more shrinkage.

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45
Q

Nano filler size composite properties

A 
Less shrinkage
Stronger bond
Better aesthetics bc small particles reflect light more
Can be polished
More wear resistant
More homogenous mixture
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46
Q

Composite resin setting methods

A 
Light-cured
Chemical cured (activator and free-radical initiator)
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47
Q

How to classify composite resins

A

Filler size
Initiation/curing method
Viscosity
Clinical application

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48
Q

Adhesion benefits for composite resins

A

More conservative.
Can support the remaining tooth structure and undercuts.
Better adaptation to tooth material = less microleakage.
Allows for bevelled margins and better aesthetics.

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49
Q

Benefits of having beveled margins for composite restorations.

A

More surface area so more exposed tubules so stronger bond and better aesthetics bc junction between restoration and tooth tissue are less evident.

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50
Q

Indications for use of composite

A 
. Can't create retentive features
. Where aesthetics important
. Incisal edges
. Conserving tooth structure
. Small cavities
. If the patient allergic to metals.
. Repairing enamel/dentine fractures and tooth wear
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51
Q

Contraindications for composite

A 
. Can't have good moisture control
. Not enough tooth structure to bond to
. Too large restoration
. Time constraints
. Lots of force/pressure on restoration
. Patients with high caries risk or grinding habits
. If allergic to the materials.
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52
Q

How to acid etch

A

35% phosphoric acid for 20-30s

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53
Q

Benefits of acid etching.

A
  • Removes pellicle layer so exposes enamel surface which allows for complete wettability bc enamel surface energy > adhesive surface tension.
  • Removes contaminants
  • Makes enamel surface rougher by partial desolation of HA prisms increases SA and undercuts and creates a more terentive surface so stronger bond to adhesive/more intimate contact.
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54
Q

Why does bonding area for composite restorations need to be kept dry

A

Water is polar and resin in not polar so if water was in the way it would stop complete intimate contact between resin and enamel so the bond would be weaker.

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55
Q

Steps to a composite restoration

A
  1. clean with pumice and slurry 30s
  2. wash and dry
  3. acid etch 20-30s
  4. wash and dry until a frosted white appearance
  5. apply bond
  6. light cure for 15s
  7. apply the composite in small increments and light cure for 30s in between.
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56
Q

Why is it important to clean before acid etch and what is the process

A

Clean with pumice and slurry and then rinse and dry.

To remove debris so that the acid can act on the enamel surface.

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57
Q

How to reduce shrinkage/stress in composite restorations

A

Reduce the C-factor (Configuration factor = bonded surfaces: open surfaces in the cavity. Large means more bonded surface so more stress and a higher C-factor).
Oblique packing for rebuilding cusps or curing in small increments.

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58
Q

Bulk fill composites and benefits

A

A Sonic device changes the viscosity of the composite and makes it more flowable. Better adaptation, less polymerisation shrinkage, better seal and better aesthetics.

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59
Q

Instruments used to finish and polish composite restorations

A

Finish with microfine diamond burs and polish with polishing strips and soflex discs.

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60
Q

Resin bonding to dentine benefits

A
  • Seals the dentine tubules and enhances retention and strength.
  • Stops internal gaps so stops hydrodynamic effect and post-op sensitivity/pain.
  • Stops marginal gaps which allow bacterial invasion and secondary caries.
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61
Q

Problems/challenges with resin-dentine bonding

A
  • Dentine is hard to dry/is hydrophilic whereas resin is hydrophobic so need a primer.
  • Smear/pellicle layer needs to be removed
  • Complex heterogenous substrate (dentine).
  • Fluid flow from resin into tubules and to the pulp (toxic).
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62
Q

Dentine conditioner

A

Acid etch to remove the smear layer and to dissolve the dentine leaving a collagen meshwork.
Stronger etch/acid = wider tubules.

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63
Q

Dentine primer structure and example

A

A polar group that binds to the collagen/HA
A methacrylate group that binds to the resin via polymerisation
A spacer that is long enough to make molecule and bonds flexible so the bond is stronger.
E.g. HEMA
In a solvent that carries the monomers deep into the tubules and chases out the water and evaporates e.g. acetone.

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64
Q

Sealer

A

Binds to the primer and hardens to seal tubules..

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65
Q

Causes and negatives of polymer shrinkage

A

VdW bonds get replaced by covalent bonds during polymerisation so molecules are brought closer together = total shrinkage. Causes stress and tension on the tooth structure and can lead to bond failure and poor marginal adaptation = gaps.

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66
Q

Wet dentine bonding

A

Highly volatile solvent chases out the water and carries monomer deep into the collagen so don’t need to dry.
Drying too much collapses the collagen so weaker bond bc primer can’t go in.

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67
Q

3 stage dentine bonding

A

Etch -> prime -> seal. Most complicated and technique sensitive and lots of stages for error. Strongest bond.

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68
Q

2 stage dentine bonding

A

Etch + Primer = a good bond, simple and don’t need to dry. The etch dissolves the smear layer and the HA but the particles aren’t removed so remain in the hybrid layer and can weaken the bond.
Primer + sealer = still need to dry, weaker bond.

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69
Q

All in one dentine bonding

A

Easiest to use but weakest bond.

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70
Q

How can you increase amalgam restoration retention

A 
Grooves
Ledges
Slots
Amalgapins - need to have healthy surrounding dentine and not go into pulp or roots etc.
Bonding
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71
Q

Bonded amalgam

A

Material that bonds to metal and tooth material e.g. HEMA.
Only sets in anaerobic conditions e.g. when under the restoration so good working times and sets as the amalgam is condensed into it.
Increases retention, less sensitivity and less iatrogenic damage.

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72
Q

Problems with bonded amalgam

A

Is soluble in saliva so dissolves out and leaves a gap.
Binds to metal matrix bands.
If some left uncovered then it won’t set.
Reduces mechanical strength of amalgam.

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73
Q

Classification of caries (not Black’s classification)

A 
Early not detectable.
Only detected by caries diagnosis aids.
D1 = Non cavitated enamel lesion
D2 = Enamel caries
D3 = Enamel and dentine caries
D4 = Enamel and dentine and pulp
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74
Q

Methods of diagnosing caries

A

Radiographically.
Tactile (for hard to see places, using blunt explorer).
Visually (need good lighting and dry, clean teeth).
Transillumination.
Electric (caries have more water and ions so altered electrical conductivity).
Interproximal imps.

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75
Q

Why is caries detection difficult

A

Hard to see areas
Different opinions
Early lesions hard to detect

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76
Q

DMF uses

A

Compare populations
Helps determine risk factors/causes and evaluate treatments and effectiveness.
Chart trends in caries.

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77
Q

DMF problems

A

Age-related
Cumulative, irreversible
Non-specific e.g. can’t tell between small restoration or active caries or crown.
Can’t add secondary caries or replaced restorations
Doesn’t take into account other reasons for tooth loss e.g. trauma.

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78
Q

Types of tooth tissue loss

A 
Attrition
Erosion
Abrasion
Trauma
Enamel/dentine abnormalities
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79
Q

Aetiology of attrition

A

Grinding, malocclusion (cross-bite, class 3), crowns affecting opposing tooth, loss of posterior teeth (anterior do more work)

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80
Q

Aetiology of abrasion

A

Tooth brushing, nail biting

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81
Q

Aetiology of erosion

A

Diet, acid reflux, bulimia

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82
Q

Treatment of TSL

A

Diet advice, mouth guard, restore, fluoride

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83
Q

Effects of bad occlusion

A

Attrition, TMJ problems, tooth drifting, localised periodontitis/pulpitis, fractured cusps.

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84
Q

ICP and benefits

A

Max intercuspation bw upper and lower teeth. Protects anterior teeth bc less contact here.

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85
Q

What to use if ICP is unacceptable

A

Use CR

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86
Q

Anterior guidance benefits

A

Disocclusion of posterior teeth.

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87
Q

CR

A

The most superior position of the condyle in the fossa.

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88
Q

RCP

A

The first contacts when the mouth is closed from CR

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89
Q

Ideal occlusion

A

RCP = ICP
Dis-occlusion of posterior teeth when not in ICP
Force applied in axial direction e.g. not lateral.

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90
Q

Indications for preformed metals crowns

A

Primary teeth with RCT or some caries
Enamel/dentine abnormalities e.g. amelogenesis imperfecta (children and adults)
When can’t do other treatment e.g. amalgam can’t be used in under 15s.
Infraoccluded teeth (shorter crowns)

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91
Q

Contraindications for preformed metal crowns

A

Large caries
The tooth about to be exfoliated
Unrestorable teeth

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92
Q

When to not use Halls technique

A

Symptomatic tooth
Endodontic lesion
Risk of endocarditis
V carious tooth

93
Q

Halls technique

A

A good seal will arrest caries so no prep. Place cement in the crown and get the child to bite down hard. Remove excess cement. Use occlusal separators 2 days beforehand to create interproximal space. No occlusal reduction so might have a bit of an open bite but in children, they will be okay.

94
Q

Conventional preformed metal crowns techniue

A

LA, Remove caries, RCT, prep tooth.

Cement PMC and remove excess cement.

95
Q

pros and cons of preformed metal crowns

A

Quick, cheap, easy, longevity, easily corrected if fails.

Not good aesthetics, GIC cement can cause gingival inflammation.

96
Q

Current classification of periodontal disease

A 
Gingivitis
Chronic periodontitis
Aggressive periodontitis
Due to systemic illnesses
Necrotising
Abscessing periodontitis
Endodontic lesion
Development/aquired conditions.
97
Q

Changes to the periodontal disease classification

A

Staging and grading (grading tells you the rate of progression). Takes into account risk factors and defines health.

98
Q

Sub-gingival plaque

A

Darker, harder to remove. Rough surface allows more plaque to form. More anaerobic and gram-negative bacteria that get nutrients from the crevicular fluid.

99
Q

Supra-gingival vs sub-gingival calculus.

A

Supra is paler, forms faster but is easier to remove.
Sub is darker, forms slower but is harder to remove.
Both are brittle and layered, calcified material.

100
Q

Barriers to communication in a dental surgery

A

Patient - nervous, in pain, language, jargon
Dentist - time constraints, lack of training, empathy or sensitivity.
Social/ethnic

101
Q

Calgary-Cambridge framework stages

A
  1. Initiation of session
  2. Gathering information
  3. Examination
  4. Planning and explanation
  5. Closing
    + building a relationship the whole time.
102
Q

Role of inflammation

A

Bring healing factors to the site
Carry and kill bacteria etc away
Stop the spread of infection

103
Q

Why is there pain during inflammation

A

Oedema
Toxic substances released
Activation of nerves via inlammatory mediators e.g. bradykinin

104
Q

Acute inflammation key points and stages

A

Resolves itself and is temporary and single episode e.g. abscess, acute pulpitis, laceration.
Main immune cells are neutrophils and granulocytes - pain, swelling, hot, red.
1. Vasoconstriction
2. Vasodilation and oedema - due to histamine or serotonin.
3. Vascular stasis

105
Q

The role of Oedema

A

Innate immunity bc complements.
Dilute toxins
Increased immune cells
Opsonisation - easier for phagocytosis (C3b also does this).
Cytotoxic T helper cells
Involves clotting cascade so fibrin barrier can form and stop the spread of infection.
Kininogens -> kinins have similar effect as histamine (vasodilation)

106
Q

Complements involved in oedema and their actions

A

C3 and 5 = Histamine secretion, vasodilation/vascular permeability, attract phagocytes, leukotrients atract neutrophils, prostoglandins for vasodilation.
C5-9 = Membrane attacking complex can change channels in the membrane of pathogens and cause cell lysis and death.

107
Q

Cellular response during acute inflammation

A

Vasodilation increases the viscosity of blood so flows slower so neutrophils have more time to adhere to the epithelium of blood (pavementation, via selectin adhesion molecules) and then bond stronger via integrins on their surface and then emigrate through the gap junctions (via chemotaxis and chemotactic gradient) and aggregate and phagocytose.

108
Q

Action of neutrophils

A

Phagocytosis.
Degranulation.
NETS - before it dies it releases its DNA and traps microbes.

109
Q

Outcomes of acute inflammation

A

Complete resolution = function restored
Healing by fibrosis - Scar tissue/granulation tissue formed
Continued inflammation - chronic

110
Q

Chronic inflammation key points and features

A

No resolution e.g. bc of low-grade inflammation or a foreign body or restricted blood supply. Gradual onset, prolonged ad frustrated healing. Cells involved are lymphocytes, macrophages. Systemic features e.g. fever.

111
Q

Action of macrophages

A

Phagocytosis.
Antigen-presenting cells stimulate T-cells e.g. helper T-cells (= B cells and plasma cells and Ig), or cytotoxic. T-cells.
Cytokines and chemokines released which attract inflammatory cells.

112
Q

How is tissue destruction caused during chronic inflammation

A

Products of activated macrophages e.g. proteases, free oxygen radicals.
Cytotoxic T-cells
Products of microbes.

113
Q

How is repair brought about during chronic inflammation

A

Regeneration - normal tissue.

CT or scar formation.

114
Q

Granulomatous inflammation and cells involved

A

Macrophages and giant cells collect and form a granuloma. Macrophages merge to form giant cells e.g. foreign body giant cells w disorganised central mass of nuclei or Langhan giant cells w nuclei arranged around the edge in a semi-circle. Lymphocytes surrounding the granuloma.

115
Q

Example of granulomatous inflammation

A

Tuberculosis - macrophages continue to be activated until granuloma formed.

116
Q

Results of stimulus on enamel

A

Pain. On heating or cooling or mechanical or chemical.

117
Q

Stimulus on dentine

A

Mechanical, drying, hydrostatic pressure and thermal = pain.
Chemical stimuli only cause pain if change osmotic pressure.
Smear layer reduces sensitivity.
Outer dentine not innervated but still sensitive.

118
Q

Types of nerve fibres in tooth

A

A-beta = in dentine, cold sensitive
A- delta = in tubules and give sensation and pain if fluid movement.
C-fibres in pulp

119
Q

A beta fibres

A

Mechano-sensitive normally but only feel pain in tooth.

120
Q

Cold vs heat sensitive neurons

A

cold sensitive = fast acting, respond quickly to cold stimuli and also respond to other stimuli.
Heat sensitive = respond slowly to hot stimuli and don’t respond to other stimuli.

121
Q

Hydrodynamic theory

A

Movement of fluids in tubules disrupts odontoblast and underlying layers and causes pain in cold-sensitive nerve fibres.

122
Q

C-fibres

A

Sensitive to direct heating.

123
Q

Treatment for non-noxious stimuli on tooth e.g. TSL or erosion

A

Prevention e.g. diet advice, OHE, fluoride, de-sensitising agents. Reduce dentine permeability (size and no. of tubules). Stop fluid movement in tubules or depolarisation of nerve fibres.

124
Q

Role of nerves in the tooth

A

Sensation and allow repair and protect the tooth.

125
Q

Demineralisation in root caries signs

A

No colour changes e.g. no white spot lesion. Can stain.
An arrested lesion is dark, shiny, clean, hard.
The active lesion is paler, soft, matt, plaque and inflamed gums.
If collagen not broken down then the process is reversible.

126
Q

Detection of root caries

A

Radiographs, tactile sensation

127
Q

Treatment of root caries

A

Prevention.
Operate if the lesion is cavitated, or plaque retentive or can’t be cleaned by pt.
Shorter recall time.
Instrumentation may be difficult if v subgingival - use retraction cord (bc rubber dam won’t work) to access.
Don’t need a fast handpiece unless it has reached the enamel - chemomechanical or air abrasion can be used.
GIC if poor moisture control or not enough healthy dentine/no enamel and aesthetics aren’t important but composite would be ideal.

128
Q

Vascular events of pulp inflammation

A

Increased vascular permeability causes increased tissue pressure (oedema) and collapses the thin-walled, low-pressure veins.
Increased viscosity of blood means waste can’t be removed = cell death.
Increased absorption from the lymphatic system and periphery vessels (to limit the spread of infection)
Blood flow redirected to areas that need it more.

129
Q

Role of dendritic cells in pulp

A

Initiate immune/inflammatory response in pulp by alerting the immune system.

130
Q

How can tubular fluid and tubules protect against bacterial infiltration into pulp

A

Less and thinner tubules in outer dentine = reduced permeability.
The tubular fluid has a positive pressure from pulp to outside so doesn’t let fluid flow down/flushes bacteria and by-products away.

131
Q

A-delta fibres

A

In dentine tubules, cause a sensation

132
Q

Types of tertiary dentine

A 
Reactionary = Primary odontoblasts responding to mild stimuli. Dentine has a regular structure e.g. tubules. Oodontoblasts don't die.
Reparative = Odontoblasts die and secondary odontoblasts make irregular, fast dentine. Porous bc more impurities and no tubules, less sensitive and less protective.
133
Q

Causes of damage to the pulp

A

Trauma
Mechanical e.g. during restorations, drying, TSL.
Bacteria - caries, secondary caries, from periodontal defects
Pathologies cause resorption.

134
Q

Bisphosphonates’ effect on treatment planning

A

Inhibit Oc e.g. if have osteoporosis or bone cancer. Avoid XLA bc risk of bone necrosis/won’t heal and pain.
Can cause oestomyelitis - infectious inflammation in the bone.

135
Q

Intra-oral examination to diagnose pulp pathology

A

Soft tissues, Gum health, teeth, occlusion, tooth discolouration (yellow/cream = tertiary dentine, grey/black = blood necrosis)

136
Q

Special investigations to diagnose pulp pathology

A

Sensibility testing
Vitality testing
Radiographs
Periapical tests e.g TTP and palpation

137
Q

Sensibility testing of pulp

A

Cold test e.g. ethyl chloride
The hot test is harder e.g. wax or GP
No response = dead
Electric pulp tester - false negatives common bc teeth’s resistance affects stimulation and can only be used on tooth tissue.

138
Q

Vitality testing of the pulp

A

Tests to see if can detect pulsing of blood (pulse oximetry) or if blood present it will scatter the light (laser Doppler).

139
Q

Types of pain responses of the pulp and what they indicate

A

Dull ache pain = C fibres in the pulp

Sharp temporary pain - A fibres in dentine.

140
Q

Reliability of pulp testing

A

Affected by restorations, caries, the thickness of enamel, gum health, pulp size/age, trauma

141
Q

Sensitivity vs specificity of tests

A 
Sensitivity = % of true positives
Specificity = % of true negatives
142
Q

Types of periapical tests

A

TTP - if tender than inflammation of PDL (total or partial necrosis).
Palpation - palpate at the apex for signs of abscess or pus.
Tooth sloth used to test each cusp.
Pain on pressure = PA/periodontal pathology, pain on the release of pressure = tooth fracture.

143
Q

Additional testing for determining pulp pathology

A

Inserting GP extra-oral through the sinus and see which tooth it leads to.
Selective anaesthetic to see where the pain is coming from.
Beginning tooth prep without LA and seeing if tooth sensitive (only if sure that it is necrotic)
Transillumination to detect cracks, fractures or pathology.

144
Q

Causes of root caries

A

Caused by recession/periodontitis, hyposalivation, drugs, brushing technique, poor oral hygiene, systemic diseases.

145
Q

Properties of an ideal pulp tester

A

Effective on all teeth and roots, restored or carious teeth, transplanted and re-implanted teeth.
False positive and negative results aren’t common.

146
Q

Types of periapical pathology

A 
Inflammatory = periapical periodontitis - chronic or acute.
Reactive = osteosclerosis, hypercementosis, ankylosis, cemento-osseous dysplasia
Neoplastic = benign cementoblastoma
Degenerative = fibrosis, calcification, internal resorption or idiopathic
147
Q

Symptomatic periapical periodontitis symptoms/ signs

A

Acute.
Localised and pain on pressure and aching pain.
Not detected radiographically if hasn’t been around long enough to erode the bone.

148
Q

Acute periapical abscess

A

May or may not be detected radiographically
Doesn’t drain and is v painful esp on pressure - localised.
Inflammation and swelling of tissues and patient may get systemic symptoms e.g. a fever.

149
Q

Chronic abscess

A

Draining so fewer symptoms and detected radiographically as a radiolucent area.
Pus from dead and dying neutrophils

150
Q

Where can pus from an abscess spread to

A

Oral through the apex or PDL, or go through the thin bone or cellulitis if it spreads to facial tissue.
Drain into sinuses.

151
Q

Asymptomatic periapical periodontitis symptoms

A

Chronic, not painful but can be detected radiographically as a radiolucent area.
Also known as a periapical granuloma.
Is a space filled w a mass of inflamed granulation tissues that replace resoprbed bone.

152
Q

Asymptomatic periapical periodontitis histology

A

Fibrous capsule w granulation tissues e.g. macrophages, fibroblasts and blood vessels.
Inflammation Stimulates rests of Mallasez to proliferate and make epithelium.

153
Q

Radicular cysts and histology

A

Periapical granuloma can become a cyst as the rests of Mallasez in PDL become activated and breakdown the proliferated epithelium in the granuloma to leave a cyst lumen lined by epithelium. Can become infected and less defined histologically. Always associated w a non-vital tooth.

154
Q

Reactive periapical pathology types.

A

Osteosclerosis, hypercementosis, ankylosis, cemento-osseous dysplasia

155
Q

Osteosclerosis

A

Radioopacity around the periapical lesion to try and stop the infection spreading and can be left behind after XLA = focal sclerosing osteitis.
Rarefying osteitis = radiolucent

156
Q

Hypercementosis

A

Extra cementum laid down, can be naturally due to age or other reasons e.g. loss of tooth or inflammation. Make XLA harder.

157
Q

Ankylosis

A

Bone and tooth fuse/loss of PDL

158
Q

Cemento-Osseous dysplasia

A

Areas of radioopaque in radiolucent areas. Trabecula laid down and areas of necrosis or cementum laid down in edentulous..
Fibro-osseous = fibrous tissue replacing bone.

159
Q

Cementoblastoma

A

Benign cementum mass under the tooth.

160
Q

Condensing osteitis

A

Radioopaque lesion around apex of tooth - scerlosed or mineralised or localised bony reaction to a low grade stimulus.

161
Q

Features of pulp that make it sensitive to infection

A

Enclosed in dentine - not enough space to expand when inflammation
Limited blood supply - cut off easily
Surrounded by bone - infection can spread here

162
Q

Pulp diagnoses

A

Reversible pulpitis
Irreversible pulpitis - symptomatic or asymptomatic
Pulp necrosis

163
Q

Reversible pulpitis

A

Not localised, a sharp pain on sweet or cold stimuli that goes away when stimulus removed.
Not detected radiographically
Intervention can lead to it being resolved e.g. removing caries.
Analgesics manage the pain.
Exaggerated response to sensibility testing.

164
Q

Irreversible pulpitis

A

Symptomatic - not localised dull achy pain that can be spontaneous and lasts a while. Trouble sleeping.
Needs RCT.
Can be asymptomatic e.g. tooth responds normally to testing.

165
Q

Pulp necrosis

A

The pulp is dead and needs to be removed to stop byproducts and toxins going into the periapical area. Bacteria don’t go into periapical space at first bc there’s an immune response here. Asymptomatic.

166
Q

Types of post-eruption dentine

A

Secondary - laid down throughout life

Tertiary - in response to a stimulus. Can be reactionary (low grade) or reparative.

167
Q

Pulp stones

A

Bit of dentine in the pulp that makes it harder to do RCT. Natural can be due to age.

168
Q

Degenerative pulp pathology examples

A

Internal resorption
Calcification
Fibrosis
Idiopathic

169
Q

Causes of pulpitis

A

Caries/bacteria
Trauma - mechanical, chemical, physical
Abrasion, attrition, erosion.

170
Q

What can lead to dental caries (caries is a secondary effect)

A

Invaginating of crown/odontoma = holes that can lead to the pulp.
Bacteria in circulation go into pulp.
Lateral root canals/roots exposed due to periodontitis.

171
Q

How does hypoxia of the pulp happen

A

Vasodilation and increased permeability = oedema and swelling of the pulp in a constricted space = pressure buildup. This collapses the low-pressure veins and may block the apex. Blocked apex (+ viscous blood bc of oedema) means blood supply is compromised so waste can’t be carried away and no more blood so hypoxic tissues and apoptosis.

172
Q

Protective responses of the pulp

A

Scerlosed tubules - dentine laid down inside tubules so are narrow so reduce toxins travelling down them etc.
Tertiary dentine.
Oedema and immune response/cells.

173
Q

Chronic hyperplastic pulpitis

A

When apex is open means that blood supply isn’t compromised so pulp will stay vital even if caries in crown continues. Will lead to (clinically) minimal crown and exposed pulp, covered by epithelium/fibrin/neutrophils and ulceration. Normally asymptomatic and manage by stimulating dentine by applying Calcium hydroxide onto pulp.

174
Q

Functions of pulpal tissue

A

Provide nutrients and oxygen and immune factors and carry waste away.
Nerve supply
Maintains structural integrity
Maintains fluid flow in enamel and dentine.
Important in mineralisation

175
Q

Why is it important to preserve pulp vitality

A

Without it tooth becomes non-vital
Loss of structural integrity
Irreversible
Loss of some proprioception
Brittle weakened tooth structure and poor prognosis.
To keep the tooth and prolong its durability.

176
Q

Consequences of loss of pulp vitality on the patient

A

Pain and dental treatment and infection and inflammation.

177
Q

Consequences of RCT on the tooth

A

EDTA and sodium hypochloride (chemical cleaning during RCT) breakdown the walls of the pulp and make the dentine brittle.
Removal of tooth tissue makes it less strong against occlusal forces and changes the distribution of forces bc of the cavity.
Eugenol increases microhardness of tooth.
Loss of pulp roof reduced fracture strength.

178
Q

Benefits of RCT

A

Preserve aesthetics and some function

Less damage to neighbouring teeth e.g. via bridges and RPD.

179
Q

How do we know that bacteria is needed for pulp pathology

A

Germ-free and normal animals feed cariogenic diet. Germfree’s pulp remained vital even when food reached it.

180
Q

Routes of entry to the pulp and routes bacteria can spread

A

From periapical blood vessels
Through dentine tubules due to caries
Exposure of pulp e.g. fracture
Exposure of dentine tubules due to gum recession.

Bacteria in the pulp can also spread out in these ways.

181
Q

Mechanism of invasion of bacteria through tubules.

A

Bind to type 1 collagen in tubules via adhesion antigens and then spread up by replication and via the fluid in tubules.

182
Q

Dentoalveolar infections and what do clinical observations/severity depend on

A

Inflammation and pus forming = abscess which can spread to surrounding tissues by the easiest route. Clinical observations depend on the virulence of bacteria, host’s inflammatory response and anatomy in that area.

183
Q

What can periapical periodontitis lead to

A

Acute inflammation = acute abscess = bacteraemia (in blood)

Chronic inflammation = chronic abscess or granuloma = cyst

184
Q

Pathogenic features of bacteria

A

Enzymes that attack the host’s tissues e.g. proteases that degrade Ig, C’ and phospholipases that degrade cell membranes.
Metabolic by-products e.g. acids or H2S.
Bacterial structures e.g. capsules, endotoxins, adhesions.

185
Q

Remaining dentine thickness

A

Minimum of 0.7mm of healthy dentine needed to ensure pulpal protection.

186
Q

Chlorhexadine

A

Disnefcts cavity and pulp surface and can be used to achieve haemostasis and stops breakdown of collagen in dentine so improves its durability.

187
Q

Conservative approach to pulp treatment

A

PCR
Direct pulp capping on exposure to form dentine bridge.
Clean w disinfectant and saline and check haemostasis.
Review and check sensibility.
Partial or coronal pulpotomy means u only remove the inflame pulp tissue.

188
Q

What is the hinge movement of the jaw

A

Movement of the jaw when in CR

189
Q

What instrument can you use to find contact points

A

Shimstock foil or GHM paper (better than articulating paper)

190
Q

How to undertake a detailed occlusal analysis

A 
ICP
RCP
RCP sliding to ICP
Anterior guidance
Lateral/side-to-side movements
191
Q

CR vs RCP

A

CR is the position of the condyle in the fossa. RCP is the first contacts when condyle in this position.

192
Q

Host’s defenses against periodontal disease

A

Saliva
Epithelium
Inflammatory response
Immune response

193
Q

How does saliva defend against perio disease

A

Contains IgA.
Washes away the bacteria so less bind.
Contains antibacterials e.g. hydrogen peroxide, lactoferrin.

194
Q

How does the epithelium defend against perio disease

A

Impermeable barrier on the oral side
On junctional epithelium, permeable to allow macrophages and neutrophils out.
Old cells and bacteria removed from surface epithelium.
Can release IL-1 and stimulate an inflammatory/immune response.

195
Q

Features of the inflammatory response that defend against perio disease

A

Crevicular fluid
Neutrophils
Macrophages

196
Q

How does crevicular fluid defend against perio disease

A

Contains C’ (C3 leads to opsonisation, inflammation and cell lysis, C3-C5 cause vascular changes, histamine release and attract/aid phagocytosis, C9 MAC)
Antibodies
Flushes stuff out of gingival margin
Kininogens converted to kinins and act like histamine to promote an inflammatory response.
Clotting cascade = fibrin barrier to stop spread of infection and thrombin promotes inflammation.

197
Q

Neutrophils’ and macrophages’ role against perio disease

A 
Neutrophils = Phagocytosis, NETS and enzymes that attack bacteria.
Macrophages = phagocytosis, release chemokines and GF to promote immune response and healing and antigen presenting so induce the active immune response.
198
Q

How does the immune response defend against perio disease

A

Plasma cells make antibodies, and lymphocytes.
If some pathogens swallowed, detected by MALT cells in the gut and activate cells that release IgA into the saliva.
Or antigen penetrates epithelium and goes to lymph nodes and initiates an immune response and antibodies.

199
Q

Destructive periodontitis and causes

A

True pocketing.
Imbalance of host (enzymes, IL-1 stimulate bone resorption, unregulated immune response, bystander cell damage) and bacterial products (endotoxins damage epithelium and fibroblasts and enzymes break down CT and can cause bone resorption).

200
Q

Gums in health

A

Pale pink, stippled appearance. Can be inflamed a bit, and some plaque present is fine. No pocketing (0.5-2mm is healthy) or attachment loss.

201
Q

Early gingivitis

A

Increased crevicular fluid, some perivascular collagen loss but PDL still inserting into cementum and junctional epithelium attached to the tooth and at ACJ. Increased vascular permeability and oedema = neutrophils.

202
Q

Early lesion in gingivitis

at 2 weeks

A

Increased crevicular fluid and neutrophils and macrophages and lymphocytes. Damage to fibroblasts = some collagen loss but PDL still inserting into cementum. Some proliferation of the epithelium but still attached to the tooth and the ACJ.

203
Q

Chronic marginal gingivitis

2-3 weeks

A

+ Chronic inflammatory cells - lymphocytes and plasma cells. Junctional epithelium not attached to the tooth but still attached at ACJ and may be ulcerated = false pocketing. More collagen loss but PDL still inserting into cementum.

204
Q

RSD advantages and limitations

A

For pockets >4mm only bc under = more attachment loss than gain, and v v small reduction in pocketing. Use curettes/periodontal hoes or ultrasonic scaler + LA. To remove the plaque retentive features e.g. calculus, and plaque and bacterial toxins from under the gum and allow the junctional epithelium to proliferate and reattach to the cementum (long epithelial attachment). But no/v little signs of bone gain or PDL reattachment to cementum and is fragile.

205
Q

Destructive perio disease vs gingivitis

A

Gingivitis = reversible, no attachment loss or pocketing or bone resorption, acute then chronic inflammation. Due to plaque accumulation.
Destructive periodontitis = irreversible attachment loss and alveolar bone resorption. Loss of collagen fibres which insert into cementum. True pocketing/migration of the junctional epithelium.

206
Q

Traditional view of infection

A

Pathogen found in all organisms suffering from the disease, and not found in health.
The pathogen can be isolated and grown and then cause disease in a healthy model and be reisolated again.

207
Q

Keystone hypothesis

A

One pathogen can cause dysbiosis in a community

208
Q

Loose vs firmly attached sub-gingival plaque and the microbial layers

A

Loose can break off and get to other areas. Firmly attached = the down-growth of supragingival plaque.

209
Q

Why is it hard to establish which bacteria are in plaque and cause disease

A

They grow in different environments and are present in health too.

210
Q

3 organisms always associated with periodontitis

A

Red-complex pathogens.
P. gingivalis
T. denticola
T. forsythia

211
Q

P. gingivalis

A

Anaerobe, black pigmented (bc of FE deposits). Has lots of attachment/adhesion proteins and can infect cells and releases enzymes that break down host cells and proteins.

212
Q

T. forsythia

A

Anaerobe. S-shaped adhesion things. Secretes toxins and glycosidases which break down host glycoproteins.

213
Q

T. denticola

A

Spiral-shaped.

214
Q

How does the invasion of pathogens cause tissue damage in gums and what is this exception

A

Cytokines released due to inflammation stimulate bone resorption, and
Enzymes from bacteria cause soft tissue damage e.g. to the fibroblasts.
Toxins from bacteria and invasion of cells = evade host’s defences.
NUG is exception bc needs weaker host defence and less peripheral blood to papillae and invaded by specific bacteria.

215
Q

At what age in children is plaque most present

A

~8 bc that’s when they start brushing their own teeth and mixed dentition hard to clean (lots of pockets etc)

216
Q

BPE exam for mixed dentition

A

0-2 score bc of false pockets bc of exfoliating/erupting teeth that haven’t formed tight contacts.
Test around the 6’s, and incisors.

217
Q

Gingival disorders in children

A

Chronic gingivitis
Acute gingivitis (infection)
Gingival hyperplasia
Traumatised lesion

218
Q

Chronic gingivitis in children

A

Plaque buildup - poor OH, ortho-device, poor occlusion, cleft-palate, etc means they find it hard to brush teeth.
Can be worsened if on certain drugs, or some genetic conditions, if exfoliating teeth.
Can cause localised gingival recession e.g. if misaligned teeth, bad brushing or injury.

219
Q

Hyperplasia of gingiva in children

A

Due to medication e.g. anti-epileptic, immunosuppresors (affect fibroblasts).
Systemic diseases e.g. lack of WBC.

220
Q

Traumatic lesions in children

A 
a = trauma due to underlying irritation
b = trauma secondary to a previously established habit
c = complex, due to underlying emotional disturbance.
221
Q

Acute gingivitis (infection) in children

A

Acute herpetic gingivostomatitis - fever, sore throat, small irregular ulcers, saliva. Manage by keeping them hydrated and good OH.
Necrotising ulcerative gingivitis - gingiva ulcered and necrosed. If systemic illness e.g. HIV, uncontrolled diabetes, malnourished, stress. Manage by giving hydrogen peroxide mouthwash, OHI and antibiotics if worried about spread to soft tissues.

222
Q

Aggressive periodontal disease in children

A

Not common but can be due to family history, genetic conditions e.g. Down’s = more susceptible, phagocyte abnormalities/host defences. Rapid attachment/bone loss = mobile teeth and v deep pockets. Destruction inconsistent w local factors e.g. plaque.

223
Q

Goals of periodontal treatment

A

Restore function, stop further damage, reduce probing depths and stop bleeding and reduce plaque, improve QoL. Allow healing of gingiva.

224
Q

Treatment strategy for periodontitis

A

Management of acute problems e.g. pain, XLA, draining an abscess.
OHI and RSD
Review probing depths, BoP and plaque score after 3 months and monitor recession and mobility.
Can give systemic antibiotics if aggressive/severe or NUG.

225
Q

Limitations of periodontal assessment methods.

A

BoP depends on drugs, smoking and can flow to other sites.

Probing depths and plaque score can be subjective/have errors.

226
Q

K-files shape and size. Techniques for using them to prep the canal.

A

Have a 2% taper. 10 sized file = 0.1mm width at tip.

Watch-winding or circumferential filing (up and down to smooth the walls)

227
Q

Steps to managing the treatment of a patient

A

Acute care -> prevention -> stabilisation -> rehabilitation -> maintenance

228
Q

What can be used to finish amalgam restorations

A 
Steel finishing burs
Brownies then greenies
White stones
Rubber cup +abrasive paste
Soflex aluminium oxide abrasive discs
interproximal abrasive strips
ZnO powder

BODC (4 decks)

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