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Dentistry BDS 2 Sem 2 > EXAMS > Flashcards

EXAMS Flashcards

1
Q

Why didn’t early hunter gatherers have a large presence of dental caries?

A

Due to the fact that hunter gatherers did not have a source of simple carbohydrates. This means that cariogenic bacteria were unable to develop, as cariogenic bacteria feast on simple carbohydrates.

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2
Q

What are the steps to radio-graph assessment?

A
  1. Exposure
  2. Detector orientation
  3. Horizontal detector positioning
  4. Vertical detector positioning
  5. Horizontal beam angulation
  6. Vertical beam angulation
  7. Central beam position
  8. Colimator rotation
  9. Sharpness
  10. Overall diagnostic value
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3
Q

What are the steps to gingival assessment?

A

C - colour
C - contour
C - consistency
T - texture
E - exudate

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4
Q

What are the steps to ILA?

A
  1. Patient
  2. CC
  3. MHx
  4. SHx
  5. DHx
  6. Exam
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5
Q

What is TRIM?

A

TRIM is an acronomy for:
Timing
Relevance
Involvment
Method

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6
Q

What is differential diagnosis?

A

It is a process where a physician is able to assign probability of one illness in comparison to others accounting for patients sympotms.

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7
Q

What is a white spot lesion?

A

A white spot lesion is an incipient caries lesion, it has a dull opaque chalky appearance and occurs due to demineralisation of enamel caused by cariogenic bacteria

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8
Q

What is the pathogenesis of caries?

A
  1. Cariogenic bacteria requires simple sugars for anaerobic respiration
  2. Glucose is processed through glycolysis in the cariogenic bacteria
  3. Glucose is converted into 2 pyruvate
  4. In order to than convert NADH electron carrier into NAD+, pyruvate is converted into lactic acid
  5. Lactic acid accumulates in the cariogenic bacteria and is released into the oral environemnt
  6. Lactic acid has pH of about 2.35 which is slower than the critical pH of hydroxyapatite which means Lactic acids is able to cause dissociation of hydroxyal groups in hydroxyapatite which leads to demineralisation of the enamel
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9
Q

How can we remineralise a tooth?

A

In presence of Calcium, Phopshate and/or Fluoride in the biofilm or in salivary pool, if pH of above 4.5 is restored the tooth would be immediatley remineralised

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10
Q

Why is fluoride so effective?

A
  1. It is able to stop cariogenic bacteria metabolism
  2. Drive remin
  3. Create fluoride salivary pool
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11
Q

Why are incipient carious lesion look so much opaque?

A

Due to increased porosity. Increased posicity of enamel traps water which has a different refractive index which makes it look more dull

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12
Q

Why is calcium still needed for fluoride incorpiration?

A

Fluoroapatite still needs calcium and phosphate

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13
Q

How would you describe WSL

A

L - location
C - colour
T - texture
C - contour

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14
Q

How is calculus formed?

A
  1. Acid attack occurs
  2. Statherin releases Ca
  3. Excess calcium is able to percipitate on the biofilm as it can be used as an epitatic agent
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15
Q

What are the steps of rubber dam critique?

A
  1. Dam preperation (hole positionin, punching)
  2. Clamp selection (choice, gingival trauma, retention)
  3. Clamp placement (gingival trauma)
  4. Dam placement (alignment of dam)
  5. Frame placement (positioning of frame)
  6. Dam finish (isolation of appropriate teeht, moistture control)
  7. Dam removal
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16
Q

What are the major salivary glands?

A

Parotid (serous), Submandibular (mixed) sublingual (mixed).

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17
Q

Where are the Von Ebners glands located?

A

Circumvallate papillae and they are serous.

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18
Q

What are the functions of the salivary proteins and dissolved materials?

A

1.Acid neutralisation

2.Promotion of remineralisation

3.Creation of pellicle

4.Antibacterial properties

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19
Q

What type of buffer does stimulated saliva?

A

Bicarbonate

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20
Q

What type of buffer is in unstimulated saliva?

A

Phosphate

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21
Q

In what conditions can enamel remineralise?

A

In super saturated conditions of the close system

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22
Q

What is the sialo-microbial-dental complex?

A

They are interaction between saliva, biofilm and tooth.

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23
Q

What can change the balance of the oral environment?

A

1.More refined, softer foods

2.Refined CHO

3.Increase in fermentation

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24
Q

Why is erosion so effective?

A

Because it occurs in an open system, where acid is able to remove the minerals used for remineralisation entirely

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25
Q

What is the diffenrence between intrinsic/extrinsic acids and plaque acid?

A

Plaque acid is less strong than intrinsic/extrinsic acids, thus take longer to effect enamel

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26
Q

Summarise the factors that show that the patient is not at risk of caries.

A

1.High biodiversity in the biofilm

2.Low amount of acidogenic & aciduric bacteria

3.High numbers of Alkali producing bacteria

4.High resting pH of biofilm

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27
Q

What is the main driver of caries?

A

Lifestyle changes

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28
Q

What is the mode of action of APF?

A

It is able to use it’s acidity to dissolve hydroxyapatite and use calcium for creation of fluorapatite – this is great for xerostomic conditions.

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29
Q

What is the mode of action of CPP-ACP?

A

Calcium is intact with a CPP and is able to penetrate deep into the caries lesion and release calcium for remin due to acidity produced by cariogenic bacteria

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30
Q

What are the three steps to re-establish a healthy oral health environment?

A

1.Change the ecology of the biofilm

2.Improve the saliva

3.Remove cause and re-establish new biofilm

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31
Q

Who is involved in treatment planning?

A

Patient and dentist work collectively to develop a plan that satisfies the patient’s needs.

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32
Q

What do we need to explain to a patient?

A

1.Their oral health status

2.Waht will happen if nothing is done

3.Treatment options

4.What patient is required to do

5.IF they want to proceed

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33
Q

What info do we need for treatment planning?

A

Full examination, with all histories and potential extra test like bitewing radiographs

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34
Q

What are the basic principles of Soft tissue health & preventative treatment?

A

Focus on hygiene instructions and removal of plaque and stains. Could potentially make a diet diary

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35
Q

Why is GV not as advantageous?

A

Because it requires a removal of a large amount of healthy structure thus it is not ideal for a long term prognosis of the tooth.

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36
Q

What is the significance of MI philosophy that relates to the histology of the tooth?

A

MI philosophy indicates that maximum amount of tooth structure and affected dentine can remain intact IF infected dentine is removed and affected dentine is sealed.

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37
Q

What is Site 1?

A

Pits, fissures and enamel defects on occlusal surfaces of posterior teeth and cingulum and other smooth surfaces of the interiors

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38
Q

What is Site 2?

A

Approximal surfaces in relation to areas in contact with adjacent teeth

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39
Q

What is Site 3?

A

The cervical one-third of the crown, or following gingival recession, the exposed root

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40
Q

What are the desired properties of resin composites ?

A

1.Aesthetics

2.Handling properties

3.Biocompatibility

4.Protect tooth bioactive

5.Function

6.Longevity

7.Radiopacity

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41
Q

Where would we use resin composites?

A

1.Aesthetics

2.Toothstructure to bond

3.Strengthen tooth structure

4.Blood and moisture can be controlled

5.Where occlusal loads are not sever

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42
Q

What is the basic composition of composites?

A

Synthetic Organic resin (which is a viscous liquid) that is bonded to inorganic filler particles with a silane coupling agent made to set or light cured.

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43
Q

What particles may give resin radiopacity?

A

Barium or Strontium

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44
Q

What are the steps to bonding resin to enamel?

A

1.Prophylaxis

2.Acid treatment – for microporosities – increase of surface area for interlocking in the area and create a macromechenical bond – increase of surface area by 2000 times

3.Wash and dry – stop the demin process and remove moisture

4.Fluid (unfiled) resin – flow into microporosities to create resin tags – chemical bonding

5.Unfilled resin polymerised

6.Composite resin placed

7.Polymerised

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45
Q

What are the steps to bonding to dentine?

A

Etching – this will expose collagen – may cause pulpal fluid to flow up which can compromise the bond – etch for a little less

Use a primer – wet or dry – dry: collagen is collapsed which rehydrated – wet: small amount of water remains – creation of hybrid zone

Unfilled resin

Polymerise

Filled resin

Polymerise

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46
Q

How do GIC bond?

A

They bond chemically throguh ion exchange and can exchange ions with tooth and oral environment.

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47
Q

How does acid-base reaction occurs in GIC?

A

1.Polyacid attacks glass particles – calcium, strontium and fluoride are released

2.Precipitation of salts occurs = gelatation and gathering occurs

3.Maturation phase = acid/base reaction continues for a few days

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48
Q

Why do we need to protect the GIC during the maturation phase?

A

GIC are vulnerable to take-up of extra water or water loss. This may create a loss in physical properties. This can be avoided by layering of unfilled resin of G-coat over the top.

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49
Q

What are the steps in applying GIC?

A

1.Clean the surfaces with pumice and water – for better ion exchange

2.Use Polyacrylic acid – depending on % - to remove the smear layer and exposure the clean tooth surface for ionic exchange

3.Wash it off – stop the reaction

4.Dry but do not desiccate – stop flow of dentinal fluid

5.Place GIC

6.Protect in the moisture sensitive phase

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50
Q

How does amalgam set?

A

When certain alloys are processed like silver or tin, they can harden when mixed with liquid mercury

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51
Q

What are the steps of amalgam placing?

A

1.Remove caries or remove failed amalgam

2.Consider depth of cavity – at least 2 mm into dentine

3.Remove unsupported enamel

4.Retention - macromechanical retention

5.Liner/base

6.Pack amalgam using a plugger – permite ect amalgam used in sim

7.Burnish

8.Carve using cuspal inclines

9.Articulating paper and adjustment

10.Polish 24 hours later

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52
Q

What are some of the techniques for caries diagnosis?

A

1.Visual Examination – clean, dry, illuminate well and use the tip of the explorer

2.Radiographs - just remember of superimposition, it is probably bigger than it is on radiographs

3.DIAGNOdent - measuring reflected light – little to no florescence in clean, healthy teeth

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53
Q

What are some of causes of damage to the dentine and pulp?

A

1.Caries - through bacterial acids, toxins and enzymes

2.Micro-leakage – due to unsealed margins – could cause sensitivity and recurrent caries – seal so bacteria can go into a dormant state

3.Mechanical damage – fracture, cavity preparation, cracked cusps, dehydration

4.Thermal damage – during cavity preparation friction, polishing, absence of insulation (base & liner)

5.Chemical damage – Hema & Tegma & other acids

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54
Q

What type of questions can we ask the patient about their pain?

A

1.Location

2.Commencement of pain

3.Character of pain

4.Frequency

5.Duration

6.Time

7.Precipitation factors

8.Other complains

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55
Q

Explain hydrodynamic theory.

A

Dentinal tubules contain an extension of the odontoblasts (odontoblastic process) in the part of the tubule that is proximal to the pulp. Around the odontoblastic process, coiled are small nerve extensions. The rest of the space inside a dentinal tubule is filled by dentinal fluid.

If the fluid is disturbed through heat, cold, dehydration and even touch and pressure, it causes the fluid to move which activates the pulpal nociceptros around the odontoblastic processes this cause an action potential and signals for pain.

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56
Q

Why don’t we advocate to polish the amalgam restoration less than 24 hours after placement?

A

Because amalgam would not reach it’s set, meaning it may chip away and create ecological niches for bacteria to thrive.

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57
Q

Is caries a one way street?

A

NOPE. Even if we have early demin, we can actually remineralise the enamel by changing conditions in the oral cavity to supersaturated condition! We can do it all the way upto cavitation!

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58
Q

When can we remineralise the enamel?

A

1.When the demin is exclusive to the enamel

2.When there is affected dentine but no infected dentine

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59
Q

How do we assess the fractures?

A

1.Tissue exposed – enamel only, enamel and dentine or exposed pulp

2.Surfaces involved

3.Check occlusion

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60
Q

What is a bevel?

A

It is a process of cutting the enamel, at 45%, to increase the surface area of enamel for bonding. This could be created with high speed diamond burs.. Make sure that the transition is smooth. Pls do both palatal and labial.

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61
Q

What is the pattern of erosion relating to intrinsic sources?

A

1.Upper posteriors are affected first

2.Diffuses and affects the upper anterior next

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62
Q

What is the pattern of erosion relating to extrinsic sources?

A

1.Occlusal of lower affected first

2.Palatal of upper anterior

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63
Q

How would you assess the teeth on the radiograph?

A

1.Identify teeth present, unerupted/missing, not imagted and restorations
2.Identify abnormalities that are present

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64
Q

How would you identify gingivitis?

A

1.Localised - 10% - 30% BOP
2.Generalised - >30% BOP
No pain or no clinical attachment loss

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65
Q

How would you identify periodontitis?

A

Proximal clinical attachment loss of equal or above 2 teeth, non-adjacent

OR

Buccal/oral clinical attachment loss of 3mm with 3mm pocketing at 2 teeth or more

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66
Q

What are the steps to occlusal analysis?

A

1.Teeth present/missing
2.Morphology of teeth
3.Wear - mild, moderate, sever
4.Crowding,spacingrotations
5.Axail inclanations
6.Shape of dental arch
7.Cruve of spee and wilsons curve
8.Angle molar classification/canine classification
9.Overbite (%) / overjet (mm)
10.Mediolateral

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67
Q

What is the 4A’s framework?

A

Ask, assess, acknowledge and address that can be used to adress a patient with dental anxiety

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68
Q

What is ALARA?

A

It stand for as low as reasonably possible - which is a concept used in radiography in order to reduce radiation exposure for both the operator and patient.

1.Keep your distance
2.Shield
3.Do not take unnecessary radiographs

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69
Q

What is the significance of dental pelicle?

A

It is able to provide some protection to the enamel. It also allows for binding of bacteria to the surface of the tooth

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70
Q

What is the needle stick inury protocol in dental emergencies?

A
  1. Stop
  2. Place needle/sharp aside
  3. Take off gloves
  4. Wash hands with soap and water
  5. Dry and cover with non-stick dressing
  6. Apply pressure if bleeding
  7. Let tutor know
  8. Contact SADS registered nurse for risk assessment
  9. Write up incident report - SLS
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71
Q

What is stage 1 periodontitis?

A

1.1-2mm attachment loss

2.Coronal third bone loss

3.No tooth loss

4.Maximum probing depth of below 4mm

5.Mostly horizontal bone loss

6.Extent variable

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72
Q

What is stage 2 periodontitis?

A

1.3-4mm attachment loss

2.Coronal third bone loss

3.No tooth loss

4.Maximum probing depth of below 5mm

5.Mostly horizontal bone loss

6.Extent variable

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73
Q

What is stage 3 periodontitis?

A

1.5mm or more attachment loss

2.Bone loss extending to middle or apical third of the root

3.Tooth loss due to periodontitis of 4 or less teeth

4.Probing depth of 6 mm or more

5.Vertical bone loss of 3 mm or more

6.Class II or III furcation

7.Moderate ridge defect

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74
Q

What is stage 4 periodontitis?

A

1.5mm or more attachment loss

2.Bone loss extending to middle or apical third of the root

3.Tooth loss due to periodontitis of 5 or more

4.Probing depth of 6 mm or more

5.Vertical bone loss of 3 mm or more

6.Class II or III furcation

7.Moderate ridge defect

8.Mastication disfunction

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75
Q

What is Grade A periodontitis?

A

When there are no evidence of loss over 5 years

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76
Q

What is Grade B periodontitis?

A

When there is a below 2 mm loss over 5 years.

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77
Q

What is Grade C periodontitis?

A

When there is an above 2mm loss over 5 years

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78
Q

How to do treatment planning?

A
  1. Differential diagnosis presentation
  2. Consent for further tests
  3. Further investigation and tests pefromance
  4. Presentation of treatment with products and justification and potential timeline
  5. Recall to check the results of the treatment
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79
Q

How do we manage a patient with dental anxiety?

A

1.Recognise and acknowledge your patient’s anxiety/fear
2.Invite your patient to talk about their anxiety/fear e.i. anything in particular that concerns them
3.Offer some piratical suggestions - try to work with a patient to accommodate for their needs.

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80
Q

How to deal with a dissatisfied patient?

A

1.Acknowledge the distress and the person’s experience
2.Say wha has been, or will be, done to investigate the complaint
3.State wat has been done could be done to address the concerns
4.Mention any changes or action taken

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81
Q

What is acute pain?

A

Occurs at tissue damage before treatment. There is an emidiate onset which creates psychological response. It goes with resolution unlike chronic pain.

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82
Q

Why do we experience pain?

A

1.Warning about something
2.Reminding - for example healing promotion

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83
Q

Why does swearing increase pain tolerance?

A

Swearing can cause sympathetic response e.g. arousal - stressed induced analgesia due to increased fight or flight

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84
Q

Why does saying “Ow” increase pain tolerance?

A

There is a theory that motor activation has a modulatory effect in addition to arousal

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85
Q

Why do athletes continue playing even after receiving an injury?

A

The potential explanation is induced analgesia from stress

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86
Q

What is the clinical significance of anxiety for LA anaesthetic?

A

There are studies that show that local anaesthetic is more likely to fail in patient with high dental fear

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87
Q

How do we approach pain?

A

Using biophsycosocial model

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88
Q

What are two types of local anaesthetic?

A
  1. Amino esther - broken down by enzymes
  2. Amide type - metabolised in the liver
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89
Q

What is the mechanism of action of anaesthetics?

A

The molecules bind to amino acids on amino acids, and simply blocking the channel. This does not allow for depolarisation thus stop the propagation of action potential.

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90
Q

What is the main problem that LA needs to overcome prior to blocking the sodium ion channel?

A

To get through the phospho-lipid bi-layer of the cell membrane

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91
Q

How do we modify local anathetic to overcome the phospho-lipid bilayer?

A

We design it to be amphiphatic

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92
Q

What does the pKa in local anaesthetic represent?

A

It represent the balance between charged and uncharged molecles of the solution. I.E. at pKa 7.6 there is equal number of molecules, thus at pH 7.6 there will be am equal number of molecules

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93
Q

What is the importance of RN in local anaesthetic?

A

The uncharged RN molecules, represent the number of molecules that can pass through the phospho-lipid bi-layer as they are water soluble. Turns to RNH+ which actually bind to sodium channel.

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94
Q

Why is the pH of injecting site important?

A

The pH at the injecting site may alter the numbers of RN making it unable to diffuse into the cells.

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95
Q

What happens when the pKa of LA is high?

A

This can decrease the number of RNs at the injection site thus will prolong the onset of the anaesthetic.

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96
Q

What is the objective of vasoconstrictors in LA?

A

1.Decrease blood flow
2.Slow absorption of LA into blood stream
3.Maintain higher local concentrations of LA
4.Longer duration of LA action
5.Reduced bleeding

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97
Q

What are the most common local anaesthetics and their vasoconstrictors?

A
  1. 2% Lignocaine (Xylocaine) with 1:80000 adrenaline
  2. 3% Prilocaine (Citanest) with 0.03 iu/ml octapressin
  3. 3% Mepivacaine (Scandonest Plain) - no vasocontrictor
  4. 4% Articaine (Articadent) with 1:100000 adrenaline
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98
Q

What is the standard local anaesthetic equipment?

A
  1. Aspirating and non-aspirating syringes
  2. Short (25mm) and long (40mm) needles
  3. 25, 27 (the usual size, and 30 gauge needles
  4. Glass cartridges
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99
Q

What are 3 commonly used LA techniques?

A
  1. Topical
    2.Block
    3.Infiltration
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100
Q

What are the landmarks that help to locate teh site of IAN?

A

1.Level - coronoid notch, 1cm above lower occlusal plane, midway between arches with mouth wide open, buccal pad
2.Angle - opposite premolars
3.Entry point - pterygotemporal depression

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101
Q

When was there a dramatic increase of dental caries?

A

Around industrial revolution due to production of sucrose

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102
Q

What is the main active pathogen in caries?

A

Acid produced by bacteria

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102
Q

What is the main active pathogen in caries?

A

Acid produced by bacteria

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103
Q

What are the 4 Koch’s Postulates

A
  1. The microbe should be found in all cases of the disease
  2. The microbe can be grown on artificial medium
  3. A pure culture of the organism should produce the disease in a susceptible animal
  4. A high antibody titre to the microbe should be detected during the infection - may provide protection from subsequent re-infection
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104
Q

What are modified Koch’s postulates for biofilm induced diseases?

A
  1. The microbe should be present n sufficient numbers to initiate the disease
  2. The microbe should generate increased levels of specific antibodies
  3. The microbe should possess relevant virulence factors
  4. The microbe should cause disease in an appropriate animal model
  5. Elimination of the microbe should result in clinical improvement
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105
Q

What is the non-specific plaque hypothesis?

A

1890 hypothesis by Prof. Miller that said that non-specific bacteria and plaque on teeth as awhole is the reason for occurance of dental carries

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106
Q

What is the specific organism that causes dental caries?

A

Streptococcus mutans

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107
Q

What is a specific plaque hypothesis?

A

1960s hypothesis by Prof. Keys, which states that dental caries relates to prevalence for Streptococcus mutans and diet

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108
Q

What is the ecological plaque hypothesis?

A

Disease results from shifts in the balance of the resident plaque microflora. Sugar = increased in pH = increase in acidoduric Streptococcus mutans

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109
Q

What is the association between Mutans Streptococci and fissure caries?

A

Around 71% of fissure caries have a high number of Mutans streptococci

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110
Q

What is S. sanguinis?

A

It is a group of bacteria that is able to increase the pH of the nvironment. It is has an inverse relationship to Mutans streptococci

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111
Q

What bacteria is more commonly found in caries on rough surfaces?

A

Lactobacilli

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112
Q

What happens to the levels of Streptococcus Mutans when a subsurface lesion forms?

A

They dicrease with the depth of the lesion

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113
Q

What is a pathogen?

A

The ability of an organism to cause infectious disease

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114
Q

What are the 4 main abilities of pathogenesis?

A

1.Attache to host
2.Entry into host
3.Colonisation and growth within the host
4.Ability to avoid host defenses

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115
Q

What are opportunistic pathogens?

A

They cause disease in compromised individuals

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116
Q

What are pathobionts?

A

They are bacteria that can become pathogenic if environment changes

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117
Q

What is virulence of an organism?

A

It is the pathogens abilityt o cause disease

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118
Q

What are the two main benefits from causing cell damage for a pathogen?

A

1.Release of nutrients
2.Allow spreading to the next host, by inducing coughing or diarrhoea

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119
Q

What is an example of receptor adhesin binding in the mouth?

A

When bacteria attaches to the pellicle in order to create biofilm. Bacteria has a receptor and pellicle has an adhesin

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120
Q

What is a non-specific invasion?

A

Breaks in skin

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121
Q

What is a specific invasion?

A

Type III secretion

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122
Q

What are some of the evasion mechanism available to pathogens?

A
  1. Trace element shortage. Pathogen remove iron from iron binding proteins found, in transferrin and lactoferrin which creates competition for resources
  2. Bacteria sense cell density and express virulence genes only when their numbers reach a certain quorum (quorum sensing)
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123
Q

What are gingipans?

A

They are enzymes that are produced by P. Gingivalis. They produce many virulence factors. Gingipains are aggresive endopeptidases (protein distruction)

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124
Q

What are the two cells of adaptive immunity only?

A

T and B cells

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125
Q

Can you tell the differences between CD4+ and CD8+ T cells?

A

Nope, that is why we have the CD system

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126
Q

How does innate immunity recognise pathogens?

A

Through INNATE-PAMPS which are structure that are common to all bacteria but are not present on host cells

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127
Q

How does adaptive immunity recognise pathogens?

A

Through use of different types of marking using immunoglubulins or cytokines

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128
Q

What happens when there is no discrimination between self and non-self?

A

This leads to autoimmunity

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129
Q

What are the two modes of adaptive immunity?

A

1.Humoral immunity - using immunoglobulins
2. Cell mediated - using different T cells

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130
Q

Where are White Blood Cells originate from?

A

Bone marrow, B cells stay in bone marrow or spleen. T cells go to the thymus

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131
Q

What is the difference between the structure of the receptors on B and T cells?

A

T cells have a straight, alfa+beta chain receptor. B cells have an immunoglobulin as a receptor

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132
Q

Where usually do mature B and T lymphocytes reside?

A

T lymphocytes reside in blood and lymph. B lymphocytes just in blood

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133
Q

What is the purpose of the TCR receptor?

A

It is the major receptor on T cells that use used to recognise antigens. It is one of the most important receptors in adaptive immunity and without it the entire adaptive immune system would not be able to function.

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134
Q

What is the function of each MHC class of receptors?

A

MHC class I used used for activation of CD8+ cytotoxic pathway. MHC class II used for activation of helper CD4+ pathway

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135
Q

What is the acronym that can be used to remember all the immunoglobulin classes?

A

MADE in Germany

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136
Q

What is the most common immunoglobulin found in saliva

A

IgA

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137
Q

What are some of the functions of immunoglobulins?

A

1.Neutralisaiton
2.Opsonisation - labeling
3.Cross linking and immobilisation

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138
Q

What is interesting about GIC restorations and Mutans Streptococci?

A

GIC main contain protective components that lower the number of Mutans Streptococci than with amalgam

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139
Q

What bacteria is the main cause of root caries?

A

It is actually belived that root caries have a polymicrobial aetiology, meaning it is usually not just one type of bacteria

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140
Q

What are the 5 Pathogenic Determinants pf Cariogenic Bacteria?

A
  1. Sugar transport - high and low affinity transport systems
  2. Acid production for proliferation
    3.Aciduricity - ability to survive in acidic environments
    4.EPS production - contributions to plaque matrix
    5.IPS production - allows for production of acit when sugar is not available
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141
Q

What are the three sugar transport systems available for S. Mutans?

A

1.Sucrose-PTS
2.Trehalose-PTS
3.Multi Sugar TS

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142
Q

In the EPS metabolism by S. Mutans, what is the function of a Mutan?

A

It aids in attachment to the biofilm structure to the tooth

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143
Q

What is the of glucosyltransferase?

A

They are extracellular enzymes that have a glucan-binding domain that aids in adherence

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144
Q

Why is sucrose so cariogenic?

A

Because it allows for the binding mechanism relating to GTFs to start unlike glucose

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145
Q

Explain ecological plaque hypothesis?

A

1.Increase sucrose consumption
2.Resulting in increasingly acidic environment
3.This favours acidoduric bacteria
4.This drive demineralisation

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146
Q

Name the following structures

A
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147
Q

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148
Q

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149
Q

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150
Q

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151
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152
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154
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155
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156
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157
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158
Q

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159
Q

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160
Q

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161
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162
Q

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163
Q

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164
Q

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165
Q

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166
Q

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167
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168
Q

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169
Q

How would you assess the teeth on the radiograph?

A
  1. Identify teeth present, unerupted/missing, not imagted and restorations
  2. Identify abnormalities that are present
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170
Q

Describe the process of odontogenesis

A

Odontogenesis - formation of tooth germ from primary epithelial band and dental lamina

Bud stage: Formation of epithelial bud surrounded by condensing ectomesenchyme

Cap stage: Formation of enamel organ and initiasl differentiation of enamel cell types. Dental sac and papilla form and begin genesis of dentine and PDL/cementum respectively.

Bell stage: Occlusal shape is now formed IEE cells, all cells of the enamel organ are now differentiated, communication with epithelial band is severed and tooth germ is embedded in ectomesenchyme

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171
Q

What are the stages of amelogenesis?

A

Morphogenic: IEE cells gain polarity

Histodifferential: IEE cells differentiate into preaameloblasts - stimulate odontoblasts from DP cells - differentiate into ameloblasts

Initial secretory: formation of initial layer of aprismatic enamel on dentine

Secretory: Formation of Tome’s processes, secrertion of enamel matrix. Proximal end of Tome’s process forms interod enamel, distal portion forms rod enamel.

Protective: Ameloblasts lay dormant, 50% of the initial population has now apoptosed

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172
Q

What is hypoplasia?

A

It is the reduction in the amount of enamel matrix produced - presents as pitting, may caause sensitivity

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173
Q

What is hypomineralisation?

A

It is the inability for sufficient organic material to be removed during maturation stage of amelogenesis - presents as variation in colour from white-yellow-brown, teeth are highly vulnerable to staining and tooth wear

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174
Q

What is hypocalcification?

A

It is insufficient inorganic material deposition during maturative stage - teeth adopt chalky, yellow appearance, highly vulnerable to staining and tooth wear

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175
Q

What are 3 types of amelogenesis imperfecta?

A
  1. Hypoplasia
  2. Hypomineralisation
  3. Hypocalcification
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176
Q

How would you identify gingivitis?

A

1.Localised - 10% - 30% BOP
2.Generalised - >30% BOP
No pain or no clinical attachment loss

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177
Q

How would you identify periodontitis?

A

Proximal clinical attachment loss of equal or above 2 teeth, non-adjacent

OR

Buccal/oral clinical attachment loss of 3mm with 3mm pocketing at 2 teeth or more

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178
Q

What is the aetiology of periodontitis

A
  1. Bacterial build in biofilm - dominance of gram negative and opportunistic bacteria
  2. Gram negative bacteria release LPS
  3. This triggers an inflammatory response
  4. Influx of neutrophils (due to release of IL-8 by epithelial tissue) to form palisade
  5. Release of pro-inflamatory cytokines and enzyme - chemotaxic agents for leukocytes & marcophages
  6. Need for creation of space for cells - break down of collagen fibres and lateral prolifiration + apical migration of the junction epithelium - creation of the pseudo pocket due to oedema
  7. End result - damage to collagen but no damage to periodontal attachmnet
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179
Q

Give example of two local and two systemic factor for gingivitis and periodontitis.

A

Local: calculus and over hangs - more sites for harbouring of bacteria, xerostomia - reduciton in anti-microbial effect of saliva

Systemic: Smoking - reduction in blood flow and immune function - more periodontopathogens arise,; Diabetes - increased formation of Advanced Glyation End Products - increased osteo clast function and oxidative stress - increased tissue destruction

180
Q

What are some of the treatment for perio?

A

Debridment.

Remember that long axis to the tooth should be parallel to the terminal shank

181
Q

Describe the problem with syncope of a patient with type I diabetes?

A

Syncope can occur in patient when insulin administration is mistimed.

Brain has an absolute need for oxygen, glucose and neural signalling.

If a patient has type I diabetes and they miss their breakfast and take their medication, it can lead to hypoglycemia because the residue glucose will be taken up from the blood.

Because brain requires a constant supply of glucose and is unable to do so in this situation, it shuts down.

182
Q

What to do if a patient faint due to hypoglycemic syncope?

A
  1. Stop treatment
  2. Lay patient in supine position
  3. Provide refined carbohydrates
  4. Monitor and supervise - get help if needed
183
Q

What are the affects of aging on endocrine function?

A

Reduction in:

  1. Oestrogen
  2. Growth hormone
  3. Aldosterone
  4. Melatonin
184
Q

What happens when oestrogen production decreases?

A

Decreased production occurs upon completion of menstruation, leading to two distinct outcomes for 2 systems.

For bone:

  1. Reduced apoptosis of osteoclasts
  2. Decreased IGF-1 formation leading to decreased formation of osteoblasts
  3. Reduced osteoprotegerin formation

For vasculature:

  1. Reduced formation of coagulation factors
  2. Reduced function of platelets
185
Q

What happens when growth hormone production decreases?

A
  1. Reduced muscle mass
  2. Increased adiposity
186
Q

What happens when aldosterone production decreases?

A

Reduce secretion leads to hyponatremia or hyperkaleamia

187
Q

What happens when melatonin production decreases?

A

Reduced secretion which causes advanced sleep phase syndrome

188
Q

What is the pattern for erosion for intrinsic acids?

A

Palatal of maxillary posteriors and anteriors as the tongue covers the lower teeth relatively well

189
Q

What is the pattern of erosion for extrinsic acids?

A

Mostly lower posteriors

190
Q

What is the 4A’s framework?

A

Ask, assess, acknowledge and address that can be used to adress a patient with dental anxiety

191
Q

What is ALARA?

A

It stand for as low as reasonably possible - which is a concept used in radiography in order to reduce radiation exposure for both the operator and patient.

  1. Keep your distance
  2. Shield
  3. Do not take unnecessary radiographs
192
Q

What happens to unpolarised resin?

A

It may damage the pulp because it is toxic thus it needs to be polymerised. Becomes a problem in wet environment or when placed in large increment.

193
Q

What are the steps to bonding resin to enamel?

A
  1. Prophylaxis
  2. Acid treatment – for microporosities – increase of surface area for interlocking in the area and create a macromechenical bond – increase of surface area by 2000 times
  3. Wash and dry – stop the demin process and remove moisture
  4. Fluid (unfiled) resin – flow into microporosities to create resin tags – chemical bonding
  5. Unfilled resin polymerised
  6. Composite resin placed
  7. Polymerised
194
Q

What are the steps to bonding to dentine?

A

Etching – this will expose collagen – may cause pulpal fluid to flow up which can compromise the bond – etch for a little less

Use a primer – wet or dry – dry: collagen is collapsed which rehydrated – wet: small amount of water remains – creation of hybrid zone

Unfilled resin

Polymerise

Filled resin

Polymerise

195
Q

How do GIC bond?

A

They bond chemically throguh ion exchange and can exchange ions with tooth and oral environment.

196
Q

What are the steps of placing resin of top of GIC base?

A
  1. Cute the GIC and create space for resin
  2. Etch
  3. Put unfilled resin on the GIC and etch enamel – GIC has irregular shape = micro-mechanical bonding
  4. Cure
  5. Place resin
  6. Cure
197
Q

What is a closed sandwich technique?

A

When GIC if covered around with another material

198
Q

What is an open sandwich technique?

A

When GIC is exposed outside the tooth – to the oral environment

199
Q

What are the steps in applying GIC?

A
  1. Clean the surfaces with pumice and water – for better ion exchange
  2. Use Polyacrylic acid – depending on % - to remove the smear layer and exposure the clean tooth surface for ionic exchange
  3. Wash it off – stop the reaction
  4. Dry but do not desiccate – stop flow of dentinal fluid
  5. Place GIC
  6. Protect in the moisture sensitive phase
200
Q

Why do amalgam may need liners & base?

A

Due to their thermal properties

201
Q

What are the steps of amalgam placing?

A
  1. Remove caries or remove failed amalgam
  2. Consider depth of cavity – at least 2 mm into dentine
  3. Remove unsupported enamel
  4. Retention - macromechanical retention
  5. Liner/base
  6. Pack amalgam using a plugger – permite ect amalgam used in sim
  7. Burnish
  8. Carve using cuspal inclines
  9. Articulating paper and adjustment
  10. Polish 24 hours later
202
Q

What are the steps of resin based fissure sealant placement?

A
  1. Clean surface – remove debris
  2. Etch (orthophosphoric acid 37%)
  3. Wash - stop reaction
  4. Dry well – frosty appearance
  5. Flow in fissure – no bubbles
  6. Light cure it
  7. Check occlusion
203
Q

What are the steps of GIC/RMGIC based fissure sealant placement?

A
  1. Clean surface – pumice
  2. Condition with polyacrylic acid
  3. Wash
  4. Dry - leave moist
  5. Place in fissure
  6. Apply protective coat
  7. Cure
  8. Check occlusion
204
Q

What theory are we using to describe dentine hyper sensitivity?

A

Hydrodynamic theory

205
Q

Explain hydrodynamic theory.

A

Dentinal tubules contain an extension of the odontoblasts (odontoblastic process) in the part of the tubule that is proximal to the pulp. Around the odontoblastic process, coiled are small nerve extensions. The rest of the space inside a dentinal tubule is filled by dentinal fluid.

If the fluid is disturbed through heat, cold, dehydration and even touch and pressure, it causes the fluid to move which activates the pulpal nociceptros around the odontoblastic processes this cause an action potential and signals for pain.

206
Q

What are some of the materials are used in pulp protection?

A
  1. Varnishes - copalite – used to block dentine tubules – bad longevity
  2. Liners - cover the dentine – placed under restorations – used for shallow cavity – CaOH cement (Life) - very alkaline - GIC line bond LC
  3. Bases - similar to liners but are thicker – use as dentine replacement – ZnPO4 cement is an example – Zinc Oxide-Eugenol is another example – GIC like the Fuji series
207
Q

What are the steps of placing the liner in a relatively small cavity? Why so?

A
  1. Prepare cavity
  2. Condition the cavity
  3. Mix Fuji Bond LC 1:1
  4. Apply
  5. Cure
  6. Etch the enamel
  7. Wash dry
  8. Use unfilled resin
  9. Cure
  10. Add filled resin

This will make sure that RMGIC is able to release fluoride and create a chemical bond with resin

208
Q

Name 3 components of saliva that have anti-bacterial properties.

A
  1. Non-immunological defences
  2. Physico-chemical barriers
  3. Immunological barriers
209
Q

What role does lactoferrin play in reducing bacterial growth?

A

Lactoferrin is an iron binding found on mucosal surfaces. Lactoferrin is able to deprive microbes of essential iron by binding iron in saliva, lowering the ability to aquire oxygen. Lactoferrin also enhances lysozyme action.

210
Q

What role do salivary mucins play in reducing numbers of oral bacteria?

A

Mucins are able to agglutinate microbe and aid their removal

211
Q

What anti-bacterial enzyme is found in high concentration on tears and saliva? What is it’s mechanism of action against bacteria?

A

Lysozyme. It is able to hydrolyse peptidoglycans which are present on bacterial cells walls. It than triggers autolysins which cause bacterial degradation.

212
Q

What are histatins and how do they interfere with the growth of oral bacteria?

A

Histatins are small peptides which are secreted by submandibular and parotid glands. They are able to interfere with membrane integrity of the bacterial membrane.

213
Q

What are defensins?

A

Defensins are small antimicrobial peptides that are present in the granules of phagocytic cells thus are able to kill bacteria there

214
Q

How does the flow rate of saliva vary during 24hr cycle?

A

The rate of saliva production is relatively high during the day and decreases significantly during the night time

215
Q

Name 3 Gram negative bacteria which are thought to lay a significant role in periodontal disease.

A
  1. P.Gingivalis
  2. P. Intermidia
  3. T. Forsythia
216
Q

Name 3 functions of gingipans.

A
  1. Adherence to and colonisation of epithelial cells
  2. Disruption and manipulation of the inflammatory response
  3. Degradation of host proteins and tissues
217
Q

What is the main nutritional source in healthy periodontium?

A

Gingival crevicular fluid

218
Q

Is there an identified pathogen that causes gingivitis?

A

No. Gingivitis is a result of bacterial accumulation which could be the same type of bacteria or transition of bacteria from gram positive to gram negative.

219
Q

What role does GCF play in gingivitis?

A

It is able to remove tissue breakdown products, introduce inflammatory mediators and antibodies

220
Q

How do we approach treatment planning?

A
  1. Diagnosis presentation
  2. Consent
  3. Further investigation and tests
  4. Recall to check the results of the treatment
221
Q

What is a phenotype?

A

It is our genotype + environment

222
Q

What is the main difference between somatic cells and gametes?

A

Somatic cells have a diploid number of chromosomes. Gametes have a haploid number of chromosomes

223
Q

What is dominance/recessiveness?

A

Differences in the DNA code between alleles at the same locus may give rise to dominance or recessivness which couple with sex linkage, may give rise to simple modes of inheritance.

224
Q

What is the law of segregation?

A

The two alleles for a heritable character segregate during gamete formation and end up in different gametes

225
Q

What is the law of independent assortment?

A

Each pair alleles segregates independently of each other pair of alleles during gamete formation

226
Q

What are the phases of mitotic divisions?

A

Growth 1 phase

S phase – genetical replication phase

Growth 2 pahse

Mitotic phase – PMAT

Cytokinesis

227
Q

What are the 2 types of alterations?

A
  1. Somatic – only affects the host.
  2. Germline - may affect the offspring.
228
Q

Where does the exchange of genetic material occur during synapsis?

A

It occurs on non-sister chromatids.

229
Q

What are the genetic and phenotypic outcomes from single gene segregation in pure breeding parents?

A

The potential traits of the offspring can be predicted.

230
Q

What are homeobox genes?

A

They are genes that regulate the development of structure in the embryo. They perform they are functions on and off and are unequally distributed throughout the embryo in terms of effect.

231
Q

What are transcription factors?

A

They are molecules that upregulate or downregulate the activity of certain genes

232
Q

What are morphogen gradients?

A

They are positional cues for cells during development; this establishes cell signalling networks to control gene expression

233
Q

How many homeobox clusters are there?

A

4 – C-7,-17,-12 and -2.

234
Q

What is a Hardy-Weinberg equilibrium law?

A

It is a law that is used to calculate allele frequencies in non-evolving populations, with assumption that shuffling of alleles has no effect on the overall gene pool. Deviations from this law result in evolution. Due to limitations above this law cannot be used in natural populations but it help us to understand how the evolution occurs.

235
Q

What are the necessary conditions for Hardy-Weinberg equilibrium?

A
  1. No new mutations
  2. No migration in or out of the population
  3. No selection
  4. Random mating
  5. Very large population
236
Q

How do we calculate genotype frequency?

A

Collect all frequency of 2 genes occuring (i.e. 2xWW, 3xWw and 1xww) and devide by the total number of samples

237
Q

How do we calculate the phenotype frequency?

A

We calculate all appearances and devide by the total number (i.e 10xwhitw 20x purple = 10/30 and 20/30)

238
Q

How do we calculate the alele frequency of aleles?

A

add the frequency of all aleles and devide by the total number (i.e. 10xW 15xw)

239
Q

What are the main features of randomised control trials?

A
  1. High level of evidence
  2. Eandom assignment
  3. Groups are exchangeable
240
Q

What are the different types of RCTs?

A
  1. Parallel-arm RCTs
  2. Cross-over RCTs
  3. N-of-1 ‘single patient’ RCT
241
Q

What is the structure of the parallel-arm RCTs?

A
  1. Selection
  2. Randomisation
  3. Treatment and control group establishment and intervention
  4. Follow up measures
  5. Analysis
242
Q

What is the structure of the Cross-over RCTs?

A
  1. Selection
  2. Randomisation
  3. Treatment and control group and intervention
  4. Washout period
  5. Swap of control and treatment groups for second intervention
  6. Outcomes of interventions
  7. Analysis
243
Q

What is the structure of the N-of-1 ‘single patients RCTs?

A
  1. One patient is selected
  2. They go through periods of treatment and non-treatments – the pattern is also random
  3. Outcomes of interventions are recorded
  4. Data is analysed
244
Q

What is the design of a cohort study?

A
  1. Time baseline
  2. Time goes on
  3. We observe
  4. Analysis
  5. Outcome
245
Q

How does a cross sectional study work?

A
  1. Select a group
  2. See if they were exposed or not
  3. Analyse
  4. Outcomes
246
Q

Why do we do a cross-sectional study?

A

Have a snapshot and see the prevalence of health problems in a population

247
Q

What is a perspective study?

A

The study is conducted before data is gathered.

248
Q

What is a retrospective study?

A

The study is conducted after the data is made available.

249
Q

Why do we sample?

A

Reduce costs and it is more efficient

250
Q

What are some of the sampling methods?

A
  1. Simple random sample – equal chance being selected
  2. Stratified random sample – equal participation of sexes, races and other parameters
  3. Systematic - non-random – a set process e.g. every tenth person
  4. Clustered - geographic areas are selected, after the clusters of multiple people are selected
  5. Convenience sampling – just recruit people where we actively recruit people with needed traits
251
Q

What is the main objective of case control study?

A

It is causal interference. What can we do to reduce the problem.

252
Q

What is the main objective of ecological study?

A

It is casual interference. What can we do to reduce the problem.

253
Q

What is the design of a case control study?

A

It starts with a known outcome that is classified as a “case”. Non-cases are treated as a control group.

254
Q

What is the design of a case control study?

A
  1. A group of people with a known disease are classified as cases
  2. A group of people who are known not to have a disease are used as controls
  3. Both groups are sampled and separated into exposed and none exposed
  4. We get 4 groups thus 4 data steams
  5. Odds are calculated
255
Q

What are ecological studies?

A

Ecological studies are epidemiological evaluations in which the unit of analysis is populations, or groups of people, rather than individuals. Example: Is the prevalence of dental caries lower in fluoridated areas?

256
Q

What is a systematic error?

A

It relates to the way we conduct studies. It cannot be reduced by increasing sample size.

257
Q

What is a systematic review?

A

They are a way of reviewing all the data and results from studies about a specific question in a standardized systematic way

258
Q

What is empathy?

A

It is the ability to understand and share other people’s emotions.

259
Q

What does fluoride do to bacteria?

A

It can cause cytoplasmic acidification thus unabling functions of certain enzymes.

260
Q

Why is the pKa of weak acids is important?

A

The protons in weak acids want to stay together, that is why they dissociate partially in water

261
Q

When do cleft lip and palate occur?

A

Lip - 4-7 weeks

Palate - 6-9 weeks

262
Q

What is a typical structure of a local anaesthetic solution?

A
  1. An aromatic portion that provides lipid solubility
  2. An intermediate chain with either an ester or amide linkage
  3. A terminal amide that provides water solubility
263
Q

In what form does LA exist in the solution?

A
  1. Unchanged lipid soluble molecules that are referred to as the base - more of it exist the better LA works - it can defuse through the cell membrane
  2. Positively charged molecules RNH+ - this is the molecules that is able to inhibit the work of the Sodium channels in neurons which disables the propagation of action potential - it can not defuse through the cell membrane
264
Q

What is the relationship between pH and Rn and RNH+?

A

1.When pH is low, there is a large number of RNH+ as RN is converted into RNH+
2. IF pH is high, there is a large number of RN

265
Q

How much of myelinated fibre needs to be covered by anaesthesia in order to anaesthetised the nerve?

A

8-10 mm

266
Q

What are two main objective of LA?

A
  1. The LA must diffuse through the nerve sheath
  2. The LA must bind at receptor sites in the nerve membrane
267
Q

What determines the number of basic and cationic forms of LA?

A
  1. The pKa of the solution
  2. The pH of the LA solution
  3. The pH of the site of injection
268
Q

What does methylparaben do in LA solution?

A

Acts as an anti-bacterial preservative but has the
potential to cause allergy

269
Q

What does bisulphite do in LA solution?

A

Acts as an anti-oxidant for the vasoconstrictor and
also tends to lower the pH of the LA solution. May
cause allergy problems

270
Q

What does sodium chloride do in LA solution?

A

Makes the solution isotonic

271
Q

What does sodium hydroxide do in LA solution?

A

Added to some LAs to adjust the pH

272
Q

What does distilled water do in LA solution?

A

Used to dilute the solution and increase its volume

273
Q

What does vasoconstriction do for LA solution?

A
  1. Increased rate of absorption into the blood stream
  2. Decreased duration of action and effectiveness
  3. Increased bleeding at the site of injection, and
  4. Possible overdose reactions due to high blood levels
274
Q

What are the 3 essential components of local anaesthetic equipment?

A
  1. Syringe
  2. Needles
  3. Cartridge
275
Q

What are two common needles in SA dental clinics

A

1.Short, 25 mm length, 27 gauge
2.Long, 40 mm length, 27 gauge

276
Q

What are 5 common anaesthetics in SA dental?

A
  1. Lidocaine hydrochloride - Lignospan
  2. Prilocaine hydrochloride - Citanest
  3. Mepivacaine hydrchloride - Scandanest
  4. Articane hydrochloride - Septanest
  5. Bupivacaine hydrochloride - Marcaine
277
Q

What type of topical anaesthetic is used in SA dental?

A

Benzocaine, 15-30 seconds applied to the area of anaesthetic

278
Q

What are two main technique in LA?

A
  1. Supraperiosteal infiltration - diffusion through cortical bone
  2. Nerve block - depositing solution to a nerve trunk
279
Q

What are types of infiltration can be administered?

A

Labial, buccal or palatal

280
Q

What types blocks are available for the maxilla?

A
  1. Maxillary - blockes whole of maxillary nerve
  2. Tuberosity - blocks posterior superior alveolar nerves
  3. Infraorbital - blocks anterior superior alveolar nerves
  4. Nasopalatine - anaesthetises palate back to canines
  5. Greter palatine - anaesthetises palate as far forward as canines
281
Q

What are the steps of labial or buccal infiltrations?

A
  1. Position the patient
  2. Pull lip or cheek firmly out
  3. Define the fornix
  4. Wipe if necessary, then apply small amount of typical
  5. Insert needle, bevel towards bone, in the fornix
  6. Keep close to bone without touching, insert 2-3 mm, parallel to long axis of tooth
  7. Inject slowly (1-2ml depending on the procedure)
282
Q

What are the steps to a palatal infiltration?

A
  1. Define point of entry
  2. Apply topical
  3. Insert needle, approximately at right angles to the palate, at junction of alveolar process and horizontal plate
  4. Advance needle gently 2-3 mm
  5. Inject slowly approx. 0.5 ml
283
Q

Where is the location of injection for the maxillary block?

A
  1. Buccally beyond third molar
  2. Through greater palatine foramen
284
Q

What are the advantages of palatal block?

A

Wide area of LA, including maxillary sinus

285
Q

What some of the technique for anaesthesia of the mandible?

A
  1. Infiltration that is only possible in incisor region
    2.Inferior alveolar nerve block
286
Q

How to locate the place for IANB?

A
  1. Level - palpate the coronoid notch, find the deepest point
  2. Entry point - locate pterygotemporal depression. It is between the pterygomandibular fold medially and the ramus of the mandible laterally
  3. Angle - the angle of insertion is along a line drawn from the opposite lower second premolar to the pterygotemporal depression
287
Q

What is the location of the inferior alveolar nerves?

A

It is close to the ramus between the ramus and sphenomandibular ligament that runs from the spine of the spenoid to the lingula

288
Q

What is the location of lingual nerve?

A

It is medial and anteriorly to the inferior alveolar nerve and in close proximity to the lateral surface of medial pterygoid muscle.

289
Q

What are steps to IANB?

A
  1. Position patient in chair
  2. Palpate the right ramus with the left index finger and define the coronoid notch
  3. Slide finger medially so that the ball of the finger lies in the retromolar area between the external and internal oblique ridges
  4. Hold syringe in right hand, with the barrel parallel to the occlusal plane. Insert the needle halfway between the fingertip and PMF, with the barrel over premolars on the left hand side
  5. Advance the needle with minimum force until it touches bone
  6. Withdraw slightly, aspirate, inject 1-2 ml
  7. Move barrel towrds midline, withdraw half the amount of insertion, inject for lingual nerve about 0.5 ml
  8. Complete withdrawal
290
Q

How to perform anaesthesia of buccal nerve?

A
  1. Inject just medial to anterior border of mandible, distal buccal to the last molar tooth around the level of the lower occlusal plane
  2. Hold the syringe parallel with the occlusal plane on the same side
  3. Advance the neddle until the needles gently touches the mucp[eriosteum/bone, then slightly withdraw and then inject
291
Q

What are the steps for a mental block?

A
  1. Hold lip between finger and thumb and pull anteriorly and downwards
  2. Insert needle just lateral to the fornix, distal to second premolar
  3. Direct the needle medially, anteriorly and inward into the canal. Inject slowly
292
Q

What nerve innovate the upper molars?

A

The posterior superior alveolar nerve

293
Q

What nerve innovates the upper premolars?

A

The middle superior alveolar nerve

294
Q

What nerve innovates the anterior upper teeth?

A

The anterior superior alveolar nerve

295
Q

What is the procedure in emergencies?

A

DRSABCD:
Danger
Response
Send help
Airway
Breathing
Circulation
Defibrillation

296
Q

During odontogenic infection, what is the path of least resistance in the mandible?

A
  1. If above the mylohyoid line, the infection would progress lingually, eroding the lingual cortical plate and entering the sublingual space. This will elevate the tongue and create diffuculties with breathing
  2. If below the mylohyoid line, the infection would progress down into the submandibular space. This may causes swelling near the angle of the ,and able to potentially causing trismus and therefore diffuculties chewing..
297
Q

How does an odotontic infection spread if it is not treated

A
298
Q

How does an odotontic infection spread if it is not treated?

A
  1. Caries reach the root
  2. Pulpal progression
  3. Root progression
  4. Progression to the apex
  5. Progression into other tissues and cavities
299
Q

What is the usual cause of infection in the sub mandibular region?

A

Usually the source is second and third molar because their roots are entirely below the attachment of mylohyoid muscle.
The infection starts in the periodontal pocket and spreads to the musculature of the floor of the mouth. Infection pierces through the lingual cortical plate of the mandible.
The infection moves lingually rather than buccally, as the lingual aspect of the tooth socket is thinner and provides the path of least resistance.
The infection than moves into sublingual space.

300
Q

How can commensal members of the oral microbiome become pathogenic when they inhabit environments that are no their primary ecological niche?

A

Oral commensal flora includes opportunistic bacteria, which can cause disease in compromised situations.

For bacteria to become pathogenic they must:
1.Avoid host defences - both specific and non-specific
2.Adhere to host surfaces
3.Gain entry to the pulp and periapical soft tissues
4.Gain adequate nutrients in the new environment

301
Q

What are the most frequently isolated bacteria in pulpal disease?

A
  1. Gram positive streptococci
  2. Peptostreptococci
  3. Staphylococcus aureu
302
Q

What are common routes of pulpal entry for bacteria?

A
  1. Exposed dentinal tubules
  2. Cavitated carious lesions
  3. Micro leakage of restoration
  4. Injury
303
Q

What is the function of odontoblasts during the defence of pulp against bacterial infections?

A

1.Express Pattern Recognising receptos
2.Secrete antibacterial products
3.Release cytokines for chemo attraction of defence molecules

304
Q

What is the process of tertiarry dentine formation?

A

When odontoblasts receive signal about presence of bacteria near the pulp they are able to react by up regulating the production of reactive dentine (tertiary dentine) which creates a barrier between the pulp and the bacteria.
If odontoblasts die, pulp is able to create reperative dentine. The main cells in deploying reparative dentine are the pulp fibroblasts or stem cells.

305
Q

What is the function of neurovascular network in protection of pulp during bacterial infection?

A

Secretion of neuropeptides causing vasodilation, vascular permeability increased, and promotion of immune cells. This also promotes tertiary dentine formation

306
Q

What are some of the way to treat an odontogenic infection?

A

Reffere to V3 of therapeutic guidlines

307
Q

What type of tissue is labial mucosa?

A

Non-keratinised stratified squamous epithelium. Labial mucosa has many elastic finred for flexibility and blood supply.

308
Q

What type of tissues are in the vermillion zone?

A

Thin orthokeratinised stratified squamous epithelium followed by a lamina propria.

309
Q

What is the main arterial supply to the lips?

A

It is predominantly supplied by external carotid artery, specifically via the facial artery.

310
Q

What is the main venous drainage from the lips?

A

Through superior and inferior labial veins into the facial vein into external jugular and into subclavian vein

311
Q

What is the main nerve supply to the lips?

A

The supply to the muscles is via the facial nerve and sensory via trigeminal nerve

312
Q

What mechanism does the cell regulate for prior to S phase?

A

1.Cell size
2. DNA damage

313
Q

What mechanism does the cell regulate for prior to M phase?

A
  1. DNA damage
  2. DNA replication completeness
314
Q

What mechanism does the cell regulate for prior to end of mitosis?

A

Chromosomes attachment to spindle

315
Q

What are some external factors that regulate the cell cycle?

A
  1. Physical signals - contact inhibition - when cell inhibit replication when they come in contact
  2. Chemical signals - availability of growth factors or other hormones
316
Q

What are some internal factors that regulate cell cycle?

A
  1. Cyclins
  2. Cyclin-dependent kinases
317
Q

What are some common risk factors for oral cancer?

A
  1. Tobacco use
  2. Excessive sun exposure to the lips
  3. Heavy alcohol use
  4. HPV
  5. Immune deficiencies
318
Q

Why does tobacco increase the likely hood of cancer?

A
  1. Epigenetic alteration of oral epithelial cells can cause abnormal expression of genes such as GLUT-1 transportes and diwn expression of p53 anti-tumor gene
  2. Inhibits systemic immune functions of the host, causing defects in CD4+ and CD3+ T cell activity
  3. Oxidative stress on tissues
319
Q

Why does excessive sun exposure to the lips increases the likely hood of developing cancer?

A
  1. UV rediation is carcinogenic
  2. Causes excess bond to form between DNA, this lead to mutations in cells
320
Q

Why does heavy alcohol use increas the probability of developing cancer?

A

The mechanism by which alcohol consumption causes cancer are not fully understood but maybe oxidative damage

321
Q

Why does heavy alcohol use increase the probability of developing cancer?

A

The mechanism by which alcohol consumption causes cancer are not fully understood but maybe oxidative damage

322
Q

Why does HPV increases the probability of developing cancer?

A

HPV affects the gene p16, which regulates the cell cycle - causes it to be overexpressed

323
Q

Why do immune deficiencies increase the probability of developing cancer?

A

Depressed immune function means that immune surveillance amd recognition of cancer cells is also depressed. This decreases the likely hood that early malignant cells are recognised and terminated by white blood cells

324
Q

What is an effective communication and Patient managment plan for treatment with LA?

A
  1. Information gathering
  2. Diagnosis explanation
  3. Informed consent
  4. Post op instructions
325
Q

What is an effective way to manage an individual with dental anxiety?

A
  1. Acknowledge the fear, show empathy
  2. FInd out what is the pt particularly feel fearful about
  3. Familiarized with the procedure as the operator and show confidence
  4. Familiarise patient with the procedure in order to minimise surprise and pain
  5. Positive encourgment during the procedure
  6. Using topical gel to minimise the paint at injection site
  7. Use method of distractions
326
Q

What are the four main anatomical sites to consider when trying to administer IANB?

A
  1. Pterygotemporal depression
  2. Pterygomandibular fold
  3. Lingula
  4. Coronoid notch
327
Q

What is the rationale for direct IANB?

A
  1. Anaesthesia is supplied to the gingiva, mucoperiosteum, lower lip and mandibular teeth
  2. Useful for procedures such as root canals, extraction of teeth and periodontal treatment
328
Q

What are some common anatomical deviations and common reasons for failure of IANB?

A
  1. Accessory innervation from other nerves, such as nerve to mylohyoid nerve
  2. Long buccal nerve is unable to be anaesthetised
  3. Type 4 bifid mandibular canal, an anatomical variation causing difficulty for IANB to effecgtively anaesthetise as there are two mandibular foramina where IAN enters at the same time
  4. Mandibular prognathism where the lingula is located higher, making a larger height difference between the lingula and coronoid notch
329
Q

What are some common complications with IANB?

A
  1. Pain during administration
  2. Insufficient Anaesthesia
  3. Iatrogenic and Self-Inflicted Damaged of Anaesthetised Tissues
330
Q

What are some rare complications with IANB?

A
  1. Needle Breakages
  2. Skin paleness
  3. Tissue Necrosis
331
Q

What are causes for pain during administration during IANB?

A
  1. Increased tissue pressure
  2. Injection performed too quickly
  3. Injecting too large a volume
  4. Incorrect technique
  5. pH/temp of anaesthetic
332
Q

How to manage a patient with pain when administering IANB?

A

If the patient expresses one of the key signs/symptoms, pull the needle back slightly and if necessary to increase patient comfort, the direction of needle insertion should be altered before injecting the anaesthetic

333
Q

What are causes for insufficient anaesthesia during IANB?

A
  1. Incorrect technique
  2. Incorrect site
  3. Injection into an inflammed area
334
Q

How to manage a patient with insufficient anaesthesia during IANB?

A

Carefully explain potential reasoning for insufficient anaesthesia and gain informed consent for examination and possibly a second dose

335
Q

What are causes for Iatrogenic and Self-Inflicted Damage of Anaesthetised tissues during IANB?

A
  1. Accidental damage due to numbness
  2. Burn wounds caused by smoking or hot foods thay go unnoticed
336
Q

How to manage a patient with Iatrogenic and Self-Inflicted Damage of anaesthetised tissues during IANB?

A

The companions of these patients should be warned of the possible injuries and should be told to keep watch on them for anaesthetic period. They should not allow them to smoke, eat or drink during this time.

337
Q

What are reasons for failure of IANB besides anatomical variation?

A

Operator factors: Technical errors - poor technique

Patient factors:
1. Pathological processes
2. Infection/inflammation
3. Psychological causes
4. Accessory innervation

338
Q

What is anaesthesia?

A

It is the absence of all sensory modalities

339
Q

What is paraesthesia?

A

An abnormal sensation (tingling) whether spontaneous or evoked

340
Q

What is dysaesthesia?

A

An unpleasant abnormal sensation, wether spontaneous or evoked

341
Q

What is hyperesthesia?

A

Increased sensitivity to stimulation, excluding special senses

342
Q

What is trismus?

A

The restriction of range of motin of the jaws

343
Q

What are some of steps for management of trismus?

A
  1. Heat therapy
  2. Analgesics
  3. Muscle relaxants
  4. Physiotherapy
  5. No further dental treatment
  6. Antibiotic therapy potentially
  7. Reference to oral surgeon
344
Q

What is rheumatic heart disease?

A

Rheumatic heart disease is a condition in whch rheumatic fever causes damage to the heart tissue or any of the valves

345
Q

What is ineffective endocarditis?

A

It is when bacteria are able to infect heart tissue. This disease is strongly associated with rheumatic heart disease

346
Q

What is rheumatic fever?

A

It is a multi system disease that results from mistreatment of Scarlet Fever, which is caused by Type A streptococcus bacteria

347
Q

What is the concentration of fluoride in fluoridated water supply?

A

About 1 ppm

348
Q

What type of bacterial growth inhibitor is chlorhexidine?

A

It is a broad spectrum mouth rinse. It has bacteriostatic levels and is able to stick around the mouth for around 5 hours. It blocks adherence and interferes with ATP’ase ion channels. IT DOES NOT UPSET THE NORMAL MICROBIAL ECOLOGY. DO NOT USE WITH FLUORIDE.

349
Q

What is selective cytotoxicity?

A

It is a process in which there is preference to targeting bacteria without causing damage to host cells

350
Q

What are antibiotics, chemotherapeutic substances and semisynthetic antibiotics?

A

Antibiotics - natural substances produced by certain groups of microorganisms
Chemotherapeutic substances - they are chemically synthesised in a lab
Semisynthetic antibiotics - hybdri compounds, chemically modified antibiotics

351
Q

What are two types of action of antibiotics?

A

Cidal - killing the bacteria
Static - gives immune system time to attack by stopping the bacteria from dividing

352
Q

What are some of the desirable properties of a clinically useful antibiotic?

A
  1. Non-toxic to host
  2. Spectrum which does not include normal microflora
  3. Bactericidal rather than bacteriostatic
  4. Bacterial resistance not readily induced
  5. Does not induce allergic reaction in host
  6. Retains activity in body tissues and fluids
  7. Soluble and stable in water
  8. Inexpensive to produce
353
Q

What does penicilin do?

A

Penicilin, is a b-lactama antiobiotic, which inhibits X-linking of peptide side chains by targeting the enzyme transpeptidase. Penicillin is a suicide inhibitor.

354
Q

What are the major difference between different beta-lactams?

A

Standard stuff like spectrum of activity, toxicit, stability in body and so on.

355
Q

What are some of the protein synthesis inhibiting anti-biotics?

A

Macrolides, aminoglycosides, lincomycin & clindamycin

356
Q

What is an advantage and disadvantage of inhibitors of nucleic acid function?

A

Disadvantage: They are not selectivity toxic
Advantage: Some of them can be used in cancer treatments

357
Q

What are some examples of inhibitors of nucleic acid function?

A

Quinolones, rifampicin, 5-nitroimidazoles

358
Q

What are cell membrane inhibitors?

A

They are antibiotics that disorganise structure or inhibit function of bacterial membranes

359
Q

What are advantages of penicillin and ampicillin?

A

They are relativley broad, targeting both gram positive and gram negative bacteria. Even tho, these antibiotics could cross react with cephalosporins, but at a very low probability.

360
Q

What is the advatage o flucloxacillin?

A

It maintaince slightly less of broad spectrum of work, but it is good for patient with B-lactam allergy

361
Q

What is the advantage of cepjalosporins antibiotics?

A

They reduce activity of gram-positive bacteria and are good for treating multi-resistant organisms.

362
Q

What are three main mechanisms of bacterial drug resistance?

A
  1. Altered permeation/Efflux
  2. Altered target site
  3. Drug inactivation
363
Q

What are the 10 steps to effective antibiotic use?

A
  1. Is an antibiotic indicated on clinical grounds?
  2. Have appropriate investigations been performed?
  3. What organisms are most likely to cause this infection?
  4. Which agent is best?
  5. Is an antibiotic combination appropriate
  6. Are any host factors relevant?
  7. What is the best route of administration?
  8. What is the appropriate dose?
  9. Can therapy be modified when lab results are obtained?
  10. What is the optimal duration of therapy?
364
Q

What are some of the causes for cell injury?

A

1.Oxygen deprivation - hypoxia
2. Physical agents - mechanical trauma, temperature extremes, radiation
3. Chemical agents
4. Infectious agents
5. Immunological reaction - collateral damage, autoimmune reactions
6. Genetic changes - deficiency of functional proteins, susceptibility of cells
7. Nutritional imbalances

365
Q

What are basic principals of cell injury?

A
  1. Cell response depends on type, duration and intensity of injury
  2. Consequences of injury depend on the type, state and adaptability of the cell
  3. Cell injry has detrimental effects on several cellular/biochemical mechanisms
366
Q

What are some of the mechanisms of cell injury?

A
  1. Nitochondrial damage - decrease in ATP production
  2. Entry of Ca2+ - loss of calcium homeostasis - activation of enzymes regulating apoptosis
  3. Membrane damage - leading to loss of cellular components and increase in enzymatic digestion
  4. Protein misfolding due to DNA damage
367
Q

What are free radicals?

A

Free radicals are chemical species that have a single unpaired electron. They are highly reactive thus are damaging to the cells. One of the free radicals is oxygen

368
Q

What are some of the pathological effects of free radicals?

A
  1. Lipid perioxidation which damage the cell membrane
  2. Protein modification - which causes breakdown and misfolding of proteins
  3. DNA damage - leading to mutation
369
Q

What are two main light microscopic changes are characteristic of reversible cell injury?

A
  1. Hydropic change - cellular swelling, cells incapable of maintaining ionic and fluid homeostasis
  2. Fatty change - hypoxic injury, metabolic injury and hepatocytes
370
Q

What are two different processes of cell death?

A
  1. Necrosis
  2. Apoptosis
371
Q

When does necrosis occur?

A

It occurs as a result of irreversible cell injury. It is unregulated form of cell death due to ischaemia, toxins, infections and trauma. Elicits a host reaction - inflammation.

372
Q

What morhological changes occur in necrosis?

A

Denaturation of intracellular proteins and enzymatic digestion of irreversibly injured cell resulta in:
Inability to maintain membrane integrity
Elicit an inflammatory response
Increased eosinophilia
Nuclear changes

373
Q

What are 3 different [patterns of tissue necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
374
Q

What happens during coagulative necrosis?

A
  1. Preservation of tissue architecture
  2. Eosinophilic, anucleate cells
  3. Removal of necrotic cells by phagocytosis
375
Q

What happens during liquafactive necrosis?

A
  1. Enzymatic digestion of necrotic cells
  2. Infections, production of pus
376
Q

What happens during caseous necrosis?

A
  1. Collection of fragmented necrotic cells
  2. Granulomatous inflammation
    Usually hapens during tuberculosis
377
Q

What is apoptosis?

A

It is programmed cell death. Activation of intracellular enzymes. Degradation of nuclear DNA and nuclear and cytoplasmic proteins.

378
Q

What are some of physiological causes of apoptosis?

A
  1. Embryogenesis
  2. Involution of hormone-dependent tissues due to hormone withdrawal
  3. Protection against autoimmune disease
  4. Resolution of inflammatory and immune response
379
Q

What are some of the morphological changes in apoptosis?

A
  1. Cell shrinkage
  2. Condensation of nuclear chromatin
  3. Formation of membrane bound apototic bodies
  4. Phagocytosis of apoptotic cells or apoptotic bodies
  5. Absence of inflammation
380
Q

What are the 5 changes in cell growth?

A
  1. Hypertrophy - An increase in the size of particular tissue by increase in cell size.
  2. Hyperplasia - An increase in the size of a particular tissue by increase in cell number. Is reversible.
  3. Metaplasia - An acquired form of altered differentiation. Transformation of one mature differentiated cell type to another. Is riversible
  4. Dysplasia - An increased cell growth with atypical morphology. May be reversible in early stages.
  5. Neoplasia - Abnormal, uncoordinated and excessive cell growth
381
Q

What are 4 different types of cell growth?

A
  1. Multiplicated growth - increase in cell number
  2. Auxetic growth - increase in cell size
  3. Accretionary growth - increase in intercellular tissue compartment
  4. Combined patterns of growth
382
Q

What is important to remember with hypertrophy and hyperplasia?

A

Important to remember that following the removal of the stimulus causing the hypertrophy or hyperplasia, the tissue return to normal. Meaning, these conditions are reversible.

383
Q

What is atrophy?

A

It is the decrease in size of an organ or cell. Could be physiological or pathological

384
Q

Why is their inflammation?

A

It is a protective process that deals with infection and injuries but it does cause damage to surrounding tissues

385
Q

What are 5 stages of respond to initial insult?

A
  1. Initial insult
  2. Inflammation
  3. Tissue damage
  4. Resolution
  5. Repair
386
Q

What are macroscopic features of acute inflammation?

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain
  5. Loss of function
387
Q

What changes in vessel calibre occur during inflammation?

A
  1. Increased vascular permeability - formation of fluid exudate
  2. Movement of neutrophils into the extravascular space - formation of cellular exudate
  3. Arteriolar vasoconstriction
  4. Capillary dilatation
  5. Arteriolar dilatationn
  6. FLuid exudation into extravascular space
388
Q

What are some of the benefits of acute inflammation?

A
  1. Dilution of toxins
  2. Entry of antibodies
  3. Transport of drugs
  4. Fibrin formation
  5. Delivery of nutrients and oxygen
  6. Stimulation of the immune response
389
Q

What are some of the harmful effects of acute inflammation?

A
  1. Destruction of normal tissues
  2. Swelling
  3. Inappropriate inflammatory response
390
Q

What is the sequelae of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Repair and organisation
  4. Fibrosis
  5. Chronic inflammation
391
Q

What is a collection of pus called?

A

An abscess

392
Q

What are granulomas?

A

A granuloma is a collection of macrophages and or their derivatives. Basically it is a small area of inflamation

393
Q

How does pulpal tissue respond to an insult?

A
  1. Inflammation
  2. Reparative dentine formation
  3. Fibrosis and reduced cellularity
  4. Granulation tissue formation
394
Q

Why does pulpal tissue die?

A
  1. Limited capacity for drainage
  2. Limited access for repair
  3. Limited space for swelling
  4. Concentrated stimulus
  5. Limitations of material to treat
395
Q

When does perioapical abcess occur?

A

It occurs due to untreated pulpal necrosis and acute inflammation in periapical tissues.

396
Q

What can happen when periapical abcess is not treated?

A

It can turn into periapical granuloma. Due to granulation process a granuloma could form.

397
Q

What is regeneration?

A

It is the replacemenet of dead or injured cells and tissues by cells and tissues of the indentical type.

398
Q

What is repair?

A

It is replacement of dead/injured cells by “repair” tissue which is usualy fibrous connective tissue - scar tissue

399
Q

What are to basic patterns of wound healing?

A

Primary intention - the wound is closed up for example using sutures - results in decreased area of repair
Secondary intention - the wound is left open - results in increased area of repair

400
Q

What is angiogenesis?

A

Increase in blood vessels. Process by which new blood vessels grow into damaged, ischaemic or necrotic tissues. Activated by vascualr endothelial growth factor (VEGF). Released by hypoxic cells and macrophages

401
Q

What are some of the factors that influence healing?

A
  1. Nutrition
  2. Infection
  3. Metabolic disorders
    other
402
Q

How does healing of bone occur?

A

Through secondary intention plus bone regeneration. It is dependent on the site of fracture, normal vs pathologic bone and type of fracture.

403
Q

What is a dry socket?

A

It is a condition where the site of extraction did not create an adequate blood clot and there is exposed bone. Could lead to necrosis of lamina dura and bone.

404
Q

What is traumatic neuroma?

A

It is a bundle or nodule of thick neural tissues that forms after injury to a nerve.

405
Q

What is neoplasia?

A

Literally means “new growth”. A neoplasm is a lesion that arises from genetic a mutations in cells. Abnormal growth of cells.

406
Q

What is a basic make up of neoplastic lesions?

A

Neoplastic cells or tumour parenchyma and tumour stroma

407
Q

What influences the growth and spread of tumour cells?

A

It is influenced by the stromal components

408
Q

What is the difference between bening tumours and malignant tumours?

A

Benign tumour have no potential for metastasis.
Malignant tumours have potential for metastisis

409
Q

What is carcinogenesis?

A

It is process of transformation of a normal cell to a neoplastic cell by causing permanent genetic alterations.

410
Q

What is viral carcinogenesis?

A

It is the integration of viral genome into host DNA or viral proteinsthat lead to interference. One of these coudl be HPV wich cuases cervical carcinoma

411
Q

What are some of physical agents that could cause carcinoma?

A

Ionisng radiation
UV radiation

412
Q

What si the relationship between dysplasia and epithelial atypia and carcinoma?

A

Many carcinomas are thought to arise as a result of progression and invasion of pre-existing epithelial dysplasia. Dysplasia could be a pre-neoplastic lesion. When dysplastic changes are maked and involve the entire thickness of the epithelium the lesion is referred to as carcinoma in situ which is a pre-invasive stage of cancer.

413
Q

What is epithelial atypia?

A

It is changes in a normal epithelial lining. Such could be architectural changes such as drop shaped rete pegs, loss of polarity of basal cells. Superficial mitoses. Irregular epithelial sratification and so on

414
Q

What are some cytological changes during epithelial atypia?

A

Nuclear pleomorphism, abnormal variation in nuclear size, abnormal variation in nuclear shape, cellular pleomorphism, abnormal variation in cell size.

415
Q

How do we collectively refer to signs of epithelial atypia?

A

Epithelial dysplasia

416
Q

What are oncogenes?

A

They encode proteins that promote normal cell growth and proliferation. Genetic alterations can alter the transcription of oncogenes or the behaviour of their products. Abnormal expression of oncogenes drive normal cells towards the neoplastic state

417
Q

What are clinical effects of benign neoplasma?

A
  1. Pressure on adjacent tissues
  2. Obstruction to the the flow of fluid
  3. Production of a hormone
  4. Transformation into a malignant neoplasm
  5. Anxiety
418
Q

What are clinical effects of malignant neoplasms?

A
  1. Pressure on and destruction of adjacent tissue
  2. Formation of secondary tumours
  3. Blood loss from ulcerated surfaces
  4. Obstruction of flow
  5. Production of a hormone
  6. Paraneoplastic effects causing weight loss and debility
  7. Anxiety and pain
419
Q

What is a squamous cell carcinoma?

A

It is the most common primary malignant neoplasm of the oral cavity. It arises from the oral mucosal epithelium.

Clinical features
Age: any age

Sex: More males than females

Hugh risk sites: lower lip, anterior floor of mouth, lateral border of tongue and other

Early clinical features: fixed white patch, exophytic papillary or wart-like lesion, speckled leukoplakia

Early lesions are usually painless while symptoms of late lesions may include: pain, parathesia, loss of function, enlarged lymph nodes, radiographic changes

420
Q

What is differentiation?

A

The degree to which the tumour tissue resembles the tissue of origin. Well differentiated - resemble mature cells. Poorly differentiated - slight resemblance to mature cells.

421
Q

What is anaplasia?

A

Refers to a lack of differentiation of tumour cells, however often equated with poor differentiation at a tissue level.

422
Q

What are the 5 grades of histological tumour differentiation?

A

Carcinoma in situ - Pre-invasive scc
Grade 1 - well differentiated scc
Grade 2 - moderately differentiated scc
Grade 3 - poorly differentiated scc
Grade 4 - anaplastic scc

423
Q

What is the universal staging system for cancers?

A

T = size of primary tumour
N = condition of regional lymph nodes
M = presence/absence of distant metastases

424
Q

What are some subdivision of T in the TNM staging system?

A

T1 = primary <2 2cm diameter
T2 = primary 2-4 cm diameter
T3 = primary > 4 cm diameter
T4 = primary > 4 cm diamtere and invading local structures

425
Q

What are some subdivision of N in the TNM staging system?

A

N0 = No nodes clinically
N1 = Palpable nodes
N2 = Contralateral or bilateral nodes
N3 = Fixed palpable nodes

426
Q

What are some subdivisions of M in the TNM staging system?

A

M0 = No distant metastasis
M1 = Evidence of distant metastasis

427
Q

What are the stages of cancer?

A

Stage 1: T1 N0 M0
Stage 2: T2 N0 M0
Stage 3: T3 N0 M0; Any T with N1
Stage 4: Any T with N2 or N3; Any T, Any N with M1

428
Q

What is immune tolerance?

A

It is the ability to recognise self from nonself, thus immune cells do not attack body’s own cells or commensal organisms

429
Q

What are two types of tolerance?

A
  1. Central tolerance - negative selection and elimination of autoreactive T cells - usually within thymus and bone marrow
  2. Peripheral tolerance - limited selection, deletion or tolerise - in the paripheral after exiting centra organs
430
Q

What are major mechanisms of T cell tolerance?

A
  1. Apoptosis - induced by pro-apoptotic proteins
  2. Clonal anergy - long-lived functional unresponsiveness
  3. Suppression - use of T cells to supress immune function in order to reduce autoimmunity
431
Q

What does the loss of immune tolerance can lead to?

A

Loss of immune tolerance lead to autoimmunity like Type I diabetes or Multiple sclerosis

432
Q

What is the etiologu of any autoimmune disease?

A

Unknown. Cqauses are heterogeneous & multifunctional

433
Q

What is hypersensitivity?

A

Immune responses can cause tissue injury and disease known as hypersensitivity disease. It is an excessive or inappropriate immune responsee. Mostly harmless. Can lead to host tissue damage

434
Q

What are the 4 types of hypersensitivity reactions?

A

Type I - Immediate hypersensitivity
Type II - Bound antigen
Type III - Immune complex
Type IV - delayed hypersensitivity

435
Q

What is a mnemonic that could be used to hypersensetivities?

A

ACID
Type I - Allergic
Type II - Cytotoxic
Type III - Immune complex deposition
Type IV - Delayed

436
Q

How to administer an epipen?

A

BLUE TO THE SKY ORANGE TO THE THIGH. Remove the blue cap, put orange to the thigh, hard squeeze and hold for 10 seconds.

437
Q

What are some of the latex products in the dental clinic?

A

Gloves, rubber dam, gutta percha, impression material, bite blocks and more

438
Q

What are the three reactions to latex?

A
  1. Irritative dermatitis - non-immunological reaction
  2. Hypersensitivity type I - immunological
  3. Hypersensitivity type IV - immunological
439
Q

What does immunodeficiency lead to?

A

Any type of immunodeficiency leads to the individual being immunocompromised

440
Q

What are the two types of immunodeficiency?

A
  1. Primary immunodeficiency - when you are born with it
  2. Secondary immunodeficiency - mostly acquired
441
Q

What is one of the most common causes of immunodeficiency?

A

Malnutrition

442
Q

What are three common immune cell defects?

A
  1. T cell defects - leading to fungi, viruses and parasites
  2. B cell defects - hypogammaglobulinemia
  3. Phagocyte defects
443
Q

What are some oral complications with T cell defects?

A

Due to lowered immune function, many opportunistic batcteria are able to thrive in an oral environment.
MHC receptors on CD4+ are unable to perform their function, thus opportunistic pathogens are able to trhive like Herpes simplex viruses.

444
Q

What is important to consider when treating a patient who is immunocompromised?

A

Aggresive preventive care.

Patient with immunodeficiency are extremely vulnerable to a range of oral opportunistic bacteria.

445
Q

What is a virus and what is a virion?

A

Virus - the tiny infectious particle. Virion - an entire mature virus particle

446
Q

What is the function of viruses?

A
  1. Virus inserts its genome into its host
  2. Takes over the host’s functions
447
Q

How are viruses divided into groups or families?

A
  1. Nucleic acid types & structure
  2. Replication strategy
  3. Capsid morphology
  4. Presence or absence of lipid envelope

Dentistry BDS 2 Sem 2 (5 decks)

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