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dentistry bds 2 sem 2 > PIA answer in text > Flashcards

PIA answer in text Flashcards

1
Q

What are the symptoms and what is the physiological mechanisms of Vasovagal syncope?

A

Sympyoms: Light-headedness, narrowed vision, nausea.
Physiological mechanisms:
1. Sudden decrease in blood pressure due to stress
2. Decreased blood perfusion to the brain
3. Results in brain shut down due to low levels of oxyegn in the brain

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2
Q

What are the symptoms and what is the physiological mechanisms of Postural hypotension?

A

Symptoms: Light-headedness/dizziness, blured vision, weakness, nausea
Physiological mechanisms:
1. Prolonged periods of being in supine position
2. Blood pools in veins of legs
3. There is a decrease in venous return
4. Decreases venous return reduces the cardiac output
5. Decrease in cardiac output results in decrease blood pressure, because blood pressure equals to the product of cardiac output and systemic vascular resistance
6. When patient rises to a sitting position and standing position, the reduced blood pressure causes a deficit of oxygen travelling to the brain
7. Brain has an absolute need for oxygen, thus when there is a deficit, it shuts down

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3
Q

What are the symptoms and what is the physiological mechanisms of Changes in BGL?

A

Symptoms: Constant hunger, nausea, blurred vision, confusion
Physiological mechanisms (possible mechanism):
1. High blood glucose levels
2. Polyuria
3. Dehydration
4. Impared cognitive functions
5. Decrease in blood volume, decrease in systemic peripheral resistance, resulting in decreased blood pressure because blood pressure equals to the product of cardiac output and total peripheral resistance
6. Syncope due to brain shutting down due to low oxygen perfusion

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4
Q

What are the symptoms and what is the physiological mechanisms of hyperventilation syncope?

A

Symptoms: Weakness, confusion, dizziness, shortness of breath
Physiological mechanisms:
1. Ventilation exceeds body’s metabolic needs for CO2 removal
2. Partial pressure of CO2 in blood decreases
3. Blood pH increases due to respiratory alkalosis
4. Hypocapnia
5. Cerebral vasoconstriction
6. Lowered cerebral perfusion
7. Syncope due to reduced cerebral perfusion

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5
Q

What are the procedures in SADS to deal with a syncope?

A
  1. Stop dental treatment
  2. Implements DRSABCD:
    Danger
    Response
    Send for help
    Airway
    Normal Breathing
    CPR
    Defibrilaetor
  3. Call your tutor
  4. After incident, require dental record documentation including completing SLS incident report & debriefing with tutor
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6
Q

What to do in SADS if a patient shows symptoms of syncope?

A
  1. Stop dental treatment
  2. Elevate patient’s legs to achieve a position where their head is lower than the heart. If patient is in dental chair, tilt the chair back to a horizontal angulation
  3. Allow patient to recover slowly
  4. Measure patient’s blood pressure & heart rate
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7
Q

What are systemic manifestations of diabetes?

A
  1. Micro & Macro vascular damage
  2. Retinopathy
  3. pEripheral Vascular Disease
  4. Cardiac Disorders
  5. Kidney Problems
  6. Nerve Damage
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8
Q

What are oral manifestation of diabetes?

A
  1. Caries risk & Periodontal disease
  2. Xerostomia
  3. Slow healing ability
  4. Susceptibility to developing oral mucosal disease
  5. Taste disturbance
  6. 2-way interaction of oral infections & increased BGL
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9
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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10
Q

What are the steps to gingival assessment?

A

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

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11
Q

What are the steps to ILA?

A
  1. Patient
  2. CC
  3. MHx
  4. SHx
  5. DHx
  6. Exam
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12
Q

What is TRIM?

A

TRIM is an acronomy for:
Timing
Relevance
Involvment
Method

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13
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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14
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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15
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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16
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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17
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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18
Q

Why is calcium still needed for fluoride incorpiration?

A

Fluoroapatite still needs calcium and phosphate

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19
Q

How would you describe WSL

A

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

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20
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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21
Q

What type of buffer does stimulated saliva?

A

Bicarbonate

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22
Q

What type of buffer is in unstimulated saliva?

A

Phosphate

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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

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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25
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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26
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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27
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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28
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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29
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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30
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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31
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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32
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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33
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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34
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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35
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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36
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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37
Q

How would you assess the teeth on the radiograph?

A
  1. State what radigraph and side you are looking at
  2. FDI: notatation with restorations and radioopacities
  3. Pathology: radiolucencies, extent and causes
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38
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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39
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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40
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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41
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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42
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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43
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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44
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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45
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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46
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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47
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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48
Q

What is Grade A periodontitis?

A

When there are no evidence of loss over 5 years

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49
Q

What is Grade B periodontitis?

A

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

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50
Q

What is Grade C periodontitis?

A

When there is an above 2mm loss over 5 years

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51
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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52
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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53
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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54
Q

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

A

We design it to be amphiphatic

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55
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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56
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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57
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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58
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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59
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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60
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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61
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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62
Q

What are 3 commonly used LA techniques?

A
  1. Topical
    2.Block
    3.Infiltration
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63
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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64
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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65
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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66
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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67
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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68
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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69
Q

What are 3 types of enamel defects?

A
  1. Hypoplasia
  2. Hypomineralisation
  3. Hypocalcification
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70
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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71
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

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72
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

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73
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.

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74
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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75
Q

What is a closed sandwich technique?

A

When GIC if covered around with another material

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76
Q

What is an open sandwich technique?

A

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

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77
Q

Why do amalgam may need liners & base?

A

Due to their thermal properties

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78
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
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79
Q

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

A
  1. Non-immunological defences
  2. Physico-chemical barriers
  3. Immunological barriers
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80
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

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81
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.

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82
Q

What are the main features of randomised control trials?

A
  1. High level of evidence
  2. Eandom assignment
  3. Groups are exchangeable
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83
Q

What are the different types of RCTs?

A
  1. Parallel-arm RCTs
  2. Cross-over RCTs
  3. N-of-1 ‘single patient’ RCT
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84
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
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85
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
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86
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
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87
Q

What is the design of a cohort study?

A
  1. Time baseline
  2. Time goes on
  3. We observe
  4. Analysis
  5. Outcome
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88
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
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89
Q

Why do we do a cross-sectional study?

A

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

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90
Q

What is a perspective study?

A

The study is conducted before data is gathered.

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91
Q

What is a retrospective study?

A

The study is conducted after the data is made available.

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92
Q

Why do we sample?

A

Reduce costs and it is more efficient

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93
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
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94
Q

What is the main objective of case control study?

A

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

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95
Q

What is the main objective of ecological study?

A

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

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96
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.

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97
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
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98
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?

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99
Q

What is a systematic error?

A

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

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100
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

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101
Q

What is empathy?

A

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

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102
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
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103
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

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104
Q

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

A

8-10 mm

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105
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
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106
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
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107
Q

What does methylparaben do in LA solution?

A

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

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108
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

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109
Q

What does sodium chloride do in LA solution?

A

Makes the solution isotonic

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110
Q

What does sodium hydroxide do in LA solution?

A

Added to some LAs to adjust the pH

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111
Q

What does distilled water do in LA solution?

A

Used to dilute the solution and increase its volume

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112
Q

What does vasoconstriction do for LA solution?

A
  1. Decreased rate of absorption into the blood stream
  2. Increased duration of action and effectiveness
  3. Decrease bleeding at the site of injection, and
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113
Q

What are the 3 essential components of local anaesthetic equipment?

A
  1. Syringe
  2. Needles
  3. Cartridge
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114
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

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115
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
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116
Q

What type of topical anaesthetic is used in SA dental?

A

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

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117
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
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118
Q

What are types of infiltration can be administered?

A

Labial, buccal or palatal

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119
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
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120
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)
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121
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
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122
Q

Where is the location of injection for the maxillary block?

A
  1. Buccally beyond third molar
  2. Through greater palatine foramen
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123
Q

What are the advantages of palatal block?

A

Wide area of LA, including maxillary sinus

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124
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
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125
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
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126
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

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127
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.

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128
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
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129
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
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130
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
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131
Q

What nerve innovate the upper molars?

A

The posterior superior alveolar nerve

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132
Q

What nerve innovates the upper premolars?

A

The middle superior alveolar nerve

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133
Q

What nerve innovates the anterior upper teeth?

A

The anterior superior alveolar nerve

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134
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..
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135
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
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136
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.

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137
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
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138
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

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139
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.

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140
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

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141
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.

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142
Q

What is the main arterial supply to the lips?

A

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

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143
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

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144
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

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145
Q

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

A

1.Cell size
2. DNA damage

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146
Q

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

A
  1. DNA damage
  2. DNA replication completeness
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147
Q

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

A

Chromosomes attachment to spindle

148
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
149
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
150
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

151
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

152
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
153
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

154
Q

What is anaesthesia?

A

It is the absence of all sensory modalities

155
Q

What is paraesthesia?

A

An abnormal sensation (tingling) whether spontaneous or evoked

156
Q

What is dysaesthesia?

A

An unpleasant abnormal sensation, wether spontaneous or evoked

157
Q

What is hyperesthesia?

A

Increased sensitivity to stimulation, excluding special senses

158
Q

What is trismus?

A

The restriction of range of motin of the jaws

159
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
160
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

161
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

162
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

163
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.

164
Q

What does penicilin do?

A

Penicilin is a beta-lactam. β-Lactam antibiotics are bactericidal agents that interrupt bacterial cell-wall formation as a result of covalent binding to essential penicillin-binding proteins (PBPs), enzymes that are involved in the terminal steps of peptidoglycan cross-linking in both Gram-negative and Gram-positive bacteria.

165
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.

166
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

167
Q

What are two different processes of cell death?

A
  1. Necrosis
  2. Apoptosis
168
Q

What are 3 different [patterns of tissue necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
169
Q

What happens during liquafactive necrosis?

A
  1. Enzymatic digestion of necrotic cells
  2. Infections, production of pus
170
Q

What happens during caseous necrosis?

A
  1. Collection of fragmented necrotic cells
  2. Granulomatous inflammation
    Usually hapens during tuberculosis
171
Q

What is apoptosis?

A

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

172
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
173
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
174
Q

What are 5 stages of respond to initial insult?

A
  1. Initial insult
  2. Inflammation
  3. Tissue damage
  4. Resolution
  5. Repair
175
Q

What are macroscopic features of acute inflammation?

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain
  5. Loss of function
176
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
177
Q

What are granulomas?

A

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

178
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
179
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
180
Q

When does perioapical abcess occur?

A

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

181
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

182
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.

183
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
184
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
185
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

186
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

187
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

188
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

189
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

190
Q

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

A

M0 = No distant metastasis
M1 = Evidence of distant metastasis

191
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

192
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
193
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

194
Q

What is the difference between sign and symptom?

A

Symptom - are reported by the patients
Signs - are detected by the physician

195
Q

What would your brushing instruction would be for a person between ages of 0-1.5

A

No fluoride

196
Q

What would be your recommendation for an individual 1.5-6 years old for brushing?

A
  1. Low fluoride tooth paste to minimise fluorosis
  2. peasize
  3. Supervised
  4. Spit not rinse
197
Q

What would your recommendation for an individual 6+ years old?

A
  1. Standard dose fluoride
  2. Peasize
  3. Spit not rinse
  4. Supervise if needed
198
Q

What are the four classic biomedical principles?

A
  1. Non-maleficence
  2. Beneficence
  3. Autonomy
  4. Justice
199
Q

What does informed consent include?

A
  1. Alternatives and all options for treatment
  2. Information surrouding the nature and what the treatment involves
  3. Risks of treatment
  4. Pros and Cons of treatment and No intervention
  5. Cost of treatment
200
Q

What does PICO stand for?

A

Patient

Intervention

Comparison

Outcome

201
Q

What are contra indications for use of lignospan special?

A

It should not be used with patients with epilepsy, bradycardia, sever shock or heart block

202
Q

What are contra indications for use of Septanest?

A

It should not be used on patients with allergy to articane or epilepsy

203
Q

What are contra indications for use of Scandanest?

A

No major contraindications, good for people with sulfite

204
Q

What is the trigemanimal pathway for pain, temperature and crude touch?

A
  1. Stimulus occurs
  2. Action potential from a receptor in the tooth travels to the trigeminal ganglion
  3. The action potential travels to PONS
  4. The action potential switches the neurons at the spinal nucleus
  5. Action potential travels again from the spinal nucleus to the midbrain and into the thamalamus
  6. Last synapses occurs between the thamalus and post-cntral gyrus
205
Q

What is the trigeminal pathway for fine touch and vibration?

A
  1. Stimulus occurs
  2. Action potential from a receptor in the tooth travels to the trigeminal ganglion
  3. The action potential travels to PONS
  4. At the chief nucleus there is a cross over into the pontine nucleus
  5. Action potential travels again from the pontine nucleus to the midbrain and into the thamalamus
  6. Last synapses occurs between the thamalus and post-central gyrus
206
Q

What is the trigeminal pathway for propriception in muscle of mastication?

A

1.Stimulus occurs
2. The receptors in the muscles of mastication travels through the motor brunch of trigeminal ganglion, through the pons and into the mesencephalic nucleus in the midbrain
3. A cross over occurs in the mesenceohalic nucleus and action potential travels into the thalamus
4. A cross over occurs in the thalamus and travels into the post-ctrl gyrus

207
Q

What is the trigeminal pathway for movement of muscle of mastication?

A
  1. The action potential occurs in the pre-central gyrus
  2. It travels through a upper motor neuron to the motor nucleus in the PONS
  3. There is usually a cross over occuring here, meaning the signal of the right pre-central gyrus affect the the left muscle of mastication
  4. From the motor nucleus, lower motor neuron propagates the action potential to the corresponding muscle mastication.
208
Q

What is gingivitis?

A

Gingivitis is generally regarded as a site-specific inflammatory condition initiated by dental biofilm accumulation and characterized by gingival redness and oedema and the absence of periodontal attachment loss.

209
Q

What are signs of gingivitis?

A
  1. Bleeding on probing
  2. Erythema
  3. Oedema
  4. Halitosis
  5. Presence of biofilm
  6. Discomfort on probing
  7. NO EVIDENCE OF RADIOGRAPHIC BONE LOSS
210
Q

What are symptoms of of gingivitis?

A
  1. Bleeding on brushing or flossing
  2. Red gums
  3. Swollen gums
  4. Bad taste, bade breath
  5. Soreness
  6. Usually not painful
  7. Difficulty eating, altered taste
211
Q

What does it mean by reduced periodontium?

A

In certain situttion there are no evidence of previous periodontal disease, but the periodontium is reduced due to other factors such as genetical factors, injury or trauma or other. In this case, we can state that the healthy gingiva on a reduced periodontium.

212
Q

How do we define the severity of gingivitis?

A

0 = Normal gingiva
1 = Mild inflammation - slight change in color and slight edema
2 = Moderate inflammation - redness, edema and glazing
3 = Sever inflammation - marked redness and edema, ulceration with tendency to spotaneous bleeding

213
Q

How to write a diagnostic statement for gingivitis?

A
  1. Extend - localised or generalised depending on the BOP
  2. Disease - gingivitis
  3. Specification - biofilm induced, mediated by pregnancy or leukemia
214
Q

What happens when oral hygine is removed in cases of gingivitis?

A

Gingivitis develops in 10-21 days

The quantitity of microorganisms increases and changes in the biofilm occur to favour inflammatory bacteria. This occurs due to the fact that the biofilm is not removed appropritaley, causing biofilm accumulation.

When appropriate oral hygiene is reintroduced, within around 7 days gingivitis resolves.

215
Q

What is a risk factor?

A

Health risk factors are attributes, characteristics or exposures that increase the likelihood of a person developing a disease health disorder

216
Q

What are modifying factors?

A

They modify disease expression and may influence disease progression by altering the host’s immune response

217
Q

What are some systemic risk factors that mediate gingivitis?

A
  1. Smoking
  2. Hyperglycemia
  3. Nutritional factors
  4. Pharmacological agents
  5. Sex hormones - puberty, menstrual cycle, pregnancy, oral contraceptives
  6. Hematological conditions
218
Q

What is the impact of smoking on periodontal health?

A
  1. Chronic reution in blood flow and vascularity
  2. Increased prevalance in pathogens
  3. Reduced growth facot production
  4. Inhibition of fibroblast growth, attachment and collagen production
219
Q

What is a clinical impact of smoking on gingivitis diagnosis?

A

Smoking reduces vascularity thus reduces bleeding on probing

220
Q

What is the pathological significance of diabetes, as a systemic factor for gingivitis?

A

It increases the amount of advanced glycation end products. Advanced glycation end products can cause oxidative stress and chronic inflammation of the periodontal tissues

221
Q

What can be seen intraoraly in a person with diabetes?

A
  1. Enlarged red, velvety gingival tissues
  2. Increased gingival bleeding
  3. Periodontal abscesses
  4. Granulation tissues
  5. Slow resolution of gingivitis
  6. Complaints about dry mouth
222
Q

What do sex hormones mostly effect during gingivitis?

A

They usually affect the work of fibroblasts. That is why for pregnant women for example, there is a large change of developing gingivitis in the third trimester of their pregnancy

223
Q

What are some of the predisposing factors for gingivitis?

A
  1. Supra- and sungingival calculus
  2. Anatomical factors: enamel projections, grooves, concavities, furcations, root proximity, recession, frenal insertion etc.
  3. Iatrogenic factors: insufficient resoraton margins, overhangs, surface texture, open contact, denture desing etc.
  4. Motoric problems
224
Q

What can cause mouth dryness?

A
  1. Iatrogenic causes: Drugs, irradiation, graft vs host disease
  2. Disease: Salivary gland disease, dehydration, psychogenic
225
Q

What are oral manifestations of mouth dryness?

A
  1. Mirror sticks to mucosa/tongue
  2. Frothing of saliva
  3. No saliva pooling
  4. Loss of gingival architecture
  5. Glasse appearance of mucosa
  6. FIssured, lobulated tongue
  7. Active cervical caries
  8. Debris on palate
226
Q

What is DIGO?

A

Drug Induced Gingival Overgrowth.

227
Q

What can cause DIGO?

A

Calcium channel blockers that are used in treatment of cradiovascular disease, immunosuppressants or anticonvulsants

228
Q

What are oral manifestations of DINGO?

A
  1. Onset within 2-4 months
  2. Predilection for anterior gingiva, not present in edentulous areas
  3. Starts as painless, beadlike enlargement of papilla
  4. Candevelop massive tissue fold
  5. Mulberry shape, firm, pink and resilient with no BOP
  6. Spontaneous dissappearance after discontinuation of a drug
229
Q

What are some treatments for DIGO?

A
  1. Meticulous biofilm control can not prevent development of lesions but may reduce their extent and severity by preventing a secondary infection
  2. In sever cases surgcal excision and/or drug substitution may be required
230
Q

What are signs of necrotising gingivitis?

A
  1. Central necrosis of interdental papilla
  2. Large amounts of bleeeding on probing
  3. Pain on probing
  4. Halitosis
  5. Lymphodenopathy - swelling of lymph nodes
231
Q

What are the symptoms of necrotising gingivitis?

A
  1. Pain
  2. Bleeding of gums
  3. Gums appear different
  4. Bad taste, bad breath
  5. Malaise
  6. Fever
232
Q

How do we treat necrotising gingivitis?

A
  1. Debridment under LA (removal of biofilm, calculus and necrotic tissues)
  2. Local irrigation with chlorhexidine 0.2%
  3. Antibiotic therapy - Metronidazole 400 mg orally, 12-hourly, 3-5days
  4. Review and reffer when needed
233
Q

What are two major Herpes reactions for the oral cavity?

A

Gingivostomatitis herpetica and herpes labialis

234
Q

What is supra- and subgingival debridement?

A

It is the removal or disruption of dental deposits and plaque-retentive dental calculus from tooth surfaces and within the periodontal pocket space without deliberate removal of cementum as done in root planning and often in dental scaling.

235
Q

What are the steps for debridment using Gracey curettes?

A
  1. Choose a tooth and side specific curettes
  2. Identify the cutting edge
  3. Orientate the cutting edge at 20 degress in order to apply lateral pressure
  4. Adapt the toe
  5. Make sure that the terminal shank is paraller to the long axis of tooth and get going
236
Q

What is the disadvanatge of blunt instruments in debridement?

A
  1. Reduced tectile sensitivity and instrument control
  2. Increased operator fatigue
  3. Insufficient calculus removal
237
Q

How do we identify biofilm and calculus?

A
  1. Using GC tri Plaque ID Gel
  2. Using a dry field of view with use of probes both the periodontal and 11/12 probe
  3. Radiographs
238
Q

What is recession?

A

It is an apical shift of the gingival margin

239
Q

What are clinical significance of recession?

A
  1. Dentine hypersensitivity
  2. Non carious cervical lesion
  3. Impaired oral hygine
  4. Caries
  5. Esthetics
240
Q

What is the aetiology of recession?

A

Could be separated into two main brunches

  1. Anatomical influences: Periodontal phenotype, fenestrations, dehiscene, position of tooth and frenal attachment
  2. Inflammation: biofilm and trauma (such as brushing)
241
Q

How do you measure recession?

A

Recession is measured from the cemento-enamel junction to the gingival margin

242
Q

What are different types of recession?

A

Type 1 - gingival recession with no loss of inter-proximal attachment

Type 2 - Gingival recession associated with loss of inter-proximal attachment that is lower in the inter-proximal than in true buccal

Type 3 - Gingival recession associated with loss of interporximal attachment that is greater in the inter-proximal than in true buccal

243
Q

What are steps to treatment of recession?

A

1.Assessment/documentation
2. Identify and modify etiologic factors
3. Consequences of root surface exposure
4. Treatment options

244
Q

What are some of the treatments for recession?

A
  1. Monitor and careful OHI
  2. Orthodontics
  3. Surgical correction
245
Q

What is periodontitis?

A

Periodontitis is a multifactorial inflammatory disease associated with dysbiotic microbial dental biofilm and characterised by non-reversible progressive periodontal tissue destruction.

It manifests through clinical attachment loss, radiographically assessed alveolar bone loss, presence of periodontal pocketing and gingival bleeding, and leads eventually to tooth loss.

246
Q

What are some signs of periodontitis?

A

On top of gingivitis signs:
1. Periodontal pocketing
2. Recession
3. Clinical attachment loss
4. Evidence of radiographic bone loss
5. Increased mobility
6. Tooth loss

247
Q

WHat are symptoms of periodontitis?

A

On top of gingivitis symptoms:
1.Receding gums
2. Gaps between the teeth
3. Increased food debris
4. Mobil teeth
5. Change in teeth position
6. Speech alteration
7. Tooth loss
8. Pain in acute conditions

248
Q

How to write a diagnostic statement for periodontitis?

A
  1. Type of periodontal disease - periodontitis
  2. Disease extent - generalised or localised
  3. Stage - I, II, III, IV
  4. Grade - A, B, C
  5. Current disease status - stable, remission, unstable
  6. Risk profile smoking, diabetes, etc

E.g. Periodontitis; generalised, Stage III, Grade C, currently unstable. Risk factors: smoking 20cig/day

249
Q

What is the normal distance between the cemento-enamel junction and the alveolar crest in a radiograph?

A

1-3mm

250
Q

What are the stages of periodontitis in reference to ragiographic bone loss?

A
  1. No bone loss - no periodontitis
  2. <15% - Stage I
  3. 15-33% or coronal 1/3 - Stage II
  4. Middle to apical 1/3 - Stage III or Stage IV
251
Q

What is horizontal bone loss?

A

When the alveolar bone crest lowered, parallel with a line between adjacent CEJs

252
Q

What is vertical bone loss?

A

When alveolar bone crest lowered, irregular, V-shaped, not parallel with a line between adjacent CEJs

253
Q

What are some of the limitations of using radio-graphs to periodontal health assessment?

A
  1. Viewing a 3D object through a 2D image
  2. ALARA
  3. No information about periodontal pocket depth or disease activity
  4. Early signs of attachment loss not detectable and bone loss is underestimated
  5. Poor quality and technique in taking radiographs
254
Q

What are the two main components in diagnosing periodontitis?

A
  1. Comprehensive examination
    2.Radiographs
255
Q

What are the objetives of preventative dental treatments?

A

To prevent the ocurence or progression of disease and ‘heal’ the damage. This is done by reestablishing healthy oral conditions.

256
Q

What are some of the steps to treatment planning?

A
  1. A comprehensive examination with taking of all histories, extra-intraoral examinations and relevant tests and radiographic images
  2. Evaluation, proposing treatment to the patient, patient consent
  3. Oral health instructions using TRIM framework
  4. Sub/ supra gingival scaling
  5. Prophylaxis
  6. Diet evaluation
  7. Use of extra products
  8. Recall depending on patients needs
    COMMUNICATING WITH THE PATIENT IS KEY
257
Q

What are the 2 froms of detecrtors available to digital imaging?

A
  1. Solid state (direct) detectors
  2. Photostimulable phosphor plate detectors
258
Q

What are some advantages of digital radiography?

A
  1. Reduced patient radiation dose
  2. No ongoing purchase/storage of films, processing soluting
  3. Work health safety issues reduced: no chemical hazards
  4. Large dynamic range
  5. Dark room no longer needed
  6. Decreased process time
  7. Elimination of processing errors
259
Q

What are disadvantages of direct solid state sensors?

A
  1. Expensive and easily damaged
  2. Require specialised holders
  3. Rigid and bulky
  4. Patient discomfort and gagging
  5. Viewable surface area is smaller than size of the sensor
  6. Not universal
  7. Can’t withstand heat sterilisation - require coverage with disposable plastic sleeves
260
Q

What are the different types of solid state director detectors?

A

Wireless (more expensive and bulky) and wired (smaller and but has a wire). Similar quality image

261
Q

What is the advantage of indirect digital imaging over direct digital image and the disadvantage?

A

Advantages: various pate types, and less expensive plates

Disadvantages: needs a scanner, last for shorten lifespan (debatable), not as fast at processing the image

262
Q

What are two main techniques for periapical radiographs?

A
  1. Bisected angle technique
  2. Paralleling technique
263
Q

What are some of the indications for a periapical radiograph?

A
  1. Detection of apical pathology
  2. Periodontal assessment
  3. Endodontics
  4. Assessment of tooth and alveolar bone following trauma
  5. Pre/post-extraction assessment
  6. Pre/post implant evaluation
264
Q

What are the advatages of paralleling technique in periapical radiographs?

A
  1. Simple
  2. Minimal elongation or shortening of image
  3. Bone level is well represented
  4. Use of film holders ensure that the image is stable, reduces cone cutting, angulation problems and makes sure that the image can be fairly reproducible
265
Q

What are disadvantages of paralleling technique?

A
  1. Possibility of patient discomfort
  2. Tooth apices images near edge of film
  3. Not stable holders, some need to be held by hand
  4. Unsuitable of you have short cone equipment
  5. Added equipment sterilisation
266
Q

What is the technique in taking the pariapical radiograph?

A
  1. Set exposure factors
  2. Seat patient upright
  3. Establish rapport, show patint detector/film etc
  4. Remove jewlerry, dentures, glasses as required
  5. Occlusal plane of interest is horizontal
  6. Mid-sagittal plane vertical
  7. Head support for the patient
  8. Position detector in the mouth
  9. Stabilise detector - ask patient to bite gentley
  10. Align the beam
  11. Rotate collimator to correct position
  12. Advise [atient to remain still
  13. Expose film
267
Q

How do you align the film and detector in parallel periapical radiograph?

A
  1. FIlm needs to be parallel to long axis of tooth
  2. Film as close to tooth as possible
  3. Vertical beam alignment at 90 degrees to film & tooth
268
Q

What are some of the indicators of bisecting angles technique?

A
  1. Shallow palatal vault
  2. Large tori
  3. Shallow floor of mouth
  4. Short lingual frenum
269
Q

What are 4 important aspect of minimal intervention?

A
  1. Conserving tooth structure
  2. Maintaining a marginal seal
  3. Internal reminelasation of affected dentine
  4. Knowledge of properties of dental materials
270
Q

What are some of the disired properties of resin composites?

A
  1. Aesthetics
  2. Easy to handle
  3. Relativley biocompatible
  4. Protect tooth bioactive
  5. Bond to tooth structure with strength
  6. Huge repair potential
  7. Radiopacity
271
Q

What are the three clinical consideration when choosing to work with composite resigns?

A
  1. Biocompatability - unpolymeraised resin is toxi to the pulp due to HEMA & TEGDMA
  2. Water sorption and solubility - wayer is sensetive to water thus can be very soluble
  3. Polymerisation shrinkage and shrinkage stress - whe polymerised it reduces in size due to the fact that dimensional rearrangment with monomer to polymer - resulting in likage - this can also lead to shrinkage stress and breakdown of the material
272
Q

What is a C factor?

A

It is the number of bonded surface divide by the number of free surfaces. This helps to understand the shrinkage stress. Higher the c-factor higher the shrinkage stress.

273
Q

What reduces the C factor?

A

The c-factor is reduces with incirmental layering of the resin material

274
Q

Compare bonding to enamel vs bonding to dentine histologically.

A

Enamel:
1. Relativley homogenous
2. High mineral content of hydroxy apetite
3. Low protein content
4. Low water content

Dentine:
1. Reduced hydroxy apetite content
2. Increase protein content
3. Increased water content
4. Dentinal pulp complex

275
Q

What is the difference between wet and dry primer?

A

Wet - the dentine does not need to be desicated . Primer is used to reduce the water content from dentinal tubules.

Dry - the dentine needs to be desicated. Primer is used to rehydrate the collapsed collagen framework.

276
Q

What are some of the advantages of GICs?

A
  1. Biocompatible with the pulp and soft tissues
  2. Acts as a fluoride reservoir
  3. Bonding via ion exchange is strong
277
Q

What are disadvantages with GIC?

A
  1. Brittle
  2. Prone to change physical properties if not protected and used in patient with xerostomic conditions
  3. Not as strong as other materials
278
Q

How would you mix poder and liquid for GIC for the following: Luting, restoration and lining+base

A

Luning - 1/1.5:1
Restorative - 3:1
Lining or Base - 1:1 for lining and 3:1 for base

279
Q

Where would you not put amalgams?

A

Do not place it in thin layers that expose it to “pulling” or “bending” forces

280
Q

What are three disadvantages of amalgam?

A
  1. Thermal properties - need liner or base
  2. Corrosion over time
  3. Questionable biocompatibility
281
Q

Where would you place an amalgam filling?

A
  1. Where aesthetics are not an issue
  2. Where occlusal stress is high
282
Q

What are the two types of fissure sealant?

A
  1. Resin based sealants - good retention
    2.GIC/RMGIC - poorer retention but great in moist environments and fluoride release
283
Q

What are the 5 causes of damage to the dentine and pulp

A
  1. Caries
  2. Micro-leakage - unsealed margins
  3. Mechanical direct physical damage to odontoblasts
  4. Thermal - during cavity prep
  5. Chemical - restorative materials hema, tegdma and acids
284
Q

What are some of the ways we can test pulp vitality?

A
  1. Electirc pulp testing
  2. Cold test
  3. Heat tests
  4. Transillumination
  5. Percussion
  6. Wedge test
  7. Radiographs
  8. Muscle & TMJ palpation
285
Q

How do we treat hypersensitivity?

A
  1. Block dentinal tubules - using restorations or protective coverings
  2. Block nerve activity - stanous fluoride and potassium nitrate
  3. Remove the cause - erosion and toothbrushing technique change
286
Q

How do we manage dentine hypersensitivity?

A
  1. Occlude dentinal tubules to reduce impact of stimuli on fluid movement - can be done through chemical occlusion (fluorides) or physical occlusion (sealed resorations)
  2. Reduce sensitivity of nerves - using potassium nitrate
287
Q

What are indications for indirect pulp capping?

A
  1. Deep cavity
  2. No pulpal exposure
  3. Removal of all infected dentine may result in pulpal exposure
  4. No signs or symptoms of irreversible pulpits
288
Q

What is the most important aspect of indirect pulp capping?

A

CORONAL SEAL IS VITAL.

289
Q

What happens to the pulp during direct pulp capping?

A

The varnish that is used is able to neutralise necrotic tissue and cause the deposition of tertiary dentine

290
Q

What is the basic principal of polishing?

A

Go from most abrasive to least abrasive

291
Q

What is DMG ICON?

A

It is a low viscosity resin based product that is used in order to feel white spot lesions in the inter proximal surfaces at early stages.

Very similar to normal resin but has no clinical data on success

292
Q

When would you use a ‘closed’ tunnel technique?

A

Clinically, if the enamel on the proximal surface is not cavitated, you may leave it in situ

293
Q

When would you use a tunnel prep?

A

When there are evidence that a marginal ridge is not compromised and has retained appropriate thickness

294
Q

How do we detect cavitations in site 2 anteriors?

A
  1. Clinical examination
  2. Transillumination
295
Q

What is the purpose of the bevel and how do you make it?

A

Bevel - is used to increase the bonding area to enamel. Using a diamond bur like 838, at 45 degree angle make a small cuts in enamel only

296
Q

What happens to dentine as we age?

A

There is an increase in dentine quantity with age, but there is a decrease in the amount of dentinal fluid produces, thus with age we are more likely to use a primer rather than the liner.

297
Q

What are three main forms of tooth wear?

A
  1. Abrasion
  2. Attrition
  3. Erosion
298
Q

What is erosion?

A

Loss of dental hard tissue by a chemical process not involving bacteria

299
Q

How do we manage erosion?

A
  1. Isolate and eliminate the cause
  2. Re-stablish biofilm
  3. Neutralise the acid
  4. OHI
  5. Potential protective covering
  6. Monitor
300
Q

What is abrasion?

A

Wear that results when exogenous material is forced over tooth surfaces.

301
Q

What is NCCL?

A

It is a non-carious cerviacal lesion. Results from both erosion and abrasion. Has a dish-shaped, cupper, scooped appearance

302
Q

What is attrition?

A

It is wear that occurs when microfine fragment of enamel prism get caught between opposing tooth surfaces. Good treatment is a nightguard

303
Q

What is abfraction?

A

It is the development of ‘wedge-shaped’ lesions from the flexing of the tooth under load

304
Q

What are the steps for management of site 3 lesions?

A
  1. Identify aetiology
  2. Determine if process is active or historic
  3. Treat underlying aetiology or have a plan for this and start implementation
  4. Determine need for restoration
305
Q

When would you use an open sandwhich technique?

A

You would use an open sandwhich technique where there is no more remaining enamel at the gingival margin

306
Q

What are indications of cusp capping?

A
  1. Undermined cusp with caries removal
    2.Cracked cusp
307
Q

What are indications for cusp replacement?

A

The cusp has been lost due to fructure or other

308
Q

What are pins used for?

A

Pins are used to provide retention for an amalgam restoration where convetion forms of retention are inadequate. Pins do not provide strength.

309
Q

What are rules in placing a pin?

A
  1. Place in dentine
  2. Pin hole parallel to external contour of the tooth
  3. 1 pin per cusp
  4. Must not be too high
  5. Must have access to condense amalgam around pin
  6. idially, 2mm of amalgam need to cover the pin
310
Q

What is a bonded amalgam?

A

When you lute the cavity and than place amalgam in there

311
Q

Why can facial paralysis occur during IANB administration?

A

Cause: needle was positioned too far posteriorly & LA administered instead in the body of the parotid gland where facial and tympanic nerve run through

Signs + sympotms: Facial paralysis, unilateral, drooping of eyelid and upper lip / corner of mouth

Managment:
1. Tell patient this is temporary
2. Tell patient to not rub their eye
3. Cover the affected eye with eye patch
4. Keep under observation until better
5. No driving back home
6. IF not recovered in 12 hours - will need a medical review

312
Q

Why can truisms occur during IANB application?

A

Causes: Trauma to the muscles or blood vessels, often caused by withdrawing the needle through tissue distension

Signs + symptoms: may present as a prologned spasm of the jaw muscles with limited or complete inability to open the mouth, or pain associated with mouth opening

Managment: Usual improvement within 48-72 hurs with up to 6 weeks for complete recovery. Patient may seek heat therapy, wamr saline rinse, soft diet & jaw exercises.

313
Q

Why can soft tissue damage occur during IANB administration?

A

Cause: It is usually self-inflicted injury by the aptient themselves; induced trauma or burn

Sings + symptoms: May present as a soft tissue lesion, accompanied by localised pain and swelling. More noticeable once LA has worn off.

Managment: Provide appropriate post-operative insructions. If sever, antibiotics may be prescribed to void infection. Warm saline rinses.

314
Q

Why can temporary blidness occur during the IANB administration?

A

Cause: Intravascular administaton. Pathway: Inferior alveolar nerve into middle meningeal artery into opthalmic artery causing loss of vision

Signs + Symptoms: Loss of vision a few minutes post IANB administration.

Managment: Stop dental treaatment. Call 000 because patient needs to go to the emergency department. CPR if patient is unconcious.

315
Q

Why can persisten anaesthesia occur when administering IANB?

A

Cause: Direct sensory nerve damage caused by the needle. Injecting too much LA at high concentrations. Haemorrhage from around/near the neural sheath put pressure on the nerve

Signs + symptoms: paraesthesia will vary depending on structures involved - usually drooling, numbness, pins & needles. If damage to lingual nerve there can be altered taste sensation.

Management: Paraesthesia resolves within approx 8 weeks, if above 8 weeks refer to oral surgeons. Reassure patient and reassess

316
Q

Why can heart palpitations occur during administration of IANB?

A

Cause: Intravascular injection may cause an excitation of the cardiovascular system

Signs + symptoms: Tachycardia, palpitations and headache

Management: Typically only short in duration. Ensure to stop procedure and monitor the patient.

317
Q

Why can oedema occur during IANB administration?

A

Cause: May be caused by physical trauma, an allergic response, haemorrhage or irritation

Signs + symptoms: Present as a swelling tissues on the medial side of the ramus after deposition of LA

Managment: Pressure and cold compress applied to the area for 3-5 minutes, acoompanied by warm saline rinse

318
Q

Why can tingly in the trap and throat happen during IANB administration?

A

Causes: 1) LA travelling down the brachial plexus (unlikely)
2) LA deposited too far back into the fascia surrounding pharyngeal muscles -> anaesthetised supraclavicular branch of cervical plexus that innervates ur traps -> arm numbness (more likely)

Sing + symptoms: Tingling in the throat and trap

Managment: Reassure patient it is temporary. Monitor. If the paraesthesia is persistent, need to get medical care.

319
Q

When does the development of primary dentition begin?

A

It begins at around 4th fetal month

320
Q

When does the formation complete for deciduous central incisors and when do they erupt?

A

Both Maxillary and mandibular central incisors full calficiation occurs at around 18-24 months.

Eruption: Mx 6-10 months, Md 5-8 months

321
Q

When does the formation complete for deciduous lateral incisors and when do they erupt?

A

Both Maxillary and mandibular lateral incisors full calcification occurs at around 18-24 months

Eruption: Mx 8-12 months, Md 7-10 months

322
Q

When does the formation complete for deciduous canines and when do they erupt?

A

Both Maxillary and mandibular canines full calcification occurs around 30-39 months

Eruption:
Mx 16-20 months, Md 16-20 months

323
Q

When does the formation complete for deciduous first molars and when do they erupt?

A

Both Maxillary and mandibular first molars full calcification occurs around 24-30 months

Eruption:
Mx 11-18 months, Md 11-18 months

324
Q

When does the formation complete for deciduous second molars and when do they erupt?

A

Both Maxillary and mandibular second molars full calcification occurs around 36 months

Eruption:
Mx 20-30 months, Md 20-30 months

325
Q

When does calcification, crown completion, root completion and eruption occur for permanent central incisors?

A

Calcification begins at: 3-4 months

Crown completes: 4-5 years

Roots completes at: 9-10 years

Eruption: Mx 7-8 years, Md 6-7 years

326
Q

When does calcification, crown completion, root completion and eruption occur for Maxillary permanent lateral incisors?

A

Calcification begins at: 10-12 months

Crown completes: 4-5 years

Roots completes at: 11 years

Eruption: 8-9 years

327
Q

When does calcification, crown completion, root completion and eruption occur for Mandibular permanent lateral incisors?

A

Calcification begins at: 3-4 months

Crown completes: 4-5 years

Roots completes at: 10 years

Eruption: 7-8 years

328
Q

When does calcification, crown completion, root completion and eruption occur for permanent canines?

A

Calcification begins at: 4-5 months

Crown completes: 6-7 years

Roots completes at: 12-15 years

Eruption: Mx 11-12 years, Md 9-11 years

329
Q

When does calcification, crown completion, root completion and eruption occur for permanent first premolars?

A

Calcification begins at: 18-24 months

Crown completes: 5-6 years

Roots completes at: 12-13 years

Eruption: Mx 10-11 years, Md 10-12 years

330
Q

When does calcification, crown completion, root completion and eruption occur for permanent second premolars?

A

Calcification begins at: 24-30 months

Crown completes: 6-7 years

Roots completes at: 12-14 years

Eruption: Mx 10-12 years, Md 11-13 years

331
Q

When does calcification, crown completion, root completion and eruption occur for permanent first molars?

A

Calcification begins at: Birth

Crown completes: 30-36 months

Roots completes at: 9-10 years

Eruption: Mx 5.5-7 years, Md 5.5-7 years

332
Q

When does calcification, crown completion, root completion and eruption occur for permanent second molars?

A

Calcification begins at: 30-36 months

Crown completes: 7-8 years

Roots completes at: 14-16 years

Eruption: Mx 12-14 years, Md 12-14 years

333
Q

What is a material risk?

A

Material riks is a resonable risk depending on a person and procedure. FOr example, fluoride tray is not a risk for an adult but it is for a child

334
Q

What is the action of calcium channel blockers in DIGO?

A
  1. Reduced production of matrix metalloproteinases & increased production of extra cellular matrix
  2. Increased production of collagen by enhancing the proliferation of fibroblasts through the blockage of Ca2+ channels
335
Q

What is the action of immunosuppressants in DIGO?

A
  1. Ciclosporin – increased protein synthesis by subgroup of fibroblasts when stimulated by ciclosporin
  2. Generic predisposition or protection to action of ciclosporin
  3. Enhanced collagen production and collagen production when fibroblasts also exposed to pro-inflammatory cytokines such as IL and IL6
  4. Increased production of platelet – derived growth factor, which stimulates production of extra cellular matrix
  5. Reduces production of matrix metalloproteinases and or/ increases production of inhibitors of these enzymes
336
Q

What is action of anticonvulsants in DIGO?

A
  1. Increased collagen and protein production by specific subpopulations of reactive fibroblasts
  2. Increased production of platelet derived growth factor that enhances production of connective tissue
  3. Inactivation of metalloproteinases
337
Q

What are the steps for periodontal disease management?

A
  1. Treating pain
  2. Evaluation of the gingival health
  3. Phase I - hygine phase
  4. Re-evaluation after 8-12 weeks
338
Q

What framework can be used to assess fissure sealants?

A

CAMST.
Coverage - is the fissure fully covered
Amount - is there enough FS material
Margins - are the margins sealed & flush
Surface - is the surface smooth
Tooth - at future appts check the tooth

339
Q

What is oral lichen planus, signs and management?

A

Oral lichen planus is a chronic inflammatory condition affecting skin & mucous membrane including oral mucosa.

Signs: Wickham striae patterns, vascular features

Management: short term - management of discomfort and pain and use of corticosteroids to reduce inflammation, long term - management of triggers

340
Q

What is angular cheilitis, signs and management?

A

Angular cheilitis is a localised inflammation of the skin at the labial commissure.

Signs: redness, painful patches, blistering, crusting.

Management: short term - cool compresses, lip balm, topical antiseptics. Long term - avoiding skin irritants, avoiding the sun & extreme cold.

341
Q

What is amlogenesis imperfecta?

A

It is a series of genetic conditions causing change to normal enamel deposition.
It affects all teeth, both deciduous and permanent dentition and occurs due to mutation of enamel proteins.
Results in hypoplastic, hypomineralised and/or hypocalcified enamel.
Symptoms and signs vary between subtypes - include discolouration, sensitivity, increased caries risk, disintegration.

342
Q

What is dens in dente?

A

It is a cap stage anomalities. It refers to whena smaller tooth exist within a larger tooth.

343
Q

What is gemination?

A

It is a cap stage anomaly. It is the formation of two crowns from a single root.

344
Q

What is fusion?

A

It is a cap stage anomaly. Fusing of two individual crowns.

345
Q

What a diagnostic statement?

A

It is when you write clinical problems in order of most importance

346
Q

What are the 5 moments of hand hygiene?

A
  1. Before touching the patient
  2. Before cleaning
  3. After fluid exposure
  4. After touching the patient
  5. After touching the patient’s surroundings
347
Q

How do identify the age of an individual by using an OPG radiography?

A
  1. If the If the sixes are erupted - the individual is over 6 years old
  2. If the second molars are not through they are under 12
  3. If the lateral incisors are through the patient is above 8
  4. If the deciduos molars are still present the patient is between 8-9
  5. If the first deciduous molar is exfoliated they are 9-10
  6. If both of the premolars are out, but the second molars are not out than a person is 10-11 years old
348
Q

What are the steps for the prevention plan?

A

Prevention plan:
1. Patient education:
a. Diagnosis
b. Causes
c. Consequences
d. Management: control of causative factors, restorative options, products
2. Consent
3. Further information/tests:
a. Try to discover cause – diet, medical history
b. Saliva test
c. Tri-plaque gel
d. Diet diary??
e. Scratch test
f. Radiographs
4. Professional care:
a. Debridement
b. Prophy
c. Professionally applied topical agents
d. Post op instructions
5. Home care:
a. OHI advice – be specific, how, when, how often
b. Products – fluoride, CHX gel, MW, proximal cleaning aids, TB, TP plus instructions of use
6. Recall/monitoring:
a. 3/12-6/12, review/repeat tests, review home care and make adjustments where required

349
Q

What is an example of headings used n a treatment pla>

A
  1. Diagnoses
  2. Chief concern
  3. Radiographs
  4. Preventative care
    5.Periodontal care
    6.Restorative care
    7.Recall/review
    All appoitments
350
Q

How do you express emoathy?

A

Just literally say you understand the patient’s emotions. E.g. I understand that you are upset about this situation

351
Q

How to deal with the patient in a PCC way?

A

Taylor the information on what the patient want to know
Use trim framework:
Time - ask the patient if thy have time to discuss the issue
Relevance - asses the patient starting poitn. Ask what information they would like to know
Involvement - encourage patient to ask questions. Ask the patient open questions. Ask if that is helpful. Ask what their expectations are.
Method - sigposting, check undertsanding, recalll, use visual aids

352
Q

What is supragingival calculus, what is the characteristcs and aeiology?

A
  1. Supragingival calculus is a form of a mineralised tooth deposit that is associated with precipitation of calcium and phosphate in saliva
  2. It has an appearance of a creamy white/yellow ruff bolging in ecological niches, which can tak eup staining
  3. It occurs due to nucleation event between the oral environment and pellicale or biofilm
353
Q

What is subgingival calculus?

A
  1. Subgingival calculus is a form of a mineralised tooth deposit that is associated with precipitation of calcium and phosphate in gingival cruvicular fluid
  2. It has an appearance of a creamy dark, flint ruff bolging in ecological niches, which can take up staining
  3. It occurs due to nucleation event between the gingival crevicular fluid and cementum
354
Q

What si the appropriate use of the sickle scaller?

A
  1. Terminal shank parralel to the long axis of the tooth
  2. USe the end 2 mm of the tip
    3.Apply lateral pressure appropriate tfor the removal of the deposit
  3. Supragingival, atnterior teeth use only
355
Q

What is the appropriate use of the McCall’s scaller?

A
  1. Terminal shank parralel to the long axis of the tooth
  2. USe the end 2 mm of the tip
    3.Apply lateral pressure appropriate tfor the removal of the deposit
  3. Supragingival, any tooth in the mouth teeth use only
  4. The handle should point outside the oral cavity
356
Q

What is the difference between the scaller and a gracies curette?

A
  1. Scaler have 2 working ends and 4 cutting edges, gracies have 2 working end and 2 cuttign edges
  2. Gracies blade is positioned at 70 degreess, scallers at 90 degrees
  3. Gracies are used subgingivally, scallers supra gingivallly
    4.Gracies have a rounded toe with half moon crossection, scallers have a pointed toe with a triangular corss section
357
Q

How to use a gracies curette?

A
  1. Choose appropriate curette for an appropriate tooth and site
  2. Use appropriate finger rest
  3. Terminal shank to the long axis of the tooth
  4. Appropriae lateral pressure
  5. Use overlapping strokes, 1-2 mm
  6. Make sure not to burnish the calculus
  7. Similar procedure with powered scalers
358
Q

What are signs and symptosm of dry socket?

A

Signs:
1. Bone exposure 1 weeks after extraction
2. Halitosis
3. Pain on palpation or air
4. Debri in the socket

Symptoms:
1. Pain like crazy
2. CHange is taste
3/ FOod gets stuck there

359
Q

What are risk factors for dry socket?

A
  1. Haematological conditions
  2. Smoking
  3. Diabetes
  4. Sex hormones
  5. Physical distubances to clot formation
360
Q

What are the groups that are the most susceptible LA toxicity?

A
  1. Both of the extremes of age, pregnant ndividuals and drug users
  2. People with previous history of renal disease, cardiac disease, hepatic problems
361
Q

What are the signs and symptoms of LA toxicity?

A
  1. Confusion
  2. CNS excitation to depression
  3. Loss of reflexes
  4. Loss of consciousness
  5. Head aches
362
Q

What is the importance of the bavel?

A
  1. Reduces the probability of stripping the perioosteum
  2. Direction of the LA injection
363
Q

What are some of the reasons for LA failure from an operator perspective?

A
  1. Technique failures
  2. Failure to check for expiration date of the LA
  3. Failure to check for free flow of the LA
  4. Failure to administer the appropriate ammount
  5. Facing the babel the wrong way
  6. Needle breakage
  7. Not administrating enough LA
364
Q

What are post operative instructions for LA?

A
  1. Do not eat or drink anything too hot too cold until the sensation returns
  2. Make sure to be aware of your cheek to not bite it
  3. After LA there might be some soreness for 1-3 dyas, take ibuprofen or panadol to medigate
  4. If discomfort persists please come back for further investigation
365
Q

What are the contra indications for power scalers?

A
  1. Dentinal sensitivity
  2. Problems with swallowing or COPD
  3. Incipient carious lesions
  4. Old pacemakers
  5. Do not use on porcelain and composite resins because damage can be made
  6. Infectious disease patients

dentistry bds 2 sem 2 (5 decks)

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