GP/LA/Cariology Flashcards
1
Q
Clinical process
A
- History
- Examination
- Diagnosis
- Treatment planning
- Patient consultation
- Treatment plan
- Treatment
- Review
2
Q
What is a symptom?
A
Changes that may be discerned by the patient, and obtained by inquiry during history
3
Q
What are signs?
A
Functional and structural changes that may be seen by the patient or dentist
4
Q
Patient history
A
- Medical history
- Dental history
- Family and Social history
5
Q
How to take the best-possible medical history?
A
- Comprehensive conditions/allergies and drug history
- Includes thorough history of all regular medications used, including non-prescription and complementary medicine
- Verified by more than one source
- Structured process for taking history
- Verifies the history with information from a number of different sources
6
Q
Which medications are you currently or have taken?
A
- Name
- Dosage form
- Amount
- Strength
- Route
- Times taken
- What reason
- Have they stopped or continuing
7
Q
Adverse reactions and/or allergies
A
- Ask about previous adverse events
- confirm details of allergic/adverse event
8
Q
Reason for Presenting
A
- “What brings you here today?”
2. Write in patients own words
9
Q
Pain history
A
SOCRATES
S-site O-onset C-character R-radiating A-associations T-timing E-exacerbating/relieving factors S-severity
10
Q
History of Presenting complaint
A
- SOCRATES
11
Q
Previous dental experience
A
- Last visit (who, where, why, when what)
- Procedures
- Last cleaning
- Most recent radiographs
- Past treatments
- Cleaning/home care habits
- Dental phobia/anxiety
- Complications during prior care
12
Q
Family history
A
- Immediate family
- Dental status of family
- Medical conditions in the family
13
Q
Social history
A
- Place of birth
- Accommodation
- Occupation
- Smoking and alcohol history
- Drug use
- Sugar intake
14
Q
What are the characteristics of normal pulp?
A
A clinical diagnosis in which the pulp is symptom-free and normally responsive to pulp testing.
15
Q
What are the characteristics of reversible pulpitis?
A
A clinical diagnosis based on subjective and objectives findings indicating that the inflammation should resolve and the pulp return to normal.
Symptoms may include discomfort/pain in response to cold or sweet, pain does not linger and is relieved within seconds.
16
Q
What are the characteristics of symptomatic reversible pulpitis?
A
A clinical diagnosis based on subjective and objectives findings indicating that the vital inflamed pulp is incapable of healing.
Symptoms include lingering thermal pain (to cold and heat), delayed ache, spontaneous pain, referred pain, nocturnal and positional pain.
17
Q
What are the characteristics of asymptomatic irreversible pulpitis?
A
A clinical diagnosis based on subjective and objectives findings indicating that the vital inflamed pulp is incapable of healing.
Additional descriptors, include no clinical symptoms, however, inflammation from deep caries, or trauma may be observed.
18
Q
What are the characteristics of pulp necrosis?
A
A clinical diagnostic category characterised by death of the dental pulp. The pulp is usually unresponsive to pulp testing.
19
Q
What are the characteristics of previous endodontic treated teeth?
A
A clinical diagnostic category indicating that the tooth has been endodontically treated. The tooth does not response to pulp testing - for obvious reasons.
20
Q
Difference between previously treated and previously initiated therapy?
A
For previously initiated therapy, the tooth many respond to pulp testing depending on the level of therapy.
21
Q
What are the characteristics of normal apical tissues?
A
Teeth with normal periradicular tissues that are not sensitive to percussion of palpation testing.
The lamina dura surrounding the root is intact, and the periodontal ligament space is uniform.
22
Q
What are the characteristics of symptomatic apical periodontitis?
A
Inflammation of the apical periodontium, resulting in clinical symptoms such as a painful response to biting and/or percussion or palpation.
May or may not have an apical radiolucent area.
23
Q
What are the characteristics of asymptomatic apical periodontitis?
A
Inflammation and destruction of the apical periodontium which appears as a radiolucent area with no symptoms.
24
Q
Characteristics of acute apical abscess?
A
An inflammatory reaction to pulpal infection and necrosis characterised by rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus formation and swelling of associated tissues.
There may be no radio-graphical signs of destruction, however, the patient may experience malaise, fever and lymphadenopathy.
25
Characteristics of chronic apical abscess?
An inflammatory reaction to pulpal infection and necrosis characterised by gradual onset, little or no discomfort, and intermittent discharge of pus through an associated sinus tract.
Radiographically, radiolucency may be observed.
26
Characteristics of condensing osteitis?
A diffuse radio-opaque lesions representing a localised bony reaction to a low-grade inflammatory stimulus usually seen at the apex of the tooth.
27
What are LA cartridges made of?
Glass or polypropylene
28
What is the volume of an LA cartridge?
1.8 - 2.2ml volume of LA agent
29
What type of needles are used for LA?
2 needle lengths: 20mm and 35mm
2 gauges: 27 and 30
They are pre-sterilised and single use needles
30
What is the sterilizations process of needles?
- Needles are pre-sterilised
- Cartridges containing LA are pre-sterilised
- Syringe is reusable and must be autoclaved before every use
- Use aseptic technique when assembling and using equipment
31
Process of LA infiltration
Deposit LA solution close to the to the tissue to be anaesthetised - which allows the solution to diffuse around the fine branches of the sensory nerves in that area.
32
Regional nerve block process
Deposit LA solution around the main trunk of the sensory nerve, facilitating a block to all the branches of the nerve.
33
What are the types of LA techniques?
1. Maxillary infiltration
2. Palatal infiltration
3. Mandibular infiltration
4. Inferior alveolar nerve block
5. Buccal nerve block
34
Process for surface anaesthesia
1. Use topical anesthetic to reduce discomfort of needle entering the tissues - use cotton bud to apply to point of injection
2. Wait a few minutes for it to work
35
General tips for LA administration
1. Hold the mucosa taut
2. Inject slowly
3. Aspirate to ensure not inside a BV
4. LA solution at room temperature is less painful than cold solution
5. Place a small amount of LA then aspirate before depositing the bulk
6. Avoid injecting subperiosteally, we want to inject supra-periosteally.
36
Maxillary infiltration technique
1. Use a short needle
2. Advance the needle through the mucosa to the apex of the tooth
3. Stay supraperiosteal
4. Always aspirate before injecting
37
Palatal infiltration technique
1. Inject at junction of the alveolus and hard palate
| 2. Be mindful of the greater palatine artery
38
Incisive canal - palatal infiltration technique
1. This infiltration aneastethise the naso-palatine nerve- essential a type of nerve block
2. Can be uncomfortable to inject this area - place small drop to slight aneasthetise and then gradually place more
39
Mandibular infiltration technique
1. Most effective anesthesia for the incisors - as the cortical bone is thick anteriorly compared to posteriorly (inject into mucosa)
2. Also used to anaesthetise the buccal mucosa for surgical purposes
40
Inferior alveolar nerve block technique
1. IAN enters the mandible at the mandibular foramen by the lingula - LA must be deposited ay this site before it enters bone, in the pterygomandibular space
41
Direct technique for inferior alveolar nerve block
1. Lingula is often halfway between the anterior and posterior border of the ramus of the mandible
2. Aim above the lingula to stay lateral to the sphenomandibular ligament
3. Needle should be parallel to the occlusal plane
4. Angle the syringe across from the premolars on the contralateral side, pierce mucosa at a point 1cm above the occlusal plane
5. Advance until touching bone, withdraw slightly
6. Aspirate
7. Deposit into the pterygomandibular space
42
Indirect technique for inferior alveolar nerve block
1. Needle in line with teeth on ipsilateral side
2. 1cm above and parallel to the occlusal plane
3. Touch the internal oblique ridge, edge past it then swing the syringe to contralateral side and advance to position above the lingula
43
Buccal nerve block
1. Buccal nerve supplies the lateral mucosa of the molars
2. Targets the buccal nerve as it passes over anterior aspect of the ramus
Insert needle distal and lateral to the last molar tooth
44
Infraorbital nerve block
1. Blocks cheek, gingiva, incisors, canine and first premolar
2. Palpate the infraorbital rim with index finger
3. IO foramen is approximately 1cm below this rim
4. Direct percutaneous approach possible
5. Oral approach high in sulcus at level of the canine
6. Advance needle superiorly, external finger will feel the swelling as injection is performed
45
Maxillary nerve block
1. Cheek, gingiva and maxillary dentition will become anaesthetised
2. Infiltrate around the greater palatine foramen - at the level of the second molar
3. Needle at 45 degrees to palate
4. Advance up the GP foramen for approx. 30mm
5. Aspiration and very slow injection
6. To help help find GFP - follow the line from hamulus to the lateral incisor and the GFP is most likely to be at the distal aspect of 7
46
What are the complications of a maxillary nerve block?
1. Regional CN VI block - diplopia on lateral gaze
2. Haematoma
3. Retrobulbar block
4. CN II block - temporary blindness
47
CN V3 blocks technique types
1. Gow Gates Mandibular nerve block
| 2. Varizani-Akinosi Technique
48
Gow-Gates Mandibular block
1. Developed by Dr Gow-Gates in the 70's
2. Commonly aneasthetises IA, Lingual and long Buccal branches
3. LA delivered at the neck of the condyle just under insertion of the lateral pterygoid muscle
4. Advantages include; less pain on injection due to less muscle tissue in the path of the needle. This reason is also less vascularised, so LA is not cleared quickly
49
Gow-Gates mandibular nerve block technique
1. Open mouth widely to bring the condlye forward
2. Place middle finger over intertragal notch
3. Thumb retracts the cheek palpating coronoid and external oblique ridge
4. Needle comes from the contralateral premolars, pierces mucosa posterior to tuberosity
5. Advance towards the intertragal notch until you hit bone - approx 2.5mm
50
Varizani-Akinosi block principles
1. Described by Varizani in the 60's
2. Closed mouth technique
3. Commonly anaesthetises IA, lingual and long buccal branches
4. Advantages include that it is good for people with trismus, ankylosis and large tongues, it is also pain free due to musclular relaxation
51
Varizanai-Akinosi Technique
1. Mouth closed and cheeck retracted
2. Long needle advanced parallel to maxillary occlusal plane at the level of the mucogingival junction
3. Needle advanced until hub at level distal to 7 so that needle depth is 2.5mm
52
What are the types of LA used in Australia?
1. Lignocaine 2% with adrenaline
2. Prilocaine 3% with Felypressin
3. Articaine 4% withe Adrenaline
4. Mepivicaine 3%
53
When to use a type of LA?
1. Lignocaine with adrenaline - multipurpose and useful
- be careful for people with arrhythmia or liver disease
2. Prilocaine with Felypressin is a good alternative.
- Be cautious during the 3rd trimester of pregnancy, pulmonary disease and those with ischaemic heart disease
3. Articaine with adrenaline - good bony penetration
- Cautious with block technique due to potential for neurotoxicity
- Currently TGA recommends as infiltration only
4. Mepivicaine - good alternative to all LAs, especially if the patient has a medical issue with the use of vasoconstrictors
54
What are systemic complications of LA?
1. Psychogenic
2. Overdose
3. Allergy
4. Drug interactions
5. Vasoconstrictors
6. Medical conditions
55
Psychogenic side effects
1. Common side effect
2. Related to perceived stress by patient
3. Often vaso-vagal response
56
Overdose side-effects
1. Dose-related phenomenon
| 2. Direct extension of normal pharmacological effects
57
Maximum dose of LA
1. Lignocaine with adrenaline 7mg/kg
2. Prilocaine with felypressin 9mg/kg
3. Bupivicaine with adrenaline 2mg/kg
4. Articaine with adrenaline 7mg/kg
5. Mepivicaine with adrenaline 7mg/kg
58
Patient factors that influence overdose
1. Age: decrease dose for young and elderly patients
2. Weight: decrease dose for low weight patients
3. Presence of disease: hepatic of renal disease
4. Genetics: atypical psudocholinesterase
5. Drug interactions
59
Drug factors that influence overdose
1. Vasoactivity - most LA's vasodilate, so vasoconstrictors are added to slow clearance
2. Concentration
3. Dose
4. Route
5. Rate of administration
6. Vascularity of site
60
Signs and symptoms of overdose
| 1. Excitation phase - Depression of inhibitory centres
1. Cortical signs
a) restlessness
b) slurred speech
c) localised muscular twitching
d) dizziness
e) difficulty focusing eyes
f) cirumoral numbness
2. Medullary signs
a) Increased heart rate
b) Increased blood pressure
c) . Increased respiratory rate and depth
61
Signs and symptoms of overdose
| 2. Depression phase
1. Cortical signs
a) Lethargy
b) Drowsiness
c) Unresponsiveness
d) Muscular weakness
2. Medullary signs
a) Decreased heart rate
b) Decreased blood pressure
c) Decreased respiratory rate and depth
62
Management of overdose
1. Stop dental treatment
2. Put patient in recovery position
3. Support with oxygen
4. Reassure patient
5. Monitor vital signs
6. Call ambulance and perform CPR principles if respiratory arrest
63
Allergic reactions of LA
1. Hypersensitivity state due to exposure to an allergen causing release of histamine by mast cells
2. Allergic response is not dose related
3. Ester linked LA's implicated due to their breakdown to PABA
4. Amide linked LA allergies are rare
5. Patient may be allergic to preservatives used in the solution - methylparaben is most common
64
Reduce LA dose is patient is taking;
1. Narcotics
2. Antihistamines
3. Benzodiazepines
4. Barbiturates
5. NO
6. Alcohol
The interaction may lead to enhances CNS and CVS depression
65
Function of vasoconstrictors in LA
1. Reduces toxic dose of LA
2. Confines LA to the area of injection
3. Reduces bleeding into the surgical field
66
Commonly used types of LA
1. Adrenaline
- Has a strong effect on beta-receptors as well as alpha-receptors
- B1 - increases cardiac output
- B2 - dilates arteries in skeletal muscle
- A1 - vasoconstriction of vessels in skin and GIT
2. Felypressin
- Non-catecholamine, derivative of oxytocin and displays some actions similar to vasopressin
- Causes smooth muscle contraction
- Potent coronary artery constrictor
- Induces uterine contractions during pregnancy
67
Local complications of LA
1. Pain on injections
2. Trismus
- Due to LA being deposited into the medial pterygoid or a haematoma formed in the medial ptyergoid due to blood vessel injury
3. Spread of infection
4. Sloughing of tissues
5. Lip and tongue chewing
6. Facial nerve paralysis
7. Needle breakage
68
Reasons for failure of anaesthesia
1. Anatomical variations between patients
2. Intravenous injection
3. Injection into muscles
4. Neural anastomoses
5. Injection into infected areas - lower pH
6. Patient perception of noxious stimuli
69
When to conduct saliva test
1. All patients with at least one opposing pair of natural teeth should have a saliva test
2. A good time would be at the beginning of the 2nd appointment
3. Do not eat, smoke, brush teeth or use mouthwash one hour prior to appointment
70
Major factors that affect unstimulated salivary flow in healthy people
1. Degree of dehydration
2. Body position
3. Exposure to light
4. Previous stimulation
5. Smoking
5. Circadian rhythms
6. Drugs
71
Minor factors that affect unstimulated salivary flow in healthy people
1. Gender
2. Age
3. Body weight
4. Gland size
72
1. Assessing hydration levels
1. Evert the lower lip and gently blot the labial mucosa with gauze
2. Droplets of saliva form at the orifice of major glands
3. Time how long it takes for the droplet to form - record the value and category
Greater than 60s - Low
Between 30-60s - Normal
Less than 30s - High
73
2. Visual examination of viscosity of unstimulated saliva
Red - Sticky, frothy, saliva residues
Yellow - frothy, bubbly saliva with increased viscosity
Green - watery, clear, normal viscosity
74
3. ph of unstimulated saliva
1. Ask patient to expectorate any pooled saliva into the collection cup
2. Place pH test strip into saliva for 10 seconds
Resting pH of saliva is 6.2
75
4. Quantity of stimulated flow
1. Ask patient to chew wax pellet for 30s and expectorate into spittoon
2. Continue chewing for 5 minutes, collecting saliva in the collection cup at intervals
3. Read scale to get stimulated volume
<3.5ml - very low
3.5-5.0 ml - low
>5.0ml - normal
76
5. Quality of stimulated flow - Buffering capacity
1. Draw saliva with pipette and dispense a drop onto the test pad
2. Read result after 2 minutes
3. Add up the points to interpret the results
0-5 - very low
6-9 - low
10-12 - normal
77
Risk indicators for root caries
1. Medical conditions
2. Medications
3. Radiotherapy of head and neck
4. Institutionalised
5. Dependent on others for daily care
6. Altered cognitive function
7. Onset of illness
8. Altered lifestyle
9. High frequency of sugar
10. Wearing a partial denture
11. Recently root planed teeth
12. Presence of periodontal pockets >3mm in depth
78
Three strongest indicators of root caries
1. Previous root caries
2. Increased number of root surfaces at risk
3. Poor oral hygiene
79
Diagnosis of root caries
1. Presence
| 2. Activity
80
Identifying the presence of root caries
Clinical examination
1. Thorough plaque removal is essential to allow visualisation of the root surface
2. Probes should not be pushed into the surfaces to assess hardness
Radiographic examination
1. Bitewings are useful for detecting approximal and sub-gingival root caries which is difficult to detect with a probe
81
Differentiating between root caries and free coronal smooth surface caries
Root caries
1. Gingival margin of root caries lesion is in dentine
2. Also, evidence of gingival recession
Coronal caries
1. Gingival margin of coronal caries is in enamel
2. No gingival recession
82
Radiographic appearance of root caries
1. Situated at or apical to the CEJ
2. Associated with gingival recession, therefore there will be radiographic signs of bone loss
3. Radiolucency has diffused rounded inner border
4. Absence of root edge
83
Differentiating between cervical burnout and root caries
Cervical burnout
1. Diffuse radiolucent areas with ill-defined borders between the cervical edge of the enamel cap and crest of the alveolar ridge
2. Results from decreased x-ray absorption in the thinner outer portion of the convex root surface
84
Differentiating between active and inactive lesions
Active lesions
1. Location reflects areas of plaque stagnation - CEJ and adjacent to the receding gingival margin
2. Plaque covered
3. Dull surface
4. Light to mid-brown colour
5. Soft
Inactive lesions
1. Plaque free
2. Often some distance from the gingival margin
3. Shiny surface
4. Hard
85
Process of arresting root caries
1. Eliminate/modify risk factors and increase protective factors
- Site/lesion specific oral hygiene instructions
- Regular use of 5000ppm toothpaste
- Consider use of CPP-ACP
- Dietary assessment and modification to reduce consumption of sugars and acids
- Salivary modification
- Monitor regularly and include professional cleaning and application of fluoride at recall.
86
Evidence of the remineralising effect of fluoridated toothpaste
1. Study by Baysan et al (2001)
- 201 subjects participated in a 6 month study. Verbal and written instructions were given to brush at least once a day with the assigned toothpaste
- In 6 months, more lesions hardened with the 5000ppm F- toothpaste. More subjects using 5000ppm F- toothpaste had one or more lesions that become hard. The colour of the lesions remained similar to that at baseline.
2. Ekstrand et al (2013)
- 125 residents in nursing homes in Copenhagen who were not able to brush their teeth themselves. An 8-month study. Nursing home staff brushed the subjects teeth 2x/day. Control group has 1450ppm F toothpaste, while the intervention group had 5000ppm F toothpaste.
- After 8 weeks the intervention group had significantly fewer active root caries lesions and more arrested lesions than the control group
87
What are the mechanisms of action of high concentration topical fluorides?
1. A precipitate of calcium fluoride forms
2. Acts as a reservoir for fluoride ions which is released into the area in low concentrations
3. Remineralisation - incorporation of fluoride into the apatite crystals after periods of demineralisation
4. Disrupts bacterial metabolism in plaque
88
What are the effects of CPP-ACP in dentine, as shown by in-vitro studies?
1. Rahiotis et al (2007)
- CPP-ACP provoked significantly lower demineralisation and significantly higher remineralisation of dentine
2. Yamaguchi et al (2007)
- CPP-ACP effectively prevented demineralisation of bovine dentine
89
Remineralisation program in surgery for active root caries
1. OHI
- Disclosing solution
- Demo of toothbrushing
- Interdental brushed
2. Initial full mouth application with 9000 ppm neutral fluoride gel (2%NaF)
3. Spot application of Duraphat varnish (22,600 ppm NaF)
4. Dietary assessment and modification
5. Salivary modification
90
Remineralisation program at home for active root caries
1. Toothbrushing using 5000ppm
| 2. Toothmousse application
91
Which root caries lesions require restoration?
1. Lesion anatomy or position makes plaque control impossible
2. Lesions visible as a semi-circular radiolucecny on approximal surfaces in radiographs
3. Lesions jeopardising the integrity of the pulp
4. Lesions affecting aesthetics
5. Lesions which show signs of progression after OHI and the use of remineralising agents
92
Potential sequelae to restoration of root caries
1. Gingival inflammation
2. Gingival recession
3. Deterioration of restorative materials
4. Secondary root caries
93
Does GIC prevent secondary caries?
1. Study by Randall and Wilson (1999)
- No conclusive evidence for or against the inhibition of secondary caries
2. McComb et al (2002)
- 45 patients were instructed to use neutral pH sodium fluoride gel in custom trays daily. Patients were observed for 24 months. The subjects were categorized as compliers and non-compliers. In the compliers, there was no recurrent caries found for any of the restorations.
94
Management of secondary root caries
Apply the same rules as those for primary root caries
95
Signs of dental erosion
1. Loss of tooth structure
2. Smooth, shiny surfaces
3. Loss of surface detail such as perikymata
4. Tooth may become rounded
5. Dentine erodes more rapidly than surrounding enamel
6. Fillings may be proud
96
Symptoms of erosion
1. In enamel - nothing
2. In dentine - sensitivity to hot/cold
3. Pulp - acute or chronic pain
4. Often patients with erosion will have no symptoms until tissue loss is extensive
97
Aetiology of tooth erosion
1. Intrinsic
- stomach acids (gastric reflux, vomiting, eating disorders)
2. Extrinsic
- dietary
- environmental
- medicines/drugs
98
Biochemistry of erosion
The protons and chelators (anions) in the erosive agent create an under-saturates environment wrt to the apatite - causing it to dissolve to maintain equilibrium.
The anion chelator binds calcium ions reducing the free calcium available.
99
What is chelation?
1. Polydentate anions may binds cations
2. An anion can therefore form a complex with calcium and remove it from the oral environment decreasing Ca2+ activity, creating an undersaturated environment wrt to calcium phosphate solids and cause dissolution of the crystals
3. Therefore, chelators can cause erosion
100
Difference between erosion and dental caries
Erosion
1. Acids of non-bacterial origin
2. chelators
3. Surface loss of mineral
4. Surface softening
5. Undersaturated wrt HA/FA
Dental caries
1. Acids of bacterial origin
2. Subsurface loss of mineral
3. Undersaturated wrt HA but not FA
101
What is titratable acidity?
1. The total amount of protons present
2. It is the sum of free protons in solution and those bound to other molecules
3. Agents with high titratable acidity will be able to resist buffering towards neutral and are therefore more likely to maintain an acidic undersaturated environment
4. Saliva has difficulty neutralising agents with high titratable acidity
102
Chelation of saliva
1. Citrate is a powerful chelator of calcium. Citric acid is erosive over a broad range if pH values
2, Up to 32% of calcium in saliva can be complexed by citrate at concentrations common in fruits - reducing supersaturation of saliva and increases the driving force for dissolution of apatite
103
Temperature of acidic agent
1. As temperature increases erosive potential of acidic agent increased
104
How does ion content influence erosion?
1. The calcium, phosphate and fluoride content of the agent can influence its erosive potential
2. If the beverage is saturate of supersaturated wrt to enamel or dentine - then it will not erode
3. Fluoride is also unable to prevent erosion as erosive agents tend to be highly undersaturated even wrt to fluorapatite
105
Biological factors of erosion
1. Saliva
2. Anatomy of soft tissue vs teeth
3. Soft tissue movement
4. Tooth anatomy
5. Structure
106
Salivary flow rate and erosion
- Important in diluting, clearing, neutralising, buffering, resupplying proteins necessary for pellicle formation and the ions necessary to inhibit demineralisation and promote remineralisation
- Salivary flow rate increases before the acid challenge as a response to extra-oral stimuli such as odour and sight.
- Likewise, hyper-salivation also occurs before vomiting which is co-ordinated by the 'vomiting centre' in the brain
- However, as reflux is involuntary, salivary output does not increase
107
Saliva buffering
1. Bicarbonate
2, Phosphate
3. Proteins
108
Salivary proteins
1. Mucins
2. Proline rich proteins
3. Statherin/proline rich proteins
109
Salivary pellicle and erosion
1. 0.3-1.06um layer of adsorbed protein
2. Presence of the pellicle has been shown to reduce enamel erosion by up to 61% and dentine erosion by 31% in situ
3. An inverse relationship has been observed between pellicle thickness and degree of erosion
4. The pellicle may act as a diffusion barrier, a perm-selective membrane and crystal stabilisers.
110
Soft tissue movement and erosion
- The tongue has been shown to remove enamel and dentine softened by erosion
- Therefore, the size of the tongue and the dental arches, the positioning of teeth may contribute to the progression of erosion
111
Tooth anatomy/structure and erosion
1. Tooth anatomy
- shape and contour of the teeth relative to drinking and swallowing
- eroded enamel is more susceptible to attrition
2. Tooth structure
- composition of human teeth is highly variable. Some people's teeth may have more soluble apatite which will be at higher risk of erosion
112
Behavioural factors of erosion
1. Source of acid
2. How does it contact the teeth?
3. What do they do after the acid exposure?
113
Source of acid/chelator
1. Extrinsic - erosion seen on labial of anterior teeth
- erosive drinks and foods have been strongly associated with erosion on the facial and occlusal surfaces
2. Intrinsic - erosion seen on palatal of maxillary anterior teeth
114
Type of contact with erosive agent
High erosion has been associated with methods of drinking/eating that keep the beverage in the mouth for longer periods
1. Negative (swishing, sipping, holding beverage in mouth, drinking slowly)
2. Positive (straw behind teeth, drinking quickly)
115
Activities that wear teeth after erosive exposure
Tooth wear from abrasion and attrition can be accelerated following erosive exposure
1. Abrasion
2. Attrition
116
Toothbrush abrasion and waiting time
1. Previous evidence suggests waiting at least 30-60 minutes after an erosive agent before brushing
2. Recent findings question whether saliva can remineralise acid softened enamel/dentine in such a short amount of time
3. Must consider the importance of exposure to fluoride
117
Alteration of erosive agents
If the agent is saturate or supersaturates wrt dental apatite, then it will not erode.
1. Ribena toothkind (higher pH and calcium)
2. Sukkie (higher pH and calcium)
3. Addition of casein phosphopeptide-amoprphous calcium phosphate to acidic beverages
118
Effects of adding CPP-ACP to acidic drinks
Significant decrease in the erosive depth with the addition of CPP-ACP. Also a reduction in titratable acidity as the CPP-ACP will buffer and remove some of the acid - however, there is a change in taste
119
Difficulties of altering erosive agents
1. Taste
2. Cost
3. Claims
4. Consumer demands
120
Ways to preventing erosion
1. Promote salive
2. Load oral environment with ions pre- or post-exposure
3. Enhance pellicle
121
Pre-exposure (to acidic drinks) techniques
| Biological factors
1. Assess saliva quantity and quality
2. Increase buffers and ions present intra-orally
3. Do not brush aggressively prior to exposures
4. Use a stannous fluoride toothpaste
- Current evidence shows SnF2 is the most effective fluoride salt for preventing erosive demineralisation
122
What is the mechanisms of Stannous fluoride?
1. Following contact with SnF2, a tin-containing layer forms on the tooth surface; tin gets incorporated into the tooth structure up to 10um below the surface.
2. This tin-containing layer increases fluoride uptake and resists demineralisation by acid
3. Primary effect is inhibition of demineralisation, although evidence has shown SnF2 toothpastes also increase hardness of eroded enamel compared to NaF toothpaste
123
Post-exposure (to acidic drinks) preventative approaches
| Biological factors
1. Neutralise acid quickly after exposure
- baking soda rinse - effective
- dairy products
- water
2. Stimulate saliva
- sugar-free gum
3. Promote remineralisation
- fluoride
- CPP-ACP
124
Pellicle-like therapeutics
In a study by Hemingway it was found that casein and ovalalbumin mimic the pellicle protein - casein is more protective than the ovalalbumin
125
Behavioural prevention of erosion
1. Eliminate/avoid erosive agent
2. Modify erosive exposure
3. Modify behaviours after erosive exposure
126
How to eliminate and avoid erosive agents
1. Avoid low pH agents
2. Be aware of food acids - food labels
3. Avoid foods containing strong calcium chelators
4. Avoid reflux triggers
127
How to modify exposure to erosive agents and behaviour afterwards?
1. Drink quickly
2. Reduce frequency of consumption
3. Consume cold
4. Do not expose teeth to excessive abrasion or attrition immediately after erosive challenge
128
Management of patients with erosion
1. Early identification
2. Collect information
- Medical history (reflux, medications, salivary flow)
- Social history
- Dietary record
3. Determine cause
- Extrinsic
- Intrinsic
4. Explore other exacerbating factors
5. Obtain baseline records (photos)
129
Patient management to prevent erosion challenge
1. Educate
2. Eliminate or modify cause
- Diet advice
- Medical care
3. Eliminate or modify
exacerbating factors
- Improve saliva
- Prevent attrition
- Prevent attrition
4. Recommend preventative agents
5. Restorative treatments
6. Review
