Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BDS2 > ICP > Flashcards

ICP Flashcards

1
Q

What are 5 protective reactions of Dentine (2) and Pulp (3) when faced with Caries?

A

DENTINE:
1) Tubular Sclerosis - Odontoblasts retract from acid stimulus and begin forming Peritubular dentine via Sclerotic dentogenesis. This is more mineralised, so appears as a radiopaque “Zone of Tubular Sclerosis” closer to EDJ
(Dead Tracts, empty tubules from Odontoblast retraction lie between this Sclerotic occlusion and EDJ)
2) Reactionary Dentine - Formed by Odontoblasts at pulp-dentine interface, visualised as reduced pulpal chambers in radiographs.
Low grade stimulus = Regular tubules slowly laid
High grade = Irregular tubules laid down rapidly

PULP

3) Eburnoid Layer - If odontoblasts die and leave dead/empty tracts, Pulp cells will form an atubular calcified hyaline layer
4) Reparative Dentine - Formed by Progenitor cells (odontoblast-like cells produced by pulpal stem cells when Odontoblasts die)
5) Pulpitis - Increased vascular flow to pulp (more inflammatory cells present) but associated Oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

At what stage is Tubular Sclerosis destroyed?

A

Final Stage: Advanced Carious Lesion

may be some destruction in previous stage once cavitation occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens in the initial (first) stage of caries, when enamel is still intact?

A

Odontoblasts retract to acid stimuli in enamel and Tubular Sclerosis and Reactionary Dentine formation occurs.
This is visualised radiographically as enamel becomes demineralised (blueish/white) and there is a reduced pulpal volume (reactionary dentine formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 2 main bacteria types involved in early cavitation and how do they function?

A

1) Acidogenic (e.g. Lactobacilli)
Penetrate dentine tubules, diffuse on acid to cause further demineralisation
2) Proteolytic
Destroy organic matrix and produce “Liquefaction foci” (soft area of dentine which join to form cracks at right angles to dentine tubules)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is “Liquefaction foci”? What type of bacteria cause its production?

A

Soft area of dentine which join to form cracks at right angles to dentine tubules.
This is the (infected) dentine which should be removed
Caused by Proteolytic bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why is Dentine caries not present in germ-free animals?

A

It requires the production of acid by bacteria (e.g. in plaque) and relies on its ability to attach to surfaces, ferment sugars and produce acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the difference between “Infected” and “Affected” Dentine?

A

INFECTED = Irreversible demineralisation and denaturing of dentine from bacterial invasion (Proteolytic bacteria forming “Liquefaction foci” soft dentine)

AFFECTED = NO bacteria present, reversible demineralisation and collagen denaturing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In an Amalgam filling, what is the MINIMUM width, depth and length of a 2 surface cavity?

A

2mm
This must be paired with Macroscopic modifications: 90 C cavosurface angle, rounded internal line angles, undercuts, slots/grooves and a flat surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q 
What is Caries? 
What is meant by the following: 
1) Primary Caries? 
2) Secondary/Recurrent Caries? 
3) Residual Caries? 
4) Active Caries? 
5) Arrested Caries? 
6) Rampant Caries?
7) Hidden Caries
A

Caries = Tooth surface loss from the METABOLIC production of acids (e.g. by bacteria)

1) Primary = Occurs on unrestored tooth
2) Secondary = Occurs on/around previously restored tooth
3) Residual = Demineralised tissue left behind before filling (e.g. affected dentine - minimally invasive techniques)
4) Active = Progressive (cariogenic bacteria continue to live off intracellular polysaccharides)
5) Arrested = No longer progressing (darker colour)
6) Rampant = Multiple active carious lesions in 1 Px
7) Hidden = In dentine, detectable by radiograph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between Reparative and Reactionary dentine?

A

Reactionary Dentine - Formed by Odontoblasts at pulp-dentine interface, visualised as reduced pulpal chambers in radiographs.
Low grade stimulus = Regular tubules slowly laid
High grade = Irregular tubules laid down rapidly

Reparative Dentine - Formed by Progenitor cells (odontoblast-like cells produced by pulpal stem cells when Odontoblasts die)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a ______ Lesion?

1) White Spot
2) Brown Spot

A

1) WHITE = Initial sign of early caries, sub-surface demineralisation of enamel prisms (holes) causes light to be scattered, giving dull/opaque/white appearance in contrast to enamel’s usual translucency
2) BROWN = Often inactive/arrested previous WSL which has been darkened by uptake of dye (e.g. food/drink intake)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between Proximal and Approximal areas of the teeth?

A 
Proximal = Contact area between adj teeth 
Approximal = BENEATH this contact area (interproximal space)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q 
What is the resting pH of saliva? 
What is the critical pH of: 
1) enamel? 
2) dentine? 
What is significant about this difference?
A

Resting pH = 7.9 (+/- 0.3)
1) Enamel CpH = 5.2-5.7 (5.5)
2) Dentine CpH = 6-6.7
Dentine critical pH much higher, so more readily demineralised, e.g. root caries risk in gingival recession

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the mean Calcium ion concentration in saliva?

A

12.5 ppm (+/- 0.7)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What 2 factors is the balancing act between demineralisation and remineralisation primary based on?

A

1) pH
2) calcium ion concentration
Demineralisation = Low pH and calcium conc
Remineralisation = High pH and calcium conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Saliva is “supersaturated” with respect to Calcium and Phosphate ions - name the main caries protection protein in saliva and how it functions to prevent demineralisation or excess precipitation.

A

“Statherin” - Type of Tyrosine-rich protein (acidic)
Bind to excess calcium ions (SXE motif) to prevent precipitation
Release stored calcium ions in low pH environment
Can also bind to HAP to prevent primary (crystal nucleation) or secondary precipitation (crystal elongation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is meant by DMFT?

A

DMFT = Decayed Missing Filled Teeth

Method of recording oral epidemiology, assessing dental caries prevalence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Root Caries?

What is an easy mistake for clinicians to make when faced with these cases?

A

Root Caries = Caries (tooth surface loss from metabolic acid production) at or apical to the CEJ
Clinician may be confused between Root Caries (dentine origin ) and Cervical Caries (enamel origin)
Furthermore “Cervical Burnout” on radiographs may show radiolucency in these areas where there is infact NO CARIES (simply due to thin area where enamel ends and cementum begins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are 4 clinical problems we face with Root Caries (risk, presentation and treatment)?

A

1) Elderly Px most at risk (increased periodontal disease and gingival recession with age - root exposure)
2) Similar presentation to Cervical Caries
3) Dentine has higher critical pH (6-6.7) vs enamel (5.2-5.7) so undergoes demineralisation more readily
4) Restoration treatment often difficult due to location - hard to access and get moisture control (made worse as lesions often spread subgingivally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What patients are most at risk of root caries and why (2)?

A

Elderly!

1) Increased gingival recession with age (e.g. periodontal disease)
2) Increased prevalence of acidogenic microorganisms (e.g. lactobacilli) in plaque - due to decreased salivary secretion and higher denture usage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What 3 features can distinguish Active from Arrested Caries?

A

1) Active = Yellow/light brown. Arrested = Darker
2) Active = Soft (and leathery when slowly progressing
Arrested = Hard
3) Active = Covered by visible plaque
Arrested = No microbial deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Root Caries is a multifactorial disease, what are 7 possible factors?

A

1) Root exposure (e.g. periodontal disease or age)
2) Reduced OH/Plaque control
3) Certain occlusions/Denture Px (affects plaque control)
4) Diet
5) Xerostomix
6) Low fluoride level intake
7) Cariogenic microorganism presence (e.g. in periodontal disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 3 Non-Invasive treatments for Root Caries?

Why might these be favoured over Invasive treatment (Intra-Coronal Restorations)?

A

1) No treatment! (if minimal caries and good Px compliance)
2) Convert Active –> Arrested Caries (via diet/OHI)
3) Topical Fluoride, Chlorhexidine or Triclosan application

Favoured as 1st line due to difficulty in gaining access and achieving moisture control in Intra-Coronal restorations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How can the following techniques detect caries:

1) Electrical Caries Monitor (ECM)?
2) Fibre-Optic Transillumination?
3) Laser Fluorescence Systems?

A

1) [Based on principle that sound tooth = good insulator]
Carious tooth = Poor insulator (contains more water)
2) Increased opacity of tooth from holes in enamel rods scattering light (enamel normally translucent)
3) Sound tooth = Little or no fluorescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the definition of a Fissure Sealant and what are the 3 Px indications for use?
Fissure Sealant = Material (unfilled/filled composite resin or GIC) placed on the pits and fissures of teeth to prevent or arrest the development of caries. 1) Special needs children (reduced dexterity or diet - sugary medication) 2) Children w/caries in primary teeth (likely to spread to permanent, esp if caries risk factors continue unchanged) 3) Children w/ caries in permanent molars (6s most common as first to erupt)
26
What are the 5 main teeth Fissure Sealants are carried out on? Why might FS be carried out on a: 1) Molar (3)? 2) Incisor (1)?
2's (deep cingulum), 4's, 5's 6's & E's 1) Molars: - Deep pits & fissures - Complex fissure pattern - Stained fissures 2) Incisors: - Deep cingulum pits
27
What are the 3 main materials used for Fissure Sealants and Preventative Resin Restorations? Which is the least moisture sensitive?
1) Unfilled Resin 2) Filled Resin 3) GIC - least moisture sensitive
28
What are the 5 main steps in placing a Fissure Sealant? | What would happen if Px licked during prep?
1) Clean tooth surface (pumice slurry abrasive and wash away) 2) Isolate tooth (moisture sensitive! e.g rubber dam/cotton rolls) 3) Acid-etch w/ 37% Phosphoric acid (run buccally) 4) Re-isolate (If well isolated, use 1 step bond and apply FS, if Px licks glycoproteins in saliva reduce bond strength and bacteria can contaminate - RESTART - etch/prime/bond) 5) Apply fissure sealant to 1/3rd cuspal incline and cure
29
What is a PRR?
PRR = Preventative Resin Restoration "Small Composite/GIC restoration carried out on stained fissures with caries beneath that has formed cavity extending NEAR/SLIGHTLY into dentine. Preventative restoration with Fissure sealant placed on top, minimally invasive -prevents caries extending any lower"
30
How do you know whether to give Px: | Fissure Sealant, PRR or Conventional Filling?
USE BITEWING RADIOGRAPHS! Fissure Sealant = Micro-cavitation PRR = Visible shadow under enamel (caries near or only slightly into dentine) Conventional Filling = Clearly visible dentinal caries
31
What is the "Hall Technique"? :))
Method of Stainless Steel Crown application, good for difficult Px (paeds, special needs or "lickers") Requires NO LA, NO tooth prep and NO caries removal! 1) Assess tooth shape and contact area (use wedges to separate slightly) 2) Sit Px upright and size crown 3) Load crown with cement, press down firmly and remove excess
32
What are the 2 main contraindications for SSC use?
1) In primary molar where tooth is about to be exfoliated/lost (over half of tooth root resorbed) 2) Px allergy or sensitive to Nickel
33
What are 9 Indications for SSC use?
1) More than 2 carious surfaces OR one extensive carious lesion 2) Above on Px who usually undergoes GA (Hall technique can be used instead) 3) Special needs Px with reduced OH & high caries risk (same as FS) 4) Px with high risk caries and no change in risks habits 5) Space maintainers (e.g. as abutment for certain appliances or to maintain mesio-distal spaces in infra-occluded primary molars) 6) Developmental defects (e.g. Hypoplasia, Amelogenesis Imperfecta etc) 7) Excess tooth surface loss (e.g. Attrition/ Abfraction/ Erosion) 8) Fractured primary molar 9) After primary molar pulp treatment
34
Outline the main steps in placing a SSC (Non-Hall Technique) | 8 main steps
1) Give LA and place Rubber dam 2) Remove necessary caries 3) Place wedges mesially and distally to separate tooth 4) Remove mesial and distal tooth surface using fine bur 5) Remove occlusal surface to 1-1.5mm below that of the adjacent tooth 6) Try on crown and see position within gingival crevice: - Sits on Gingival Crevice: Crimp inwards and reapply - Extends below GC = Cut back, smooth edges and reapply 7) Wash/Dry tooth, cement crown and seat down (lingual to buccally) and press firmly 8) Remove excess cement and assess occlusion (occlusion can adjust for about 1mm height increase)
35
What are the 2 main (different) preparation steps in placing a SSC normally vs. Hall Technique?
1) Remove mesial and distal tooth surface with bur | 2) Remove occlusal surface by 1-1.5mm below that of adjacent tooth
36
What is the difference between the following (give an example intervention at each stage): 1) PRIMARY Prevention? 2) SECONDARY Prevention? 3) TERTIARY Prevention?
1) Keeps teeth in healthy state and PREVENTS disease initiation (e.g. Brush teeth twice a day/limit acid attacks to 4 times a day/fluoridated toothpaste 1350-1500ppm) 2) DETECTION of disease and prevention of further development (e.g. Bitewing Radiograph and PRR) 3) TREATMENT of disease and prevention of further development (e.g. Conventional restoration or extraction)
37
What 4 main factors place a (paediatric) Px at high caries risk?
1. Three or more carious lesions in one year 2. Orthodontic treatment 3. Chronic illness: medically or physically impaired 4. Social History: Low motivations
38
How can a Px be categorised into the following Caries risk based on carious lesions: 1) Low risk? 2) Moderate risk? 3) High risk?
1) No Caries 2) 1 or 2 new carious lesions per year 3) 3 or more carious lesions each year
39
What is the difference between Retention and Resistance (in cavity design)?
``` Retention = Restoration resists displacement in direction of insertion Resistance = Restoration resists displacement in all other directions (e.g. prevented by dove-tail lock in Amalgam) ```
40
How does caries appear in a radiograph?
radiolucent (dark shadow)
41
What is the difference between the "Secondary/Recurrent" and "Residual" Caries?
Secondary Caries = Causative bacteria are (initially) EXTERNAL and then break through (e.g. restoration overhang stimulates plaque retentive environment) Residual Caries = Causative bacteria is INTERNAL (left within the cavity, deep in restoration-tooth interface
42
What is meant by: 1) Occlusion? 2) Articulation?
1) STATIC relationship between teeth, can be described as an: Incisal, Molar or Skeletal relationship 2) Describes the DYNAMIC movement of teeth (e.g. lateral, protrusive or retrusive)
43
What are the 3 (/4 with subdivisions) main classifications of occlusion, based on incisal relationship?
Class I = Mandibular incisor rests palatally on maxillary incisor Class II = Mandibular incisor sits more posterior -> Over bite (Div 1 =Maxillary incisors more palatally inclined) Class III = Maxillary incisors retroclined /sit more posterior -> Underbite
44
What is the "ideal" occlusal class? What is this (incisal and skeletal class definition)?
Class I "Mandibular incisors sit palatally on maxillary incisors" "Incisors sit slightly ahead on maxillary teeth)
45
What is meant by "ICP"? | What number is it represented by on Posselt's Diagram?
ICP = (Maximal) Intercuspal Position "Occlusal position where the patient bites down and you have maximal contact between maxillary and mandibular teeth" Posselt's Diagram = 2
46
What is Posselt's Diagram/Triangle (what does it show)?
Diagram outlining the Sagittal plane movements of the jaw (up and down at midline)
47
What are 3 types of Occlusal/Articulating papers? | How are they used in practice and what is the thickness of each?
1) GHM Foil - Held in "Miller's forceps" between teeth, Px bites down into ICP (leaves coloured mark) - Select GHM foil of alternative colour, mark lateral/protrusive movements from ICP (2) Single Sided = 16-20 Microns thick Double Sided = 40 Microns thick 2) Shimstock - Held in "Shimstock needles" between teeth and Px asked to bite down onto it - Dentist attempts to pull out, contact outcomes are: "Tight" = Cant pull out/tears "Light" = Moves with resistance "None" = No resistance 12 Microns thick 3) Horse-shoe articulating paper THICKEST (250 Microns)
48
Which articulating paper is used to examine Px ICP? | How is this carried out?
GHM Foil - Held in "Miller's forceps" between teeth, Px bites down into ICP (leaves coloured mark) - Select GHM foil of alternative colour, mark lateral/protrusive movements from ICP (2) Single Sided = 16-20 Microns thick Double Sided = 40 Microns thick
49
What is meant by "Non-Working Side Interference"?
Non -working side = side of mouth mandible DOESNT move to (E.g. If you move jaw to right, working side = right and non-working side = left) "Non-Working Side Interference" = When any tooth on this opposite side makes (first?) contact
50
What is meant by the "Working Side" (what type of articulation does this describe)? What are the 2 main classifications for working side articulation?
Working Side = Side mandible/jaw moves to in LATERAL movement 1) Canine Guidance 2) Group Function
51
What is meant by "Working Side Interference"?
Working side = side of mouth that mandible moves to (E.g. If you move jaw to right, working side = right) "Working Side Interference" = When a single posterior tooth makes first contact
52
What is the difference between: Canine Guidance and Group Function (on working side during lateral articulation)?
Canine Guidance = When contact and overlap between maxillary and mandibular canines disengage posterior teeth (less posterior contact) Group function = Multiple contacts between maxillary and mandibular teeth (posterior teeth still in contact)
53
What are the 3 main components of a "Bridge" (fixed prosthetic)?
1) Abutment (tooth supporting the crown) 2) Pontic (fake tooth in-between) 3) Retainer (crown that goes over "abutment" tooth)
54
What is the only reproducible border movement on Posselt's Diagram (name and number)? What is the definition?
1 - Centric Relation (CR) or Retruded Contact Position (RCP) "Bilateral unstrained position of the mandible where the condylar disc assembly is in the most superior and anterior position in the glenoid fossa and where pure hinge axis opening can occur for the first few mm (20-25mm) of incisal opening"
55
In Posselt's Diagram, what is denoted by the line between II and III (what muscle controls this?what is II/III)?
``` II = Maximal hinge jaw opening from ICP (20-25mm) III = Maximal jaw opening - under muscle control ``` Line between II and III = Translation of the mandible (under control of Lateral Pterygoid muscle, and some Temporalis) Condylar process slides down Glenoid fossa, forwards and downwards.
56
On Posselt's Diagram, what is the distance (mm) between: 1) CR and ICP? 2) ICP and rest position? (how is this affected if the Px's head is tilted forwards or tilted back?)
1) 1.25mm (+/- 1mm) CR can = ICP!! 2) 4mm If head tilted backwards = OVER 4mm (r further from ICP) If head tilted forward = LESS THAN 4mm (r closer to ICP)
57
What is shown by H on Posselt's diagram? | Which dots/marks does it connect?
H = Px habitual opening and closing pattern, avoids the slide between CR and ICP by closing straight to ICP. Connects ICP (2) to III (maximal jaw opening)
58
What is the "Ideal" Occlusion (4) ?
- CR = ICP (with maximal contact and tighter contact on posterior teeth) - "Mutually protected occlusion" = Anterior and Posterior teeth protect each other - Canine Guidance - Protrusive movement gives even anterior contact and complete disclusion (no contact) on posterior teeth
59
Why do Canines provide ideal articular guidance (3) ?
1) Longest rooted tooth (good crown to root radio) 2) Palatal surface morphology allows for smooth guidance 3) Weaker force applied to them due to anterior position in mouth (further away from masseter muscle) so less risk of restoration/tooth fracture
60
What is the difference between: 1) Anterior Guidance? 2) Posterior Guidance?
1) ANTERIOR GUIDANCE Tooth movement that is guided by the tooth-to-tooth contact (influenced by morphology and steepness of cusps) - can be present on ALL teeth but IDEALLY should be present on anterior teeth Anterior Guidance is on Posterior teeth in Class II div 2 and Class III occlusions 2) POSTERIOR GUIDANCE Tooth movement guided by the TMJ and muscles of mastication ("at the level of the condyles") Influenced by the Glenoid/Mandibular fossa shape and movement of the condylar head Present in edentate Px or when Px protrudes jaw fully (as protrusion has no influence from teeth!)
61
Anterior Guidance can be present on any teeth but is IDEALLY on anterior teeth. In what 2 types of occlusion (class) is it present on posterior teeth?
Class II div 2 | Class III
62
What is "Balanced Articulation" and in what cases do we aim to reproduce it? What is this called if occurs in Px's natural dentition?
Balanced articulation = Where teeth on both working AND non-working sides are in contact during lateral movement. We aim to create this in removable denture Px - to stabilise dentures during chewing! Known as "Non-Working Side Interference" if this occurs in natural Px
63
What is meant by Bennett: 1) Angle? 2) Movement? How are the 2 related?
1) BENNETT ANGLE (15º!!!!!!) Angle formed between the sagittal plane and movement of condyle during lateral mandibular movement (as seen from the horizontal plane) 2) BENNETT MOVEMENT The bodily lateral movement of the mandible resulting from condyle movements along the lateral inclines of the mandibular fossa during lateral mandibular movement. 3 Main types to know: Immediate, Early and Distributed side shifts Both are viewed from the horizontal plane and Bennett Movement dictates Bennett Angle produced
64
What are the 3 main types of "Bennett Movement" and how do they differ?
Bennett Movement = Lateral movement of the mandible viewed form horizontal plane (looks at non-working side condyle movement) 1) IMMEDIATE Side Shift Non-working side condyle moves immediately inwards with little or no anterior movement 2) EARLY Side Shift Condyle moves inwards (medially) and anteriorly, where most medial movement occurs over the 4mm anterior movement 3) DISTRIBUTED Side Shift Condyle moves inwards (medially) and anteriorly in even distribution
65
What are 6 common Paediatric dental complaints/conditions?
1) Caries - "Bottle caries" 2) Double/"Shark" teeth 3) Eruption cyst/pain 4) Gingival operculum (overlaps erupting tooth) 5) Supernumeries/Mesiodens (extra tooth) 6) Anterior open-bite (dummy/sucking)
66
What is the difference (symptoms) between Reversible and Irreversible Pulpitis?
REVERSIBLE PULPITIS = Short, sharp pain to a STIMULUS (e.g. hot/cold stimuli) which is elevated with stimulus removal or analgesics IRREVERSIBLE PULPITIS = Longer, dull throbbing pain - spontaneous and may not be elevated by analgesics
67
When can BPE's be given on children? How do they differ to Adult BPE's?
Can be given at 7+ y/o (when permanent dentition begins) - based on 6 reference teeth (1s and 6s): UR/L6, UR1, LL/R6 and LL1 Px 7-12 y/o = Only BPE codes 0-2 used (0 = Healthy, 1 = Bleeding, 2 = Calculus) Px over 12 = ALL Codes used!
68
How many teeth in Primary/Deciduous dentition (vs. Adult)? | When does eruption begin and when is it complete?
``` 20 teeth (A-E) - Vs. 32 Adult Eruption begins = 6 months Eruption complete = 2.5 years ```
69
When does permanent tooth eruption begin and what tooth is (normally) first to erupt? In general, what teeth erupt between what ages?
``` 6 years (+/- 18 months) 1st tooth = 6s at 6 ``` 6-8 y/o = Incisors and 6s (lowers before uppers) 10-12 y/o = Canines, pre-molars and molars
70
What is the most common _____ source of fluoride? 1) Natural 2) Artificial (Give an example of its presence)
1) NATURAL = Sodium Fluoride (NaF) - water | 2) ARTIFICAL = Sodium Monofluorophosphate (Na2PO3F) - toothpaste/mouthwash
71
What is the level of fluoride in: 1) Water? 2) Milk?
1) 1ppm | 2) 2.5-7ppm
72
What are 3 adverse affects of too low fluoride levels?
1) Abscess formation around root 2) Decreased enamel development 3) Increased tooth mottling at fluoride levels 0.05-0.1mmol
73
What is the Acquired Enamel pellicle? How thick is it and what are the Host-derived (5) vs. Bacteria-derived factors (2) that make it up?
1μm thick layer deposited onto clean tooth surface within 2 hours. Host-derived components: 1) Acidic, proline-rich proteins (promote bacteria adherence) 2) Amylase 3) Lysozyme 4) Albumin 5) Immunoglobulins (IgG most common in GCF. Bacteria cleave IgA via IgA protease) Bacteria-derived components: 1) Glycosyl/Fructosyl Transferase 2) Glucans/ Fructans (Extracellular Sucrose storage produced by above bacterial enzymes) 3) Bacterial cell fragments
74
What is the "Pioneering Species" of plaque? - - What 4 main bacteria are present? - What do they attach to and by what interaction (2) - give equation? - How do they travel to attachment site?
"Pioneering Species" = Early colonisers that adhere directly to the Acquired pellicle (A SOM): 1) Actinomyces (closer to Ac. Pellicle) 2) Streptococci Mitis 3) Step. Oralis 4) Streo. Sanguinis Travel to enamel acquired pellicle via Passive Transport (as most non-motile) and attach via Van der Waals forces of attraction (Va) and Electrostatic repulsion (Vr) between negatively charged bacterial cells and positively charged pellicle surface Vt = Va + Vr
75
Outline the DVLO Theory in Pioneering species attachment to the Acquired Enamel Pellicle (give relevant equation)
``` Vt = Total interactive energy Va = Total attractive energy (from Van der Waals) Vr = Total repulsive energy (from electrostatic repulsion between negative bacteria and positive enamel pellicle) ``` Vt = Va + Vr
76
What is the "Confluent Layer"?
Multiplying of the Pioneering layer, involves co-aggregation of various bacteria, fermentation of salivary glycoproteins and cleaving of IgA
77
Which Bacterium marks the end of Pioneering Species + Confluent Layer in plaque formation? When does this occur and what comes after it?
Fusobacterium Nucleatum Occurs at around 2 days (day 2-7 = Accumulated "late" bacterium growth) After it Late bacterium grow, more anaerobic bacterium and increased diversity.
78
What is meant by bacterial Co-aggregation? What is the main aggregation that occurs in the plaque Confluent Layer with the following bacteria (to others) : 1) Streptococcus sanguinis/Mitits with..? 2) Fusobacterium nucleatum with...? 3) Eubacterium with...?
Co-aggregation = Cell-to-cell bacterial interactions 1) Streptococcus Sanguinis/Mitis -> Actinomyces (also Pioneering Species), Corynebacterium matruchotii and Proprionibacterium acnes 2) Fusobacterum nucleatum --> Streptococci, Actinomyces or Privotella melaninogenicus/gingivalis (Co-aggregates with P.gingivalis to promote tooth adherance) 3) Eubacterium --> Veillonella
79
What are 4 main functions of a stable and established Plaque? (Think about functions of bacteria within it)
1) Protection from stressful environments 2) Exclusion of exogenous organisms (Bacteria outcompete and host defenses include: Lysozyme, Lactoferrin and Peroxidases) 3) Recycling of nutrients (e.g. Streptococci and Actinomyces produces lactate, which is used as carbon source by asaccharolytic Veillonella) 4) Metabolic function
80
In a stable/established dental plaque, what are the host (3) and bacterial (2) defences against exogenous microorganisms entering and colonising?
HOST: 1) Lysozyme (bacterial lysis) 2) Lactoferrin (iron sequestration) 3) Peroxidase (inhibit glycolysis) BACTERIAL : 1) Competition for nutrients or receptor sites 2) Un-inhabital environment (e.g. through acid production)
81
What is the main acid produced by caries bacteria? | Name 4 other acids they can produce?
``` Lactic Acid! "FAPS" 1) Formic acid 2) Acetic acid 3) Propionic acid 4) Succinic acid ```
82
What are meant by the terms Acidogenecity and Acidduricity? | Name a bacteria that is both Acidogenic and Aciduric?
ACIDOGENECITY =
83
What are meant by the terms Acidogenecity and Acidduricity? | Name 3 bacterium that are both Acidogenic and Aciduric?
ACIDOGENECITY = Ability of bacteria to produce organic acids from fermentable carbohydrates (Main Acids: Lactic, Formic, Acetate, Propionoic and Succinic) ACIDURICITY = Ability of bacteria to survive in low pH environment E.g. Streptococci Mutans, Actinomyces and Lactobacillus are Acidogenic and Aciduric
84
What are the 2 main divisions of Acidogenic bacterium in terms of their acid produced?
HOMOfermentative Bacteria = Produce over 90% Lactic Acid (E.g. Streptococci and Lactobacillus) HETEROfermentative Bacteria = Produce mixture of organic acids (Formic, Acetic, Propionic, Succinic) and Ethanol
85
How can bacteria store Sucrose for continuous metabolism: 1) INTRACELLULARLY? 2) EXTRACELLULARLY?
1) INTRACELLULAR = Stores Sucrose as Glycogen-amylopectin (via Invertase enzyme) 2) EXTRACELLULAR = Stores Sucrose as Glucans or Fructans via Glucosyl or Fructosyl Transferase Glucans = longer half life
86
In what 5 main ways can bacteria maintain their intracellular pH? (Think methods against both increased acidity and alkalinity)
1) Cytoplasm buffering ability 2) Increased acid production (inc. glycolysis) 3) Increased alkali/base production (inc. Ureolysis, Strickland reaction or Arginine deiminase to produce Ammonia and/or CO2) 4) Thick cell, less permeable to protons 5) Ability for protons to be moved out of cell via Active Transport
87
Bacteria can maintain intracellular optimum pH by production of bases when becomes to acidic. What are these bases? What 3 reactions can produce them (USA)? What bacteria carry out each of these 3 reactions?
Bases = Ammonia and/or CO2 1) Ureolysis = Streptococcus salivaris 2) Strickland Rection = Pepto-streptococcus 3) Arginine Deiminase = Streptococcus sanguinis + gordonii
88
Why is Sodium Monofluorophosphate used as F source in toothpaste rather than Sodium Fluoride?
Ca used as mild abrasive in toothpaste. Reacts with NaF to form CaF which is insoluble, setting hard and blocking tube. Instead Ca reacts with Na2PO3F to form CaPO3F, which is soluble - PO3F ions remain available.
89
What is the main difference between NaF (Sodium Fluoride - most common natural F form) and Na2PO3F (Sodium Monoflurophosphate - most common artificial F form)? What compositional similarity allows them to have similar properties?
Sodium Monofluorophosphate = F is covalently bound (in PO3F-) Both have similar properties due to Alkaline Phosphatase presence.
90
What is the width of Enamel: 1) Crystals? 2) Prisms?
1) 30 nm | 2) 4μm
91
What are the possible HAP substitutes for: 1) Calcium (Ca2+)? 2) Phosphate (PO4 3-)? 3) Hydroxyl (OH-)?
1) Calcium --> Magnesium or Manganese 2) Phosphate --> Carbonate 3) Hydroxyl --> Fluoride or Chloride
92
At what stage in Enamel development (Amelogenesis) is Fluoride incorporated into enamel crystals? (therefore Fluorosis risk)
Maturation
93
What are 3 Post-eruptive effects of Fluoride?
1) Inhibit demineralisation, Increase remineralisation 2) Inhibit glycolysis in cariogenic bacteria (less acid production) 3) F in Plaque --> Inhibits extracellular glucan/fructan synthesis (Sucrose storage)
94
What are 4 Pre-eruptive effects of Fluoride?
1) Increases crystal production and size 2) Decreased enamel acid solubility (FAP is less soluble than HAP due to increased hydrogen bond strength) 3) More rounded cusps 4) Improved fissure pattern
95
What type of Fluoride source is present in Fluoride rinse? | At what 2 main levels is it given to Px's?
NaF (Sodium Fluoride) Daily = 0.05% 4night/week = 0.2%
96
What are the Fluoride concentrations (in ppm) in: 1) Outer crystallites of sound enamel? (MOST!) 2) Outer 2μm enamel? 3) Bulk (inner) enamel? 4) White spot lesion?
1) 6000ppm 2) 1000ppm 3) 100-350ppm 4) 1000-3000ppm
97
What makes F- ions toxic in excess? (what reaction do they invade) What are some symptoms of: 1) CHRONIC Toxicity? 2) ACUTE Toxicity? What is the fatal fluoride dose in Adults?
``` Forms complexes with transitional elements in mitochondrial ETC and enzyme cofactors Fatal dose = 1-2g 1) CHRONIC - Extoses (bony growth) - Stiffness and pain in joints 2) ACUTE - Poisoning - Nausea and vomiting - Decrease in BP - Limb spasms, tetany or convulsions - Respiratory depression --> Unconsciousness ```
98
What fluoride levels should be in toothpaste of Px aged: 1) 0-3? 2) 3-6? 3) Adults?
1) SMEAR of no more than 1000ppm 2) PEA SIZED amount MORE than 1000 (1350-1500) 3) 1350-1500ppm All should brush twice a day.
99
What are the 3 main sites of caries?
1) Pits/Fissures of posterior teeth or Cingulum 2) Approximal (Interproximal space) 3) Cervical 1/3rd of crown (gingival recession)
100
What are the 5 Cavity Classifications (Blacks)?
Class I = Pits/Fissures of occlusal posterior or Cingulum Class II = Proximal surface of Posterior Class III = Proximal surface of Anterior Class IV = Proximal surface of Anterior WITH INCISAL EDGE Class V = Cervical 1/3rd of Crown
101
What is meant by Salivary: 1) Highways? 2) Byways? Which is most at risk of caries (give example)?
1) Highways = Areas of easier and faster salivary flow 2) Byways = Areas of reduced and slower salivary flow BYWAYS most at caries risk (e.g. Buccal aspect of upper incisors)
102
What are "Iatrogenic Stagnation Areas"?
Areas at increased risk of food debris trapping due to medical intervention - e.g. Orthodontics!
103
What are 5 systemic features of Xerostomia?
1) Dryness and Hoarse throat 2) Fatigue 3) Dry eyes and nose 4) Joint pain, swelling and stiffness 5) Weight loss (from difficulty eating)
104
What are the 3 major salivary glands? | Is their saliva production greater when Stimulated or Unstimulated?
1) Parotid - Stimulated 2) Submental - Stimulated 3) Submandibular - UNStimulated
105
What Vitamins are: 1) Water Soluble? 2) Lipid Soluble?
1) Vitamin B groups and C | 2) Vitamin A,D,E and K
106
What teeth have: 1) Oblique Ridge? 2) Transverse Ridge? And what are these?
Oblique Ridge = Ridge between mesiolingual and distobuccal cusps - Maxillary Molars only!! Transverse Ridge = Ridge between 2 cusps on same side (e.g. mesiolingual and mesiobuccal) Found on ALL molars (Maxillary and Mandibular)
107
What tooth has a buccal pit?
Mandibular first molar
108
How many roots and cusps on: 1) Maxillary 6s? 2) Mandibular 6s?
1) 3 roots and 4 cusps (BUT Cusp of carabelli found mesiopalatally) 2) 2 roots and 5 cusps (3 buccal)
109
How do Local Anaesthetics work? | What does this depend on?
Blocks Action Potential conduction in nerve fibres by blocking sodium ion channels and preventing Na+ entry Must be non-ionsed to pass through lipid bilayer and must become ionised to "activate" and block channel
110
Why are Local Anaesthetics often combined with a Vasoconstrictor (3)? What Vasoconstrictor is paired with: 1) Lidocaine? 2) Prilocaine? What are some contraindications for their use?
As LAs cause Vasodilation (by blocking SNS 𝝰1 activation) Vasoconstrictors combat this by activating 𝝰1: - Reduced bleeding at site - Reduced drug systemic absorption and toxicity - Prolonged drug duration of action: reduced dose needed 1) Lidocaine = Adrenaline/Epinephrine (contraindicated in Px with heart conditions as increases HR and CO) 2) Prilocaine = Felypressin (contraindicated in pregnancy)
111
What is the % or mg/ml of: 1) Lidocaine? 2) Prilocaine? 3) Articaine?
1) 2% or 20mg/ml 2) 3% or 30mg/ml 3) 4% or 40mg/ml
112
``` What is the volume of a generic LA cartridge? How much is used in: 1) Infiltration? 2) Nerve Block? 3) Long Buccal or Palatal? ```
2. 2mg 1) 0.5-1ml 2) 2ml 3) 0.2-0.5ml
113
What is the duration of action for Lidocaine and Prilocaine: 1) Pulpally? (same) 2) Soft tissues? (different)
1) 45-60 mins 2) Lidocaine = 3-5 hours Prilocaine = 2-3 hours
114
What is the max dose (mg/kg) for Lidocaine and Prilocaine? Using this (and other knowledge) work out max CARTRIDGE dose for 60kg Px?
``` Lidocaine = 4.4mg/kg Prilocaine = 10mg/kg ``` 60kg X 4.4mg/kg = 264 mg (max) 264mg ÷ 20mg/ml = 13.2ml 13.2ml ÷ 2.2ml (cartridge) = 6 cartridges max
115
How and why does Inflammation affect LA efficacy?
``` Inflammation = Increased acidity and LA is a weak base Difference = More ionised so less able to penetrate lipid barrier (should be non-ionised) to have action - reduced efficacy! ``` Also Inflammation leads to increased blood flow so LA is more readily removed
116
What 7 factors affect the onset and duration of Local Anaesthetics?
1) Soft tissue/oral pH 2) LA pKa 3) LA lipid solubility 4) Drug concentration 5) Nerve morphology Time of diffusion: 6) Needle -> Tip 7) Away from nerve
117
What is meant by "Cleaning"? | When might it be used and what are the 2 main goals of Pre-Sterilisation Cleaning?
Cleaning = Physical removal of microbes Used on low-risk items (those not used on Px or in contact with intact skin only) 2 main Pre-Sterilisation Goals: 1) Physical removal - decrease bacterial load by thousand fold 2) Removal of any biomasses - improve sterilisation effectiveness and prevent permanent material attachment
118
What is the difference between Resistance and Retention? | What are 3 Macroscopic restoration modifications that restoration resistance or retention?
``` RETENTION = Cavity/restoration that resists displacement in the opposite direction in which it was placed RESISTANCE = Cavity/restoration that resists displacement in apical or oblique (other) directions ``` 1) Undercuts (areas of narrowing) - Both Resistance and Retention 2) Slots and Grooves - mainly Resistance 3) Flat surface - Resistance
119
What is the difference between Macro and Micro -scopic modifications? Name 6 Macroscopic modifications, which restorative materials would you find them used with?
MACRO = Large-scale modifications made with bur MICRO = Small-scale modifications made with chemicals (ETCH!!!!!!) 1) Rounded internal line angles - All (Amalgam, Composite + GIC) 2) 90º Cavosurface angle - All, mainly Amalgam 3) Undercuts - All, mainly Amalgam 4) Slots and Grooves - All, mainly Amalgam 5) Flat surface - All, mainly Amalgam 6) (Partial) Enamel Margin Bevel - GIC + Composite only
120
What is the: 1) Cavosurface angle? 2) (Internal/External) Line angle?
1) Angle between surface of cavity and tooth surface, ideally 90º and should follow enamel prisms 2) Angle between two surfaces of the tooth ROUNDED Internal Line Angles are macroscopic modifications which reduce tooth fracture risk and are formed from bevelling of internal line angle, between pulpal and axial wall
121
What are microscopic modifications? Give 2 examples... Why does Amalgam have NO microscopic modifications?
Small-scale modifications created using chemicals 1) Acid-Etch (Enamel) 2) Dentine Conditioner (Another form of Acid Etch) Amalgam has no microscopic modifications as it cannot bond chemically to the tooth. Only GIC + Composite have Microscopic modifications...
122
What muscles (3) Influence the shape of an upper impression border?
1) Buccinator 2) Levator anguli oris 3) Incisivus superioris
123
``` What muscles (6) Influence the shape of a lower impression border? (Hint: first 3 = same as upper!) ```
1) Buccinator 2) Levator anguli oris 3) Incisivus superioris 4) Mentalis 5) Mylohyoid 6) Superior Pharyngeal constrictor muscle

BDS2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions