ICP Flashcards
What are 5 protective reactions of Dentine (2) and Pulp (3) when faced with Caries?
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
At what stage is Tubular Sclerosis destroyed?
Final Stage: Advanced Carious Lesion
may be some destruction in previous stage once cavitation occurs
What happens in the initial (first) stage of caries, when enamel is still intact?
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)
What are the 2 main bacteria types involved in early cavitation and how do they function?
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)
What is “Liquefaction foci”? What type of bacteria cause its production?
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
Why is Dentine caries not present in germ-free animals?
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.
What is the difference between “Infected” and “Affected” Dentine?
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
In an Amalgam filling, what is the MINIMUM width, depth and length of a 2 surface cavity?
2mm
This must be paired with Macroscopic modifications: 90 C cavosurface angle, rounded internal line angles, undercuts, slots/grooves and a flat surface
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
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
What is the difference between Reparative and Reactionary dentine?
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)
What is a ______ Lesion?
1) White Spot
2) Brown Spot
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)
What is the difference between Proximal and Approximal areas of the teeth?
Proximal = Contact area between adj teeth Approximal = BENEATH this contact area (interproximal space)
What is the resting pH of saliva? What is the critical pH of: 1) enamel? 2) dentine? What is significant about this difference?
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
What is the mean Calcium ion concentration in saliva?
12.5 ppm (+/- 0.7)
What 2 factors is the balancing act between demineralisation and remineralisation primary based on?
1) pH
2) calcium ion concentration
Demineralisation = Low pH and calcium conc
Remineralisation = High pH and calcium conc
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.
“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)
What is meant by DMFT?
DMFT = Decayed Missing Filled Teeth
Method of recording oral epidemiology, assessing dental caries prevalence.
What is Root Caries?
What is an easy mistake for clinicians to make when faced with these cases?
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)
What are 4 clinical problems we face with Root Caries (risk, presentation and treatment)?
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)
What patients are most at risk of root caries and why (2)?
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
What 3 features can distinguish Active from Arrested Caries?
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
Root Caries is a multifactorial disease, what are 7 possible factors?
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)
What are 3 Non-Invasive treatments for Root Caries?
Why might these be favoured over Invasive treatment (Intra-Coronal Restorations)?
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 can the following techniques detect caries:
1) Electrical Caries Monitor (ECM)?
2) Fibre-Optic Transillumination?
3) Laser Fluorescence Systems?
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
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)
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
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
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
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”
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
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
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
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
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)
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
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)
What 4 main factors place a (paediatric) Px at high caries risk?
- Three or more carious lesions in one year
- Orthodontic treatment
- Chronic illness: medically or physically impaired
- Social History: Low motivations
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
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)
How does caries appear in a radiograph?
radiolucent (dark shadow)
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
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)
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
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)
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
What is Posselt’s Diagram/Triangle (what does it show)?
Diagram outlining the Sagittal plane movements of the jaw (up and down at midline)
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)
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
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
