MI Preventive Flashcards
Caries pathogenesis
On the teeth, bacteria live within biofilms adhered to surface of teeth and receive nutrients from the oral environment. When cariogenic/acidogenic bacteria metabolise sugars in the oral environment, they produce lactic acid as a by-product of fermentation (anaerobic respiration).
When amount of acid exceeds saliva buffering capacity, pH of biofilm decreases. When pH falls below 5.5, the critical pH of hydroxyapatite (which is what enamel is made of), position of equilibrium favours the dissolution of HAP, known as demineralisation of enamel.
Acid percolates down the lamellar pores of enamel and creates a subsurface demineralisation, causing spaces between HAP crystals to widen and increased porosity, while the surface is remineralised by supersaturated conditions of the biofilm (dissolved Ca and PO4 are trapped in the biofilm).
If caries continues to progress, microcavities form in the enamel until the surface lesion collapses, forming a cavity.
If caries enters dentine, acids degrade the collagen framework as well as dissolve mineral.
Demin remin cycle
and factors that tip the balance
Demin
1) Cariogenic bacteria metabolise sugars found in oral environment (from diet), forming by-product of lactic acid
Remin
2) Saliva buffers the acid and returns it to resting pH 6-7
contains Ca and PO4 ions and is supersaturated with respect to tooth enamel, thus favouring remineralisation. Stimulated saliva also contains bicarbonates which act as buffers of acids.
3) But sustained periods of acid production overwhelms buffering system - an unsaturated solution causes equilibrium to shift in favour of demineralisation. when pH drops below critical pH of hydroxyapatite, 5.5, hydroxyapatite dissolves.
4) Ca and PO4 ions released from tooth surface remain trapped within the biofilm (closed system) are still available for remineralisation of tooth structure in supersaturated conditions
The pH of the oral environment drops whenever food is eaten as oral bacteria begin to metabolise the sugars in food, causing demineralisation. It takes about an hour for saliva to return the pH to resting pH and remineralise enamel. This cycle continues every time food is taken in. This is known as the Stephan’s curve.
Feast and famine states?
Things that can tip balance
Diet
Medication
Saliva
Affected dentine vs infected dentine
Infected
Soft, cottage cheese consistency
Degraded collagen framework
Bacteria present
No potential for remineralisation
Affected
Leathery, firm
Intact collagen framework
Some dissolved mineral???
Bacteria absent
Potential for remineralisation - to be conserved
Enamel dvptal defects
- what it is
- what does it look like
Hypomineralisation: disruption of calcification of enamel leads to insufficient mineralisation of matrix. Qualitative defect - results in increased enamel translucency
Fluorosis is a type of hypomin, but is a definite diagnosis- taking into account SHx.
Fluoride interacts with mineralising tissues, causing alterations in mineralisation process
Severe fluorosis = High concentrations of fluoride at time of eruption disrupts ameloblast function→ weakened enamel leads to likelihood of chipping
Hypoplasia: disruption of matrix formation of enamel leads to insufficient matrix, but normal mineralisation. Quantitative defect - results in changes to enamel thickness - chipping, pitting
Tooth wear
Attrition - opposing teeth
Abrasion - extrinsic agents - brushing, tool use
Erosion - acids
Caries vs erosion
Caries:
Source of acid
Bacteria (in the form of metabolic byproducts)
Pathogenesis
Bacteria within biofilm on teeth metabolise
Acids percolate down lamellar pores, leading to increased porosities, enamel rod length maintained
Remineralisation
Possible
Closed system
Demineralised ions are trapped within biofilm
Location
Confined to areas of plaque accumulation
Appearance
White spot lesion-
Chalky white spot, rough and dull when dried
Exposure period
Over a long period
Erosion:
Intrinsic agents: gastric acid from reflux
Extrinsic agents:
Dietary acid, acid from environmental exposure
Acids dissolve enamel rods
Irreversible shortening of enamel rods
Possible to remineralise surface, but lost tooth structure cannot be regained,
Open system - ions are lost to environment
Anywhere on tooth, particularly on areas where acid may come into contact
Scooped, glossy appearance
Loss of anatomical features
White, may appear translucent or yellow if dentine showing through
Short period and repeated
Incipient caries
Arrested caries
Active caries
Developmental defect
refer to gil
Fluoride
- how does it help to prevent caries
- types of mechanisms
Remineralisation → strengthens tooth by formation of fluoroapatite by substituting hydroxyl group in hydroxyapatite. Fluoroapatite has a lower critical pH of 4.5 compared to HA (5.5). This
Delays demineralisation (increased resistance to demin)
Enhances remineralisation
Also
Bacteriostatic effect ([F]<190ppm): disrupts bacterial metabolism, raising pH → selects against acidogenic bacteria
Bactericidal effect ([F]>190ppm): completely arrests metabolism of bacteria
Mechanisms: pre and post-eruptive. More significant effects post-eruptively
Fluoride
- toxicity
- what concentration threshold for systemic fluorosis?
- toothpaste concentrations
- what to consider abt pt wrt their fluoride exposure
Toxicity and possible risks
Dental fluorosis - type of hypomin as a result of high fluoride exposure at time of tooth eruption. Qualitative defect- aesthetic concern, unless severe.
Systemic fluorosis - when F > 5mg/kg body weight → poisoning, triggers fluorosis of GIT and skeleton, brittle bones. Mgmt - give oral Ca (milk) and observe, admit to hospital if more than 5mg/kg/
A low and continuous dose of fluoride in water, 0.6 < F < 1.2ppm, is ideal for caries protection and avoids risk of fluorosis.
Toothpaste F concentration:
Standard (adult): 1000-1500ppm
Low F (children): 500-550ppm
High F (professionally prescribed for high caries risk): 5000ppm
Consider pt’s location and access to fluoridated water
Expected: brush 2x/day with fluoride toothpaste + fluoridated water to introduce fluoride dentifrices
Oral health instruction
- what to consider about pt
- consider about oral hygiene products - characteristics of toothbrush eg.
Consider pt’s manual dexterity, age, likely compliance, presence of appliances, crowded teeth, gaps
Type of toothbrush
Manual or electric, Size of head, bristles type
Toothpaste
Age (F toothpaste to be kept out of children’s reach, adult supervision)
Spit not swallow
Modified bass technique
Senstivity, caries risk
Interdental cleaning
Type: floss, picks, interdental brushes
Technique
Frequency
Note braces and retainer wires that get in the way
Professional MI products
- what why and how
- trim - timing relevance involvement method
Professional
Spot application
Varnishes. 5% NaF (22,600ppm F)
Colgate Duraphat
GC MI Varnish (CPP-ACP casein phosphopeptide-amorphous calcium phosphate)
CI: milk protein allergy (rare) (lactose intolerance not counted)
3M Clinpro Varnish: tricalcium phosphate
Tray application
Gels and foams - 1.23% (12,300ppm F) acidulated phosphate fluoride (APF).
Acid etches away enamel, allows deeper penetration of fluoride
4min application
Not suitable for children <10y due to poor spitting ability
Home care (consider pt’s accessibility, motivation & compliance)
GC Tooth mousse/tooth mousse plus 900ppm (adjunct to daily tp)
Colgate Neutrafluor (5000ppm - high caries risk)
Clinpro Creme 950ppm (replaces normal tp)
Saliva
Biotene mouthrinse/gel
Sugar-free gums (limited- not helpful for radiotherapy patients, as salivary glands are not functional)
Bicarbonate mouthrinse?
Gingivitis
Chlorhexidine mouthrinse - controls plaque
But long term causes staining and calculus - try to only prescribe for 2 weeks
Tooth brushing instruction: brush along gum line
Rubber dam critique
Dam prepearation
- Hole positioning
Clamp selection and preparation
- Size, type of jaws, safety floss
Clamp placement
- Gingival trauma, retention (below maximum convexity, four point contact)
Dam placement
- bunching/deficiency
Frame placement
- Frame present
- Frame orientation
Dam finish
- Contacts flossed, dam inverted
- Anterior ligature
- Gingival exposure
Fissure sealant
- what it does
- indications
- mechanism
What fissure sealant does: physically alter tooth morphology to reduce caries risk by sealing fissures with LOW VISCOSITY MATERIAL and thus reducing plaque-retentive areas
Indications: Deep pits and fissures not easily cleaned, high caries risk
Deep and narrow fissures cause food to fall in that cannot be removed by normal masticatory movements and brushing → sheltered area for bacterial growth → leads to plaque accumulation and stagnation
Mechanism:
Acts as mechanical barrier so food cannot fall in
Cuts of nutrient and oxygen supply to any bacteria that may be in fissures, eliminates conducive environment for bacterial growth
Creates easier surface for cleaning by brushing and mastication
- contraindications of FS
Contraindications:
Low caries risk
Shallow, self-cleansing pits and grooves
Teeth with occlusal caries into dentine, proximal caries
Partially erupted teeth - difficult to clamp, some fissures may be covered by gums
Previous occlusal restorations
Composition of FS + importance
Composite resin: better retention
Glass ionomer: less moisture-sensitive
Self curing and visible light cure
No polymerisation shrinkage vs can manipulate setting time and remove excesses before setting and no mixing of resins which could incorporate air bubbles
Clear and opaque
Can see if caries has developed underneath vs can assess coverage more easily and if sealant is worn
Fluoride-releasing sealants
