Cariology Flashcards
(100 cards)
1
Q
Cariology
Definition:
A
The study of caries and cariogenesis
2
Q
CARIES definition:
A
decay, in bone or teeth
3
Q
CARIES definition: decay, in bone or teeth
* — disease
* Leads to (2)
A
BACTERIAL
demineralization of inorganic components
destruction of organic components
4
Q
Dental Caries
* — disease (3)
A
- INFECTIOUS disease
- MANAGEABLE disease
- PREVENTABLE disease
5
Q
Caries Requirements
(4)
A
- Susceptible host
- Bacteria
- Food Source
- Time
6
Q
Etiology of Caries
* Specific plaque hypothesis
(5)
A
◦Biofilm is responsible for the disease
◦Plaque is pathogenic when disease is present
◦Specific Microbes are the cause
◦Strep Mutans
◦Lactobacillus and Actinomyces V. (acid producers, can live in acid)
7
Q
Control the pathogens=
A
control the disease
8
Q
Previous Theory- outdated
A
- Nonspecific Plaque Hypothesis
◦Says ALL plaque is detrimental
◦More plaque= more decay - THIS IS NOT THE CASE
9
Q
Biofilm definition:
A
Community of bacteria, bacterial by-products, extracellular matrix, and water
10
Q
Accumulation of biofilm on teeth is HIGHLY ORGANIZED
(2)
A
- Few microorganisms are able to adhere to oral surfaces
- Streptococci prominent group
11
Q
Normal saliva biofilm made up mostly of
A
Strep sanguis and Strep mitis
* Non-pathogenic
12
Q
Strep Mutans
(2)
A
- Primary bacteria in Caries
- Begin caries formation
13
Q
Strep Mutans
* Primary bacteria in Caries
* Begin caries formation
* Followed by
A
Lactobacillus
* Responsible for progression of caries
14
Q
Caries does have a genetic component
A
- Bretz WA 2005 Twins Study
Found genetics play a significant role in caries
Up to 40% - Specific information is unknown
- Genes involved unknown
- Gene-gene and gene-environmental factor interaction role unknown
- Many factors: predisposition to sweet foods, bacteria in the body, enamel makeup, saliva
makeup - ?Grand Rounds project
15
Q
Caries does have a genetic component
* THIS DOESN’T MEAN YOUR PATIENT IS OFF THE HOOK IF THEY HAVE CARIES. It means
A
they must be MORE DILIGENT to prevent future caries.
* Dentist has a responsibility to help them overcome the genetic component.
16
Q
PROGRESSION of caries:
pulp/dentin reaction
(6)
A
- Tubular sclerosis
* dentinal tubular obturation(opening gets smaller) - Tertiary dentin formation
* formed in response to stimuli (caries)
* reactionary or reparative - Inflammatory reaction when encroaching on pulp
* within 1.0mm of pulp - Pulp infection and exposure
- Pulp necrosis
- Periapical lesion
17
Q
DEMINERALIZATION:
(4)
A
-Bacteria living in plaque feed off “leftovers” (sugars,
fermentable carbohydrates)
-Bacterial waste product is ACID (lactic)
-Acid demineralizes enamel
-Phosphates and Calcium are lost
18
Q
REMINERALIZATION:
(4)
A
-Saliva rinses away sugars
-Saliva buffers acids
-Minerals in saliva (calcium, phosphate) re-enter
tooth
-Presence of fluoride facilitates process
19
Q
A CARIOUS LESION occurs when:
A
Demineralization is greater than Remineralization over time
20
Q
Carious Lesion Progression
* Enamel (pH below 5.5)
(4)
A
- calcium, phosphate ions leave enamel
- =demineralization
- =white spot lesion
- ->cavitation
21
Q
Carious Lesion Progression
* Dentin demineralizes at —
(3)
A
~6.2 pH
* Lose minerals below surface (just like in enamel)
* In addition, proteolytic activity to remove the organic portions (remaining collagenous matrix)
* Remineralization may not be possible
22
Q
What about Fluorapatite?
* pH for demineralization?
A
23
Q
Remineralization requires:
(4)
A
- Saliva
- Plaque removal
- Diet modification
- Fluoride
24
Q
Remineralization: Saliva
(4)
A
- Buffers
- Cleanses
- Antibacterial
- Calcium and Phosphate Ions
25
Remineralization: Saliva
* Buffers
(4)
◦Raises pH to non-demineralizing levels
◦> 5.5 enamel
◦>6.2 dentin
◦Bicarbonate ion
26
Remineralization: Saliva
* Cleanses
(2)
◦Flushes away free-floating organisms
◦1-1.5L/day
27
Remineralization: Saliva
* Antibacterial
(2)
◦Salivary proteins: lysozome, lactoperoxidase, lactoferrin, agglutins
◦Shown NOT to have huge impact on caries
28
Remineralization: Plaque Removal
(4)
* Removes bacteria’s habitat
* Plaque must ADHERE to cause damage
* Home care
* Professional dental visits
29
Remineralization: Diet Modification
* Starve bacteria
(2)
◦Preferred food source: fermentable carbohydrates
◦Strep Mutans loves sugar
30
Remineralization: Diet Modification
* FREQUENCY OF --- IS MOST IMPORTANT FACTOR
(2)
CONSUMPTION
◦More important than amount of sugar consumed
◦Aim to REDUCE frequency
31
Remineralization: Fluoride
(4)
* Replaces Hydroxyl groups in hydroxyapatite
* Increases rate of Remineralization
* Inhibits bacterial activity
* Fluoride should be on the surface of the tooth for these mechanisms to work
32
* Replaces Hydroxyl groups in hydroxyapatite
(3)
◦Renders enamel more resistant to DEmineralization
◦Strengthens crystalline structure
◦Forms fluorapatite
33
* Increases rate of Remineralization
(2)
◦Attracts Ca ions
◦Ca ions attract phosphate ions
34
Different habitats= different bacteria
(4)
* Pits and fissures
* Root surface
* Facial, lingual smooth surfaces and interproximal surfaces
* Bacterial communities may differ from one another in different areas on the same tooth
35
* Pits and fissures
(1)
◦Simple streptococcal bacteria
36
* Root surface
(4)
◦Complex bacterial community
◦Mostly filamentous and spiral bacteria
◦Additional complication-anatomy of root may render hygiene practices ineffective
◦Unable to reach concavities with floss
37
CARIES PATHOGENESIS
* Bacteria
◦Strep mutans initiates lesion
◦Produces lactic acid
◦Survives in low pH
◦Able to store and use intracellular glycogen
◦Produces glucans or dextrans
◦Allows it to stick to tooth
◦Forms barrier so remineralization can’t occur
38
◦--- follows and leads to progression of caries
(2)
Lactobacilli
◦High acid producer
◦Found in advanced dentinal caries
39
Dietary --- is the most important factor in producing cariogenic plaque
(3)
sucrose
◦Leads to growth of highly acidogenic bacteria
◦Strep mutans doubles in only 1.32 hours in sucrose
◦Doubles in 20 hours in saliva
40
--- frequency exposure is more damaging that --- frequency, --- volume
High
lower
high
41
CARIES PATHOGENESIS
* Layers of bacterial invasion
(3)
◦Bacterial front-closest to oral environment
◦Discoloration front
◦Softening layer-closest to pulp
42
* INFECTED vs. AFFECTED DENTIN
(4)
◦Infected must be removed
◦Bacteria present
◦Affected may remain TO PREVENT PULP EXPOSURE
◦No bacteria present
43
* Acid production plays important part
(3)
◦Acid destroys tissues
◦Acid output in caries active plaque is twice that of caries inactive plaque
Diets high in sucrose= high caries rate
44
* REDUCE CARBOHYDRATE CONSUMPTION=
REDUCE ACID
PRODUCTION
45
* Cavitation occurs when:
◦Tooth surface becomes anaerobic and acidic
46
* Once tooth is cavitated
◦Bacterial (lactobacilli) that adhere poorly are now able to more easily adhere to more
retentive (SURFACE AREA) of cavity
47
* Decay expands rapidly in more organic part of tooth
◦DEJ and dentin
48
CARIES PATHOGENESIS
* Where it all begins: white spots
(5)
◦First clinically detectable stage of caries
◦Surface level of enamel is still intact
◦Initial lesion depth at ~1 week= 20-100μm
◦Visible energy change ~2 weeks
* Lesion depth= 400-500μm
49
CARIES DIAGNOSIS
(3)
Clinical visualization
Tactile
Radiographs
50
* Clinical visualization
(2)
◦Good light
◦Air dry
51
* Tactile
(3)
◦Gently feeling occlusal surface for soft areas may be appropriate
◦Avoid using explorer on smooth surfaces
◦Could cavitate an area that could have remineralized
52
* Radiographs
(4)
◦BITEWING radiographs
◦For interproximal lesions
* NOT Pas
* Angulation misleading
53
Classify caries three ways:
site
activity
severity
54
* Site
(5)
◦Pit and fissure
◦Interproximal
◦Free smooth surface
◦Root surface
◦Cusp tip
55
* Activity
(2)
◦Active
◦Arrested
56
* Severity
◦Enamel:
◦Dentin:
◦Rampant Caries
◦Initial, Cavitated, E1-E2
◦Non-cavitated, Cavitated, D1-D2-D3
57
* Poor oral hygiene and diet can produce white spot lesion in
3 weeks
58
* Fluoride slows rate of progression in
pit and fissure
◦After fluoride was introduced in 1950’s, progression of caries from enamel to dentin slowed from ~ 1 year, to
~2-4 years
59
* Fluoride slows rate of progression on
smooth surfaces
◦Smooth surface progression is already slower than fissure
60
ON AVERAGE it takes --- for caries to progress from outer surface of enamel to DEJ
43 months
61
Pit and Fissure Caries
◦---% of caries
85
62
ACTIVE
(4)
◦White spots
◦Matte, frosted
◦Cavitated
◦Visible dentin
63
ARRESTED
(3)
◦White or brown spot
◦SHINY surface
DO NOT NEED TO TREAT SURGICALLY
64
CARIES DIAGNOSIS
* Interproximal caries
◦Rely primarily on radiographs to diagnose
(3)
◦Clinical exam may show
(2)
◦NO radiolucencies present= 98% chance of no caries
◦Radiolucency does not always mean that cavitation is present
◦Radiolucency present= 40-70% chance of no caries
◦Opaque and discolored
◦Cavitated
65
CARIES DIAGNOSIS
* Radiographs
◦By level of cavitation
◦Outside->inside
(2)
◦E1, E2
◦D1, D2, D3
66
CARIES DIAGNOSIS
* Initial Carious lesions
◦Non-surgical treatment
(4)
◦Fluoride varnish
◦Oral hygiene instructions
◦Dietary counseling
◦Resin infiltration
67
CARIES DIAGNOSIS
* Moderate Carious Lesions
(4)
◦Restore with amalgam or composite
◦= surgical treatment
◦Supplement with nonsurgical treatment
◦education, fluoride, etc.
68
CARIES DIAGNOSIS
* Advanced Carious Lesions
(4)
◦May be treated with restoration (surgical)
◦Increased patient education is necessary because:
◦Will likely require additional treatment
◦endo, fixed, OS
69
CARIES DIAGNOSIS
* Recurrent Caries
(2)
◦Remove old restoration and restore with amalgam or composite
◦Supplement with non-surgical treatment
70
Traditional surgical model
(8)
◦A condition or a cavity
◦Detection of cavity
◦No susceptibility assessment and modification
◦Restoration of function and/or relief of pain
◦Does not stop disease progression
◦Results in repaired but unhealthy mouth
◦Frequent recurrence and often replacement, eventually lose teeth
* OUTDATED
71
How we are currently managing caries:
* Medical Model
(7)
◦We’re treating an infectious disease
◦Diagnosis of a disease
◦Risk assessment and modification
◦Disease control and prevention of the disease and absence of disease occurrence
◦Stop disease progression
◦Results in a managed and healthy mouth
◦Prevention of recurrence and minimal replacement, save teeth for life
72
CARIES MANAGEMENT-Risk Assessment
* Low Risk
(2)
no disease indicators, <2 risk factors, has
protective factors
73
CARIES MANAGEMENT-Risk Assessment
* Moderate Risk
(2)
no disease indicators, > 2 risk factors (but no
caries)
74
CARIES MANAGEMENT-Risk Assessment
* High Risk
(2)
Cavitated lesions/disease indicators OR >3 risk
factors
75
* What is the single best risk predictor for dental caries?
* Other significant factors:
(7)
A: Current caries
*Parent and siblings with caries
*Extensive restorative work
*Orthodontic appliances
*Multiple medications
*Recession
* Nutritional habits
*Poor OH
76
CARIES MANAGEMENT-Low Risk Patients
(3)
* Toothpaste 2x day (F 1000ppm)
* Sealants for all Molars
* Age-related Oral Hygiene Education
◦Between meal snacks
◦Acidic or sugary drinks, like sports drinks
77
CARIES MANAGEMENT-Medium Risk Patients
* All of the previous AND:
(3)
* Add interventions based on patient need. For example,
◦OTC Fluoride rinse (ACT or Fluorigard); must rinse for 1 minute!
◦F varnish @ 6 months
78
CARIES MANAGEMENT-High Risk Patients
* All of the previous AND:
◦Surgical treatment of caries
◦Professional Fluoride varnish at recall appointments/ 3 month intervals
◦Prescribe Fluoride toothpaste
◦Dispense: Prevident5000 (1.1% NaF) Sig: Brush with small amount for 2 minutes before bedtime,
expectorate excess DO NOT RINSE
◦Nutrition Counseling
◦Xylitol chewing gum
◦2 pieces for 30 minutes 3-5 times per day
79
CARIES MANAGEMENT
* Newer player:
* Resin Infiltration (Icon®)
Use etch to “chemically drill”
◦15% hydrochloric acid gel
◦etch for 2 minutes
◦up to three times
Infiltrate with Icon® resin
Indicated for Smooth surface lesions
◦very good for small white spot lesions after ortho treatment
80
CARIES MANAGEMENT
* Develop YOUR philosophy
◦WHEN to restore
◦Not every stick needs to be restored
◦May be stain, may be narrow fissure
◦Is treatment worse than the problem?
◦Use common sense and ethical standars
◦YOU ARE NOT A SALESPERSON, YOU ARE A HEALTH CARE PROVIDER
81
CARIES MANAGEMENT
* Is there cavitation?
(2)
* Is dentin involved?
(2)
* Is enamel involved?
(2)
◦No= don’t need to drill
◦Manage non-surgically
◦Usually needs restoration
◦Unless worn dentin
◦May be able to do enameloplasty and seal
◦Or manage non-surgically if it has not extended into dentin
82
CARIES MANAGEMENT
*Manage surgically◦YOU KNOW HOW TO DO THIS STUFF!
(3)
◦THIS IS THE BULK OF WHAT YOU’VE BEEN LEARNING IN OPERATIVE
◦No further slides on this matter!
83
CARIES MANAGEMENT
* Manage non-surgically
◦Education
◦Oral hygiene instructions
AND
◦Nutrition counseling
◦Remineralization
◦Fluoride
◦Varnish, prescription toothpaste, OTC rinses
84
CARIES MANAGEMENT
*PATIENT EDUCATION IS ---
TREATMENT
* Insurance codes
D1310 nutritional counseling
D1320 tobacco counseling
85
CARIES MANAGEMENT
*Conservative
(3)
◦Sealant
◦Enameloplasty and seal
◦Preventative Resin Restoration
86
Sealant procedure side-track
(6)
* Pumice tooth
* May or may not enameloplasty
* Etch
◦Rinse and dry
* Place sealant
◦Light cure
* Check for voids, check occlusion
◦Adjust if necessary
* Suction is OFF (or it would
suction the sealant material)
87
What is PRR side-track
* PRR= Preventative Resin Restoration
* One tiny step beyond a sealant
May even PRR small area (pit) and seal the remaining occlusal surface
* The carious lesion has STARTED but not progressed into dentin
or so we think...
88
REMINERALIZATION
* --- surfaces respond best to remineralization
(3)
Smooth
◦Root surfaces are second, followed by proximal surfaces
◦Early lesions have best results
◦Silver diamine fluoride being used more
89
* The body is ideally doing this naturally, we can offer suggestions to improve:
(3)
Fluoride- varnish, rinse, or toothpaste
Reduced sugar (ESPECIALLY DRINKS)
Oral hygiene instructions
90
REMINERALIZATION
* Types of fluoride
(5)
◦0.05% NaFmouthrinse
◦8% Stannous Fluoride
◦1.23% acidulated fluoride
◦5% fluoride varnish
* ◦1.1% NaF toothpaste
91
◦8% Stannous Fluoride
◦stains
92
◦1.23% acidulated fluoride
◦Used in trays
93
◦5% fluoride varnish
◦Painted on teeth at dental office
94
REMINERALIZATION
* Indications for self-applied fluoride:
(6)
*High caries risk
*Rampant enamel or root caries
*Xerostomia
*Exposure to radiation therapy
*Root surface sensitivity
*Orthodontic bands or bonded appliances
95
EMINERALIZATION
* Self Applied Fluoride methods:
Custom tray
Tooth brushing
◦Regular toothpaste
◦Prescription toothpaste
◦Spit only, do not rinse after brushing
Rinses
◦Contraindicated for children under 6 years of age
Fluoride gels
◦Use after normal tooth brushing and flossing
◦Brush for 1 minute with gel
96
REMINERALIZATION
* Silver diamine fluoride
* Contraindications:
(3)
Patient desires esthetic treatment in the area
Silver Allergy
Ulcerative gingivitis, stomatitis
97
REMINERALIZATION
* SDF Application:
(3)
Isolate tooth well, apply petroleum jelly to lips/face of child
Apply SDF liquid to dry tooth for one minute
◦Gently rinse and remove isolation
98
* SDF WILL CAUSE
AREAS TO TURN BROWN
◦They will be hard
◦SDF will also stain fabric, etc. (i.e.your patient’s favorite
shirt)
99
REMINERALIZATION
* Xylitol Gum
(4)
Non-cariogenic
Antibacterial
Enhances remineralization
Patient must chew 3-5 times/day
100
IN CONCLUSION
Dental Caries
* Still a high prevalence
* Most common chronic ---
* By age 17, ---% of people have had a carious lesion
* Fewer than ---% of adults are caries-free
* Elderly patients experience substantially more --- caries
* ---% of the population bears 75% of the caries burden
disease of childhood
89
5
root
10-20
