Unit 1 Flashcards
(113 cards)
1
Q
What is a Dental Carie?
A
Multifactoral, transmissible, infectious oral disease. Caused by biofilm(flora) + fermentable carbohydrates.
2
Q
What 3 things are needed for caries pathogenesis (traditional)
A
1) Tooth Structure
2) Bacteria
3) Carbohydrates
3
Q
Primary modifying factor for caries (8)
A
1) Tooth anatomy
2) Saliva
3) biofilm pH
4) Use of fluoride
5) Diet
6) oral hygiene
7) Immune system
8) Genetic factors
4
Q
Secondary modifying factors for caries (7)
A
1) socioeconomic
2) Education
3) Lifestyle
4) Environment
5) Age
6) Ethnic
7) Occupation
5
Q
Caries on what 2 surfaces would indicate rampant caries throughout the mouth
A
Occlusal
Interproximal smooth surface
6
Q
How does bacteria demineralize tooth structure?
A
Metabolize carbohydrates–> produce organic acid by products–>lower biofilm pH–>calcium and phosphate leave tooth
7
Q
How does remineralization occur?
A
1) When pH in biofilm returns to neutral,
2) concentration of calcium and phosphate is supersaturated (relative to tooth)
–> Then mineral can be added back
8
Q
Pathological Factors
A
Acid producing bacteria
Subnormal saliva flow/function
Frequent eating/drinking fermentable carbs
Poor hygiene
9
Q
Protective Factors
A
Saliva flow components
Remineralization (F, Ca, Phosphate)
Antibacterial (fluroide, chlorhexidine, xylitol)
Good oral hygiene
10
Q
Ecological Plaque Hypothesis
A
PH effects both dominance and how the flora acts
11
Q
3 Critical pH levels
A
Enamel 5.5
Dentin 6.2
Hydroxyfluroapitite 4.5
12
Q
Carie therapeutic treatment
A
Biofilm control
Elevating biofilm pH
Enhancing remineralization
13
Q
Caries lesion
A
Tooth demineralization as a result of the caries process
14
Q
Smooth surface caries
A
A caries lesion on a smooth tooth surface
15
Q
Pit and fissure caries
A
Lesion on a pit or fissure
16
Q
Enamel caries
A
A lesion in enamel typically indicative that the lesion has not penetrated dentin
17
Q
Coronal caries
A
A lesion in any surface of the anatomical tooth crown
18
Q
Root caries
A
Lesion on root surface
19
Q
Primary caries
A
A caries lesion not adjacent to an existing restoration or crown
20
Q
Secondary caries
A
A caries lesion adjacent to an existing restoration crown or sealant
CARS caries adjacent to restoration or sealant
21
Q
Residual caries
A
Refers to various tissue that was not completely excavated prior to restoration. Difficult to differentiate from secondary caries
22
Q
Cavitation caries lesion
A
A caries lesion that results in the breaking of the integrity of the tooth or cavitation
23
Q
Noncavitated caries lesion
A
A caries lesion that has not been cavitated. In enamel referred to as white spots. Blunt prope must be able to enter but usually sharp explorer finds roughness
24
Q
Active caries lesion
A
A caries lesion that is considered to be biologically active at time of examination
25
Rampant Caries
Presence of extensive and multiple cavitated and active caries lesions in the same person. Meth mouth radiation therapy caries baby bottle caries
26
Dental Plaque
Soft film accumulating on the surface of teeth-->biofilm
Composed of bacteria, by products, ECM, Water
27
No pathogenic bacterial plaque
Pellicle composed of salivary proteins and free cells. Protects, reduces friction, remineralization
28
Mucosa flora
S. mitis
S sanguis
S salviarius
Aerobic
PH 7
Oxidative reduction is positive
29
Tongue Flora
S salviarisu
S mutans
S sanguis
Aerobic
PH 7
Oxidation reduction positive
30
Teeth Flora (non carious)
S Sanguis
Ph 5.5
Aerobic
Oxidative reduction negative
31
Gingival Crevice Flora
Fusobacterium
Spirochatea
Actnomyces
Veillonella
Anaerobic
Variable pH
Very Negative Oxidation reduction
32
Enamel Caries
S mutans
An aerobic
PH less than 5.5
Negative
33
Dentin Caries
S mutans
Lactobacillus
PH less than 5.5
An aerobic
Oxidation negative
34
Root Caries flora
Actinomyces
Anaerobic
PH less than 5.5
Oxidation reduction
35
Caries originating on root are alarming (4)
Rapid progression
A symptomatic
Closer to pulp
Difficult to restore
36
Saliva Enzymes
Amylase
Lactoperoxidase
Lysozyme
Lipases
37
Non Enzyme Proteins Of Saliva
Lactoferrin
Secretory immunoglobulin
Glycoproteins
38
When enamel caries penetrates to the DEJ....
Rapid lateral expansion of the caries lesion occurs because dentin is much less resistant to acid demineralization
39
3 Distinctly different clinical sites for caries initiation
Pits and fissures
Smooth enamel surfaces
Root surface
40
Pits and Fissures Caries
Bacteria: MS usually found in carious pits and fissures
Physical Properties: narrow fissure prevents biofilm removal
Difficulty: appear smaller than the actual lesion. Inverted v appearance. Covers more surface area than smooth
41
Smooth Enamel Surface Caries
Less favorable
Usually under sites of contact
Board area of origin. Pointed or conical extension towards DEJ. Parallel to enamel rods
42
Root Surface Caries
Roots surface much rougher than enamel
Increasing prevalence because older are retaining more teeth
43
Progression of Carie Lesions
Caries development in healthy individuals is usually slow compared to compromised persons
18 +/- 6months from noncavitated to clinical caries
- occlusal less time than smooth surface
- 3 weeks with poor hygiene acidic food and sucrose
- 3 months from onset of dry mouth
44
Hypocalcified Enamel
Developmental white spot
Same WET OR DRY
Do no restore!
45
White Spot Lesion (noncavitated enamel caries)
- Disapears when wet
- Do not restore
- Noncavitated can remineralize
- chalky white hard external surface
46
Cavitated Enamel Lesions (Active Caries)
- Surface is disturbed or missing
- Soft, chalky surface
- Into dentin
- Can not remiineralize must be restored
47
Remineralized Enamel Lesion (Inactive Caries)
- Should not be restored
- Intact but discolored usually brown or black.
- Supersaturation of saliva with calcium and phosphate ions Is the driving force
48
Every time a tooth remineralizes...
It becomes a little more resistant to decay
49
Normal Enamel
Hydrated: translucent
Desiccated: Translucent
Surface Texture: Smooth
Surface Hardness: Hard
50
Hypocalcified Enamel
Hydrated:Translucent
Desiccated:Opaque
Surface Texture:Smooth
Surface Hardness:Hard
51
Noncavitated Caries
Hydrated:Translucent
Desiccated:Opaque
Surface Texture:Smooth
Surface Hardness:Softened
52
Active Caries
Hydrated: Opaque
Desiccated: Opaque
Surface Texture: cavitated
Surface Hardness: Very soft
53
Inactive Caries
Hydrated: Opaque dark
Desiccated: opaque dark
Surface Texture: roughened
Surface Hardness: hard
54
Normal Enamel (clinical significance)
Plaque: Normal
Enamel Structure: normal
Therapeutic Treatment: NA
Restorative: NA
55
Hypocalcified Enamel (Clinical sig)
Plaque: Normal
Enamel Structure: abnormal not weakened
Therapeutic Treatment: NA
Restorative: Only for aesthetic
56
Noncavitated Caries (clinical sig)
Plaque: Cariogenic
Enamel Structure: pours weakened
Therapeutic Treatment: Yes
Restorative: NA
57
Active Caries (clinical sig)
Plaque: Cariogenic
Enamel Structure: Cavitated very weak
Therapeutic Treatment: Yes
Restorative: Yes
58
Inactive Caries (clinical sig)
Plaque: Normal
Enamel Structure: Remineralized very strong
Therapeutic Treatment: NA
Restorative: Only for esthetic
59
Dentin Composition
50% HA (75% wt)
25% Collagen (20% wt)
25% water (5% wt)
60
Reaction to long term low level acid
Repair demineralize dentin by remineralization
Direct exposure of pulp tissue to micro organisms is not a prerequisite for inflammatory response
Hypermineralized areas may be seen
61
Moderate intensity attack
Bacterial invasion of dentin
Can cause degeneration and death of odontoblasts; information of pulp
Cause formation of secondary odontoblasts(mesenchyme derived)
62
Severa advancing caries
High levels of acid production
Abscesses
Death of pulp due to impaired blood supply
63
Zones of Dentin Caries
1) weak organiz acids demineralize dentin
2) The organic material of dentin practically collagen degenerated and dissolves
3) the loss of structural integrity Is followed by invasion of bacteria
64
3 Zones of dentin caries
Zone 1: Normal
Zone 2: Affected Dentin
Zone 3: Infected Dentin
65
Zone 1: Normal Dentin
Deepest area is normal dentin
Has tubules with odontoblasts processes smooth and no crystals
Intertubular denint has normal cross banded collagen
66
Zone 2: Affected Dentin
-Inner carious dentin
Zone of demineralization of interubular dental
Initial formation of fine crystals in the tubules lumen at the advancing front
Odontbalsitc procees damage evident
Painful when stimulated
Uninflected
1)Subtransparent dentin 2) transparent dentin 3) turbid dentin
67
Zone 3: Infected dentin
"Outer carious dentin"
Layer that the clinician would encounter first when opening Lesion
Bacterial invasion and is marked by widening and distortion of dentin tubules
Non sensitive
68
What is Dentistry?
The Evaluation, diagnosis, prevention, and or treatment of diseases disorordr and conditions of the oral cavity, maxillofacial area and or adjacent structures
69
Composition of Enamel
90-95% HA
4-8% Water
1-2% Protein
70
Enamel Vs. Dentin/pulp Development
Enamel is epithelial origin and the ameloblasts extinct after deposition
Dentin/pulp complex mesenchymal origin but the odontoblasts remain in the pulp
71
Enamel Organization
Interlocking rods with he tails closer to the dentin
The rods are surrounded by organic sheath
Millions of crystallites make up rods. Each crystalline is surrounded by a film or matrix.
- composed of calcium phosphate (Hydroxyapitate)
- Needlike irregular shape
72
Cystyallite Organization
The crystallites themselves are irregular in shape but they are arranged in patterns within a rod.
Body:
-long axis of crystal parrallel to rod direction
Periphery and tail:
-up to 65 degree from pirsim or rod direction
The rods will follow a way spiraling path...very rarely straight
73
Properties of Enamel: Parallel to Rod Direction
Very Hard, brittle, stiff
74
Properties of Enamel: Perpendicular to Rods
Low Tensile strength
75
Isotropic Vs. Anisotropic
ISO: Same in all direction (Isotropic)
Ani: depends on direction (Enamel)
76
Dentin Composition
50% HA
25% Collagen
25% Water
77
Function of the Dentinal Tubule
Allow fluid movement and ion transport
- Remineraliztion
- Apposition of peritubular dentin
- Pain perception
78
Dentin Organization
Dentin is not uniformly organized
Peritubular dentin is more mineralized than intertubular
Less and smaller tubules in roots
79
Dentin Structure
Long rope like protein (organic) adds toughness
HA crystals contained within that collagen
Crystals are smaller than in enamel
80
Properties of Dentin
20% less hard than enamel
Higher tensile strenght and lower stiffness than enamel
Isotropic properties
-Dentin stops the propagation of most cracks in enamel
81
Types of Dentin
```
Primary Dentin
Secondary Dentin
Presenting
Reparative Detnin (tertiary)
Sclerotic Dentin
```
82
Primary Dentin
Forms up to 3 years after tooth eruption
83
Secondary Dentin
Without any obvious stimulus, dentin direction changes and deposition slows
84
How is dentin different from enamel?
```
Less mineral content
Small tubules run throughout
-more fluid and ion transport
Ability to repair or regenerate
-physical chemical response
-cellular response
```
85
4 Functions of Dental Pulp
Formative or developmental
Nutritive
Sensory or protective
Defensive or reparative
86
Dental Pulp:Formative
Production of primary and secondary odontoblasts
87
Pulp: Nutritive
Supplies nutrients and moisture to detnin through the blood vascular supply to odontoblasts and their processes.
88
Pulp: Sensory
Nerve fibers within the pulp--Pain
| ONLY PAIN
89
Pulp: Defensive/Reparative
Deposition of reparative dentin in response to stimuli
| Inflammatory reaction to severe irritation...may result in death of pulp
90
Cementum Composition
5-10% mineral content
45-50% HA by weight
50-55% organic matter and water by weight
91
What Tissue has the highest fluoride content of all mineralized tissue
Cementum
92
Cementum Structure
Hard, avascular dental tissue covering anatomy roots
Formed continuously throughout life: acellular and cellular
Formed by cementoblasts--->from mesenchymal cells in CT of dental follicle
93
CDJ
Attachment of cementum to dentin
94
CEJ
Cervical line
| Cementum joins enamel
95
Cementum Properties
Slightly softer than dentin(less minerals)
Permeable
Can undergo self repair
96
Tooth Centered vs Patient Centered
Tooth centered is surgical intervention to eliminate cavitated lesions
Patient centered is to use a medical model to control the disease process
97
Caries Risk Assessment
Gather data on current and recent dental history
- interview
- conduct test to determine status of saliva, bioload, and any other pertinent data
- Establish a risk level for each patient that indicates their level of risk
- Establish a caries treatment plan or protocol
98
Social, Economic, and Education Status
- Not directly involved in the disease
- Affect the expression and management of the caries disease
- Compliance and behavioral changes
Predictive at the population level but are inaccurate at the individual level
99
Dietary Analysis
- Sugar in the form of fermentable carbohydrates and frequency increase risk
- Candies lozenges increase risk
- Acidic beverages, sport drinks, juice, and soft drinks provide energy to the acidogenic and aciduric bacteria and change biofilm pH
- Snacking frequency lower pH environment
100
Salivary Anaylsis
Flow, rate, buffering capacity, and pH all can be measured by tests
- Predicitve for these tests is not supported in all circumstances
- Patients can still have caries
101
A salivary test in cases of xersotomia is predictive of risk for what
- Root caries in older patients with recession
| - For increased caries in the general population
102
Effects of saliva
```
Inhibition of bacteria and substrates
Diluting
Elimination
Buffer bacterial acids
Offering a reparative environment with necessary ca and phosphate
```
103
Patients with dry mouth are at higher risk why?
Saliva effects are diminished and therefore the fermentable carbs, low pH food and beverages have more effect
104
Dental Clinical Analysis to determine risk factors
Current caries
White spots
Brown Spots
Visible plaque
Exposed root surfaces
Deep Pits, grooves, fixed, removable prosthesis/orthodox
Poor restorations-with open contacts, markings, or overhangs
105
Risk considerations for children under 6
Age specific
- active caries in primary caregiver
- bedtime bottle or snippy cup
- no supervised brushing
- severe enamel hypoplasia
106
In a modern practice model
The restoration of a caries lesion should no longer be considered a cure dental caries. Rather, the practioner must identify patients who have active caries lesions and patients at high risk for caries and institute appropriate preventive and treatment measures
107
Caries Management
1) Limiting pathogen growth and altering metabolism
2) Increasing the resistance of the tooth surface to demineralization
3) Incresasing biofilm pH
108
Primary goal of caries prevention program
Redeuce the number of cariogenic bacteria and create an environment conducive to remineralization
109
Factors Influencing Caries Risk
```
General health
Diet
Oral Hygeine
Fluoride Exposure
Immunization
Function of Saliva
Antimicrobial agents
Calcium and Phospahte Compounds
Probiotics
Sealants
Restorations
```
110
Caries Control Restorations
Removing the infected tooth structure
Medicating the pulp
Restoring the defects
111
Large Carious lesions with healthy pulp a and periodical tissues should
Be managed via partial caries excavation and indirect pulp capping
112
4 Strategies for prevention of root caries
1) Improve salivary flow rates and increase buffering capacity
2) Reduce numbers of cariogenic bacteria (s. Mutans)
3) Reduce quantity and numbers of exposures of carbohydrates
4) Attempt to remineralizes
113
How to restore root caries
With a fluoride-releasing material
Resin modified glass ionomer materials are preferred for definitive restorations primarily because they bone effectively to both enamel and dentin.They act as reservoirs for fluoride which can be re-released into mouth
