Dental Caries Introduction

Two Diseases in Dentistry

Caries - non-communicable

Periodontal

Caries Form With

Microorganisms

Host and teeth

Time

Substrate

Dental Caries

Localized destruction of susceptible dental hard tissue by acidic by products from bacterial fermentation of dietary carbs

Disease can be arrested at any time

Dental Caries Formation

Bacterial driven, chronic, site-specific, multifactorial disease process

Results from the imbalance in the physiologic equilibrium between the tooth mineral and the plaque fluid

pH drops results in net mineral loss over time

Enamel Critical pH

5.5

Below Critical pH

Demineralization

Mineral loss

Above Critical pH

Remineralization

Mineral gain

Dentin Critical pH

6.2

Dentin pH

Closer to neutral

More susceptible to dissolution as the pH drops in an acid challenge

Demineralization

Ingest fermentable carbs causing cariogenic bacteria to breakdown and form acid

Acid lowers pH of bioofilm below 5.5

H+ protonates hydroxyl group of hydroxyapatite crystals

Mineral leaves enamel causing pores

Active White Spot Lesion

Ongoing demineralization with loss of CaHPO- from H+

Crystals lost superficially causing rough and large pores

Chalky white opaque

Arrested White Spot Lesion

Demineralization has stopped

Shiny smooth small pores

Remineralization

Begins with demineralized enamel with pH lower than 5.5

Carbs removed causing pH to increase through saliva (around 7)

Demineralization stops allowing for minerals to be added to crystals - calcium and phosphate

Move into porous enamel - usually begins superficial

Allows for hydroxyapatite to be replaced with fluorapatite

Biofilm

Diverse community of microorganisms found on the tooth surface

Express properties which are not exhibited by the same organisms in individual culture

Properties are more than the sum of their parts

Pellicle

Bacteria free, organic layer between enamel and biofilm

Derived from saliva, gingival crevicular fluid, and bacteria

High affinity for enamel

Absorbs within seconds to clean enamel/newly erupting tooth

Layers

Enamel

Pellicle

Biofilm

Removing Pellicle

Trophy cups

Acid etch

Toothbrushing using SLS toothpaste

Bacteria with Pellicle

Adhere, colonize, and multiply

Biofilm formation

Biofilm Formation

Attachment

Growth

Removal

Reattachment

Cariogenic Features of Biofilm

Ability to rapidly transport fermentable sugars

Conversion os sugars to acid via glycolysis

Ability to maintain sugar metabolism under extreme conditions - low pH

Production of EPS and IPS

Transporting Fermentable Sugars

Multiple transport systems

Scavenge sugars even in low concentrations

EPS

Glucans and fructans (contribute to biofilm matrix)

Concentrate acids in regions of biofilm

IPS

Glycogen like storage compounds that are used for energy production and converted to acid when sugar is not available

Metabolism of this prolongs the period over which biofilm can generate acids

Specific Plaque Hypothesis

Single or small number of species cause disease

Non-Specific Plaque Hypothesis

Disease is the outcome of the overall activity of the total plaque microflora

Ecological Plaque Hypothesis

Disease is the result of a shift in the balance of the resident microflora driven by a change in the local environment - diet and chemistry of enamel

Repeated conditions of low pH in plaque following frequent sugar intake (or decreased sugar clearance following salivary secretion) will favor the growth of acidogenic and aciduric species

Repeated low pH

In plaque following frequent sugar intake (or decreased sugar clearance following salivary secretion) will favor the growth of acidogenic and aciduric species

Acidogenic Bacteria

Other than S. Mutans can make a significant contribution to the strength of the cariogenic challenge at a site

Disease Organisms

May be present at sound sites but at levels to low to be clinically relevant

S. Mutans

When found in high numbers in plaque may be an absence of demineralization

S. Mutans Absence

Structure of the biofilm/location of the bacteria in the biofilm

Presence of lactate consuming species (Veillonella)

Production of alkali to raise the pH - ammonia production of S. Salivarius from urea)

Caries Reversible Stages

Dynamic stability stage

Acidogenic stage

Aciduric stage

Events can be reversed at any stage by normalization of the acidic environment via sugar restriction/substitution

Dynamic Stability Stage

Bacteria produce acid by sugar fermentation during meals

Homeostasis is maintained because the acids are rapidly neutralized by saliva and microbial production of alkali

Balance of demineralization and remineralization - no mineral loss

Acidogenic Stage

Acid-induced adaptation of microbes increases their acidogenicity

Environment is acidified

Balance favors demineralization - low pH strains

Dynamic Stability Stage Bacteria

S. mitis

Actinomyces

Acidogenic Bacteria

Low pH strains of non-mutans strep and Actinomyces

Aciduric Stage

Acid-induced adaption of microbes selects for more bacteria that survives in such conditions

Environment experiences severe and prolonged acidification

Accelerates progression of caries

Aciduric Stage Bacteria

S. mutans

Lactobacilli

bifidobacterium

Control of Disease

Target pathogens (S. mutans and other acidogenic/aciduric species) through interference with the factors that drive the deleterious shifts in the balance of the microflora

Glycolysis

Glucose broken down into lactate

Lactic Acid

Causes demineralization of the tooth and caries formation

Fermentable Carbs

Sugars - monosaccharides, disaccharide, sucrose

Starches

High fructose corn syrup

Processed and convenience foods

Monosaccharides

Glucose

Fructose

Galactose

Rhamose

Xylose

Disaccharides

Sucrose

Maltose

Lactose

Starches

Not direct substrates for fermentation but they are hydrolyzed to maltose, isomaltose, and glucose in the mouth

Salivary and bacterial amylase

Cariogenic Sweeteners

Mono and disaccharides

High fructose corn syrup

Starches

Plaque Accumulation

1 week - dissolution of outer surface (20-100 um)

• lesion is not visible

2 Weeks - Whitish, opaque, subsurface lesion

• White spot lesion visible with air drying

3-4 Weeks - chalky, rough surface, opaque

• Marked dissolution of mineral

• White spot lesion visible without air-drying

1 Week of Plaque Accumulation

Dissolution of outer surface (20-100 um)

• lesion is not visible

2 Weeks of Plaque Accumulation

Whitish, opaque, subsurface lesion

• White spot lesion visible with air drying

3 Weekw of Plaque Accumulation

Chalky, rough surface, opaque

• Marked dissolution of mineral

• White spot lesion visible without air-drying

Proper Plaque Removal

1 Week - reduced chalkiness

2-3 Weeks - hard and shiny

Protective Factors of Caries

Saliva

Fluoride

Antibacterials

Risk Factors of Caries

Acidogenic bacteria

Frequent carbs

Sub-normal saliva

Other Conditions in Loss of Tooth Structure

Erosion

Abrasion

Demastication

Attrition

Abfarciton

Fluorosis

Erosion

Loss of tooth structure from chemical wear

Caused by extrinsic or intrinsic acids acting on plaque free tooth surfaces

Loss of surface structure, cupping on occlusal surfaces, shallow concavities coronal form the CEJ

Abfarction

Loss of tooth structure from physical and fatigue wear

Abrasion and eriosion

Caused by tensile or shear stress in the CEJ provoking micro-fractures in enamel and dentin

Wedge shaped defects

Attrition

Loss of tooth structure from physical and two body wear

Caused by action of antagonist teeth

Antagonist plane facets with sharp margins

Abrasion

Loss of tooth structure from physical and three body wear (external)

Caused by oral hygiene procedures,, habits, and exposure to abrasive particles

Depends on the surface and agent

Dental Erosion

Physical result of a pathologic, chronic, localized, loss of dental hard tissue chemically etched away from the tooth surface by acid and or chelation without bacterial involvement

Intrinsic Acids

Stomach acid

GERD

Bulimia

Pregnancy

Extrinsic Acids

Foods and drinks

Citrus fruits and juice

Soda, kombucha

Erosion with pH

Critical pH is not defined

Depends more on concentration of caclium and phosphorus ions

Features of Erosion

Concavities

Loss of occlusal anatomy

Rounded cusps and grooves

Silky-glazed appearance on surface

Restorations rising above the level of adjacent tooth structure

Lifestlye Erosion

Use of alcohol and drugs

Occupation - wine tasters, chemical industry, service industry

Health conscious - athletes (sports), dietary (kombucha)

Fluorosis

Can occur in primary and permanent teeth

Caused by excessive fluoride ingestion during tooth development

Intrinsic, permanent stain, usually white, but can be dark brown or orange

Enamel can be damaged in severe case

Low fluoride - still can be found

Secondary Recurrent Caries

Caries adjacent to restorations or sealants (CARS)

Residual Caries

Carious lesion left in cavity preparation

Either by oversight or purposely

Incipient Caries

May be white spot or brown spot

Contained within enamel

Classification by Severity

Incipient caries

Moderate caries

Severe caries

Classification by Activity

Arrested/inactive

Active (progressive)

In transition (continuum)

Active Lesion

Dull and chalky

May or may not be cavitated

Greater likelihood of transition (progress, arrest or regress)

Arrested Lesions

Dry and shiny

Not cavitated

Less likelihood of transition

Active Lesions

Greater likelihood of transition (progress, arrest or regress)

Caries Activity Evaluation Process

Consider of the lesion is in a plaque stagnation area

Consider visual appearance

Consider gentle tactile feeling - bal ended probe

Do not press hard with sharp tip or explorer

Caries Activity

If more predicators indicating activity than predicators indicating inactivity, then the lesion is active

Vise verse

ICDAS

Visual criteria of caries detection/assessment reflecting current scientific understanding of carious processes

ICDAS Exam Protocol

Ask patient to remove any appliances

Clean teeth of all plaque

Place cotton in buccal vestibules

Remove excess saliva

Visual examination of the surface wet

Dry the surface for 5 seconds

Visual inspection of the dry surface

Dry Examination

When tooth is wet, similar refractive index to enamel

Air replaces water

Air has lower refractive index than water, thus lesions are more visible

Caries Score 0

Sound enamel

No evidence of caries with no change after air-drying for 5 seconds

Includes - enamel hypoplasia, fluorosis, tooth wear, stains

Caries Score 1

Smooth surface - nothing seen on wet tooth

Lesion visible after 5s of air-drying

Extent - lesion contained to pit and fissure

Opaque, white or brown

Caries Score 2

Smooth surface - lesion seen when both wet and dry

Extent - lesion extended beyond pit and fissures

Caries Score 3

Localized enamel breakdown due to caries with no visible dentin

When wet - may see darkening of dentin visible through enamel

5s of air drying - carious loss of tooth structure at entrance to or within pit/fissure

Extent - pit/fissure may appear wider, but dentin is not visible in the walls or base of cavity/discontinuity

Caries Score 4

Non-cavitated surfaced with underlying dark shadow from dentin

Shadow of discolored dentin through apparently intact enamel surface

Darkened area is an intrinsic shadow which may appear as grey, blue, or brown color

Caries Score 5

Frank cavitation

Distinct cavity with visible dentin

Cavitation in opaque or discolored enamel which exposes dentin beneath

Histologically - lesion extends from pit and fissure to middle 1/3 of dentin

Caries Score 6

Extensive distinct cavity with visible dentin

Obvious loss of tooth structure - involves at least half of tooth surfaces

Possibly reaches pulp

Extent - cavity both deep and wide, with dentin clearly visible on walls and base

Caries in Radiograph

Smaller than it is clinically

Incipient Lesion Treatment

Treat non-surgically regardless of caries risk

Remineralize with fluoride, MI paste, follow up

Treatment without handpiece

Moderate Lesion Treatment

Surgical

Cut tooth to remove disease then restore

Future of Dentsitry

Respecting health, function, and esthetics of oral tissue by preventing disease from occurring or intercepting its progress with minimal tooth loss

Treat the cause of disease - not the symptoms

Non-Surgical Treatment

Remineralization

Reduction in cariogenic bacteria

Surgical Treatment

Minimally invasive cavity preparation

Approapriate restorative material selection