Caries pt. 2

CEU MALOLOS DENT

Caries primary modifying factors

1. Tooth anatomy
2. Saliva
3. Biofilm pH
4. Use of fluoride
5. Diet specifics
6. Oral hygiene
7. Immune system
8. Genetic factors

Caries Secondary modifying factors

1. Socioeconomic status
2. Education
3. Life-style
4. Environment
5. Age
6. Ethnic group
7. Occupation

Dental Plaque

gelatinous mass of bacteria adhering to the tooth surface that metabolize refined carbohydrates for energy and produce organic acids as by-product.

Dental plaque exacerbation

Availability of simple carbs/sucrose which has high bacterial metabolic activity-\> low pH(acidic) -\> dissolution of crystalline structure

Dental plaque remission

Few carbohydrates\= little bacterial metabolic activity\= increase pH

What pH causes remineralization?

\>5.5

In what range of pH does demineralization(of enamel) occurs?

5.0-5.5

What may be the most important factor in producing cariogenic plaque?

High freq. sucrose exposure

Caries balance

balance between demineralization and remineralization is illustrated in terms of pathologic factors and protective factors

Pathologic factors

Acid-producing bacteria
Frequent eating/drinking of fermentable carbohydrates
Subnormal salivary flow and function
Poor oral hygiene

protective factors

Saliva flow and components
Remineralization(fluoride, calcium, phosphate)
Antibacterials (fluoride, Chlorhexidine, xylitol)
Good oral hygiene

Cariogenic

Organisms that cause caries

Cariogenecity potential

degree to which a tooth is likely to become carious

Which microorganism is more strongly associated with the ONSET of caries?

MS

Which microorganism are associated with active progression of cavitated lesions?

Lactobacilli

epidemiologic study

determines the extent of the need for and effectiveness of dental treatment

Prevalence

number of individuals in a population having a disease at a specific point in time

Incidence

number of individuals developing new cases of disease over a specific period usually 1 year

most common epidemiologic measure of caries

DMF
*important in making decisions concerning changes in caries in populations.

DMF

decayed, missing, filled
*dmf-for deciduous teeth

nonspecific plaque hypothesis

all plaque is pathogenic
goal: total plaque elimination(not possible)

specific plaque hypothesis

plaque is pathogenic only when signs of associated disease are present
-aimed at the elimination of the specific plaque pathogenic organisms

Pathogenic bacterial plaque progression

1. SM adhere to mucosa, teeth structure
2. SM prod. sticky matrix(which helps it adhere to each other, colonize tooth)
3. Proliferate and spread laterally(forming mat-like covering)
4. Vertical growth away from tooth surface
5. Allows adherence of other organisms (filamentous & spiral bacteria)
5. Mature plaque is formed

Predominant species in the MUCOSA

S. mitis
S. sanguis
S. salivarius

Predominant species in TONGUE

S. salivarius
S. mutans
S. sanguis

Predominant species in Non carious Teeth

S. sanguis

Predominant species in Gingival crevice

Fusobacterium species
Spirochaeta species
Actinomyces species
Veillonella species

Predominant species in Enamel Caries

S. mutans
*anaerobic

Predominant species in dentinal caries

S. mutans
Lactobacillus species
*pH

Predominant species in root caries

Actinomyces species

To reduce/ prevent plaque accumulation:

1. Restore cavitated carious lesions
2. Obturation of anatomic faults(P&F)-reduces number of MS
3. Correct tooth malalignment-contributes to overall oral health

Plaque succession

1. 2 hrs after oral prophylaxis, pellicle covers the tooth
2. Adhesion between pellicle and pioneering organisms
3. Maturation of plaque slows down cell & matrix prod., uses energy for total community metabolism-\> acid prod.
4. Rapid drop in pH\=increased chance for demineralization

Pellicle function

1. Protect enamel
2. Reduce friction between teeth
3. Provide matrix for remineralization

What pH does dentin demineralization happen?

Saliva

primary means by which the patient. exerts control over its oral flora

Protective mechanism of saliva:

1. Bacterial clearance
2. Direct antibacterial activity
3. Buffers
4. Remineralization

Bacterial clearance

lubricates oral tissues, bathes teeth & plaque flushing avray virtually all microorganisms not adherent to the oral surface.

Direct Antibacterial Activity

salivary glands produce antimicrobial products(lysozome, lactoperoxidase, lactoferrin and agglutinins)
*little effect on caries

Is caries susceptibility in healthy individuals is related to saliva composition?

No, its more related to decrease in salivary production

Buffer(Saliva)

volume & buffering capacity have major roles in caries protection bcs of Buffering Capacity

buffering capacity of saliva

Conc. Of bicarbonate ion(reduces potential for acid formation)
Sialin and urea, when hydrolized forms ammonia(increasing plaque pH)

Remineralization(Saliva)

calcium & phosphate ions in saliva is stabilized by statherine- a proline-rich peptide preventing excessive deposition of these fons on the teeth. Presence of these ions help remineralize enamel protecting it from caries attack.

After cavitation, remineralized portion becomes?

harder often dark brown or black in color(arrested caries)

Before cavitation, remineralized tooth surface may show carious episode by the presence of?

Brownish discoloration

Eburnated dentin

Arrested caries in dentin

Tooth habitats for pathogenic plaque

Pit & fissure, smooth surface, Root surface,

pit and fissure

highest prevalence of all dental caries
-after appearance of MS in P&F it's followed by caries 6-24 mo later
*PFS after tooth eruption- most important event to resist caries

Smooth enamel surfaces

proximal enamel surfaces immediately gingival to the contact areas are the second most susceptible areas to caries.
*More rigorous oral hygiene practices (e.g. flossing) are required to keep these proximal region free of disease

Presence of caries in what surface usually indicates a caries active mouth?

Smooth enamel surface
*as smooth surfaces are usually self-cleansing so if caries are here, imagine the other non-self cleansing surfaces

Root surfaces

exposed root surfaces is a result of gingival recession and are often unaffected by flossing and usually not rubbed by bolus of food

Caries originating on the root(characteristics)

1.Has a comparatively rapid progression
2.Is often asymptomatic
3.Is closer to the pulp
4. More difficult to restore

Subgingival areas

metabolites from plaque easily penetrate the thin epithelial lining of the sulcus-\> strong inflammatory rxn -\> eventual destruction of gingival epithelium

Pathophysiology of caries

1. Local decrease in pH\=plaque metabolism(high MS and lactobacilli)
2. Exposure to sucrose\=rapid metabolism of organic acid(lactic acid)
3. pH\=

Incipient caries

initial carious lesion limited to enamel surface
When dried\= chalky white
When hydrated\= undetectable
*may be reversed by remineralization; presence of fluoride ion is part of the remineralization process rendering the enamel more resistant to further caries attack.

How does cavitation occur?

subsurface demineralization is so extensive that the surface collapse. It is irreversible.

Pattern of caries attack

Base to base relationship- Pit and fissure caries
Apex to Base - smooth surface

Smooth enamel surface caries progression

broad ares of origin and a conical or pointed extension towards the
DEJ, parallels the long axes of enamel rods. In cross section, it is also V shaped where the apex is directed toward the DEJ.

Dentin pit and fissure, smooth surface caries progresion

caries spread laterally and pulpally.

Root surface caries progression

Less well defined margins
-U-shaped(bcs theres no enamel rods)

Progression of caries in pit and fissures

Initial lesions develop on the lateral walls of the fissure. Demineralization follows the direction of the enamel rods spreading laterally as it approaches the DEJ. In cross section, it appears as an inverted V with narrow entrance and a progressively wider area at the DEJ.

Time of progression, from incipient to cavitated cavity on smooth surfaces

Appr. 18 to more or less 6 mo

zones of incipient lesion

Zone 1: Translucent zone
Zone 2: dark zone
Zone 3: body of lesion
Zone 4: surface zone

zone 1: translucent zone(incipient caries enamel)

-deepest portion
-has pores/voids in enamel rod boundaries
-pore volume of enamel caries:1%(10x greater vs normal enamel)

Zone 2: Dark zone(incipient-enamel)

-named bcs it does not transmit polarized light(bcs of loss of crystalline structure)
-opaque bcs of air-filled/vapor-filled pores

zone 3: body of lesion(incipient- enamel)

-largest portion during demineralization stage
-pore size: 5%(at periphery) up to 25%(center)
-bacteria may be present if pores are large enough

Zone 4: surface zone(incipient enamel)

-unaffected by caries
-lower pore vol(

Zones of dentinal caries

Zone 1: normal dentin
Zone 2: subtransparent dentin
Zone 3: transparent dentin
Zone 4: turbid dentin
Zone 5: infected dentin

Zone 1:normal dentin

Deepest area
-smooth odontoblastic process(no crystals in lumen)
-no bacteria
- sharp pain in stimulation

zone 2: subtransparent dentin

-zone of demineralization of intertubular dentin
-crystals in lumen
-no bacteria
-stimulation\=pain
-can be remineralized

zone 3: transparent dentin

-zone of carious dentin
-softer vs normal dentin
-loss of mineral in intertubular dentin, many large crystals in lumen
-pain on stimulation
-no bacteria
-can self-repair(if pulp is vital)

Zone 4: turbid dentin

-zone of bacterial invasion
-wide and distorted dentinal tubules with bacteria
-little mineral, collagen denatured
-does not repair itself, cannot remineralized; must be removed before restoration

Zone 5: Infected Dentin

-outermost zone
-decomposed dentin with bacteria
-no recognizable structure
-removal is essential for a successful restorative procedure and prevention of spread of infection.

Affected dentin

Zone 2 and 3
-softened, demineralized dentin not yet invaded by bacteria

Infected dentin

Zones 4 and 5
Softened and contaminated by bacteria
-includes: superficial, granular necrotic tissue, and softened dry leathery dentin

Indirect pulp capping

placement of a thin laver of calcium hydroxide on the questionable dentin remaining over the
pulp.

direct pulp capping

placement of calcium hydroxide directly on exposed pulpal tissue (a pulpal exposure) and the surrounding deeply excavated dentinal area.

patient is at high risk for the development of new cavitated lesions if:

1. High MS counts are found.
2. Any two of the following factors are present:
• Two or more active carious lesions
• Numerous restorations
• Poor dietary habits
• Low salivary flow

Bacteriologic testing for MS should be done if:

• Patient has one or more medical health history risk factors
• Patient has undergone antimicrobial therapy
• Patient presents with new incipient lesions
• Patient is undergoing orthodontic care
• Patient's treatment plan calls for extensive restorative dental work

Proximal Caries Treatment Decision Making(Posterior)

If non-cavitated-\> no progression -\> no treatment
If non-cavitated-\> likely progression -\> antimicrobial, fluoride

If cavitated-\> restoration and antimicrobial, F

Non cavitated(Proximal surface)

-surface intact(use explorer w/ caution)
-opacity of proximal enamel may be present/seen with transillumination
-radiolucency may be present
-marginal ridge not discolored

Cavitated(proximal surfaces)

-surface broken, detectable visually/tactilely
-marginal ridge may be discolored
-opaque area on dentin on transillumination
-radiolucency is present

Pit and fissures Caries Treatment Decision Making(Posterior)

If non-cavitated-\> no progression -\> no treatment
If non-cavitated-\> likely progression -\> sealant, antimicrobial, fluoride

If cavitated-\> restoration and antimicrobial, F

Noncavitated (caries-free) P&F

• No radiolucency below the occlusal enamel
• Deep grooves may be present
• Superficial staining may be present in grooves
• Mechanical binding of explorer may occur

P&F Cavitated(disease)

• Chalky enamel on base of pit and fissure
• Softening at the base of p&f
• Brown-gray discoloration under enamel adjacent to P&F
• Radiolucency below occlusal enamel

Root surface caries diagnosis

• Usually arrested and remineralized
• Usually no pain
• Little discoloration- light brown to yellow
• Presence of softness and cavitation if progressing

Factors for potential remineralization of root caries:

• Degree of sclerosis of dentinal tubules
• Degree of bacterial infection
• Degree of lesion progression
• Location of the lesion

Caries Prevention

1. General health of patient
2. Fluoride exposure(systemic/topical)
3. Immunization
4. Salivary functioning
5. Antimicrobial agents
6. Diet
7. Oral hygiene(brushing/flossing)
8. PFS
9. Restoration

Salivary functioning

Using salivary stimulants/salivary substitutes (sialogen/cevimeline)

Antimicrobial agents

Chlorhexidine, mouthwashes

Diet

Modification of diet, less sucrose intake

Theories of caries etiology

1. Acidogenic Theory
2. Chemico-parasitic theory
3. Proteolytic theory

Acidogenic Theory

a theory of caries pathogenesis suggesting that enamel calcification is caused by acid-producing bacteria

Proteolytic Theory

Said that organic portion of the tooth serves as pathways for advancing microorganisms causing demineralization of the teeth and therefore dental caries.

Caries Risk Assessment and Management

classification criteria, and associated estimates of caries activity, are based upon the histological extension of lesions spreading into tooth tissue
*a 7-point rating scale

0 - 7 point rating scale(Caries risk assessment and management)

Clinically sound

1-2 (caries risk assessment and management)

Clinically detected "intact" enamel lesions (initial stage decay)

3-4 (caries risk assessment and management)

Clinically detectable early, shallow, or microcavitations (moderate decay)

5-6(caries risk assessment and management)

Clinically detectable late or deep cavitations (extensive decay)