Cariology- Lecture 3 Flashcards by Savannah Glenn

Where does rapid lateral expansion of caries occur?`

DEJ

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3 distinct clinical sites for caries:

Pits & fissures
Smooth enamel surfaces
Root surfaces

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Why are the root surfaces easiest to decay?

Because there is no enamel

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Large variations exist in the microflora found in pits and fissures, suggesting that each site can be considered a separate ecologic system. Numerous gram-positive cocci, especially S. sanguis, are found in the pits and fissures of newly erupted teeth, whereas large numbers of MS usually are found in carious pits and fissures.

Bacteria

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Most common bacteria in newly erupted teeth

S. Sangius

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Found in already carious pits and fissures

Mutans Streptococci (MS0

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What pattern does demineralization follow?

The direction of the enamel rods

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What happens after initial enamel lesion occurs?

A reaction can be seen in the dentin and pulp

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Where do smooth surface caries occur?

Generally near the gingiva or under proximal contacts

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Have a broad area of origin and a conical extension towards the DEJ?

Smooth enamel surface caries

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Rougher than enamel

Root surface

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Have well defined margins, tend to be U shaped in cross section and progress more rapidly because of the lack of protection from an enamel covering

Root surface caries

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The path of ingress of the lesion is roughly parallel to the long axis of the enamel rods in the region

Smooth enamel caries

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V shape in cross section with a wide area of origin and the apex of the V directed to the DEJ

Smooth enamel caries

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Covers the root surface, is extremely thin and provides little resistance to caries attack

Cementum

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These caries have increased significantly because of the increasing number of old people who retain more teeth

Root surface caries

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What factors impact the progression of caries?

Site of origin and the conditions of the mouth

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Time of progression from non-cavitated caries to clinical caries (cavitation)

18 months +- 6 months

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Peak rate for the incidence of new lesions after the eruption of a tooth

3 years

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dry mouth

Xerostomia

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Another name for noncavitated lesions

White spots

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First clinical evidence of demineralization

White spots

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Developmental white spot
Same wet or dry
Do not restore unless for esthetics

Hypocalcified enamel

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Disappear when wet

-Chalky white when desicatted

White spot lesion (noncavitated)

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Demineralized but not cavitated - Hard external surface - Do not restore

White spot lesion (noncavitated)

often remineralize in enamel

White spot lesion (noncavitated)

retain most of the original crystalline framework of the enamel rods, and the etched crystallites serve as nucleating agents for remineralization

White spot lesion (noncavitated)

Surface is disturbed or missing. | Soft, chalky surface discernible with an explorer tip.

Cavitated enamel lesion (active caries)

Lose most of the original crystalline framework of the enamel rods.

Cavitated enamel lesion

What serves as a driving force for remineralization?

Saliva with calcium and phosphate ions

Greatly enhances the precipitation of remineralization process

Fluoride

Allows remineralized enamel to become more resistant to subsequent caries attack because of the incorporation of more acid-resistant fluorapatite.

Fluoride

observed clinically as intact, but discolored, usually brown or black, spots. The change in color is presumably caused by trapped organic debris and metallic ions within the enamel.

Remineralized Enamel Lesion (inactive caries)

How long does it take to see differences in remineralization

3-6 months

Remineralized enamel lesion. Will be hard when you put explorer in there

Stain

What happens every time a tooth remineralizes?

It becomes more resistant to decay

Hydrated: Translucent Desiccated: Translucent Surface texture: Smooth Surface hardness: Hard

Normal enamel

Hydrated: opaque Desiccated: opaque Surface texture: Smooth Surface hardness: Hard

Hypocalcified enamel

Hydrated: Translucent Desiccated: opaque Surface texture: Smooth Surface hardness: Softened

Noncavitated caries

Hydrated: Opaque Desiccated: Opaque Surface texture: Cavitated Surface hardness: Very soft

Active caries

Hydrated: opaque, dark Desiccated: opaque, dark Surface texture: Roughened Surface hardness: Hard

Inactive caries

Plaque biofilm: Normal Enamel structure: Normal Therapeutic Treatment: Not indicated Restorative treatment: Not indicated

Normal enamel

Plaque biofilm: Normal Enamel structure: Abnormal but not weakened Therapeutic Treatment: Not indicated Restorative treatment: Only for esthetics

Hypocalcified enamel

Plaque biofilm: Cariogenic Enamel structure: Porous, weakened Therapeutic Treatment: Yes Restorative treatment: Not indicated

Noncavitated caries

Plaque biofilm: Cariogenic Enamel structure: Cavitated, very weak Therapeutic Treatment: Yes Restorative treatment: Yes

Active caries

Plaque biofilm: Normal Enamel structure: Remineralized, very strong Therapeutic Treatment: Not indicated Restorative treatment: Only for esthetics

Inactive caries

Why is progression of caries in dentin different from the progression in enamel

Structural differences of dentin

Contain much less mineral and posses microscopic tubules that provide a pathway for the ingress of bacteria and egress of minerals

Dentin

Has the least resistance to caries attack and allows rapid lateral spread

DEJ

Much less resistance to acid attack owing to less mineralized content

Dentin

- Epithelial origin | - Ameloblasts extinct after deposition

Enamel

- Mesenchymal origin | - Odontoblasts remain in pulp

Dentin/pulp complex

90-95% Inorganic (HA) 1-2% Protein 4-8% water Volume %

Composition of enamel

50 vol% HA (75 wt%) 25 vol% collagen (20 wt%) 25 vol% water includes tubules (5wt%)

Dentin Composition

Odontoblasts become increasingly compressed in the shrinking pulp chamber, and the number of associated tubules becomes more concentrated per unit area

As dentin grows

Where is the more recently formed dentin

Near the pulp

Has large tubules with little or no peritubular dentin and calcified intertubular dentin filled with collagen fibers

Dentin near the pulp

large tubules with little or no peritubular dentin and calcified intertubular dentin filled with collagen fibers

Newer dentin

a uniform layer of mineral

Peritubular dentin

What do horizontal lines in dentin indicate?

Predentin

What do diagonal lines indicate in dentin?

Increasing density of minerals

What do darker horizontal lines in dentin indicate

Densely mineralized dentin and increased thickness of peritubular dentin.

Characterized by bacteria filling the tubules and granular material in the intertubular space

Most superficial infected zone of carious dentin

Contains very little mineral and lacks characteristic cross-banding of collagen.

Granular material

What do carbohydrates produce to remove peritubular dentin?

Lactic acid

Found pulpal to transparent dentin

Normal dentin

1. reaction to a long-term, low-level acid demineralization associated with a slowly advancing lesion 2. reaction to a moderate-intensity attack 3. reaction to severe, rapidly advancing caries characterized by very high acid levels

Pulp-dentin complex reacts to caries attacks

What does the pulp respond with?

Inflammatory cells

Large chucks of dentin in the pulp

reparative dentin

Results in bacterial invasion of dentin by a wide variety of pathogenic materials or irritants, including high acid levels, hydrolytic enzymes, bacteria, and bacterial cellular debris.

Intense caries activity

What does the success of the dentinal reparative response depend on?

The severity of the caries attack and the ability of the pulp to respond.

The most important limiting factor to the pulpal responses

Pulpal blood supply

- High levels of acid production overpowers dentinal defenses and results in: - Infection, - Abscess, and - Death of the pulp, usually due to impaired blood supply.

Reaction to severe, rapidly advancing caries

1. Weak organic acids demineralize dentin 2. The organic material of dentin, particularly collagen, degenerates and dissolves 3. The loss of structural integrity is followed by invasion of bacteria

Caries advancement in dentin

Zone 1 Zone 2 Zone 3

1- Normal dentin 2- Affected dentin 3- Infected dentin

- Deepest area - tubules with odontoblastic processes that are smooth - No crystals are present in the lumens - No bacteria present in tubules

Zone 1: Normal dentin

Stimulation of this dentin produces a sharp pain

Zone 1: Normal dentin

- Inner carious dentin - A zone of demineralization of intertubular dentin and of initial formation of fine crystals in the tubule lumen at the advancing front.

Zone 2: Affected Dentin

- Damage to the odontoblastic process is evident. - Softer than normal dentin and shows loss of mineral from intertubular dentin and many large crystals in the lumen of the dentinal tubules.

Zone 2: Affected dentin

- Collagen cross-linking remains intact in this zone. - The intact collagen can serve as a template for remineralization of intertubular dentin, and this region remains capable of self-repair, provided that the pulp remains vital.

Zone 2: Affected dentin

- Also called outer carious dentin, this is the outermost carious layer, the layer that the clinician would encounter first when opening a lesion. - The zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules, which are filled with bacteria.

Zone 3: Infected Dentin

-Little mineral is present, and the collagen in this zone is irreversibly denatured. -The dentin in this zone does not self-repair. This zone cannot be remineralized, and its removal is essential to sound, successful restorative procedures and the prevention of spreading the infection.

Zone 3: Infected Dentin