Dental Cariology II

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Dr. Khalid AL-Tubaigy

description

Dental Cariology II. Dr. Khalid AL-Tubaigy. Early Stages of Plaque Succession. Pellicle is formed primarily from the selective precipitation of various components of saliva. Functions of the pellicle are believed to be : (1) protect the enamel, - PowerPoint PPT Presentation

Transcript of Dental Cariology II

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Dr. Khalid AL-Tubaigy

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Pellicle is formed primarily from the selective precipitation of

various components of saliva .

Functions of the pellicle are believed to be :(1 )protect the enamel ,

(2 )reduce friction between the teeth(3 )possibly provide a matrix for remineralization .

Pellicle is formed from salivary proteins that have apparently involved for this function .

These proteins have many basic groups and consequently adsorb to the phosphate ions while other acidic proteins adsorb to calcium ions.

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Microorganisms do not attach themselves directly to the mineralized tooth surface and the teeth are always covered by an a cellular proteinaceous film.

• The pellicle forms on the “naked” tooth surface within minutes to hours

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Salivary glycoproteinCarbohydrates

Lipida lesser extent

components from the gingival crevicular fluid

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Definition: A gelatinous mass of bacteria (soft, translucent, and tenaciously adherent material) accumulating on the surface of teeth.

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Attachment, growth and reattachment of bacteria to the tooth surface is a continuous and dynamic process .

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.1Formation of acquired pellicle and primary aggregation

.2Bacteria growth and development.3The mature of dental plaque

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bacteria which form 50-70% of dental plaque

glycoprotein together with extracellular polysaccharides form the plaque matrix

• Muco-poly-saccharides such as glucans and fructans

• Inorganic components calcium phosphorus fluorides .

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Supra gingival plaque ----- dental caries

Sub gingival plaque----- periodontal

diseases

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1 .Plaque on smooth surface Plaque adhere to dental surface

Middle layer condensed microbial layer

( body of plaque)2 .Plaque in pit and fissure

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Advanced lesions often have a high proportion of lactobacilli

dentinal lesions have a diverse micro-flora with many Gram positive(+), Gram negative(-) bacteria.

Root surface caries was originally associated with Actinomyces, but recent studies suggest a similar etiology to enamel caries

Rampant caries and early childhood caries can occur in xerostomic patients and infants fed with high levels of sugar in pacifiers )nursing bottle caries( the plaque contains high levels of mutans

streptococci and lactobacilli.

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Pits and Fissures: Large numbers of MS gram-positive cocci especially S. sanguis are found in the pits and fissures of newly erupted teeth. In cross-section, the gross appearance of pit & fissure lesion is aninverted V with narrow entrance and a progressively wider area of involvement closer to the DEJ .

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Smooth Enamel Surfaces:Less favorable site for plaque attachment.

Plaque develops near the gingival area or under proximal contacts.

Lesions have broad area of origin and a conical or pointedextension toward the DEJ.

Path of ingress of the lesion is roughly parallel to long axes ofenamel rods in the region.

Cross-section of enamel of the lesion shows V shape with a widearea of origin and the apex of the V directed toward the DEJ.

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Root Surface:Cementum is extremely thin and provides little resistance to caries

attack.

Lesions have less well defined margins tend to be U-shaped incross-section and progress more rapidly.

In recent years, Prevalence of root caries has significantly increasedbecause of the increasing number of older persons who retain more

teeth experience gingival recession and usually have cariogenic

plaque on the exposed root surfaces.

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The time for progression from incipient caries to cavitations onsmooth surfaces is estimated to be 18 ± 6 months.

Peak rates for the incidence of new lesions occurs 3 years after eruption of the tooth.

Both poor oral hygiene and frequent exposures to sucrose containingfood can produce incipient )white spot).

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Incipient Smooth-Surface Lesion:On clean, dry teeth, the earliest evidence of caries is white spot

(chalky white. )

Incipient caries will partially or totally disappear visually whenthe enamel is hydrated (wet) while hypocalcified enamel is

relatively unaffected by drying and wetting.

Injudicious use of explorer tip can cause actual cavitation fora previously noncavitated incipient area thus requiring in mostcases restorative intervention.

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Zones of Incipient Lesion : (a )Intact surface zone

(b )Body of lesion(c )Dark zone(d )Translucent zone

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Zone 1 Translucent Zone1. Name refers to its structureless

appearance when perfused with quinoline solution and examined with polarized light.

2 .The deepest zone.

3 .Pore volume is 1%.

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Zone 2 Dark Zone1 .Does not transmit polarized light.

2 .Light blockage is caused by the presence of many tiny pores too small to absorb quinoline.

3 .These smaller air or vapor, filled pores make the region opaque.

4.Pore volume is 2% - 4%.

5 .Size of dark zone is probably an indication of the amount of remineralization that has recently occurred.

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Zone 3 Body of the Lesion1.The largest portion.

2 .Has the largest pore volume, varying from 5% at periphery to

25% at the center.

3 .Bacteria may be present in this zone if the pore size is largeenough to permit their entry.

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Zone 4 Surface Zone1 .Unaffected by the caries attack.

2 .Has lower pore volume than the body of the lesion

<(5% )and radiopacity comparable to unaffected adjacent enamel .

3 .Surface of normal enamel is hypermineralized by contact with saliva and has a greater concentration of fluoride ion than the immediately subjacent enamel.

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* Pulp-dentin complex reacts to caries attacks by attempting to initiate remineralization and blocking off the open tubules.

* These reactions result from odontoblastic activity and the physical process of demineralization and remineralization .

* Levels of dentinal reaction to caries : (1) Reaction to long-term, low-level acid demineralization associated with a slowly advancing lesion. (2) Reaction to moderate-intensity attack. (3) Reaction to severe, rapidly advancing caries characterized by very high acid levels.

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Zone 1 Normal Dentin.1. The deepest area is normal dentin, 2. No bacteria are in the tubules. 3. Stimulation of dentin )e.g., by osmotic gradient [sucrose or salt],bur, dragging instrument, or desiccation from heat or air), produces sharp pain.

Zone 2 Sub-transparent Dentin.1. Is a zone of demineralization of the inter-tubular dentin .2. Damage to odontoblastic process is evident.3. No bacteria .4. Stimulation of the dentin produces pain, and the dentin is capable of remineralization.

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Zone 3 Transparent Dentin 1. is softer than normal dentin . 2. Stimulation of this region produces pain. 3. No bacteria are present. 4. Dentin is self repaired.

Zone 4 Turbid Dentin 1. filled with bacteria . 2. Collagen in this zone is irreversibly de-natured. 3. Dentin is not self-repaired (not remineralized ) and must be removed before restoration.

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Zone 5 Infected Dentin 1. The outermost zone . 2. consists of decomposed dentin that is teeming with bacteria. 3. No recognizable structure to dentin and collagen and mineral seem to be absent. 4. Great numbers of bacteria are dispersed in this granular material.

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The possibilities seem to be: 1. The color is exogenous stain absorbed from the mouth (e.g. from tea, coffee, red wine(. 2. comes from pigment-producing bacteria. 3. is the product of a chemical reaction called the Maillard Reaction. 4. A brown color is produced when protein breaks down in the presence of sugar .

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