histology+clinical application- mou (3)

8/3/2019 Histology+Clinical Application- Mou (3)

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Clinical considerations ofdentin

Related to

1.Dentin properties

2.Related to Caries3.Age related changes

4.Dentin hypersensitivity

5.Related to bonding6.Developmental defects


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Dentin

Pashley defined dentin as a porousbiological composite composed of apatite

crystal filler particles in a collagen matrix.


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Dentin is normally yellow white and

slightly darker than enamel.

In older patients dentin is darker.

It can become brown or black in caseswhere it has been exposed to oral fluids,old restorative materials, or slowly

advancing caries. Dentin surfaces are more opaque and

dull, being less reflective to light thansimilar enamel surfaces, which appear

shiny.

COLOR


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HARDNESS

Dentin is softer than enamel and provides greater

yield to the pressure of a sharp explorer tine, whichtends to catch and hold in dentin.

When moving an explorer tine over the tooth, enamelsurfaces provide a sharper, higher-pitched sound than dentinsurfaces.

The hardness of dentin averages one fifth that of enamel .

hardness near the DEJ is about three times greater thannear the pulp

Dentin becomes harder with age, primarily due to increases

in mineral content.MATERIAL MOH`S

HARDNESS

KNOOP

HARDNESS

VICKERS

HARDNESS

ENAMEL 5 340-431 294-408

DENTIN 3-4 70 57-60


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PROPERTIES DENTIN ENAMEL

Thermalconductivity(w/m/k)

.57 .93

Thermal diffusivity(10-4 cm2 /sec) 26 47

LCTE(ppm/k)

8.3 11.4

Tensile Strength

(Mpa)

52 10

Compressive strength(Mpa)

297 384

Shear strength

(Mpa)

30 90

OTHER PROPERTIES


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Dentin provides thermal insulation to the pulp.

Most restorative materials are not as insulating as

dentin and therefore thermal insults may occur duringintraoral temperature changes.

Need for insulation is greatest for metallic

restorations.

Thermal insulation thickness of the insulatingmaterial.

Approximately 2 mm of dentin, or an equivalentthickness of material, should exist to protect the pulp .This thickness is not always possible, but 1 to 1.5 mmof insulation is accepted as a practical thickness.


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While dentin is a hard, mineralized tissue, it issomewhat flexible, with a modulus of elasticityof 1.67 X 106 PSI. This flexibility helps support

the more brittle, nonresilient enamel.


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Any stimulus that involves the dentin whether itbe from dental caries, attrition or from operativeprocedure will affect the pulp of the tooththrough the dentinal tubules.

The surface area of dentin is much larger at thedentinoenamel or dentinocemental junction thanit is on the pulp cavity side.

The number of tubules increases from 15,000to 20,000/mm at the DEJ to 45,000 to65,000/mm at the pulp


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The lumen of the tubules varies from the

DEJ to the pulp surface. In coronal dentin,the average diameter of tubules at thedentinoenamel junction is 0.5 to 0.9 /-mm,but this increases to 2 to 3 /mm at the pulp.


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Dentin permeability

Coronal dentin is much more permeable than rootdentin.

Depends on the remaining dentin thickness (i.e.,length of the tubules) and the diameter of thetubules.

Deep dentin is a less-effective pulpal barrier than issuperficial dentin near the dentinoenamel ordentinocemental junctions


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OPERATIVE CONSIDERATIONS

Dentin must be treated with great care to minimizedamage to the odontoblasts and pulp.

Air-water spray should be used whenever cutting with

high-speed handpieces to avoid heat buildup. The dentinshould not be dehydrated by compressed air blasts; itshould always maintain its normal fluid content.

Protection is also provided by judicious use of liners,

bases, dentin-bonding agents,and nontoxic restorativematerials.

Restorations must adequately seal the preparation toavoid microleakage and bacterial penetration.


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A, Excessive drying of tooth preparations can cause

odontoblasts to be aspirated into dentinal tubules.


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Restoration requiring extensive and deep removal ofdentin would open more and larger dentinal tubules andincreases the pulpal irritation- thus the importance of

REMAINING DENTINAL THICKNESS

Clinical judgments about the need for specific liners andbases ,adhesive materials, and restorative material arelinked to the amount of remaining dentin thickness(RDT).

Approximately 2 mm of dentin, or an equivalentthickness of material, should exist to protect the pulp .This thickness is not always possible, but 1 to 1.5 mm ofinsulation is accepted as a practical thickness

OPERATIVE CONSIDERATIONS


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Dental Caries

It is an infectious microbial disease of the calcifiedtissues of the teeth, characterized by demineralizationof the inorganic portion and destruction of the organicsubstance of the tooth.

Progression of caries in dentin isdifferent from progression in the

overlying enamel because of thestructural differences of dentin.

Begins with the natural spread ofthe process along the DEJ

and rapidinvolvement of the dentinal

tubules. The dentinal tubulesact as tracts leading to

the pulp (path for micro-organisms).


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DEJ has the least resistance to cariesattack and allows rapid lateral spreading

once caries has penetrated the enamel.

Dentinal caries is V-shaped in cross-section with a wide base at the DEJ andthe apex directed pulpally.

Caries advances more rapidly in dentin

than in enamel because dentin providesmuch less resistance to acid attackbecause of less mineralized content.


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Affected and Infected Dentin:

Fusayama has reported that carious dentinconsists of two distinct layers, an outer(refer toinfected dentin) and an inner(refer to affected

dentin).

In tooth preparation, it is desirable that only

infected dentin be removed, leaving the affecteddentin, which then may be remineralized in avital tooth following the completion of restorativetreatment.


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Infected dentin has bacteria present and the collagenis irreversibly denatured. It is not remineralizable and

must be removed.

Affected dentin has no bacteria, is reversiblydenatured, remineralizable, and should be preserved.

To differentiate between remineralizable andnonremineralizable dentin, staining carious dentin wasproposed many years ago by Fusayama.


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DENTINAL FLUID

Play a role in the pain

sensing mechanism

Interfere with the

bonding .

Generally there is an

outward flow of the

dentinal fluid from

pulp.


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TERTIARY DENTIN

Also known asReactionary orReparative dentin.

Formed as a reaction tonoxious stimuli only bythose cells affected byit.

2 types:-Reactionary-formed by

preexisting

odontoblasts.Reparative-formed bynewly differentiatedodontoblast like cells.


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DEAD TRACTS

When the odontoblastsare injured beyondrepair they retract theirprocesses leavingbehind empty dentinaltubules filled with

air,these are known asdead tracts.

They appear black intransmitted and whitein reflected light.

Mostly seen in coronaldentin.

Dead tract

Reparative dentin


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INTERGLOBULAR

DENTIN These are regions of

hypomineralisation indentin where thecalcospherites fail to

fuse. Most common in

circumpulpal dentinimmediately belowmantle dentin.

Occurs due to Vit.Ddefn. or due highexposure to fluoride.


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Sclerotic dentinresults from aging or mild irritation

These areas are harder, denser, less sensitive andmore protective of the pulp against subsequentirritations.

The apparent function of sclerotic dentin is to wall offa lesion by blocking (sealing) the tubules. Thepermeability of sclerotic dentin is greatly reduced in

comparison to normal dentin because of thedecrease in the tubule lumen diameter .Therefore itmay be more difficult to bond a restorative material tosclerotic dentin

During excavation, when sclerotic dentin isencountered it represents the ideal final excavationdepth because it is a natural barrier that blocks thepenetration of toxins and acids.


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The most accepted theory of paintransmission is the hydrodynamictheory, which accounts for paintransmission through small, rapidmovements of fluid that occur within thedentinal tubules.

Many tubules contain mechanoreceptor

nerve endings near the pulp, small fluidmovements in the tubules arising fromcutting, drying, pressure changes, osmoticshifts, or changes in temperature accountfor the majority of pain transmission.

Dentin SENSITIVITY


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Stimuli that induce fluid movements in

dentinal tubules distort odontoblastsand afferent nerves (arrow), leading to asensation of pain. Many operativeprocedures such as cutting or air-drying induce such fluid movement.


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BONDING TO THE DENTIN

Bonding of resins to dentin is far more difficult& less predictable than bonding to enamel as-

More complex histologic structure than enamel, which also variesmore with location

Alterations in the mineral content and structure of dentin as in

caries-affected or sclerotic areas

Not a separate entity, but a part of a complex with the pulp


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Most dentin bonding systems remove or solubilize

smear layer, allowing resins to penetrate and form

"hybrid layer" with dentin structures. Ideally, smear

plugs should not be removed since this will provide

the pathway for microleakage and bacterial ingress

leading to pulpal irritation.


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35-37% phosphoric acid.

Dentin should not be etched for more than15 secs, as this will cause post operativesensitivity & increased microleakage, leadingto early failure.After etching, dentin should not be dried.

Blotting should be done to remove excesswater & the dentin should be left moist.

PRECAUTIONS


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The bond strength is primarily related to micro-mechanical bonding to the intertubular dentin which

occurs between tubules along the cut dentin

surface.

Bond strength for superficial dentin close to thedentino enamel and dentino-cemental junctions are

greater than those for deep dentin.

In deep dentin the greater number of tubules andthe diameter of tubules reduce the amount of theintertubular dentin available for bonding.


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INTRINSIC CHANGES

MOST COMMONLY THE RESULT OFTRAUMA.

BREAKDOWN OF BLOOD SUPPLYWHICH LEADS TO PULPAL NECROSIS

(PULP DEATH). PULPAL BREAKDOWN PRODUCTS

PENETRATE THE DENTINAL TUBULESLEADING TO DISCOLORATION.

LYSIS OF BLOOD CELLS, THE RESULTOF INTRAPULPAL HEMORHAGE, WITHSUBSEQUENT PENETRATION INTO THETUBULES LEADS TO STAINING.


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SYSTEMIC STAINING

EXAMPLE HERE WOULD BE TETRACYCLINE GIVEN

DURING TOOTH DEVELOPMENT.

IT EFFECTS THE HYDROXY-APPETITE CRYSTALSOF BOTH THE ENAMEL AND THE DENTIN.


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DEVELOPMENTALDEFECTS


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Dentinogenesis Imperfecta

Definition: A genetic disorder affecting dentinecollagen during embryogenesis.

Gray to yellowish Broad crowns with constriction of the cevical

area resulting in a tulip shape.

Radiographically, the teeth appear solid,lacking

pulp chambers and root canals


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Dentinogenesis imperfecta


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Dentinogenesis Imperfecta

Classification of DIType I: DI without osteogenesis

imperfectaTypeII: Brandywine type

a shell-like appearance andmultiple pulp exposures


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TYPE-1 DI

Caused by mutation in the DSPP gene.

Teeth are blue gray or amber brown andopalescent.

Radiographically,teeth have bulbous crowns,roots that are narrower than normal andpulp chambers and root canals that are

smaller than normal or completelyobliterated.

The enamel may split readily from the dentinwhen subjected to occlusal stress.


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TYPE-II DI

This disorder was found in the Brandywine tri-racial isolatein Southern Maryland.

Crowns wear rapidly after eruption and multiple pulpexposures may occur.

Radiographs of the deciduous dentition show very largepulp chambers and root canals whereas the permanentteeth have pulpal spaces that are either smaller than

normal or completely obliterated.


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The premature loss of enamel exposes thedentin to occlusal forces that can lead tosevere attrition. As in this patient, full crown

coverage is often used to preserve occlusalheight.


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Dentinogenesis imperfecta (note obliteratedpulp chambers & canals, short roots, relativelynormal crowns with thin enamel)


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Radiological features:--characteristic

short roots

--obliteration ofpulp chambers


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TREATMENT:

The treatment is directed primarily towards

preventing the loss of enamel andsubsequent loss of dentin through attrition.

Cast metal crowns on the posterior teeth andjacket crowns on the anterior teeth.

Fillings are not usually permanent becauseof the softness of the dentin.


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DENTIN DYSPLASIA(ROOTLESS TEETH)

A hereditary defect in dentin formation in which thecoronal dentin and tooth colour is normal; the rootdentin is abnormal with a gnarled pattern and

associated shortened and tapered roots. type I radicular dysplasia

normal crowns of regular or slightly ambertranslucency

Extreme mobility type II coronal dysplasia

semi-transparent opalescent primary teeth

thistle-shaped pulp chambers, bell shapedcrowns


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DENTIN HYPOCALCIFICATION

There is a failure of union of many of theglobules, leaving interglobular areas ofuncalcified matrix.

But there is no alteration in clinicalappearance.

Hypocalcified dentin is softer than wellcalcified dentin.

G O O O O S S


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REGIONAL ODONTODYSPLASIA(GHOST TEETH)

This is an unusual dental anomaly inwhich one or several teeth in alocalized area are affected in anunusual manner.

The etiology is unknown. It has been suggested that the

condition may represent a somaticmutation, although the possibilityhas also been raised that it could bedue to a latent virus reciding into theodontogenic epithelium, whichsubsequently becomes active duringthe development of the tooth.


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