enamel clinical consideration

GOOD MORNING

ENAMEL DEFECTS

AND

CLINICAL CONSIDERATIONS

OF

ENAMEL

ENAMEL DEFECTS

ENAMEL DEFECTS

CARIOUS

PIT

&

FISSURE CARIES

SMOOTH SURFACE CARIES

NON-CARIOUS

WEAR DEFECTS

DEVELOPMENTAL DEFECTS/HYPOPLASIA

STAINING/

DISCOLORATION

CARIES

Definition – Dental caries is an infectious microbiological disease of the teeth that results in localized dissolution and destruction of the calcified tissues .

It is of two types -1.pits and fissure caries. 2. smooth surface caries .

PIT & FISSURE CARIES

Shape- Contributes to their high susceptibility to caries Appears inverted v-shaped.

Undermining: Pit and fissure caries expand as it penetrates into the enamel. Thus the entry site may appear much smaller than the actual lesion. base is towards DEJ and apex is towards enamel surface

SMOOTH SURFACE CARIES The earliest evidence of caries on the smooth enamel

surface of a crown is a white spot.

Translucency – LOST

Subporosity due to loss of interprismatic or

interrod substance caused by

demineralization.

SHAPE :V shape with a

wide area of origin and the

apex of the V directed towards

the DEJ.

NON CARIOUS LESIONS

• WEAR DEFECTS /REGRESSIVE CHANGES --ATTRITION

--ABRASION

--EROSION

--ABFRACTION

• DEVELOPMENTAL DEFECTS & HYPOPLASIAS:

--AMELOGENESIS IMPERFECTA(Hereditary)

--LOCALISED ENAMEL HYPOPLASIAS(Non Hereditary)

• STAINING & DISCOLORATION :

--EXTRINSIC

--INTRINSIC

ATTRITION

It is the physiologic wearing away of the tooth as result

of tooth to tooth contact occlusally,incisally and

proximally.

C/F:

Permanent dentitions affected more than deciduous.

Small polished facet on cusp tip or flattering of ridge or incisal edge.

shortening of dental arch length

(due to proximal wear).

ATTRITION• It is the physiological wearing away of the tooth as a result of tooth to

tooth contact occlusally,incisally and proximally• The most important age change associated with enamel is its loss due to

wear• It has been estimated that by age of 40as much as 1 cm can be lost from

overall circumferential length of arch in average complete dentition

C/F• -permanent dentitions affected more than deciduous.

Males > Females - Small polished facet on cusp tip or flattering of ridge or incisal edge- Gradually = reduction of cusp height and flattening of occlusal inclined Planes, there is shortening of dental arch length (due to proximal wear)-

ABRASION• The pathologic wearing away of tooth substance through

abnormal mechanical process.• Causes -

Improper tooth brushing. Occupational Habits.

C/F=• V wedge shaped ditch on root side of CEJ . Sharp angle between depth of lesion + enamel edge • Exposed dentin is highly polished. • Sensitivity and pulp exposure may occur.

T/t MODALITIES

Remove causative factors.

Lesion < 0.5mm in dentin: no restoration needed.

Lesion > 0.5mm in dentin :restoration needed.

EROSION It is wear or loss of tooth surface by chemico-mechanical

action.

C/F: Mostly facial surfaces. Enamel, dentin and cementum get affected. 3 types of erosive lesions are seen:-• Dish / Saucer shaped, • Shallow concavities -gingival 1/3 of incisors,• Wedge / notch shaped V-shaped (PM, M) .

Causes:• Extrinsic .• Intrinsic .

ABFRACTION• These are cervical wedge shaped defects , caused due to heavy

eccentric occlusal forces resulting in microfractures or abfractures .

• Under large occlusal forces

or off-axial loading of tooth

cusps,the teeth experience

microscopic level of bending

at CEJ,leading to concentration of

stress & microcrack formation.

C/F ABFRACTION• Sensitivity• Weakened tooth structure• Reduced life of restorations

(GIC,ceramic)• Possible TMD disorder.

T/t.• Diet modification,• Fluoride application,• Occlusal splint,• Consider restoring tooth.

AMELOGENESIS IMPERFECTA• Acc to Witkop and Sauk(1976), it is a group of hereditary

disorder characterized by alteration of the quantity and quality of enamel in humans and is frequently associated with significant dental disease.

Hereditary.• Types:

Non Hereditary(localized).

AMELOGENESIS IMPERFECTA

• Acc to Witkop and Sauk(1976), it is a group of hereditary disorder characterized by alteration of the quantity and quality of enamel in humans and is frequently associated with significant dental disease.

• It is a genetic disease in which enamel is poorly formed or mineralized

• Such genetic disturbance can be result of defective matrix synthesis ,defective protease formation or defect in other cellular formation

Hereditary• Types:

Non Hereditary(localized)

C/F 1. Hypo plastic: (formative stage); The

defects are in the matrix formation .

C/F : enamel does not form to its full thickness.

2. Hypo calcified:(Calcification stage): Defects is in mineralization of matrix .

C/F : enamel is soft that it can be flaked off with hand instrument.

• 3. Hypo Maturation (Maturation stage):Enamel crystals remain immature

• C/F - enamel can be pierced with an explorer tip.

TREATMENT:-• Early diagnosis is the key Two modalities of treatment can be used • In most cases –1. Selective Odontotomy2. Full Veneering – teeth should be restored at the same time

with the same materials .

In extensive conditions , lengthy , comprehensive periodic evaluation should be practiced before trying any restorative work on these patients , as the teeth are easily chipped away.

If enamel imperfections are not associated with the dentin genesis imperfecta , the restorative prognosis can be favorable .

LOCALIZED NON-HEREDITARY ENAMEL HYPOPLASIA

Also called Environmental hypoplasia.

Either of the dentitions or even just a single tooth can be defective

Causative factors:

1). Nutritional deficiency of vitamins A,C and D

2). Exanthematous fevers such measles ,

chicken pox .

C/F : Pitted, stained, unsightly teeth Incisors, cuspids & 1st molars are usually

affected.

• 3) Congenial Syphilis■ C/F: Hutchinson's teeth.

• Permanent incisors -Screw driver shaped and notched■ Mulberry molars: First molars have globular masses instead of cusps and narrow occlusal surfaces.

4) Hypocalcaemia: Pitting of enamel occurs when serum Ca+2 is very low

5) Birth Injuries: The Neonatal line is indicative of trauma at time of birth at times, enamel formation totally ceases

6) Local infection and Injury :C/F: Turners teeth occur due to periapical infection/ trauma to deciduous tooth, disturbing the underlying ameloblastic layer of permanent tooth bud. -Can manifest abstain or severe pitting -Single tooth involvement -Upper incisors and maxillary mandibular premolars are commonly affected.

• 7)Fluoride: Ingestion of fluoride containing drinking water (> 1ppm) during the time of tooth formation leads to mottled enamel formation.

• C/F: Ranges from white specks/ patch to pitting to brownish staining to a totally corroded appearance

TREATMENT MODALITIES

• 1.Narrow Lines or isolated pits – selective odontotomy .• 2.In occluding or contacting area – metallic or cast

restorations .• 3.Discolored large lesion- veneering

vital bleaching• 4. Completely disfiguring lesion -

composite resin or ceramic veneers • 5.Disfiguring lesion with tooth structure loss –P.F.M.

crowns or full ceramic crowns

STAINS or DISCOLORATIONThis can be either extrinsic or intrinsic .

• CAUSES OF EXTRINSIC STAINS:--Remnants of Nasmyths membrane-Poor oral hygiene -Plaque / calculus-Existing restorations-Gingival bleeding -Food colors-Chromatic bacteria -Tobacco stains-Mouthwashes like chlorhexidine

T/t OF EXTRINSIC STAINS

Scaling and polishing with the indicated abrasives.

Chlorhexidine stainsGreen stains

INTRINSIC STAINSCAUSES OF INTRINSIC STAINS

-Tetracycline and other drugs

-Fluoride

-Age change

Porphyria

-Systemic diseases:

Erythroblastosis fetalis

-Non vital teeth / endodontically treated teeth

-Internal resorption / “ Pink spot of mummery ”

T/t OF INTRINSIC STAINS

• Intrinsic discoloration due to tetracycline or fluoride - is treated in the same way as enamel hypoplasia or hypo calcification is treated .

• Discoloring changes in pulp root canal system :- • if non vital- endodontic therapy and non vital bleaching.

If non vital bleaching does not end with pleasing result P.F.M. Or full ceramic crowns .

Clinical considerations of enamel

COLOR & SHADE

• Enamel :NORMAL-semi translucent.

ISOLATION- whiter (opaque).

Temporary loss of loosely bound (exchangeable) water.

CLINICAL IMPLICATION:• Thus shade selection must be determined before

isolation & tooth preparation for tooth colored restoration.

ENAMEL RODS• Enamel is hardest substance in body but brittle

too, so require dentin base to support as dentin is resilient .

• CLINICAL CONSIDERATION: Unsupported enamel formed by caries or faulty

tooth preparation tends to fracture.

ENAMEL RODS• Enamel is hardest substance in body but brittle too,,so

require dentin base to support as dentin is resilient . Unsupported enamel formed by caries or faulty tooth

preparation tends to fracture Hydroxyapatite crystals in rods are oriented parallel

in head region but angled(65*)in tail region.• By virtue of this dissolution occurs more in head

region of rods whereas tail & periphery of head region are resistant to attack of

acids ..

RODS-ORIENTATION

Hydroxyapatite crystals in rods are oriented parallel in head region but angled(65*)in tail region.

• By virtue of this dissolution occurs more in head region of rods whereas tail & periphery of head region are resistant to attack of acids .

CLINICAL IMPLICATION:

Caries susceptibility.

Acid-etching.

CEMENTOENAMEL JUNCTION• In those 5-10 % of junctions where there is gap

between cementum & enamel there are increased chances of dentinal sensitivity.

Permeability of enamel:

• Enamel- Acts as semipermable membrane. • Occlusal or incisal enamel > cervical enamel.• More mineralized occlusal enamel .

less pores

less permeability

:

Permeability of enamel :• Permeability of enamel: enamel is relatively

impermeable in comparison to dentin. Pores as such do not exist in enamel

• surface enamel less permeable than inner enamel.• Similarly occlusal or incisal enamel less

permeable than cervical enamel• Acts as semi permeable membrane • Permeability of enamel decreases with age• It seems that ions are exchanged between the

surface enamel and saliva

Hardness of enamel:

• surface to deeper region.• cuspal to incisal region ,lowest at DEJ.• 5 times harder than dentin.• Base of dentin required- withstand masticatory

forces.• Clinical consideration.• Normally: hard but brittle.• If this dentin layer is destroyed by caries or improper

cavity preparation then unsupported enamel fracture easily. So for maximum strength in tooth preparation ,all enamel rods should be supported by dentin

Hardness of enamel:

• Hardness of enamel decreases from surface to deeper region and from cuspal to incisal region ,lowest at DEJ

• 5 times harder than dentin• Makes enamel brittle so it requires a base of dentin to withstand

masticatory forces.• If this dentin layer is destroyed by caries or improper cavity

preparation then unsupported enamel fracture easily

• So for maximum strength in tooth preparation ,all enamel rods should be supported by dentin

Thickness of enamel

• Clinical implication:

Colour : thick- blue tinge.

thin- yellow tinge. Thermal conductivity:

Acts as thermal insulator.

Coefficient of thermal expansion:• Clinical consideration:-

varying coeff. of thermal expansion

Percolation/micro leakage

Secondary caries

Failure of restoration

Enamel relation with fluoride:

• The reduction of caries in young individual exposed to fluoride can be explained by the higher permeability of younger enamel to fluoride ions

• The semi permeable nature of enamel enables topical application to provide a higher concentration of fluoride in surface enamel of erupted teeth fluoride ion is incorporated into HA crystals ,crystals become more resistant to acid dissolution. This reaction explain role of fluoride in caries prevention, hence remineralaization reaction is greatly enhanced by fluoride

• The replacement of hydroxyl ion with fluoride in HA decrease solubility of enamel making it more caries resistant by producing fluoroapatite

• Excessive fluoride result in result in a condition known as fluorosis .The enamel may be discolored or hypoplastic or both

Structural features

Secretory product of one

ameloblast from distal

portion of tomes process.

Extension of an odontoblast process which extend in ameloblastic layer during initial stage of matrix formation.

Hypomineralised areas of enamel near DEJ.

Developmental origin

Provide strength to enamel. Paths are important in

cavity.

Sensitivity during cavity preparation.

Present area of enamel weakness.

Clinical relation

Enamel rod

Enamel spindles

Enamel tufts

Structural features

• Hypomineralised area extending from dej to enamel.

• Twisting of enamel rods in cusp region .

•

• Found b/w cusps; represent thon areas of enamel matrix.

• Susceptible to cracking.• Pathway for bacterial

ingress. • Confers strength to

enamel. This enamel does readily to pressure Of bladed, hand cutting instrument in tooth preparation.

• Areas of caries development.

Enamel lamellae

Gnarled enamel

Enamel pits

Developmental origin Clinical relation

GNARLED ENAMEL• Mostly occur in incisal & occlusal areas as adaptation

to masticatory stress.• Gnarled enamel is not subject to cleavage as is regular

enamel• So gnarling of enamel rods provide strength by

resisting ,distributing and dissipating impact forces

• This enamel does not

yield readily to pressure

Of bladed, hand cutting

instrument in tooth

preparation.

Primary enamel cuticle:

• Enamel is incapable of repairing itself once destroyed beacause the ameloblast cell degenerates after formation of enamel rod

• The final act of ameloblast cell is secretion of nasmyth membrane or primary enamel cuticle. This membrane is replaced by an organic deposit called a pellicle.

• Microorganism may invade pellicle to form bacterial plaque, a potential precursor to dental diseases

• Enamel cuticle may remain adherent to tooth after eruption ,appearing as reddish or brown spot on crown .this may cause undue concern for parents. however this layer is soon shed or removed easily with toothbrush

RODS & ETCHING• Hydroxyapatite crystals in rods are oriented parallel in

head region but angled(65*)in tail region.• By virtue of this dissolution occurs more in head region

of rods whereas tail & periphery of head region are resistant to attack of

acids . (Sturtevant)• ETCHING PATTERN 3TYPES:

Type1prefential removal of rod cores (prismatics)

Type2preferential removal of periphery with core intact

Type3irregular and indisriminate or mixed

Primary enamel cuticle:

• Enamel is incapable of repairing itself once destroyed beacause the ameloblast cell degenerates after formation of enamel rod

• The final act of ameloblast cell is secretion of nasmyth membrane or primary enamel cuticle. This membrane is replaced by an organic deposit called a pellicle.

• Microorganism may invade pellicle to form bacterial plaque, a potential precursor to dental diseases

• Enamel cuticle may remain adherent to tooth after eruption ,appearing as reddish or brown spot on crown .this may cause undue concern for parents. however this layer is soon shed or removed easily with toothbrush

Some important clinical considerations:

• In vitamin A deficiency ameloblast fail to differentiate properly, consequently, their organizing influence on adjacent mesenchymal cell is disturbed and a typical dentin known as osteodentin is formed

• Bleaching agent increases porosity of enamel but these areas may remineralise quickly

• Length of enamel rod is greater than its thickness to which it is related due to their undulating or wavy course

• Enamel is more susceptible to fracturing or separation along at its rods boundaries due to abrupt change in orientation of crystals at its boundary. Through the use of fine chisels clinician can remove groups of rods that are unsupported by dentin during cavity preparation

Continues…….. The caries spreads more rapidly in dentin than enamel because of low organic content in

enamel

During the enamel secretion in the intercuspal areas ameloblast may become strangulated as their base become apposed.in the fully formed crown these areas become pit and fissures which are difficult to clean.pit and fissure sealants are used to keep tbacteria out of these areas

Enamel of primary and permanent teeth differ in their suspetibility to enamel defects. Permanent teeth are more susceptible to hypomineralisation or white spots than primary. Because these defects are in outer enamel they can be removed mechanically or with inorganic acid can result in removal of whit-spot lesions. This is known as micro abrasion

Certain antibiotics like tetracycline have affinity for calcified tissues. They may become incorporated during mineral phase during maturation and cause discoloration of enamel and underlying dentin. Additionally it may interfere with differentiation of ameloblasts and cause hypoplastic areas of enamel on crown of teeth

• It is important to note that inclination of rod differ in primary and permanent teeth and must be accounted for cavity preparation

• Concentration of fluoride, lead and zinc have their highest concentrations in surface layers of enamel

• Similarly concentration of magnesium ,sodium and carbonate is highest at DEJ and is almost halved in the surface layers of enamel

• magnesium ,sodium and carbonate when incorporated into HA crystals, makes enamel more soluble in water and acid –cariogenic in nature

• On the other hand fluoride, zinc ,lead and tin makes it less soluble in water and acid