zenamel wdd

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CONTENTS

INTRODUCTION

PHYSICAL PROPERTIES

CHEMICAL PROPERTIES

MICROSCOPIC STRUCTURE OF ENAMEL

SURFACE STRUCTURES

DEVELOPMENT OF ENAMEL

MOLECULAR ELEMENTS OF TOOTH DEVELOPMENT

PROTEINASES

ENAMEL DEFECTS

AGE CHANGES IN ENAMELCLINICAL CONSIDERATION

ENAMEL PRODUCTION IN VITRO

REFERENCES


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ENAMEL

INTRODUCTION:-

The literal meaning of Enamel is a vitreous, glass like coating fused on to a metallic basesimilarly the tooth enamel form an outer covering of tooth and protect the inner structure.Enamel is hardest calcified tissue of the human body and is ecto-dermal in origin.

Enamel is defined as Acellular hard mineralized tissue that forms the protective covering of

variable thickness over the entire surface of the crown.

Enamel, along with dentin, cementum, and dental pulp is one of the four major tissues that makeup the tooth .

Physical properties of Enamel:

Hardest calcified tissue. Ranks 5 on mohs scale with young`s modulus of 83 GPA & 343KHN Thickness 2-2.5 mm (cusps) to feather edge (cervical line). Brittle in nature. Act as a Semipermeable membrane. Specific gravity 2.8. Compressibilty (elastic modulus) 19 X 10^ 6 psi, tensile strength 1100 psi. Translucent & Color ranges from yellowish white to grayish white.

Incisal areas may have a bluish tinge where the thin edge consists only of a double layer

of enamel.

Enamel is avascular and has no nerve supply within it and is not renewed, however, it isnot a static tissue as it can undergo mineralization changes.
http://en.wikipedia.org/wiki/Dentinhttp://en.wikipedia.org/wiki/Cementumhttp://en.wikipedia.org/wiki/Pulp_(tooth)http://en.wikipedia.org/wiki/Toothhttp://en.wikipedia.org/wiki/Toothhttp://en.wikipedia.org/wiki/Pulp_(tooth)http://en.wikipedia.org/wiki/Cementumhttp://en.wikipedia.org/wiki/Dentin


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Chemical properties of Enamel:

Enamel

inorganic mat. organic mat.& water

96% (by wt) 4%

Inorganic

Content

Organic

Content

+ Water

Enamel 96% 4%

Dentin 70% 30%

Cementum 45-50% 50-55%

Inorganic substances in enamel - comprises of crystalline ca phosphate i.ehydroxyapatite.

Various ions- strontium, magnesium, lead , fluoride get incorporated if present duringenamel formation.

Hydroxyapatite crystal

Apatite crystals of enamel are largest & best developed of all the crystals of mineralizedtissue (dentin &bone).

Initially crystallites appear as long plates/ribbon of 15 A which grows rapidly in width& slowly in thickness.

1600 A in length, 680 A in width &260 A in thickness. Enamel crystallites are organized into basic structural units called as prisms.Composition of hydroxyapatite crystal: 10Ca++6PO4 & 2OH

By wt. 37% Ca, 52% phosphate, & 3% hydroxyl


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Organic substances in Enamel

Enamel proteinpolysacch.protein complex & acid mucopolysaccharides.

ENAMEL PROTEIN

Two types (TERMINE et al 1979):

1. Amelogenin (90%)(LMW Protein)2. Non amelogenin (10%)(HMW Protein)a) Ameloblastinb) Enamelinc) Tuftelin

STRUCTURES OF ENAMEL

Enamel Rods Striations Hunter schreger bands Incremental lines of Retzius DEJ Enamel tuft Odontoblastic process & enamel spindles Enamel lamellae Enamel cuticle

ENAMEL RODS

cylindrical in shape. Extend from DEJ to outer enamel surface. 5 million in lower lateral incisor to 12 million in upper first molars. Head is broadest part(5 m wide), elongated thinner portion or tail is (1 wide). The bodies of the rods are nearer occlusally or incisally whereas the tails point cervically. the diameter of the rods increases as they transverses the Enamel, towards the surface of

the tooth diameter becomes double while at enamel surface the rod structure is irregular

or absent (tome`s processes are lost as amelogenesis comes to an end.).

length of rod 9 m. length greater than the thickness of the enamel because of the oblique direction and

tortuous/wavy course of the rods.

Each rod formed by 4 ameloblasts. One ameloblasts forms the rod head, a part of twoameloblast forms neck & tail by fourth ameloblast


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Rods are surrounded by rod sheath & separated by inter rod substance. Rod sheath: the boundary where crystals of the rod meet those of the interod regions at

sharp angles. rod sheath contain more enamel protein than other regions.

The inter rod regions is an area surrounding each rod is which crystals are oriented in adifferent directions from those making up the rod.

The consistent arrangement of rod sheaths,with their greater protein content accounts forfish scale appearance in etched ground sections. The rod sheath can also be visualized in

undemineralised light microscope sections because of differences between refractive

indices of sheath, rod, & interred regions.

A more common pattern in a keyhole pattern or paddle shaped prism in human enamelKeyhole shape results mainly due to lateral flaring of the rod crystals which continue

uninterrupted into cervically located inter rod region till they are perpendicular to the rod

.Inter rod region which is cervical to the rod is not separated by the rod sheath.

Rod is filled with crystals which are approx. parallel to long axis of rods in head region &deviates 65 degree in tail.

In first 5 m ,next to dentin there is no rod structure because tome`s processes not yet

formed when this enamel is laid down.

Directions of rods Enamel rods are arranged circumferentially in rows around the long axis of the tooth . Rods are oriented at right angles to dentine surface. Near the cusp tip, they have a small radius and run vertically. In cervical and central part of crown of Deciduous tooth they are approximately

horizontal.

Near the incisal edge cusp tip they change gradually to an increasingly oblique directionuntil they are they are almost vertical.

The permanent teeth is similar in the overall two thirds of the crown. In the cervicalregion the rods deviate from the horizontal in an apical direction superimposed on this

row arrangements are two other patterns. S shaped course in horizontal plane and

change in direction of about 2 b/w successive rows.


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CROSS STRIATIONS:

Each enamel rod is built up of segments separated by dark line/ band. These periodic bands or cross striations occur at 4 m intervals across the rods. Striated appearance because of alternating constrictions and expansions of the rods. Indicates a daily (circadian) variation in the secretory activity of ameloblasts.

GNARLED ENAMEL

Optical appearance found at the cusps and incisal edges of teeth. The twisted appearance results from the orientation of enamel rods and the rows in

which they lie. The rods undulates back & forth within the rows. This undulation

vertically directed rods ( i.e at cusp tip) around a ring of small circumference give thisappearance.

HUNTER SCHREGER BANDS

Named after scientist who first noted band microscopically. Optical phenomena seen due to Change in directions of rods & provides enamel with

strength for mastication and biting.

Alternate dark and light bands seen in longitudinal sections and oblique reflected light These zones can be reversed by altering direction of illumination. Originate at DEJ & found in inner four fifth of enamel. The repeating pattern from cervical to incisal/occlusal areas seen along long axis of the

tooth.

Variations in calcification of the enamel coincide with the distribution of the bands ofHunter schreger..

Diazone and parazone: purely an artifact of sectioning in HSB, not a true structure. Insections vertical to HSB,decussating prisms are intersected at different angles. Layers in

which prisms are truncated were called DIAZONES by PREISWERK(1894, 1896).While layers in which prisms are intersected at low angles or longitudinally were called

PARAZONES .


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INCREMENTAL LINES

Dr. retzius first noted growth lines in Enamel & termed them the striae of retzius These are growth lines which are result of rhythmic recurrent deposition of Enamel

Appear as dark bands in longitudinal sections of the enamel, reflecting successive

Enamel forming fronts.

In longitudinal sectionssurround tip of dentin and run obliquely in cervical parts. In transverse section concentric circles.when these circle not complete, a series of

groove called line of pickerill are formed.

Decrease in number of crystals in striae & bending of the enamel rod occur as they crossstriae.

Formed as a result of temporary constriction of tomes process associated withcorresponding increase in the secretory face forming interrod Enamel.

Accentuated incremental lines are produced by systemic disturbances. Prominent in permanent teeth less prominent in postnatal deciduous teeth and rare in

prenatal teeth.

NEONATAL LINE/ NEONATAL RING

The Enamel of the deciduous teeth develops partly before and partly after birth, theboundary between the two portions of enamel in deciduous teeth in marked by an

accentuated incremental line of Retzius.

Result of abrupt change in the environment and nutrition at the time of birth. Microscopically the Enamel internal to this line is of different consistency from external

to it because internal was formed before birth and external after birth.

DENTINOENAMEL JUNCTION

Scalloped profile in cross section at junction of Dentin & Enamel. Junction is like series of ridges that increase surface area and adhesion b/w dentin and

Enamel.


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The surface of dentine is pitted at DEJ.

ENAMEL TUFTS

Project from DEJ into Enamel one fifth to one third of its thickness. Branched like tufts of grass and contain greater concentration of protein than rest of

Enamel.

Occur because of abrupt changes in direction of group of rods that arise from DEJconsidrered as adaptation to spatial conditions.

ODONTOBLAST PROCESS AND ENAMEL SPINDLES

Odontoblast processes push b/w adjoining ameloblasts and when enamel formationbegins, get trapped forming a tubule.

These small tubules may contain living process of odontoblast ,contributing to the vitalityof DEJ.

The direction of the odontoblast process and spindles in the enamel corresponds to theoriginal directions of ameloblasti.e. at right angles to the surface of the dentine.

Rods and spindle directions are divergent.

ENAMEL LAMELLAE:

Leaf like structures that extends from the Enamel surface towards DEJ and maypenetrate dentin.

Consist of organic material but little mineral content. Lamellae may develope in planes of tension, where rods cross such plane, a short

segment of rods may not calcify, if it distribution in more severe a crack may develope.

3 types of lamellaeType A - Lamellae composed of poorly calcified rod segments.

- it is restricted to enamelType B - consist of degradation cells & may reach dentin


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Type C - in erupted teeth, where cracks are filled with organic matter & reach dentin

- More common

Spaces b/w group of rods are another eg. of lamellae & may be caused by stress cracksthat occur because of impact or temp. changes

Enamel lamellae may be a site of crack in a tooth and form a road of entry for bacteriathat initate caries.

ENAMEL CUTICLE

A delicate membrane called Nasmyths membrane, or primary enamel cuticle covers theentire crown of the newly erupted tooth but a probably soon removed by masticaton.

This membrane is a typical basal lamina secreted by ameloblast when enamel formationis completed & is composed of keratin.

Enamel surface:

structureless Enamel layer Salivary pellicle Perikymata Cracks (lamellae)

Structureless Enamel layer:

Rodless enamel occurs in outermost 30 um of all primary teeth & 70% of permanent atgingival third. Crystals in these regions are perpendicular to tooth surface.

In erupted teeth both these layer are rapidly lost by abrasion attrition & erosion.

Salivary pellicle:

Organic deposit on surface of tooth always reappear shortly after teeth mechanicallypolished.


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Perikymata/imbrications lines:

Transverse, wave like grooves across the face of crown. External manifestation of the striae of Retzius. Usually lie parallel to each other and CEJ. More prominent on facial surface and cervical areas 30/mm at CEJ to 10/mm near

occlusal or incisal edge.

Course is irregular in cervical region.

Cracks:

Narrow fissure like structures. The outer edges of lamellae and at right angles to DEJ. Mostly < 1mm but sometime may be longer.

Difference in Enamel of primary and permanent teeth

Primary teeth Permanent teeth

Thin enamel .5- 1 mm 2.5 mm

More opaque & white Yellowish white

Inorganic 92% inorganic 96%

More permeable Less

Enamel rod direction in cervicalregion - Horizontal

Apical


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DEVELOPMENT OF ENAMEL

Enamel organ Life cycle of Ameloblasts Amelogenesis

ENAMEL ORGAN

Oral epithelium

6th

week IUDental lamina

proliferates

Enamel Organ

Enamel formation is part of the overall process oftooth development. The stages of tooth development are the bud stage, cap stage, bell stage, and crown, or

calcification, stage. Enamel formation is first seen in early crown stage & involves the

differentiation of cells of internal dental epithelium into Ameloblasts

FOUR LAYERS

Outer Enamel Epithelium Stellate reticulum Stratum intermedium Inner Enamel Epithelium

Outer Enamel Epithelium

It consists of single layer of cuboidal cells which get laid down into folds. B/w these folds mesenchyme of dental sac forms papillae that contains capillary loops

which provide nutritional supply to enamel organ.

Inner Enamel Epithelium

Present at concavity of enamel organ & are tall columnar cells these cell differentiate intoameloblast.

The cells of IEE have an organizing influence on underlying mesenchymal cells of dentalpapilla to differentiate into odontoblast and their product dentin becomes the initiator forfurther differentiation of inner dental epithelium cells( reciprocal induction)into

ameloblasts.
http://en.wikipedia.org/wiki/Tooth_developmenthttp://en.wikipedia.org/wiki/Tooth_development


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Stellate reticulum (enamel pulp)

Cells are star shaped & located in centre of enamel organ & assumes a branched reticularform.

The spaces in this reticular network are filled with mucoid fluid rich in albumin whichgives this layer cushion like consistency before Enamel formation starts this collapses ,

reducing distance b/w Ameloblasts and capillaries near outer Enamel epithelium.

Temporary structures enamel knot & cord present in centre of enamel organ theydisappear before enamel formation begins . they act as reservoir of dividing cells for

growing enamel organ.

.

Stratum intemedium

It Consists of flat cuboidal cells & are present b/w IEE & stellate reticulum. These cells have high alkaline phosphatase activitiy & glycogen deposits. It play a role in enamel formation either through control of fluid diffusion into and out of

Ameloblasts.

LIFE CYCLE OF AMELOBLAST

Morphologic stage

Differentiation stage

Secretory stage

Maturation stage

Protective stage

Morphologic stage

IEE cells are short columnar with large centrally located nuclei . Golgi elements & centriole present in proximal portion. Mitochondria scattered throughout.

Differentiation stage


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Cells elongates & their nuclei shift proximally toward stratum intermedium. Golgi complex increases into volume and migrates from its proximal position to centre. RER increases & most of mitochondria cluster in proximal region. Adajacent ameloblasts are closely aligned to each other & maintained by junctional

complexes.

(imp. of junc.complexes: selective passage between ameloblasts)

Secretory stage Synthesis of enamel protein occur s in RER ,packed & condensed into granules in golgi

bodies , and their contents released against newly formed mantle dentin.

Ameloblast control over passage of inorganic ions from capillaries of dental follicle toEnamel surface.

After this first structureless enamel layer is formed the ameloblasts migrate away fromthe dentin surface & permit formation of conical processes -Tome`s process.

Tome`s processes jut into newly formed enamel giving junction b/w enamel andameloblast a picket fence or saw toothed appearance .

Secretory granules are present in Tome`s process . Tome`s process persists until final new enamel increments are formed.

Maturation stage

Ameloblasts reduced in length and closely attached to enamel matrix. Cells of stratum intermedium loose regular arrangement and assume spindle shape. Cells become striated/ ruffled border. Ameloblasts display microvilli at their distal extremities. Reduction in height and decrease in volume and excess organelles digested by

lysosomse enzymes.

Water & organic material are selectively removed from enamel while additionalinorganic material is introduced by alternate bursts of activity.

Ruffle ended Ameloblast associated with introduction of inorganic material & smoothended cells with removal of protein and water.

Protective stage Ameloblast protect enamel surface from follicular connective tissue Cell layers form

stratified epithelial covering of enamel called REDUCED ENAMEL EPITHELIUM.

Ameloblast secrete material morphologically similar to basal lamina. The distal cell membrane no longer folded & has developed Hemidesmosomes which

provide a firm attatchment for the Ameloblasts to the enamel surface that is utilized to

form primary Epithelial attatchment b/w gingival & newly erupted tooth.


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MOLECULAR ELEMENTS OF AMELOBLAST DIFFERENTIATION

Amelogenesis is under the control of expression of various molecules

Gene transcription factors

a) MSX-2 gene ( homebox gene) Expressed during bud stage in epithelium localized to enamel knot region Regulates morphogenesisb) Egr-1 Expressed in the polarized ameloblasts before any matrix is produced.

Membrane receptors Receptor molecules on the cell surface recognize & bind signaling moleculea. B5b. FgFc. EGF

INTRACELLULAR RECEPTORSa. CRABP-1 Transmit signal of retinoic acid. Expressed by secretory but not maturation stage ameloblastsb. Growth hormone receptor Appear only on differentiating ameloblasts vitamin D receptor identified during differentiation.

Amelogenesis:

Organic matrix formation Mineralization


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Formation of the enamel matrix

Ameloblasts begin their secretory activity when a small amount of dentine has been laiddown.

Ameloblast lose the projection which had penetrated the basal lamina. A thin layer of enamel forms along the dentin. This has been termed the Dentinenamel

membrane.

The presence of membrane shows that the distal ends of enamel rods are not in directcontact with dentin.

Head of rod formed by one and tail by three Ameloblast thus each rod is formed by fourAmeloblast.

Bulk of developing enamel matrix is protein Amelogenin produced by Ameloblast.

AMELOGENINS

amelogenin nanospheres appear as beaded rows of electro luscent structures ali gned with

and separated ,the enamel mineral crystallites (FINCHAM et al 1995)

Dr. Alan fincham is the father of Amelogenin. Gene specific protein. Latest studies have indicated that Amelogenin exists in the form of nanospheres. Molecular wt. 25 KDa derived from gene located on x chromosome. Hydrophobic protein rich in Proline,Glutamine. Undergoes long term & short term extracellular processing. Accumulates during secretory stage. support & locate framework for developing enamel. Regulate growth of crystal in thickness & width. May also nucleate crystals. During mineralization process 90% of amelogenin in enamel matrix get removed by

proteolytic enzyme into TRAP & LRAP.


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NON AMELOGENINSAmeloblastin

Undergo rapid degradation. Promotes mineral formation and crystal elongation. Determination of prismatic pattern.

Enamelin

Protein in developing Enamel that is tightly bound to crystals and similar in compositionas that of mature Enamel matrix.

Contains Glycine, Glutamic acid, Aspartic acid & serine phosphate. Organically bound phosphate or serine phosphate play a key role in nucleation ofHydroxyapatite thus initiating calcification.

Tuftelin

Participates in establishment of DEJ. Its gene is located on autosome 1. Cell signaling. Nucleator for first Enamel crystal.


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Mineralization and Maturation of enamel matrix

Two steps

Immediate partial mineralization.

Maturation

Immediate partial mineralization

Immediate partial mineralization occur in the matrix segment and inter prismaticsubstance as they are laid down( 25% to 30% of total mineral content).

Maturation

The gradual completion of mineralization& conversion of first formed enamel which issoft or moderately hard into hardest of hard tissue.

Maturation process starts from the height of the crown and progress cervically. The incisal and occlusal regions reach maturity ahead of the cervical regions. Crystal increase in thickness more rapidly than width. Organic matrix gradually become thinned and widely spaced to make room for the

growing crystals.

Over 90% of initially secreted protein is lost during enamel maturation. Human enamel forms at a rate of around 4 m per day. Ameloblast undergo programmed cell death.

Studies involving microradiography of thin ground section indicates mineralization in 4

stages:

First stage primary mineralization

30% mineralization achieved.Second stage


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Starts at surface of enamel & sweeps rapidly into deeper layers until it reaches innermost8 m layer.

Third stage

Tertiary increase in mineral rebounding from innermost layer out toward the enamelsurface.

Fourth stage(quaternary mineralization)

outer layer mineralizes rapidly & heavily & becomes the most mineralized part ofenamel.

PROTEINASES AND TOOTH DEVELOPMENT serve two important functions:

a. processingb. degrade enamel proteins.

Enamelysin (MMP-20) is the foremost enamel matrix-processing enzyme

cleavage products reside in mature and deeper layers Full length protein reside on surface enamel. They activate the parent proteins MMP20) or enamlysin reside in recently formed tooth enamel. Enamlysin cleave amelogenin , important in early tooth development. a decrease in enamel protein content degrade the organic matrix

Enamel matrix serine proteinases 1(EMSP 1)

was cloned from the enamel organ epithelia. EMSP 1 involved in the degradation of enamel prior to its removal Accor. To USC led team of dental researchers, a gene critical for tooth formation

expresses a protein that is cleaved into two proteins with opposite functions viz.DSP

(dentin sialophosphate) and DPP (dentin phosphoprotein)


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DSP : imp. in the development of enamel and dentin.DSP protects the tooth againstcaries but over expression can lead to inc hardness of enamel.

DPP : asso.with early stages of mineralization .Over expression leads to softer enamel.

Thus, a fine balance of DSP and DPP results in delicacy of the DEJ.

ENAMEL DEFECT

Carious defect Non-carious defects Developmental defects:- Enamel hypoplasia- Amelogenesis imperfect- Enamel Pearl- Odontodysplasia- Dens evaginatus Regressive defects:- Attrition- Abrasion- Erosion- Abfraction Fractures Discolorations

CARIES

First sign- white spot due to loss of translucency which sometime get remineralized andbecomes brown.

When lesion is invaded two third of enamel it becomes visible radiographically. In fissuresstart at adjoining lateral wall. The high mineral content of enamel, which makes this tissue the hardest in the human

body, also makes it susceptible to a demineralization process which often occurs as dental

caries.

Ca10(PO4)6(OH)2(s) + 8H+(aq) 10Ca2+(aq) + 6HPO42-(aq) + 2H2O(l) As enamel continues to become less mineralized and is unable to prevent the

encroachment of bacteria, the underlying dentin becomes affected as well.

When dentin, which normally supports enamel, is destroyed by a physiologic conditionor by decay, enamel is unable to compensate for its brittleness and breaks away from the

tooth easily.

Zones of caries in Enamel
http://en.wikipedia.org/wiki/Dental_carieshttp://en.wikipedia.org/wiki/Dental_carieshttp://en.wikipedia.org/wiki/Dental_carieshttp://en.wikipedia.org/wiki/Dental_caries


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Zone 1 Translucent zone deepest zone, pore volume 1%.

Zone 2 Dark zone does not transmit light, pore volume 2-4%

Remineralization increases dark zone.

Zone 3 Body pore volume 5- 25% demineralized ,well marked striae of retzius.bacteria present.

Zone 4 Surface zone unaffected by caries, low pore volume.Hypermineralised & high fluoride.

HYPOPLASIA

Defined as incomplete or defective formation of organic matrix of enamel.

Two types:-

Hereditary:

Environmental:

Causes are: [systemic/local]

Nutritional deficiencies (Vit. A, D, C). Local infection /trauma. Congenital syphilis (mulberry molars and screw driver shaped incisor). Hypocalcaemia (pitting is seen). Birth injury (neonatal line), pre-maturity. Chemical intoxication.

HYPOPLASIA DUE TO NUTRITIONAL DEFICIENCY & EXANTHEMATOUS

FEVERS

- Vitamin A, C, D Deficiency.- Rickets most common cause.- Chickenpox, measles & scarlet fever.- Pitted variety.


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HYPOPLASIA DUE TO LOCAL INFECTION/ TRAUMA

- Turners hyoplasia.- Single tooth involved most common is maxillary incisor or maxillary/mandibular

premolar.

-

Infection from carious deciduous teeth in periapical tissue may disturb the ameloblasticlayer of permanent tooth.- Trauma to deciduous tooth injures permanent tooth bud.

Hypoplasia due to congenital synthesis.

- Hutchisons teeth in anteriors.- Screw driver shaped maxillary central incisors.- Mulberry molars.

Enamel hypoplasia due to Hypocalcemia

- In tetany (ca -6-8 mg/100 ml).- molar pitting variety of hypoplasia.

Hypoplasia due to birth injuries

- traumatic birth.- premature born children.- children who suffer hemolytic disease at birth.

Hypoplasia due to fluoride

- Mottled enamel- Fluoride conc. > 1ppm in drinking water.- There can be white flecking/ spotting on enamel, white opaque areas, pitting and

brownish staining or corroded appearance.

- They wear and even fracture easily

AMELOGENESIS IMPERFECTA

(Hereditary brown enamel, Heriditary Enamel Dysplasia)


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- Heterogeneous group of enamel defects having genetic basis.- Autosomal dominant.- MUTATION IN AMELX,ENAM,MMP20,KLK-4 GENESclini cal features:

Color ranging from yellow to dark brown. Affects all teeth of both dentition. Open contacts. Abrasion of occlusal/incisal surfaces. Smooth or may have // vertical grooves. Cheesy in consistency or may be hard.Classif ication (Witkop and Sauk)

1. Hypoplastica. Pitted, autosomal dominantb. Local, autosomal dominantc. Smooth, autosomal dominantd. Rough, autosomal dominante. Rough, autosomal recessivef. Smooth, X-linked dominant2. Hypocalcifieda. Autosomal dominantb. Autosomal recessive3. Hypomaturationa. Hypomaturation- hypoplastic with taurodontism, autosomal dominantb. X- linked recessivec. Pigmented, autosomal dominant


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d. Snow capped teeth

1) Hypoplastic type - defective formation of matrix.2) Hypocalcification type- defective mineralization of the formed matrix.3) Hypomaturation typecrystallite remain immature.

Hypoplastic amelogenesis imperfecta

- Yellow brown color.- Enamel pitted ,rough or smooth & glossy.-

Defective Ameloblast.- Reduced Enamel thickness-undersized teeth so lack of contact b/w adjacent teeth.

Hypocalcification amelogenesis imperfecta

- Colour clear to cloudy white , yellow brown.- Enamel is soft, may crack down.- Enamel thickness normal but mottled appearance.- Rarely snow capped with opaque enamel.

Hypomaturation amelogenesis imperfecta

- Poorly mineralized enamel start to fracture shortly after in function.- Increased permeability, stained & dark.- Under pressure explorer penetrate soft enamel.

Radiographic findings:

- In hypo plastic type-square shaped crown, thin opaque enamel, low or absent cusp- Pitted enamel appears as sharply localized areas of mottled density- In hypocalcified type-enamel density even less than dentine


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- With abrasion-oblitration of pulp chambersENAMEL RENAL SYNDROME

Enamel-renal syndrome (ERS) is characterized by hypoplastic amelogenesis imperfecta (AI) and

nephrocalcinosis (NC). It is listed as a "rare disease" by the office of rare diseases (ORD) of the

National Institutes of Health (NIH). This means ERS affects less than 200,000 people in the US

population. The common features of this syndrome are the presence of thin or no enamel,

delayed tooth eruption, intrapulpal calcifications, bilateral nephrocalcinosis, and normal plasma

calcium.

Enamel pearl

- Enamel pearl: Also called Enameloma or Enamel Drop.- Enamel pearl is condition where enamel is found on locations where it is not supposed to

be.- Usually present in furcation area of molars.- Thickness of enamel layer varied between 0.3-0.5 mm in different pearls and increased

pearl diameter.- Pearl enamel is loosely textured than crown enamel which is due to porosities due to

loosely packed crystals.

Odontodysplasia

- Developmental disturbance enamel & dentine thin, irregular & fail to mineralizeadequately.

- Central incisors & canine most affected.- Teeth small, mottled brown.- Caries susceptible, brittle so fracture easily.- Delayed or no eruption.- Radiographically enamel thin so not evident, pulp chamber & root canal are large &

wide.

Dens Evaginatus/Leong`premolar

- Outfolding of enamel organ resulting in tubercle of enamel on occlusal of premolar


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- Tubercle has dentin core & very slender pulp horn

REGRESSIVE DEFECT

Attrition:

Physiologic wearing away of tooth structure as a result of tooth to tooth contactocclusally and proximally.

Commonly seen in old age Permanent teeth > deciduous teeth Small polished facet on cusp tip & flattening of incisal edgeAbrasion

Pathologic wearing away of tooth substance through some abnormal mechanical process. Causes: Improper brushing technique, .Habits , Occupational, Improper flossing C/F: - Wedge shaped defect is seen at the DEJ exposed dentin is polished. Sharpe angle at the depth of the lesion and at enamel Secondary dentin formation occurs.Erosion

Loss of tooth structure resulting from chemo-mechanical acts in the absence of specificmicro-organisms. Seen mostly on facial surfaces Manifested as shallow, broad, smooth, highly polished scooped out depression.causes

Dietsoft drinks, lemon, citrus fruit juices Salivary citrates Local acidosis in the periodontal tissue Gastric reflux Vomiting

Abfraction


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Flexure of tooth under heavy lateral load which may lead to displacement or # of rods atthe CEJ.

Wedge shaped lesion seen commonly on buccal surface of mandibular teeth Produce micro fractures in the thinnest region of enamel at CEJ which predisposes to loss

when subjected to tooth brush abrasion.

Fractures

Due toTrauma Dentinal caries leading to undermining of enamel which fracture under occlusal load.

Discoloration

Extrinsic factors:1. Tobacco/tea stains2. Poor oral hygiene3. Food colors4. Gingival bleeding5. Existing restorations6. Chromogenic bacteria

Intrinsic factors:

1. Caries.2. Fluorosis.3. Tetracycline and other drugs.4. Age changes.5. Non vital teeth6. Internal resorption.7. Hereditary disorders.

Tetracycline

Discoloration of either deciduous or permanent teeth. Formation of complex with calcium ions i.e tetracycline orthophosphate. Oxytetracycline or doxycycline diminish tooth discoloration.


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Yellowishbrownish gray. Dentin is more heavily stained than enamel.

Erythropoetic prophyria

Genetic disease resulting in the deposition of porphyrins through throughout the body. These deposits also occur in enamel and leave an appearance described as red in color

and fluorescent.

Age Changes in Enamel

Attrition of occlusal surface and proximal contact point as a result of mastication. Wear facets are common. Crystal increase in size and pores diminishes. Water content of enamel decreases. Generalised loss of rod ends and flattening of perikymata. Localized increase of elements such as nitrogen and fluoride in superficial enamel layers

of older teeth.

Darker with age(due to addition of organic material from the environment or deepeningof dentin color seen through thinning layer of translucent enamel.

Reduced permeability to fluids.

Clinical Considerations

Cemento-enamel junction-Exhibits 3 types of relationships. In about 60% of teeth, cementum overlaps enamel. In about 30% of teeth, enamel and cementum meet edge to edge.


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In about 10% of teeth cementum and enamel do not meet and dentin in this area is notcovered by cementum.

Cavity cutting Unsupported enamel rods are not left at the margins, they would break and produce

leakage.

Brittleness of Enamel Enamel is brittle and does not withstand forces in thin layers or in areas where there is no

underlying dentine.

Deep enamel fissures Although these are not considered pathological, food lodgementand difficult clearance area may lead to dental caries, caries penetrate the floor of fissure

rapidly because the enamel in these areas is very thin. As the destructive process reaches

the dentin, it spread along to DEJ under rising to enamel.

Dental lamellae may also be predisposing locations for caries because they containmuch organic materials.

Bruxism, also known as clenching of or grinding on teeth, destroys enamel very quickly.The wear rate of enamel, called attrition, is 8 micrometers a year from normal factors.

The truly destructive forces are the parafunctional movements, as found in bruxism,

which can cause irreversible damage to the enamel.

Fluoride If incorporated into the hydroxyapatite crystalsbecomes more resistant to acids. Lead to precipitation of calcium phosphate . Shifts equilibrium of Ca and phosphate ions towards the solid phase. Remineralization reaction is enhanced . Interference in enzymatic action of bacteria.
http://en.wikipedia.org/wiki/Bruxismhttp://en.wikipedia.org/wiki/Attrition_(dental)http://en.wikipedia.org/wiki/Attrition_(dental)http://en.wikipedia.org/wiki/Bruxism


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Direct antibactericidal action. Formation of large appatite crystals. Lowers solubility of enamel. Recommended dosage in drinking water is 0.7-1.2 mg/L. Excessive ingestion may damage the tooth-forming cells, leading to fluorosis. Discoloration ranging from white spots to brown and black stains. Skeletal fluorosis -- bone disease caused by excessive consumption offluoride. Causes pain and damage to bones and joints.Fluoride catalyzes the diffusion of calcium and phosphate into the tooth surface, which in

turn remineralizes the crystalline structures in a dental cavity. The remineralized tooth surfacescontain fluoridated hydroxyapatite and fluorapatite, which resist acid attack much better than the

original tooth did..The acute toxic dose of fluoride is ~5 mg/kg of body weight

Effect of dental procedures Dental restorations involve the removal of enamel. the purpose of removal is to gain

access to the underlying decay in the dentin or inflammation in the pulp.

Enamel can sometimes be removed before there is any decay present. The most popularexample is the dental sealant. Sealants are unique in that they are preventative

restorations for protection from future decay and have shown to reduce the risk of decay

by 55% over 7 years.

Aesthetics is another reason for the removal of enamel. Removing enamel is necessarywhen placing crowns and veneers to enhance the appearance of teeth. In both of these

instances, it is important to keep in mind the orientation of enamel rods because it is

possible to leave enamel unsupported by underlying dentin, leaving that portion of the

prepared teeth more vulnerable to fracture.

Enamel etching- Invented in 1955,(BUNOCORE) By dissolving minerals in enamel, etchants remove the

outer 10 micrometers on the enamel surface and make a porous layer 550 micrometers

deep. This roughens the enamel microscopically and results in a greater surface area on

which to bond.

- Remove the smear layer
http://www.fluoridealert.org/health/teeth/fluorosis/mild.htmlhttp://www.fluoridealert.org/health/teeth/fluorosis/moderate-severe.htmlhttp://en.wikipedia.org/wiki/Fluoridehttp://en.wikipedia.org/wiki/Remineralisation_of_teethhttp://en.wikipedia.org/wiki/Hydroxyapatitehttp://en.wikipedia.org/wiki/Fluorapatitehttp://en.wikipedia.org/wiki/Dental_restorationhttp://en.wikipedia.org/wiki/Pulp_(tooth)http://en.wikipedia.org/wiki/Dental_sealanthttp://en.wikipedia.org/wiki/Crown_(dentistry)http://en.wikipedia.org/wiki/Veneer_(dentistry)http://en.wikipedia.org/wiki/Veneer_(dentistry)http://en.wikipedia.org/wiki/Crown_(dentistry)http://en.wikipedia.org/wiki/Dental_sealanthttp://en.wikipedia.org/wiki/Pulp_(tooth)http://en.wikipedia.org/wiki/Dental_restorationhttp://en.wikipedia.org/wiki/Fluorapatitehttp://en.wikipedia.org/wiki/Hydroxyapatitehttp://en.wikipedia.org/wiki/Remineralisation_of_teethhttp://en.wikipedia.org/wiki/Fluoridehttp://www.fluoridealert.org/health/teeth/fluorosis/moderate-severe.htmlhttp://www.fluoridealert.org/health/teeth/fluorosis/mild.html


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- increase retention of resin sealant- promote mechanical retention.- phosphoric acid is a common wet etching agentThere are three patterns formed by enamel etching :

-

Type 1 the enamel rods are dissolved.- Type 2 area around the enamel rods are dissolved.- Type 3 no evidence left of any enamel rods.type 1 - most favourable patterntype 3 - the least

The explanation for these different patterns is not known for certain but is most commonly

due to different crystal orientation in the enamel.

Tooth whitening

Effects on enamel

1. Surface texture-- Most SEM studies show no change( Haywood et al, 1991)- One study testing 16% and 35% carbamide peroxide solution showed loss of aprismatic

layer,exposure and demineralization of enamel and pitting (Bitter, 1995).

2. Surface hardness and wear resistance.- Surface hardness is unaffected(Zalkind et al, 1996)- OTHER study- decrease in hardness and wear resistance ( Seghi and Denry,1992)3. Chemical structure- Loss of organic componenets i.e. carbon, hydrocarbon and tertiary amine replaced by

oxygen

- Loss of average 1.06g/mm2 of calcium after 6 hours with carbamide peroxide(Haywoodet al , 1991)

- Tooth bleaching procedures attempt to lighten a tooths colourin either mechanical orchemical actions.

- A bleaching agent is used to carry out an oxidation reaction in the enamel or dentin.- Agents most commonly used to change the color intrinsically are hydrogen peroxide

and carbamide peroxide.

- Effects on enamel can be adverse apart from tooth whitening. It can result in lowpH,decrease in fracture toughness and no significant change in surface hardness. These

changes are due to change in organic matrix.
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- Tooth whiteners in T/P work mainly through mechanical action. They have mildabrasives which aid in removal of stains on enamel.

- Oxygen radicals from the peroxide in the whitening agents contact the stains in theinterprismatic spaces within the enamel layer. When this occurs, stains will be bleached

and the teeth now appear lighter in color. Teeth not only appear whiter but also reflectlight in increased amounts, which makes the teeth appear brighter as well.

- Studies show that whitening does not produce any ultrastructural or microhardnesschanges in the dental tissues. However, a tooth whitening product with an overall low

pH can put enamel at risk for decay or destruction by demineralization. Consequently,

care should be taken and risk evaluated when choosing a product which is very acidic.

Enamel & Microabrasion- This technique involves the rotary application of a mixture of weak hydrochloric acid and

silicon carbide particles in a water-soluble paste.

- An acid is used first to weaken the outer 2227 micrometers of enamel in order toweaken it enough for the subsequent abrasive force

- Enamel loss is lower than acid etching- Bond strength is higher for acid etching- Remove superficial stains of enamel EDTA treated Enamel- Dissolution mainly started on the peripheral borders of the prisms- Reaching laterally and then cervical portion.- complete delineation of rod cores with a decrease in interprismatic zone.- removal of calcium ions occur more in hypo mineralized sections.


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Shade- Enamel becomes temporarily whiter when isolated.- Thus shade must be selected before isolation and preparation of tooth.- This is due to temporary loss of loosely bound water.

Growth tracks in enamel :

- Enamel consists of tightly packed crystals organized by differential orientation of prismsand inter prisms.

- Crystal orientation is influenced by both cellular and physico chemical factors.- structure of enamel testifies the events that take place during enamel formation.- prisms are the fossilised tracks traced out by ameloblasts.- The tangential diameter of ameloblasts and the central distance of the prisms increase

from the DEJ to the enamel surface.

- The prisms cross striations are the light microscopic variations of the prism varicositiesor compositional variations and these are due to rhythm in enamel formation and the

variation is diurnal.

- In human Enamel, the rate of enamel formation is 3.54um and the enamel formationincreases from the inner incisal to outer enamel epithelium and decreases from incisal

area to the cusp region.

- The evenly spaced striae of retzius are the incremental lines that represent 6-11 dayrhythm in enamel formation while other lines represent the stress levels.

- The geometry of the enamel growth tracks and their chronological significance arevaluable tools in chronological mapping of dental development and for understanding

temporal and spatial patterns in tooth morphogenesis.

- The taxonomic significance of prism packing patterns, prism decussation and enamelthickness should be clarified through further systematic descriptive research.


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Regrowth of enamel from cultured cell

Can` t regenerate itself due to loss of cells so vulnerable to wear and tear. The idea of culturing technique originates from 1975 when Dr. J.G.Rheinwald and

Dr.H.Green of harvard medical school reported the use of feeder layers for culturingepithelial cells from skin.

The 3T3-J2 cells used in the culturing were gifted by Dr.H.Green. Cell scaffold approach (based on tissue engineering technology) was used to produce

artificial enamel.

Considering the crown engineering,three main parameters have been considered :

a) the relationship between crown morphology and tooth functionb)The growth of the organ which is hardly compatible with the organ scaffolds

c)Easily availiable non dental competent cell sources.

The in vitro synthesis involves : BMDC (BONE MARROW DERIVED CELLS) DENTAL

TISSUES.

The PEK(primary enamel knot) is involved in signalling crown morphogenesis andformation and fate is recognised by re association between :

a) embryonic day 14 (ED14) incisor and molar enamel organs and mesenchyme.

b) ED14 and molar enamel organs and BMDC.

The mesenchyme controls the fate of EK cells using apoptosis as criteria and function todetermine whether tooth is uni/multicusped.


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Epithelial cells extracted from developing teeth of 6 month old pigs continued toproliferate when cultured on special feeder layer of cells(3T3-J2 cells)

This study was reported at the 85th general session of the international association fordental research by a team of researchers from the institute of medical science,university

of tokyo(japan)

Now a days researcher`s are seeding cultured dental epithelial cells onto collagen spongescaffolds along with cells from the middle of tooth.

These scaffolds were then transferred into the abdominal cavities of rats where conditionswere favourable for cells to intearct and develop.

When removed after 4 weeks,the remnants of scaffolds were found to contain enamellike tissue.

The key finding of this study was that even after multiple divisions that occurred duringthe propagation of cells in culture,the dental epithelial cells retained the ability to produce

enamel as long as they were provided with an appropriate environment.

Calcium mediated differentiation of cell in vitro:

Primary human ameloblast were isolated from human fetal tooth buds. Cells were treated with calcium

cell morphology studied by phase contrast microscopy

Proliferation of cells measured by BrdU immunoassay. The effect of calcium on mRNA expression of amelogenin ,type 1 collagen

,DSPP,amelotin and KLK 4 was compared by PCR analysis.

Von kossa staining done to measure mineral formation Calcium induced cell organization and clustering at 0.1-0.3 mM concentration The addition of 0.1 mM calcium to the cultures up regulation of expression of

amelogenin,type 1 collagen and amelotin.

After pre t/t with 0.3 mM calcium,mineralised matrix could form.


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REFERENCES

ORBANS- TEXTBOOK OF ORAL HISTOLOGY TEN CATE ORAL HISTOLOGY DEVELOPMENT STRUCTURE & FUNCTION

SIXTH EDITION

SHAFERS STURDEVENT AFM STUDY OF DENTAL ENAMEL STRUCTURE AND SYNTHESIS COMPOSITION AND STRUCTURE OF DENTAL ENAMEL- JADA 1975; 91(3);594-

601

SOBEN PETER BERKOWITZ et al : oral anatomy & histology third edition James k. avery : oral development & histology Phillips` science of dental material High Levels of Hydrogen Peroxide in Overnight Tooth-Whitening Formulas: Effects on

Enamel and Pulp Journal of Esthetic and Restorative Dentistry; Volume 17 Issue 1 Page

40 - January 2005

10% or 16% carbamide peroxide did not effect the structure of enamel, whereas 35%carbamide did affect the structure Journal of Oral Rehabilitation Volume 27 Issue 4 Page

332 - April 2000

Ectopic Tooth Enamel. An SEM Study of the Structure of Enamel in Enamel Pearls byS.Risnes

The Emergence of "Nanospheres" as Basic Structural Components Adopted byAmelogenin by Janet Moradian.

Enamel Matrix: Structural Proteins by termine,torchia and conn SEM study of EDTA treated enamel by Hoffman et al


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A study on effect of bleaching agent on enamel by R.R.Seghi Functions of KLK4 and MMP-20 in dental enamel formation by Yuhe Lu, Department

of Biologic and Materials Sciences, University of Michigan School of Dentistry, 1011

North University, Ann Arbor

A study on General Histology and Cytology of Structural characteristics of staircase-typeretzius lines in human dental enamel analyzed by scanning electron microscopy by S.Risnes in the Department of Anatomy, Dental Faculty, University of Oslo, Blindern,

0316 Oslo 3, Norway

Kala Vani SV, Varsha M, Sankar YU. Enamel renal syndrome: A rare case report. JIndian Soc Pedod Prev Dent 2012;30:169-72

A study on enamel regeneration after restorative therapy by dr.kazue yamagishi

zenamel wdd

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