ENAMELINTRODUCTION

It covers the anatomical crown of the tooth and varies in thickness in different areas. Enamel provides a hard durable shape for the functions of teeth and a protective cap for the vital tissues of dentin and pulp.Both color and form contribute to esthetic appearance of enamel. Much of the art of restorative dentistry comes from efforts to stimulate the color,texture,translucency and contours of enamel with synthetic dental materials. Nevertheless, the lifelong preservation of the patient’s own enamel is one of the defining goals of the dentist.

CHEMICAL PROPERTIES

Weight (%)Weight (%) Volume (%)Volume (%)

Organic Organic 0.50.5 1.01.0

Inorganic Inorganic 95.595.5 87.087.0

Water Water 4.04.0 12.012.0

Inorganic composition

Calcium hydroxyapatite Ca10(PO4)6(OH)2 is principal mineral component of enamel. Hydroxyapatite is present in the form of crystallites about 70mm in width and 25nm thick. Calcium and phosphate form major constituent of enamel. Magnesium replaces the calcium ion and strontium, radium, vanadium and carbonate replace phosphate to modify the apatite crystal. Fluoride may substitute for hydroxyl ions, conferring greater stability and resistance to acidic dissolution. Core part of crystallites differs slightly in composition from periphery being richer in magnesium and carbonate. Chloride, lead, zinc, sodium, strontium and aluminum may also substitute into the apatite lattice.

Organic composition

A wide variety of organic molecules occurs in enamel, ranging from free amino acid (serine, glutamic acid and glycine) to large unique proteins complexes, these protein are Amelogenins and non Amelogenins (Enamelins) .50 to 90% of matrix composed of small molecules (peptide and free amino acid). Larger molecular weight material contains components rich in carbohydrate (80-95%, sugars )

Water:

The presence of water is related to the porosity of the enamel. As ions such as fluoride would, travel through the water component, its distribution is of clinical importance.

Physical characteristics

Most highly mineralized tissue in the body. Specific gravity is 2.8.Refractory index of enamel is1.6o.Enamel will wear because of attrition or frictional contact

opposing enamel or harder restorative materials, such as porcelain. Normal physiological wear of enamel is 29µm/year.

Density:

Decrease from surface of the enamel to the dentine enamel junction. It varies from 3.0 to 2.84gm/ml.The permanent upper incisors have maximum density and premolars and lower incisors have least.

Thickness

At the cusp of premolar thickness of enamel is 2.3 to 2.5mm.At the cusp of molars thickness of enamel is 2.5 to 3.0mm.At the incisal ridge of incisors 1.0mm.knife edge at the neck of tooth. Thickness is 1mm in primary tooth. Thin in occlusal pit and fissures. This forms a “V-shaped escape for food during chewing

Color & translucency

Its color is primarily a function of its thickness and the color of the underlying dentin. Color of enamel covered crown range from yellowish white to grayish white. Enamel is semi translucent .Color is determined by difference in translucency of enamel. Young enamel is white. Yellowish teeth having thin, translucent enamel. Grayish teeth having a more opaque enamel. The young anterior tooth has a translucent gray or slightly bluish enamel tint at the thick incisal edge.Caries and demineralization, anomalies of development, extrinsic stains, antibiotic therapy and excessive fluorides can alter the natural color of the teeth Enamel becomes temporarily whiter within minutes when a tooth is isolated from the moist oral environment.(temporary loss of loosely bound water)Shade must be determined before isolation and the preparation of a tooth for a tooth colored restoration.

Hardness:

Enamel is hardest biological tissue of the body. Its Knoop Hardness number is 343 (68 for dentin) .Hardness make enamel brittle. However dentin is a highly

compressive tissue that acts as a cushion for the enamel. Enamel requires a base of dentin to withstand masticatory forces. Enamel rods that fail to possess a dentin base because of caries or improper cavity preparation design are easily fractured away from neighboring rods. For maximum strength in tooth preparation, all enamel rods should be supported by dentin. Hardness vary over the external tooth surface according to the location. It decreases inward , with hardness lowest at the DEJ

Tensile strength and compressibility

Elastic modulus of enamel is 19 x 106 psi (131 GN m-2).Compressive strength is 76Nm.-2Enamel is very brittle structure with a high elastic modulus and low tensile strength, which indicates a rigid structure

Solubility:

Enamel dissolves in acidic medium. Surface enamel is less soluble in acidic media than deeper.

permeablity:

Enamel is permeable for varying degrees. The organic matrix and water contained in the enamel is in a network of microspores opening to the external surface. The microspores form a dynamic connection between the oral cavity and the systemic, pulpal and dentinal fluids Various fluids, ions and low molecular weight substances, whether deleterious, physiologic or therapeutic can diffuse through the semi permeable enamel. The dynamics of acid demineralisation,caries reprecipitation or remineralisation,flouride uptake are therefore not limited to the surface but are active in 3 dimension.

Resiliance

A substructure, organized into discrete parallel rods with the scalloped DEJ, minimizes the transfer of occlusal stress laterally and directs it anisotropically

or unidirectionally to the resilient dentinal foundation. The interwoven paths and interlocked key-hole morphology of the enamel rods help control lateral cleavage. Gnarled Enamel acts as a functional adaptation to occlusal stress. Further subdivision of enamel rods into distinct crystals separated by a thin organic matrix provides additional relief to help prevent fracture dentinal tubules fluids. Enamel thickness and degree of mineralization are greatest at the occlusal and incisal surfaces where masticatory contacts occurs. If enamel were uniformly crystalline, it would shatter with occlusal forces. Carious demineralization to the point of cavitations generally takes 3-4 years.Demineralisation of enamel is impeded because the apatite crystals 10 times larger than those in dentin. Enamel apatite crystals offer less surface to volume exposure and little space for acid penetration between the crystals. With preventive measures and exogenous or salivary renewal of calcium, phosphate and especially fluoride, the dynamics of demineralization can be stopped or therapeutically reversed

Tooth development

Tooth development divided into three overlapping phases.

Initiation: sites of the future teeth are established with appearance of tooth germ along an invagination of the oral epithelium called the dental lamina.

Morphogenesis: Shape of the tooth is determined by a combination of cell proliferation and cell movement.

Histogenesis: Differentiation of cells proceeds to give rise to the fully formed dental tissues both mineralized and non-mineralized.

Stages of Tooth Development

For descriptive purposes, tooth germs are classified into bud, cap and bell stages according to the degree of morpho-differentiation and histodifferentiation of enamel organ.

Bud stage:

The enamel organ in the bud stage appears as a simple, spherical to ovoid, epithelial condensation that is poorly morph differentiated and histo-differentiated.

Cap Stage

By the 11th week IUL the tooth bud continues to proliferate .The peripheral cells of cap stage are cuboidal cover the convexity of the “CAP” and are called the outer enamel (dental) epithelium. The cells in the concavity of the “CAP” become tall, columnar cells and represent inner enamel epithelium. Outer and inner enamel epithelium separated each other by stellate reticulum cells. Three temporary structure are seen in Cap stage

Enamel knot: The cells in the center of the enamel organ are densely packed and form enamel knot.

Enamel cord: Its vertical extension of the enamel knot.

Enamel niche: Its funnel shaped depression containing connective tissue. functional significance is not known

Enamel knots as signaling centers linking tooth morphogenesis and odontoblast differentiation

the enamel knot signals have important roles, together with mesenchymal signals, in regulating the patterning of the cusps and hence the shape of the tooth crown. It also suggest that the enamel knots are central regulators of tooth development, since they link cell differentiation to morphogenesis.Adv Dent Res. 2001 Aug;15:14-8.

Bell stage

divided into two stages

Early bell stage: By the 14th week of IUL further morphodifferentiation and histo-differentiation of the tooth germ leads to the early bell stage. The enamel organ show four distinct layer

External (outer) enamel epithelium

Stellate reticulum

Stratum intermedium

Inner enamel epithelium

External enamel epithelium: Outer layer of flatten low cuboidal cell, which limits the enamel organ ,cells of this layer contain centrally placed nuclei

Stellate reticulum: The cells are star shaped with long processes that anastomose with adjacent cells. The inter cellular spaces are fluid filled.

Stratum intermedium: This layer 1st appear at the bell stage and consist of few layer of squamous cells between inner enamel epithelium and stellate reticulum.

Inner enamel epithelium: Cells of this layer are consists of single layer which differentiate prior to amelogenesis into tall columnar cells called Ameloblasts. These cells are 4 to 5mm in diameter and 40mm high

Late bell stage: Appositional stage of tooth development is associated with the formation of the dental hard tissues, occurs at 18th week under inductive influence of developing Ameloblasts (pre Ameloblasts).

DEVELOPMENT OF ENAMEL

Enamel is an epithelial product. Other hard tissues are derived from connective tissue. Borderline b/w IEE& connective tissue of dental papilla is DEJ---determines the occlusal/incisal aspect of crown

Outer enamel epithelium

Highest convexity of enamel organ. Cells of OEE is irregular in shape .Cells of OEE develop villi & cp vesicles & large no:- of MC which help in active transport. Capillaries in contact with OEE shows area of thin walls

Stellate reticulum

Cells are star shaped .Wide intercellular spaces. Function that it acts as a buffer against physical forces that might distort DEJ.Decreasein thickness when first layer of dentin is laid

Stratum intermedium

Cells of this show mitotic division even after cells of IEE cease to divide. Are essential for enamel formation. Functionally associated with Amelogenesis. Intense alkaline phophatase activity

Inner enamel epithelium

Cervical loop-at the free boarder of enamel organ the OEE &IEE are continuous. Cervical loop cells are low columnar .As IEE traced coronally cells become tall columnar and their nuclei become aligned at the proximal end of the cells. Because Ameloblasts are distant from bv,IEEaccumulate glycogen before beginning secretory activity

Life cycle of Ameloblasts

Life span of IEE divided into 6 stages

1.morphogenic

2. organizing /differentiation

3.formative /secretory

4.maturative

5. protective

6.desmolytic

Morphogenic stage

Before the Ameloblasts are fully differentiated and produce enamel they interact with adjacent mesenchymal cells, determining the shape of DEJ & crown. Cells are short & columnar with large oval nuclei that almost fill the cell body. Golgi apparatus & centrioles move to the proximal end. Mitochondria is evenly distributed in CP. IEE separated from connective tissue of dental papilla layer is a cell free zone containing fine argyrophil fibers and the cytoplasmic process of the superficial cells of dental papilla.

Organizing

Cells of IEE & their nuclei shift proximally towards Stratum intermedium. Golgi complex increase its volume & migrate to centre.RER increases. Mitochondria cluster in proximal region. Ameloblasts become polarised cell with organelles distal to nucleus. The clear cell free zone between the IEE &the dental papilla disappears, probably because of elongation of epithelial cell towards the papilla. Thus the epithelial cells come into close contact with the of connective tissue dental papilla which differentiate into odontoblasts .During the terminal phase of organizing stage the formation of the dentin by the odontoblasts begins .As long as IEE is in contact with of connective tissue dental papilla, it receives nutrient materials from the blood vessel of this tissue. When dentin forms it cuts of the Ameloblasts from original source of nourishment .Then they are supplied by capillaries that surround & may even penetrate the OEE.This reversal of nutritional source is characterized by & gradual disappearance of Stratum reticulum. Distance between capillaries & Stratum intermedium and Ameloblasts is decreased. First appearance of dentin is critical in the lifecycle of Ameloblasts. Ameloblasts are connected by junctional complexes. Fine actin containing filament radiate from junctional complex into cytoplasm of Ameloblasts & can be distinguished as forming proximal &distal terminal web. They have ability to change the functional role to leaky or tight.

The basal lamina supporting Ameloblasts disintegrate after deposition of predentin &differentiation of Ameloblasts

Secretory stage

Ameloblasts maintain same length & arrangement .Enter formative stage after first layer of dentin has formed. Synthesis of enamel protein occur inRER passed on to Golgi complex .There they are Condensed and packed into secretory granules. They migrate to distal extremity of cell contents are released against newly formed mantle dentin. No time lapse between secretion of enamel matrix &mineralization. Hydroxyapatite are randomly packed in the first formed enamel &interdigitate with crystals of dentin. After the first structure less enamel is formed, Ameloblasts migrate away from dentin surface and tomes process formed. Cytoplasm of Ameloblasts continue into tomes process Distinction between process&cell body marked by distal terminal web jnal complex. Cell Process has secretory granules &small vesicles. Cell body has synthetic organelles. Cells of IEE (Ameloblasts) begins to secrete enamel matrix which becomes immediately partially mineralized seen as deep staining layer in demineralized H&E section. As this first increment of enamel is formed, the Ameloblasts begin to move away from dentin surface &as they do each cell form a conical projection –Tomes process just into newly forming enamel, giving the junction b/w enamel & Ameloblasts a PICKETFENCED/SAW TOOTHED APPERANCE.When Tomes process is established the sec of enamel pr becomes confined &staggered to two points. Secretion from first site with Ameloblasts forms enamel matrix wall. These walls enclose a pit into which tomes process fits. Secretion from second site later fills the pit with matrix. Wall becomes interrod. Infilling forms enamel rod.TP persist until final few layer of sturctureless increments of enamel is laid

MATURATION STAGE

Decrease in height of Ameloblasts occurs. Decrease in volume and organelle content. Excess organelles phagocytosed by autophagic vesicles containing lysozyme enzyme. Organelles shift to distal part of cell. Ameloblasts become involved in cyclical process. Cyclical nature is reflected in Ameloblasts morphology

with cell altering between ruffled &smooth boarder . Water & organic material is selectively removed from enamel to form smooth boarder. Inorganic is introduced in ruffled boarder.

protective

As enamel maturation near completion ,the Ameloblasts secrete basal lamina between flattened distal ends of cells &enamel surface.Hemidesmosomes attach Ameloblasts to enamel surface important for establishment of DENTOGINGIVAL. Ameloblasts with stratified epithelium (OEE+SI+SR ) forms REE.It protects mature enamel from connective tissue till tooth erupts. Connective tissue if it comes in contact with enamel cementum is deposited. Cell is still able to modify enamel function . fluoride if available is incorporated into enamel.

DESMOLYTIC

REE proliferates&induce atrophy of connective tissue separating it from oral epithelium leading to fusion of epithelium.Epithiliail cells elaborate enzyme that destroy connective tissue fibers by desmolysis. Premature degeneration of REE prevent eruption of teeth

Regulation of pH During Amelogenesis.

Crystal growth is modulated by changes in the pH of the enamel microenvironment that is critical for proper enamel biomineralization .mutations to genes involved in pH regulation may result in severely affected enamel structure, highlighting the importance of pH regulation for normal enamel development. This review summarizes the intra- and extracellular mechanisms employed by the enamel-forming cells, Ameloblasts, to maintain pH homeostasis and, also, discusses the enamel phenotypes associated with disruptions to genes involved in pH regulation. Calcif Tissue Int. 2010 Feb;86(2):91-103.

Amelogenesis

l.ENAMEL MATRIX FORMATION[differentiation of IEE into Ameloblast,Formation secretion of enamel matrix]

II. MINERALIZATION & MATURATION OF ENAMEL MATRIX

ENAMEL MATRIX FORMATION

Ameloblasts begin their secretory activity when a small amount of dentin laid is down. As enamel deposition proceeds thin continuous layer of enamel is formed along the dentin termed dentino enamel membrane. Four Ameloblasts involved in synthesis of each enamel rod. Organic matrix sec consists of- enamel protein, an array of enzyme-serine protease, phophatase, metalloproteinase, traces of protein analogues to various glycosylated , sulfated & phosphorelated noncollagenous protein in calcifying connective tissue

Enamel proteins—90%amelogenins

--10%enamelin,tuftelin,amelin

Amelogenins-molecular weight-22-30kda ,hydrophobic ,rich in proline, histidine, glutamine, ability to flow under pressure

Enamelin -molecular weight 48-70KDa,acidic ,rich in gutamine acid,aspartic acid,sreine

Enamelin-2%

amelin -5-10%

Tuftelin-intiation of mineralization.

Enamelins are secreted first &linked to formation of hypermineralized enamel first deposited on dentin. They are then retained in mature enamel in enamel tufts

Molecular mechanisms of dental enamel formation.

Tuftelin is an acidic enamel protein that concentrates at the DEJ and may participate in the nucleation of enamel crystals. Other enamel proteins may regulate crystal habit by binding to specific faces of the mineral and inhibiting

growth. Structural analyses of recombinant Amelogenins are consistent with a functional role in establishing and maintaining the spacing between enamel crystallites.(Crit Rev Oral Biol Med. 1995;6(2):84-108).

Mineralization &maturation

As soon as enamel protein is secreted by Ameloblasts it is instantly mineralized. Enamel protein is labile. Intial mineralization is thought to be achieved by nucleation from apatite crystals located within the dentin .After formation of partially mineralized enamel matrix, which involves production of entire volume of enamel, a process of maturation begins. Continued influx of mineral and removal of protein&water—final consistency is achieved

Mineralization involves 4 stages

I.Formation of partially mineralize en matrix(30%)

II. mineralization starts at the enamel surface proceeds into deeper layer until it reaches innermost layer

III. starts from innermost layer to surface, surface layer of 15 micron which mineralize slowly

IV.Outer layer mineralize heavily & rapidly becoming the most mineralized

STRUCTURE OF ENAMEL

ENAMEL RODS

The basic structural unit of enamel, the rods owes its existence to the highly organized pattern of crystal orientation. The rods are cylindrical in shape and are made of crystals with their long axes running for the most part parallel to the longitudinal axis of the rods. Interrod –an area surrounding each rod, crystal are arranged in different direction. Rod sheath-boundary where crystals of rod meet those of interrod at sharp angles .The consistent arrangement of rod sheath, with the protein content, accounts for the fish scale appearance of enamel matrix in demineralized/etched ground sections. in cross studies rod, interrod appear to have SHAPE OF KEY HOLE

Enamel rod head is 5micrometer wide, Tail is1micrometer wide. Rod length is 9microm.The rods vary in number from 5 million for a mandibular incisor to about 12 million for a maxillary molar .Enamel rod approximates the size of RBC .From the DEJ the rods run in a tortuous course to the surface of the tooth. Rods located in the cusps, the thickest part of the enamel are longer than those at the cervical areas of the tooth. Diameter of rods increases from DEJ towards the surface of the enamel at the ratio of about 1:2

ROD INTERRELATIONSHIP

Rods run in a direction nearly perpendicular to the surface of dentin .In deciduous tooth the rods run horizontally at the central and cervical part of the crown becoming increasingly oblique to almost vertical at the tip of cusps and incisal edges. In permanent tooth the rod arrangement is similar in occlusal 2/3 of the crown, but deviating from horizontal to a more apical direction in the cervical region.

ENAMEL PRISM

The structural components of the enamel prism are millions of small, elongated apatite crystallites. The crystallites are tightly packed in a distinct pattern of orientation that gives strength and structural identity to the enamel prisms. The long axis of the apatite crystallites within the central region of the head(body) is aligned almost parallel to the long axis of rod .The crystallites incline with increasing angles (up to 65 degree)to the prism axis in the tail region. The susceptibility of these crystallites to acid, either from an etching procedure or caries,appears to be correlated with their orientation. Whereas the dissolution process occurs in the head regions of the rod; the tail regions and the periphery of the head regions are relatively resistant to acid attack.

STRUCTURE OF HYDROXYAPATITE CRYSTALS

LENGTH 1600 Å

WIDTH 200 – 400 Å

EACH APPATITE CRYSTALS HAVE THOUSANDS OF UNIT CELLS THAT HAS HIGHLY ORDERED ARRANGEMENT OF ATOMS.CRYSTALLITE MAY BE 300 UNIT CELLS LONG, 40 CELLS WIDE AND 20 CELLS THICK

INCREMENTAL LINES OF RETZIUS

Are incremental growth lines successive apposition of enamel in discrete increments during formation of crown. In longitudinal sections it surround tip of dentin. In cervical region it run obliquely. From DEJ to surface it deviate occlusally. In horizontal sections they appear as concentric rings. Line of Retzius is due to any of the following reasons:-Variations in organic structure, Disturbances in rhythm of mineralizations, Intermittent alteration of rod course. It traverse the cuspal and incisal areas in symmetric arc pattern. When these circles are incomplete at the enamel surface, a series of alternating grooves called, the imbrication lines of pickerill are formed .Formed as a result of temporary constriction of Tomes process associated with secretory phase forming interrod enamel. Enamel rod bend as they cross incremental line

NEONATAL LINE

En of deci tooth develops partly before & partly after birth. Boundary is marked by accentuated incremental line of Retzius. Abrupt change in environment & nutrition of newborn infants is the reason. Prenatal en is better

Cross striations

En form at rate of ~4microm/day. Ground section shows periodic bands of 4micromi intervals across rods. Scanning electron microscope reveals constriction & expansion of rods. Cross striations shows daily variation in secretory activity of Ameloblasts. Incremental line of Retzius shows weekly rhythm

HUNTER SCHREGER BANDS

These are alternating dark and white band of varying widths best seen in longitudinal section under oblique reflected light. The Originate at the DEJ and pass outward ending at some distance from the outer enamel surface. In the sections cut parallel to long axis of the tooth. The bands of prism cut longitudinally are known as parazones and those cut transversely as diazones. change in the direction of rod responsible for the appearance of the hunterschreger bands. They are regarded as functional adaptation ,minimising the risk of cleavage in the axial direction under the influence of occlusal masticating forces

Gnarled enamel

Especially near dentin in the region of cusp or incisal edges rods appear twisted .Rods arranged radially in horizontal rows. Rods surround long axis of tooth like a washer .Rods undulate back & forth with in rows. This type of enamel formation does not yield readily to the pressure of bladed, hand cutting instruments in tooth preparation.

ENAMEL LAMELLAE

They are thin, leaf life structures extend from the enamel surface toward the DEJ they extend to and sometimes penetrate the dentin. They consist mostly of organic material which is a weak area predisposing a tooth to entry of bacteria and dental caries. Lamellae may develop in plane of tension, where rods cross such a plane, a short segment of the rod may not fully calcify.

Three type of lamellae are founded

Type A: Lamellae composed of poorly calcified rod segment.(restricted to en)

Type B: Lamellae consisting of degenerated cells.(reach into dentin)

Type C: Lamellae arising in erupted teeth where cracks are filled---org matter from saliva (reach into dentin)

En lamellae-cells in depth degenerate, surface may remain vital-hornified cuticle

Crack if develops disturbance is severe .in unerupted tooth it is filled by cells .after eruption it is filled by organic substance .If connective tissue invade Crack cementum is formed.

ENAMEL TUFTS

They are hypo-mineralized structures of enamel rods and inter-prismatic substance arise at the DEJ and reach into the enamel to about 1/5th to 1/3rd of its thickness. in ground section resemble tuft of grass. Contain greater con of enamel protein-Enamelin. They extend into the enamel in the direction of the long axis of the crown may be involved in the spread of dental caries. Tufts are believed to occur developmentally because of abrupt changes in the direction of groups of rods that rise from different regions of scalloped DEJ

DENTINOENAMEL JUNCTION

The interface of the enamel and dentin is scalloped in outline. The convexities of the scallops are directed toward the dentin.SEM shows it to be a series of ridges that increase the surface area and probably enhance the adhesion between enamel and dentin. It is hyper mineralized and 30µm thick interdigitation contributes to a firm attachment between dentin and enamel

ENAMEL SPINDLE

Their direction similar to Ameloblasts ,right angle to surface of dentin. Occasionally odontoblast processes pass across the DEJ into the enamel. Their ends are thickened and are termed as enamel spindles. They seem to originate from processes of odontoblasts that extended into the enamel epithelium before hard substances were formed. In gs org content replaced by air & dark in trans light

CLINICAL SIGNIFICANCE : HAS PAIN RECEPTORS WHICH EXPLAINS ENAMEL SENSITIVITY DURING CAVITY PREPARATION IN SOME PERSONS

Surface structures

Structure less enamel

Perikymata

Rod ends

cracks

STRUCTURELESS OUTER LAYER OF ENAMEL

It is about 30µm thick .seen in70% permanent teeth and all deciduous teeth. Most commonly toward the cervical area and less often on cusp tips. There are no prism outlines visible, and apatite crystals are parallel to one another and perpendicular to straie of Retzius. Layer is heavily mineralized.

PERIKYMATA

TRANSVERSE WAVELIKE GROOVES PARALLEL TO EACH OTHER AND TO CEJ.EXTERNAL MANIFESTATIONS OF STRIAE OF RETZIUS

ROD ENDS

CONCAVE AND VARY IN DEPTH AND SHAPE SHALLOWEST IN CERVICAL REGIONS AND DEEPEST AT INCISAL EDGES

CRACKS

NARROW FISSURE LIKE STRUCTURESAND RUN AT RIGHT ANGLES TO DEJ,OUTER EDGES OF LAMELLAE CONSIST OF ORGANIC MATERIAL ,SITE OF WEAKNESS THAT INITIATE DENTAL CARIES

ENAMEL CUTICLE

NASMYTH’S MEMBRANE OR PRIMARY ENAMEL CUTICLE IT IS BASAL LAMINA SECRETED BY AMELOBLASTS WHEN ENAMEL FORMATION IS COMPLETED

Ameloblasts cell degenerates following formation of enamel rod. The final act of Ameloblasts cell is the secretion of a membrane covering the end of the enamel

rod. This membrane covers the entire crown of newly erupted tooth but is probably soon removed by mastication and cleaning

PELLICLE

An organic deposit called pellicle covers the erupted enamel. It is a precipitate of salivary proteins. The pellicle reforms within hours after an enamel surface is mechanically cleaned. Microorganisms may invade the pellicle to form bacterial plaque, a potential precursor of dental caries

AGE CHANGES

Enamel is a non-vital tissue that is incapable of regeneration. With age, it becomes progressively worn away in the regions of masticatory area. Wear facets are increasingly pronounced in older people. Other age changes seen are discoloration and reduced permeability. Linked to these changes there is an apparent reduction in incidence of caries.Water content of enamel also decreases. Teeth darken with age. It may be due to addition of organic material to enamel from the environment or may be due to the deepening of dentin color seen through the progressively thinning layer of translucent enamel.

MAMELLONS ARE LOST, LOSS OF ROD ENDS AND PERIKYMATA, ATTRITION, ABRASION, EROSION, FRACTURE OR CRAZE LINES.ATTRITION OR WEAR OF OCCLUSAL SURFACE AND PROXIMAL CONTACTS – MESIAL MIGRATION.SEVERE ATTRITION RESULTS IN REVERSE CUSPING ,ARRESTED CARIES

Enamel caps and focal holes (depression):

Small elevations 10-15mm of depression (focal holes) are found particularly on lateral surfaces.

Enamel broches:

Larger surfaces elevations, 30-50mm in diameter, also occur occasionally and consists of radiating group of crystal.

CEMENTOENAMEL JUNCTION

The relation between enamel and cementum at the cervical region of the tooth is variable. In 60% of the teeth, cementum overlaps the cervical end of enamel for a short distance. In 30% of all teeth, cementum meets the cervical end of enamel in a relatively sharp line. In about 10% of teeth, enamel and cementum do not meet. This occurs when the enamel epithelium degenerates at its cervical termination, permitting connective tissue to come in direct contact with the enamel surface. Electron microscopic evidence indicates that when connective tissue cells, cement oblasts come in contact with enamel they produce a laminated, electron dense ,reticular material termed afibrillar cementum.

Pits and Fissure:

Pits and fissures are defects in the enamel surfaces usually associated with developmental grooves that mark the line of fusion between cusp or other major division of crown .As enamel formation proceed from these centers, it progresses over medial inclines of the cusps towards centre of the tooth. Strangulation occurs when Ameloblasts from adjacent cusp literally collide as they retract from DEJ. Because secretory activity ceases in these compressed cells, a fissured defects in the enamel results.

MORPHOLOGICAL TYPE OF OCCLUSAL FISSURES:

V – Wide at top and gradually narrowing towards the bottom (34%)

U – Almost same width from top to bottom (14%)

IK – Hourglass, extremely narrow slit associated with a large space at the bottom (26%).

λ – Inverted Y, bifurcating at the bottom (7%).

I – Extremely narrow slit (19%)