Seminar on chemical , physical and mechanical properties of enamel
Size: 11.21 MB
Language: en
Added: Aug 24, 2022
Slides: 123 pages
Slide Content
ENAMEL
Contents Introduction Physical properties Chemical properties Structure of enamel Rods Gnarled enamel Dentino -enamel junction Cemento -enamel junction Apri smatic enamel Hunter schreger bands Striae of retizius Microscopic details of surface enamel Perikymata Rod ends Enamel crack Investing layers associated with enamel surface
Age changes Difference b/w deciduous & permanent tooth Development of enamel Amelogenesis Life cycle of ameloblast Etiology of developmental anomalies of enamel (as per soames ) Amelogenesis imperfecta Classification (as per witkop ) Clinical features Radiographic features Enamel hypoplasia Factors In brief about each factor Clinical aspect Enamel caries Non carious lesions of enamel Effect of bleaching ( Greenwall ) Discolouration classification ( hyas , nathoo )
Consideration for cavity preparation ( marzouk ) Effects of drugs on enamel Tetracycline Minocycline Effect of micro abrasion ¯o abrasion Effect of burs Effect of fluoride on enamel Cavosurface considerations Composite Inlay Enamel etching Ectopic enamel Effects of lasers Emdogain Conclusion Reference
I NTRODUCTION Teeth is composed of 3 mineralized tissues i.e. Enamel, dentin & cementum. 1.Acellular calcified tissue covering anatomic crown & providing shape & contour to tooth. 2. Ectodermal in origin. 3. Hardest tissue of body. 4. Physiologically unrepairable tissue.
Physical properties colour Appears bluish white or greyish at the thick opaque areas & yellow-white at the thin areas reflecting underlying dentin. Translucency of enamel – increase with increasing wavelengths Dehydration decreases translucency but it was reversed on rehydration.
Hardness:- hardest structure of the body i.e.5 to 8khn. Permeability:- selectively permeable. Density:- decreases from the surface of enamel to the dentino -enamel junction. Thickness:- cusps of the molars measures 2.5 mm incisal edges of incisors 2.0 mm.
Chemical properties
Hexagonal structure with width:70nm; thickness:25nm. Ions present are magnesium, lead, fluorides. Core is more soluble than periphery Amelogenins Heterogenus group of low molecular weight proteins Hydrophobic; rich in proline , histidine , glutamine and leucine . Non amelogenins Enamelin , ameloblastin , tuftelin . High molecular weight proteins. Rich in glycine , aspartic acid, serine Inorganic Organic
WATER BY WT:2% By vol:5-10% Water lies -in b/w crystals and rods Trapped in defects of crystalline structure
Structure of enamel Rods/ enamel prism Basic structural unit of enamel. Rods are thin running from DEJ to surface in a tortures manner. Length of rods are more than width. Longer in cuspal region than cervical area Dia .of rods increases from DEJ to surface in a ratio of 1:2. Rods dimensions: width:5 µ m length:9 µ m diameter:4 µ m
Cross section of rods Type 1: circular Type2: parallel rows. Type3: key hole/paddle shaped pattern. All three type of pattern are seen in human teeth but most common is type 3.
Type3 Head and tail present in longitudinal section. Head of rod is directed occlusally ,tail is directed cervically . Millions of appetite crystals in rod running parallel to long axis at head end. At tail crystals diverging 60-70 º from long axis. Due to deviation rods are not closely packed & make space for organic matrix at these surfaces Rods are clear crystalline permitting light to pass through them. Demineralized rods resembles fish scale pattern
Directions of rods Deciduous tooth : horizontal at cervical and central part. Permanent tooth: horizontal in occlusal two third of crown and apically directed at cervical third. Permanent maxillarymolar:12 million rods. Permanent lower incisors:5 million rods .
Gnarled enamel The enamel at the cusp of the tooth generally exhibits a wavy pattern. This enamel is called gnarled enamel Optical appearance of enamel cut in oblique plane Bundles of rods appear interwine more irregularly Makes enamel stronger Seen in the incisal or cuspal region.
Hunter- schreger bands Optical phenomenon seen in reflected light Alternate light and dark bands Seen in ground longitudinal section Originate from the DEJ. Dark bands – parazones Light bands – Diazones . Angle between them is 40 degrees
Incremental lines of Striae of retzius Longitudinal section: runs obliquely from D.E.J to surface Appears as brownish band in ground section . Moderate intensity is considered as normal Etiology Periodic bending of E. rods. Variation in organic structure. Physiologic calcification rhythm.
Transverse section of striae of retzius Concentric lines like growth rings of tree Due to metabolic disturbances during matrix formations results in broad and prominent incremental lines
Surface structures of enamel Aprismatic enamel Perikymata Enamel cracks Rod ends
Aprismatic enamel About 30 µm thick. In 70% permanent teeth and all deciduous teeth. Found least often over the cusp tips. Found commonly in the cervical areas. No prisms outlines are visible All the apatite crystals are parallel to one another and perpendicular to the striae of Retzius . More mineralized than the bulk of Enamel beneath it.
perikymata Transverse wave like grooves supposed to be external manifestation of straie of retzius . On C.E.J:30perikymata/mm. On enamel:10perikymata/mm. Lies parallel to each other. Clearly seen on cervical enamel of deciduous second molar.
Perikymata (imbrication lines) Are external manifestations of Retzius striae
Rod ends Concave & vary in depth & shape Shallowest in cervical& deepest in occlusal Ultra structurally, surface of enamel – Uneven Pits of about 1 – 1.5 micrometers in diameter. Elevations of about 10-15micrometer - enamel caps
Enamel cracks The narrow, fissure like structure that are seen on almost all surface Supposed to be an outer edge of lamellae Extends for varying length perpendicular to D.E.J. Long lamellae appear thicker than shorter ones
Neonatal lines Supposed to be resulted due to abrupt change in the environment & nutrition of newborn infant prenatal enamel is better developed than post natal enamel because fetus develops in a well protected environment with adequate supply of essential nutrients Due to undisturbed development the perikymata is absent in occlusal part while present on post natal cervical part
Dentinoenamel junction Scalloped junction – the convexities towards Dentin. At this junction, the pitted Dentin surface fit rounded projections of the enamel. Crystals of enamel and dentin mix with each other. Enamel lamella Enamel spindle Enamel tufts
. TRANSVERSE SECTION SHOWING THE D.E.J. SCALLOPED APPEARANCE OF D.E.J DEJ, more pronounced in occlusal area, where masticatory stresses are greater.
Enamel lamellae . Thin leaf like extending from enamel to D.E.J. Hypo mineralized , best seen in transverse sections. Persists even after decalcification. Develops in plane of tension, rods crossing this plane do not calcify.
Types of lamellae . 3 types are present i.e. Type A Type B Type C Type A Seen in enamel . Rods are poorly calcified .
TYPE B May reach into dentin . Consists of degenerated cells . TYPE C May reach into dentin. In erupted teeth filled with organic matter.
Enamel spindles Narrow (8 µm in dia.) extending 25µm in enamel Resulted due to entrapment of odontoblastic process b/w ameloblast during early stage of tooth development. Commonly seen in region of cusp where most crowding of odontoblast would have occurred. Best seen in longitudinal section
Longitudinal section of enamel showing enamel spindles
Enamel tufts Arises from DEJ & seen 1/5 th to 1/3 rd thickness of enamel Resembles to tufts of grass in thick ground section & under low magnification Extends in long axis, so best seen in horizontal section Consist of hypocalcified E. rods and interprismatic substance
Enamel Tufts
Cemento enamel junction 3 patterns are present Pattern 1- 60%: cementum overlaps enamel Pattern 2- 30%: cementum meets enamel at butt joint. Pattern 3- 10%: cementum fails to meet enamel and exposes dentin.
Three patterns of C.E.J .
Investing layers on enamel surface Primary E. cuticle ( Nasmyth’s membrane). Afibrillar cementum . Pellicle (a precipitate of salivary proteins).
Primary enamel cuticle : Covers the entire crown of newly erupted tooth. Thickness: 0.2 µm. Removed by mastication (remains intact in protective areas). Function- protect the surface of the enamel from the resorptive activity of the adjacent vascular tissue prior to the eruption of the teeth.
Afibrillar cementum . Covered the cervical area of the enamel. Thickness: up to 10 µm. Continuous with the cementum . Secreted after Enamel Organ retracted from the cervical region during tooth development.
Pellicle: Precipitate of salivary protein Covers the crown Re-form within hours after mechanical cleaning . May be colonized by microorganisms to form a bacterial plaque. Plaque may be calcified forming calculus.
Age changes Physiological wear depending on diet, habits etc. Darker in colour due to decreased translucency, formation of secondary dentin, surface stains & thinning of enamels. Decreased permeability & water content results in harder tooth surface. Increased fluoride & nitrogen incorporation in surface of enamel results in decreased porosity & caries incidence.
Differences b/w deciduous & permanent enamel Lighter in colour , bluish white Darker in colour grayish or yellow white Thinner enamel i.e. 1mm thicker enamel i.e. 2-3 mm Rods are perpendicular to DEJ Directed gingivally in cervical direction More supplemental grooves Lesser supplemental grooves
Development Epithelial enamel organ 4 distinct layers depending on morphology, function or location -Outer enamel epithelium -Stellate reticulum -Stratum intermedium -Inner enamel epithelium
Border line b/w I.E.E & dental papillae is D.E.J of future Outer enamel epithelium Single layer of cubodial cells separated from dental sac by basement membrane Increased vascularity ensures a rich metabolism During enamel formation cells of O.E.E develops cytoplasmic vesicles & large no of mitochondria
STELLATE RETICULUM Star shaped cells are separated by inter cellular substances Connected to cells of enamel epithelium & stratum intermedium by desmosomes Provides elasticity so acts as a buffer against forces that might distort the formation of DEJ
STRATUM INTERMEDIUM Present between stellate reticulum & I.E.E Believed to play a role in enamel production . Action via fluid diffusion or by contributing necessary elements or enzymes
INNER ENAMEL EPITHELIUM Derived from basal layer of epithelium Assume a columnar shape & differentiate into ameloblast that produces enamel matrix Cell differentiation occur early in incisal edge or cuspal region than cervical loop.
CERVICAL LOOP : At the free border of the enamel organ the outer and inner enamel epithelial layers are continuous and reflected into one another as the cervical loop. When the crown has been formed, the cells of this portion give rise to Hertwig’s epithelial root sheath.
Life cycle of Ameloblast 6 stages are present . Morphogenic stage. Organizing stage. Formative stage. Maturative stage. Protective stage. Desmolytic stage.
Morphogenic stage Before the full differentiation of amoeloblast and production of enamel they interact with adjacent mesenchymal tissue shape determination of DEJ & crown Cells are short columnar, oval nuclei, with dispersed mitochondria Basal lamina separates dental papillae and I.E.E .
ORGANIZING STAGE Elongation of epithelial cells towards papillae. Close contact between papillae and epithelial cells. odontoblast At terminal phase of this stage odontoblast gives dentin
Formative stage Formation of enamel matrix. Ameloblast approx. retain the same size. Development of blunt process on ameloblast surface which penetrate the basal lamina and predentin .
Maturative / mineralization stage Starts after full thickness matrix formation on occlusal or incisal area. At cervical matrix formation is under progress. Ameloblast is reduced in size. Ameloblast display microvilli at the distal extremities and cytoplasmic vacuoles containing enamel matrix like material
Protective stage Ameloblast can’t be differentiated from S.I.&O.E.E as once enamel get fully matured. Stratified epithelium covering enamel is termed as REDUCED ENAMEL EPITHELIUM . Which protects mature enamel. Retraction of epithelium at cervical edge . Deposition of afibrillar cementum on enamel
Reduced enamel epithelium covering enamel
Desmolytic stage Reduced enamel epithelium induces atrophy of connective tissue separating it with oral epithelium thus fusion of the two epithelia can occur Premature degeneration of the reduced enamel epithelium may prevent the eruption of the tooth .
Amelogenesis Majorly composed of 2 process Organic matrix formation Development of tomes process Distal terminal bars Ameloblast covering mature enamel 2.Mineralization & maturation of enamel matrix
Formation of organic matrix Starts after dentin formation Island of enamel matrix are deposited along predentin Amelogenin degradation into smaller low M.wt fragments – specific functions in regulating crystal growth. In fully formed teeth, amelogenin is present between crystals, absence of amelogenin hypoplastic teeth
Ameloblastin and enamelin helps in nucleation and crystal growth. Amelotin, a new protein, secreted by mature ameloblast helps in enamel formation.
Development of tomes process Projection of ameloblast into matrix is called as tomes process containing abundant R.E.R. & mitochondria As per electron microscope- 4 ameloblast results in the synthesis of 1 enamel rod
Distal terminal bars Juctional complexes which encircle ameloblast at distal and proximal ends have fine radiating actin filaments extending into cytoplasm, forming webs. Serves to control substances that pass between ameloblast and enamel. separate tomes process from rest of cells.
Ameloblast covering mature enamel Shorter ameloblast covering the mature enamel Ameloblast reduce in height, enamel stops secretion, process of amelogenin removal starts. Modulation: ameloblast alternate cyclically in developing ruffled and smooth borders in the apical cytoplasm during the maturative stage .
Ruffled ended ameloblast- numerous lysosomes and endolytic activity, promotes calcium entry into forming enamel. Smooth ended ameloblast- leaks small amounts of proteins and water into forming enamel.
Mineralization &maturation of enamel matrix 2 stages. First stage : Partial mineralization of matrix & interprismatic substance. Influx of about 25-30% of total mineral content, form crystalline apatite, some studies say it is octacalcium phosphate, however it is unstable and convert into hydroxyapatite.
Second stage : starts from height of crown & proceed cervically. Rods mature from -depth to surface -cusp to cervical lines Maturation starts before matrix reaches full thickness. Advancing front is at first parallel to DEJ & later to outer enamel surface.
Primary ribbon shaped crystals increase in thickness more than width . they increase from 1.5 - 25µm during maturative phase. The rate of formation of enamel is 4µm/day Therefore to form 1mm layer of enamel it would take 240 days
Etiology of developmental abnormality of enamel Local cause : (as per soames ) Infection Trauma Radiotherapy Idiopathic Generalized cause : Environmental/ systemic Prenatal - infection -maternal disease. -excess fluoride ions
Neonatal – hemolytic disease of new born -hypo calcemia Post natal -severe child hood disease -Cancer chemotherapy -Excess fluoride ions -Ingestion of lead, tetracycline Genetic Teeth only affected- Amelogenesis imperfecta Teeth is affected in association with generalized defects –down syndrome - ectodermal dysplasia
Extent of enamel defect depends on : Intensity of etiological factors. Duration of presence of factors. Time at which factors occurring during crown development
Amelogenesis imperfecta/ hereditary brown opalescent enamel/hereditary brown enamel Ectodermal disturbance development of enamel takes places in 3 stages: Formative stage (deposition of organic matrix) calcification stage (matrix mineralization) Maturation stage (crystals are enlarged & matured)
Clinical features Hypo plastic type : enamel not formed to full thickness on newly erupted developing teeth. Hypo calcified type : enamel is soft & can be removed by prophylactic instrument. Hypo maturation type : pierced by an explorer tip under firm pressure & can be lost by chipping. Discolouration ranges from yellow to dark brown.
Enamel may be totally absent, may have chalky texture, cheesy consistency or may be hard sometimes smooth or with numerous parallel vertical grooves Open contacts & abraded occlusal , incisal edges radiographic features Enamel may be absent, may be very thin over tips of cusps & interproximal surfaces
Enamel hypoplasia Defined as an incomplete or defective formation of enamel matrix of teeth. Types: Hereditary Environmental Hereditary type Deciduous & permanent teeth are affected
Environmental type Either dentition is affected , both enamel & dentin is affected. Factors producing injury to ameloblast : Deficiency of vit.A & vit.D . Exanthematous disease like measles , chicken pox etc. Birth injury, Rh hemolytic disease Local infection or trauma Chemical ingestion Congenital syphilis Hypocalcaemia Idiopathic cause.
Mild environmental hypoplasia results in small grooves or pits on surface In severe condition presence of deep pits arranged horizontally across the tooth surface It results only in the formative stage of enamel formation
Due to nutritional deficiency Commonly seen in- central/ lateral incisors - canine - first molar Vit. D deficiency is the most common cause, may be seen due to deficiency of vit. A & vit.C pitting type of hypoplasia is present.
Due to congenital syphilis Commonly involve- max. & mand . central incisor ,first molars Anterior teeth- Hutchinson's teeth Post. Teeth- mulberry/ moon’s/Fournier’s molars Upper central incisors are screw driver shaped due to absence of central tubercle or calcification centre. 1 st molar: -irregular crown -Enamel of occlusal 3 rd of tooth appears to be an agglomerate of globules rather than well formed cusp.
Due to hypo calcemia : Pitting variety. Due to birth injuries : Traumatic birth may cause cessation of enamel formation Due to local infection or trauma : Single tooth involvement is common called as TURNER’S TOOTH & condition is called as TURNERS HYPOPLASIA Commonly involved are max. incisors & premolars
Mild brownish to severe pitting &irregularity of teeth Carries bacterial infection to ameloblast layer of tooth. Trauma to teeth inward movement of teeth disturbance in permanent teeth
Due to fluoride Mottled enamel is formed Water level of fluoride as per W.H.O should range b/w 0.7-1.2 ppm Excess may lead to fluorosis .
Ectopic enamel/ enamel pearl Presence of enamel in unusual location mainly root Hemispherical in shape , may consist entirely of enamel or may contain underlying dentin & pulp tissue. Commonly seen in furcations or c.e.j of maxillary molars followed by mandibular molars. Clinically significant for endoperio lesions
Effect of caries on enamel . Zones of enamel caries Zone1: translucent zone . Zone2: dark zone. Zone3:body of lesion. Zone4:surface zone
Zones of enamel caries
TRANSLUCENT ZONE Deepest zone. Represent advancing front of lesion Pore volume:1%, i.e. 10 times greater than normal enamel. DARK ZONE Because does not transmit polarized light. Less of crystalline structure. Total pore volume:2-4%
BODY OF LESION Largest portion Pore volume:5% -25% at periphery. Striae of retzius are marked & accentuated SURFACE ZONE Relatively stable Radiopacity comparable to adjacent enamel
Pit & fissure caries of enamel Large no. of S.Sangius are found in pit & fissure of newly erupted teeth Where as large no. streptococcus mutans are present in carious pits & fissures. Gross appearance: inverted V shaped with a narrow entrance & wider at base.
Pit & fissure enamel caries
Smooth surface enamel caries . Plaque accumulation is seen towards gingiva below the contact area. Gross appearance: V shaped lesion with wider area of origin & apex of V is directed towards D.E.J.
Non carious lesions of enamel Attrition Abrasion Erosion Localized nonhereditary enamel hypoplasia Localized non hereditary enamel hypo calcification Discolouration Amelogenesis imperfecta ( AS PER MARZOUK )
Attrition Surface tooth structure loss resulting from direct frictional force b/w contacting teeth Physiological: age dependent, continuous Type: - proximal - occlusal
Abrasion : Surface loss of tooth structure resulting from direct friction b/w teeth & external object or from frictional force b/w contacting tooth component in the presence of abrasive medium smooth polished , v shaped Etiological features:- Tooth brush abrasion -denture of porcelain teeth opposing naturals
Erosion Loss of tooth structure resulting from chemicomechanical acts in the absence of specific microorganism Glazed surface decreased caries incidence Supporting teeth are healthy etiological factors:- -acids of diet - acids of gingival crevice -acid fumes
Effect of bleaching 16-35% of carbamide peroxide results in loss of aprismatic layer, exposure of enamel prism & pitting. (BITTER 1995 ) Surface hardness & wear resistance 10% carbamide peroxide may lead to reduction in hardness which reflect the loss of mineral from enamel and decreased wear resistance ( SEGHI & DENRY1992 ) Decreased fracture toughness Loss of organic content from treated enamel
Effect of fluoride on enamel Increased enamel resistance Increased rate of post eruptive maturation Remineralization of incipient lesion
Increased enamel resistance When hydroxyapatite is exposed to F - ion concentration upto 1ppm a layer of flouroapetite is formed. Most of the fluoride ion which enter the enamel replaces the OH- ion. Increased rate of post eruptive maturatation Hypomineralised area of recently erupted tooth are mineralized as they get exposed to fluoride ion of oral cavity.
Remineralization of incipient lesion Acts by accelerating the growth of enamel crystals in incipient lesion Rate of remineralization is enhanced in the presence of calcium & phosphorus ions Preeruptive incorporation Get incorporated in fluid filled sac around the tooth Highest concentration is seen in enamel crown near surface Post eruptive incorporation Resulting into formation of flouroapetite crystals
Discolouration of enamel As per classification of DZIERKAN(1991), HYAES et al(1986)& NATHOO(1997) Extrinsic stains : - plaque - Mouthwashes e.g. chlorhexidine -Beverages e.g. tea , coffee -Foods e.g. berries, beet roots -Dietary fibers precipitate -Antibiotics -iron supplements Intrinsic stains : preeruptive disease- liver disease hematological disease e.g. Rh factor disorder Medications : tetracycline Post eruptive disease- trauma -Aging -Smoking -Dental restorations.
Effect of drugs on enamel Tetracycline: ( DCNA OCT2002& SHAFERS 4 TH ED.) In 1961 & 1963 it was suggested that tetracycline bounds to Ca ++ ion of newly formed teeth or bone in young children. Administration during pregnancy leads to deposition in fetal teeth resulting in brownish grey discolouration Teeth shows bright yellow discoloration under u.v . light. Precautions: No tetracycline before 8 yrs & oxytetracycline or doxycycline in spite of tetracycline during pregnancy
Severe tetracycline staining
Minocycline : Semi synthetic tetracycline Absorbed into dentin via pulpal blood vessels Enter into enamel defect through crevicular fluid. stains are composed of drug degradation product Minocycline - Hemosidrin complex
Consideration while making cavity Enamel rods should rest on sound dentin. Enamel rods forming cavosurface margin/ angle must have their inner ends resting on sound dentin & outer end must be covered by restorative material. Junction b/w different enamel walls should be rounded. If walls has to be inclined then outermost part of wall should follow the direction of rods & innermost is supported by dentin. In area where there is abrupt change in the direction of rods or where rods do not follow any specific direction, that part should be included in cavity & place the cavity margins in more predictable rod pattern (As per sturedvent )
Micro abrasion In 1984 MCCLOSKY recommended for removing brown stains of fluorosis by 18% HCl . In 1986 CROLL AND CAVANAUGH used HCl & pumice and termed as mircoabrasion Useful for removal of superficial 0.2-0.3 mm of enamel Rotary instrument application for stain removal allows the simultaneous abrasion & erosion of enamel surface. A generalized smoothening of enamel is documented ( BERG & DONLY ET AL 1992 ) It consists of amorphous layer of compacted mineral called as ENAMEL GLAZE abrasion effect ( GREENWALL)
Macro abrasion Some opacity of enamel which do not respond to micro abrasion & removal of them by macro abrasion do not expose dentin.( MAGNE 1997) Removal of stains from fast moving hand piece with fine grit diamond with air water spray. Final finishing & polishing is done with 30 bladed tungsten carbide bur Results in rough enamel surface ( Greenwall)
Effect of burs Higher speed results in more rougher surface Straight cut provides smoother finish than cross cut design. Tungsten carbide provide smoother finish than stainless or diamond burs. ( KIDD & SMITH )
Cavosurface consideration for enamel Bevels are generally given on gingival, occlusal or cavosurface depending on type of restoration. Bevels should follow the direction of enamel rods. Bevels in inlay restorations Flame shaped , fine grit diamond is used to bevel occlusal & gingival margins. This beveling provide seal & protect the margins resulting in stronger enamel margins with an angle of 140 º -150 º. provide marginal metal 30-40º Gingival bevel should be 30-40º & 0.5-1 mm wide.
Commonly used bevels for inlays: A- Partial bevel B- Short bevel C- Long bevel D- Full bevel E- Counter bevel F- Hollow ground/concave bevel
Bevel in amalgams : bevels in amalgam restoration are contraindicated except at the gingival surface. Bevel is given at 15-20 º. Functions of gingival bevels : Removal of weak enamel. provide burnishable metal margin in inlays Lap sliding fit is produced which improves the fit of casting.
Bevels in composite: Used in beveled conventional preparation . bevels are given at cavosurface , 45 º to the external tooth surface with flame shaped or round bur Bevel provides more surface area for end on etching of rods. Width of bevel: 0.25-0.5mm Provide more resistance to microleakage . Instruments used are : Gingival marginal trimmer Jeffery angle former Flame shaped enamel finishing bur(no.7901 or 242) Sonicys with torpedo tip. precautions bevels are not given on cementum & on lingual surface which under centric contact or heavy forces
Enamel etching The process of roughening a solid surface by exposing it to an acid and thoroughly rinsing the residue to promote micro mechanical bonding of an adhesive to surface By BUONOCORE in 1955. Silverstone suggested use of 30-40% of phosphoric acid. Removal of 10 µm of surface enamel & create a micro porous layer of 5-50µm depth. Etching pattern (SILVERSTONE 1975) Type 1: dissolution of prism cores- HONEY COMB APPEARANCE Type 2: dissolution of periphery of enamel rods- COBBLESTONE APPEARANCE Type 3: No distinct pattern or mixed
Type 1 Type 2 Type 3
Etching provide: rough surface for micromechanical bonding Increased surface area increased free surface energy Method of etching: Apply 35% of ortho phosphoric acid for 15 sec. (increased time duration for flourosed & primary teeth) Rinse it off On drying gives frosty white appearance of enamel
Acid etching in primary teeth According to Silverstone : 120sec etch necessary to establish proper enamel porosity MUELLER (1977): by increasing the etch time an increase in tag formation was seen NORDENVELL et al : 15-60 sec gave surface irregularities in primary teeth
Effect of laser on enamel Factors which affect biological effect of laser on enamel Wave length , energy, density & duration of laser radiation Absorption, reflection , transmission & scattering properties of tissues Energy needed for enamel ablation by ER:YAG is 200mjoule, Pulse/ sec-15 Hz depth of penetration :5 µ with 300µs pulse width.
Enamel surface remain rough after ER:YAG ( Frentzen et al ) Treatment of sound enamel with argon laser causes surface melting & fusion due to loss of organic content water & carbonate content resulting in marked resistance to demineralization. (HICKS ET AL) Use of fine mist does not greatly decreases ablation rate & does not cause any carbonization or melting of enamel ( Hossain Et al) [ Dcna oct 2000]
Emdogain Enamel matrix derived protein Promote regeneration of lost periodontal tissue EMD is accumulated at root surface & promote regeneration of periodontal tissue & acellular cementum of transplanted teeth Also seems to promote healing of root resorption It improves prognosis of teeth that are replanted with traumatically damaged periodontal ligament & in intentional replantation The cementum regeneration-promoting factor in enamel proteins that is clinically used for periodontal regeneration to induce cementum-promotive and osteopromotive activities Dental Traumatology (17-2001;36 ) (18-2002;12 )
Air abrasion/ kinetic cavity preparation Developed by DR. ROBERT BLACK in 1940. Air abrasion hand pieces & nozzles are sterilizable and can be used at angulation ranging from 0 to 120 º. Uses aluminum oxide particles which are irregular & sharp, needed hardness & lower cost When these particles hit enamel/ dentin ,kinetic energy is absorbed by substate resulting in cutting or abrasion of surface
Particle size: 50 µ m for primary teeth 27 µ m for permanent teeth Air pressure ranges from 40-160 pounds/ inch 2 Uses of air abrasion : Cavity preparation Preparation for sealant application Removal of temporary cement from inside of crown Removal of old restoration Removal of porcelains inlays & onlays Modifications of dentin & porcelains for bonding Stain removal Micro abrasion for enamel hypoplasia Aid in repair of acrylic, composite & porcelain
Advantage of air abrasion : Non traumatic Biocompatible Efficient No chipping & micro fracture Micro smooth margins Enhanced quality of care Lesser discomfort during cavity preparation Time saving Reduced need for anesthesia ( lambrechts et al 1997)