Enamel Seminar - Anu presented.pptx......

MICROABRASION , MACROABRASION

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2. ENAMEL Presented by, Dr. ANN MARY AUGUSTINE First Year MDS Student Dept. Of Conservative Dentistry And Endodontics PSM Dental College

3. CONTENTS Introduction Physical properties Chemical properties Structure of enamel Microscopic features Surface structures Dentino - enamel junction Cementoenamel junction Difference between deciduous and permanent tooth enamel Development of ename l Life Cycle of Ameloblast Amelogenesis Age changes Developmental anomalies of enamel Clinical Considerations Conclusion References 3

4. Previously Asked Questions RGUHS Various age changes of enamel and it’s clinical significance (May 2009, Nov 2021,Nov 2016) 20 marks Explain development, formation, structure and chemical properties & physical properties of enamel(May 2010) 20 marks Resin adhesion to enamel,its clinical implications and challenges(Nov 2013)20 marks Development of Enamel,Factors that affect physical and chemical properties of the structure during the formation of tooth(Nov 2013)20 marks KUHS Discuss in detail about stages of amylogenesis ( June 2019 )10 marks Enumerate various age changes in enamel( Jan 2020 & J an 2019)10 marks Structure , development and age changes in enamel (Jan 2017)10 marks Amelogenesis Imperfecta (Nov 2014) 10 marks Stages of tooth Development and age changes in the tooth (Nov 2014)20 marks 4

5. INTRODUCTION The anatomic crown of a tooth is covered by an acellular,avascular,highly mineralized material known as ENAMEL Ectodermal in origin Hardest calcified tissue in the human body Epithelial derived hard tissue , formed by ameloblasts which cannot be reform itself Teeth composed of 3 Mineralised Tissues – ENAMEL , DENTINE & PULP 5

6. Physical properties 1 . Colour : Yellowish white to Grayish white 2. Permeability : S emipermeable M embrane 3. Density : 2.6 -3 g/Cm2 4. Thickness: 2-2.5 mm 5 . Solubility : Dissolves in acidic media 6. Specific gravity : 2.8 7. Hardness: 343 KHN 8. Refractive index: 1.62 9. Modulus of Elasticity : 83 GPa 6

7. Chemical Properties Highly Mineralised Extracellular Matrix Inorganic material – 96% Organic material & water – 4% INORGANIC Major constituents- Oxygen- 43.4% Calcium-36.6 % Phosphorous -17.7 % Minor constituents Na-0.67% C – 0.64% Mg -0.35% ORGANIC MATERIALS Amelogenins - proline, histidine, glutamine and leucine Nonamelogenins – Enamelin , ameloblastin , tuftelin , glycine , aspartic acid and serine Water: 2% by weight or 5-10% by volume 7

8. Structure of Enamel ENAMEL RODS Basic structural unit Number ranges from 5-12 million Rod dimensions Cross Section of Rods : Type I-Circular Type II- Parallel rows Type III- Key Hole/Paddle Shaped Pattern ULTRASTRUCTURE Keyhole or paddle shaped Rods surrounded by rod sheath and Separated by interrod substance 8

9. STRIATIONS Enamel rod is built up of segments separated by dark lines that give it a striated appearance Due to diurnal rhythm of enamel matrix formation Uniform length of 4 µm DIRECTIONS OF RODS The rods are oriented at right angles to the dentin surface . Deciduous Tooth : Horizontal at cervical and central part Permanent Tooth : Horizontal at occlusal two third of crown and apically directed at cervical third Permanent Primary 9

10. GNARLED ENAMEL Optical appearance of enamel ,cut in oblique plane Inter twinning of rods following curvy irregular path HUNTER-SCHREGER BANDS D ue to change in direction of rods INCREMENTAL LINES OF RETZIUS F ormed due to temporary constriction of tome’s process Under polarized light Under reflected light 10

11. SURFACE STRUCTURES Prismless enamel S tructureless layer of enamel Perikymata External manifestation of striae of Retzius Cracks Outer ends of lamellae Rod ends and neonatal lines 11

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14. DENTINOENAMEL JUNCTION CEMENTOENAMEL 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 Scallope Structure Due to mixing of crystals of dentin and enamel with each other Best appreciated in cusp & incisal edge Convexity of scallops towards dentin & concavity towards enamel 14

15. DIFFERENCE BETWEEN DECIDUOUS AND PERMANENT TEETH ENAMEL 15

16. Development Epithelial E namel Organ 4 distinct layers depending on morphology, function or location Outer enamel epithelium Early- Single layer of cuboidal cells separated from dental sac by basement membrane. Increased vascularity ensues a rich metabolism During enamel formation, cells of outer enamel epithelium develops villi, cytoplasmic vesicles & large no of mitochondria - active transport of materials. 16

17. Stellate reticulum It forms the middle part of the enamel organ. Desmosomes connections Star shaped cells that seperates the neighboring cells by inter cellular spaces filled with intercellular substance Function- 1)Acts as a buffer against physical forces 2) Permit only a limited flow of nutritional elements 17

18. Stratum intermedium Present between stellate reticulum & Inner E namel Epithelium Play a role in enamel production via fluid diffusion or by contributing necessary elements or enzymes They are flat to cuboid in shape and are arranged in 1-3 layers. Essential for enamel formation and calcification . 18

19. Inner Enamel Epithelium Cells derived from the basal cell layer of the oral epithelium. Before enamel formation begins, these cells assume a columnar form and differentiate into ameloblasts that produce the enamel matrix. Cell differentiation occurs earlier in the region of the incisal edge or cusps than in the area of the cervical loop. 19

20. TRANSITORY STRUCTURES During the early stages 3 transitory structures may be seen: ENAMEL KNOT Function- 1) Outlining the central fissure. 2) I t soon disappears & seems to contributes cells to the enamel cord. 3) Important signaling Centre during tooth development . ENAMEL CORD ENAMEL SEPTUM ,ENAMEL NAVEL Function- I nvolved in the process by which the cap stage is transformed into the bell stage (acting as a mechanical tie) or it is a focus for the origin of stellate reticulum cells. ENAMEL NICHE It is seen where the tooth germ appears to have a double attachment to the dental lamina – buccal and lingual enamel strands. 20

21. 1.MORPHOGENIC STAGE Before the differentiation of ameloblast and production of enamel, they interact with adjacent mesenchymal tissue Shape of DEJ and the crown Cells are short columnar, large oval nuclei, with dispersed mitochondria The Golgi apparatus and the centrioles are located in the proximal end LIFE CYCLE OF AMELOBLAST 21

22. .  2.ORGANIZING STAGE Reversal of functional polarity Interaction between Inner enamel epithelium & connective tissue gives odontoblast. Elongation of epithelial cells toward papillae. Close contact between papillae and epithelial cells. odontoblast At terminal phase of this stage odontoblast forms dentin 3.FORMATIVE STAGE Messenger RNA carries the message from nucleus to cytoplasm Ribosomes translate the message Protein is synthesized in rough e ndoplasmic reticulum Protein undergoes post translation modification in golgi complex Packing of protein into secretory granules 22

23. 4.MATURATIVE / MINERALISATION STAGE Starts after full thickness matrix formation on occlusal or incisal area. At cervical matrix formation is under progress. Ameloblast is reduced in size. Cells of Stratum intermedium is spindle shaped. 5.PROTECTIVE STAGE : The ameloblast cell layers then form a stratified epithelial covering of the enamel- REDUCED ENAMEL EPITHELIUM The layer protects enamel from connective tissue till it erupts into oral cavity 6.DESMOLYTIC STAGE The reduced enamel epithelium proliferates and induce atrophy of the connective tissue separating it from the oral epithelium, so that fusion of two epithelia can take place . Pattern of mineralization during maturation Reduced enamel epithelium covering enamel 23

24. Amelogenesis FORMATION OF ORGANIC MATRIX Starts after dentine formation Ameloblast lose the projections from the basal lamina Islands of enamel matrix are deposited along predentin. This process is carrying along thin layer of enamel which is formed along the dentin called as dentino enamel membrane DEVELOPMENT OF TOMES’ PROCESSES Projections of ameloblasts into Enamel matrix 4 ameloblasts results in the synthesis of 1 enamel rod Ameloblast has rough surface during enamel formation due to enamel rods & cells they produce 24 Based on U ltrastructure and Composition two procesess are involved : Organic Matrix Formation and Mineralization

25. Distal terminal bars During formation of Tomes process, T erminal bars appear at distal end which separate tomes process from rest of cells. AMELOBLASTS COVERING MATURE ENAMEL Shorter ameloblast covering the mature enamel Villous surface is near enamel & end is packed with mitochondria. 90% of initially formed protein is lost in maturation, which ever is left form a layer around crystals MINERALISATION AND MATURATION OF ENAMEL MATRIX 2 stages. First stage: Immediate partial mineralization of matrix & interprismatic substance First mineral is in the form of a crystalline apatite Starts from dentinal end of rod . Other studies –Initial mineral : Octacalcium Phosphate 25

26. Second stage: Gradual completion of Mineralization S tarts from height of crown & proceed cervically. Rods mature from -depth to surface - cusp or incisal edge to cervical lines Primary ribbon shaped crystals increase in thickness more than width at the expense of organic matrix consuming protein & water Maturation starts before matrix reaches full thickness. Advancing front is at first parallel to DEJ and later to outer enamel surface. 26

27. Age Changes Attrition : Physiologic wearing Modification Of Surface layer: rod ends and perikymata Increase in inorganic contents: increase in Na & F Decrease in permeability: consolidation of crystals Decrease in water content: Reduced pore size Change in colour: darker 27

28. DEVELOPMENAL ABNORMALITIES OF TEETH ETIOLOGY LOCAL CAUSES Infection Trauma Radiotherapy Idiopathic GENERALIZED CAUSE Environmental/Systemic Prenatal Infection Maternal disease Excess fluoride ions Neonatal Hemolytic disease of New born Hypo calcaemia Postnatal Severe childhood disease Cancer chemotherapy Excess fluoride ions Ingestion of Lead , Tetracycline Post Genetic Effect on teeth – Amelogenesis Imperfecta Effect on teeth associated with generalised defects Down Syndrome Ectodermal dysplasia 28

29. Amelogenesis imperfecta Hereditary Enamel dysplasia, Hereditary brown enamel , Hereditary Brown Opalescent Teeth-defect Clinical features Hypoplastic type : enamel is not formed to full normal thickness Hypocalcification type : in which there is defective mineralization . The enamel is so soft that it can be removed by a prophylaxis instrument. Hypo maturation type : in which enamel crystallites remain immature. The enamel can be pierced by an explorer Radiographic features Enamel may be absent, may be very thin over tips of cusps & interproximal surfaces Treatment No treatment except for improvement of cosmetic appearance 29

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31. Enamel hypoplasia It is an incomplete or defective formation of organic enamel matrix. Local and systemic factors that interfere with the normal matrix formation can cause enamel surface defects and irregularities. It results only if injury occur during the time teeth are developing or the formative stage of enamel development. 31

32. Hereditary type Occurs during the embryonic development of enamel Deciduous & permanent teeth are affected Only enamel is affected Environmental type Either deciduous or permanent dentition is affected , both enamel & dentin is affected or single tooth is affected Factors producing injury to ameloblast: Nutritional Deficiency Exanthematous disease like measles , chicken pox etc. Birth injury, Rh hemolytic disease Local infection or trauma Chemical ingestion Congenital syphilis Hypocalcemia Idiopathic cause. 32

33. FEATURES Mild – Few small grooves, pits or fissures on enamel surface Moderate – Rows of deep pits arranged horizontally across tooth surface Severe form – Considerable portion of enamel is absent due to prolonged disturbance in the function of ameloblasts Due to nutritional deficiency Vit. D deficiency is the most common cause and can also cause due to deficiency of Vit.A & Vit . C. Pitting type of hypoplasia is present. Exanthematous diseases like measles, chickenpox and scarlet fever. Pitting type of hypoplasia is present with staining Involves teeth that are formed within 5 years of age Commonly seen in central/ lateral incisors canine first molar 33

34. Due to birth injuries : Present in deciduous teeth and first permanent molars . Caused due to trauma or change of environment at the time of birth Can also be attributed to Gastrointestinal disturbances or some other illness in the mother. Due to congenital syphilis Involves maxillary and mandibular central incisors and first molars Anterior tooth affected - Hutchinson's teeth Upper central incisor –screw driver shaped Molars referred as - Mulberry / Moon’s / Fournier’s molars Enamel of occlusal 3rd of tooth appears to be an agglomerate of globules 34

35. Due to hypocalcemia : Tetany - due to decrease level of calcium in the blood Pitting variety Seen in vit. D deficiency and Parathyroid deficiency Due to local infection or trauma : Single tooth is involved Commonly – permanent maxillary incisors maxillary/mandibular premolar . Degree of hypoplasia ranges from mild, brownish discoloration of enamel to severe pitting and irregularity of tooth surface. Teeth referred as TURNER’S TEETH Condition known as TURNER’S HYPOPLASIA . 35

36. Hypoplasia due to fluoride- (Mottled enamel) Due to ingestion of fluoride containing drinking water during the time of tooth formation . Amount of fluoride in the water that is more than 1 parts per million . Pathogenesis Disturbance of ameloblasts during stage of tooth development. Higher level of flouride -interference in the calcification process Of matrix Individual variation in causing mottled enamel Clinical Features : W hite flecking or spotting of the enamel W hite opaque areas on tooth surface area Moderate to severe changes showing pitting and brownish staining of surface Corroded appearance of teeth Tendency of wear and fracture Treatment Cosmetic management: Periodic bleaching 36

37. ENAMEL CARIES TRANSLUCENT ZONE Deepest Zone Represent advancing front of lesion Pore volume : 1% -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 Largest pore volume Pore volume : 5 % at periphery 25% at the centre Striae of retzius are marked and accentuated Bacteria may be present SURFACE ZONE Relatively unaffected Serves as a barrier Pore volume less than 5% Radiopacity 37

38. PIT AND FISSURE CARIES OF ENAMEL Large number of Streptococcus Sangius are found in pit & fissure of newly erupted teeth Where as large number of streptococcus mutans are present in carious pits & fissures. Gross appearance: inverted V shaped with a narrow entrance & wider at base near DEJ SMOOTH SURFACE CARIES OF ENAMEL Plaque accumulation is seen towards gingiva below the proximal contact area. Gross appearance: V shaped lesion with broad area of origin & a pointed extension towards DEJ . 38

39. NON CARIOUS LESIONS OF ENAMEL Attrition Abrasion Erosion Abfraction Localized nonhereditary enamel hypoplasia Localized non hereditary enamel hypocalcification Discoloration Amelogenesis imperfecta 39 ABFRACTION Stress lesion Loss of tooth structure that results from flexure that is caused by occlusal stresses The magnitude of tooth tissue loss depends on the size, duration, direction, frequency and location of the forces

40. ATTRITION ABRATION EROSION Surface tooth structure loss resulting from direct frictional force between contacting teeth Physiologic wearing age dependent, continuous Usually involve : - proximal - occlusal / incisal Pathologic wearing by mechanical forces Usually involve: exposed root surfaces Smooth polished ,V-shaped Etiological features: - Brushing habits - Iatrogenic -denture of porcelain teeth opposing naturals Chemicomechanical Glazed surface Decreased caries incidence Supporting teeth are healthy Etiology: -acids of diet - acids of gingival crevice -acid fumes -salivary citrates 40

41. 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 41

42. Intrinsic stains: Decomposition of pulp tissue Trauma Excessive haemorrhage following pulp extirpation Calcific metamorphosis Filling materials Endodontic materials Aging Iatrogenic discolorations 42

43. Lightening of discolourations of teeth through the application of chemical agents to oxidize the organic pigmentation in teeth 16-35 % of carbamide peroxide results in loss of aprismatic layer, exposure of enamel prism & pitting. (BITTER 1995) Adverse effect of 1.Intra coronal bleaching : Inhibition Of resin polymerisation 2.Extra coronal bleaching Tooth sensitivity Bleaching can result in erosive areas and increased porosity. Caustic nature of hydrogen peroxide causes reduction in enamel microhardness Peroxides can cause change in inorganic-organic ratio, rendering enamel weak Effect of Bleaching 43

44. Increased enamel resistance When hydroxyapatite is exposed to F- ion concentration upto 1ppm a layer of fluorapatite is formed Most of the fluoride ion which enter the enamel replaces the OH- ion. 2 . Increased rate of post eruptive maturation Hypomineralised area of recently erupted tooth get mineralized as they get exposed to fluoride ion of oral cavity EFFECT OF FLUORIDE ON ENAMEL 44

45. 3. 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 a) Pre eruptive incorporation Get incorporated in fluid filled sac around the tooth Highest concentration is seen in enamel crown near surface b) Post eruptive incorporation Resulting into formation of flouroapetite crystals 45

46. Effect of drugs on enamel Tetracycline: 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 discoloration. Precautions: No tetracycline before 8 years & oxytetracycline or doxycycline during pregnancy Staining First Degree : light yellow to light gray staining without banding Second degree : Darker and more extensive yellow or gray staining without banding Third degree : Severe staining-Dark gray or blue discolouration with banding 46

47. Treatment Bleaching using 30% hydrogen peroxide and thermostatically controlled heat source Intentional pulp extirpation and internal bleaching Veneers Full crown restorations Minocycline Semi synthetic tetracycline Can affect permanent dentition even in adults Theories of entry into tooth structure. Absorbed into dentin via pulpal blood vessels Enter into enamel defect through crevicular fluid. Form complexes with calcium in dentin stains are composed of drug degradation product Minocycline- Hemosiderin complex 47

48. Enamel Infarction An incomplete fracture or crack of enamel without the loss of tooth structure Dyes: Methylene blue with magnification/ Transillumination No Tenderness on percussion, luxation or root fracture-absent Treatment: Etching and sealing B. Enamel Fractures A complete fracture of enamel Loss of enamel is visible , No Tenderness on Percussion, Normal mobility RE : to rule out Luxation and root fractures Treatment: Smoothening of roughened margins Reattachment of fragment Periodic vitality test TRAUMATIC INJURIES OF ENAMEL 48

49. Consideration while making cavity in enamel Enamel rods should rest on sound dentin. Cavo surface margin/ angle must have their inner ends resting on sound dentin & outer end must be covered by restorative material. Outermost part of wall should follow the direction of rods & innermost supported by dentin. 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 unsupported enamel rods should be removed 49

50. Cavosurface consideration for enamel Bevels are generally given on gingival, occlusal or cavosurface depending on type of restoration. Should follow the direction of enamel rods. 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 50

51. 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 135º-145º. Provide marginal metal 30-40º Gingival bevel should be 20-30º & 0.5-1 mm wide. Bevel in amalgams: Bevels in amalgam restoration are contraindicated except at the gingival surface. Bevel is given at 15-20º. 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 51

52. Bevels in composite: Used in beveled conventional preparation . B evels are given at cavosurface , 45º 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. 52

53. Micro abrasion MCCLOSKY reported removing brown stains of fluorosis by 18% HCl and heat application. In 1986 CROLL AND CAVANAUGH described microabration using PREMA, an abrasive paste containing HCl, silicon gel silicon carbide and silica gel. Useful for removal of superficial 0.2-0.3 mm of enamel Procedure: Compound is polished onto the teeth using contra angled slow speed handpiece Protect the gingiva with petroleum jelly and apply rubber dam Bleached surface should be polished with graded abrasive disks and prophylactic paste Advantage: Better control over the procedure Faster and easier Disadvantages: Technique sensitive & can have negative outcome 53

54. Macro abrasion Indication: removal of localized surface enamel in fluorotic teeth Burs: 12 or 16 fluted composite finishing or fine grit finishing diamond Procedure: bur in high speed with intermittent pressure, with air-water spray. Then polish with abrasive rubber points. Advantages: Better control of removal of tooth structure Faster and easier Do not require rubber dam isolation. Disadvantages: Technique sensitive Results vary according to the clinician 54

55. Enamel etching Process of roughening a solid surface by exposing it to an acid and thoroughly rinsing the residue to promote micromechanical bonding of an adhesive to surface By BUONCORE in 1955 Silverstone suggested use of 30-40% of phosphoric acid. Mechanism: Resin microtag formation . Etching pattern (S ILVERSTONE 1975) Type A: dissolution of prism cores Type B : dissolution of periphery of enamel rods Type C: A mixture of type 1 and type 2 Type A Type B Type C 55 Type D: pitted enamel surface as well as structures that look like unfinished puzzle Type E : Flat smooth surface

56. Emdogain Enamel matrix derived protein Purified form extracted from developing embryonal enamel of porcine origin Emdogain 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 Dispersed as sterilized aqueous solution of propylene glycol alginate 56

57. TOOTH MOUSSE AND TOOTH MOUSSE PLUS 57 Topical tooth cremes that help strenghthen and rejuvenate the patient’s teeth They bind calcium and phosphate to the tooth surfaces,plaque and surrounding soft tissue Streptococcus Mutans is a common cariogenic bacterium in the oral cavity involved in plaque formation Casein phosphopeptide -amorphous calcium phosphate (CPP-ACP) has introduced into tooth mousse – RECALDENT – that prevents the biofilm formation of streptococcus mutans A special milk derived protein that replace lost minerals in the teeth, making them stronger and helps protect them from decay and erosion Tooth mousse containing casein phosphopeptide -amorphous calcium phosphate prevents biofilm formation of streptococcus mutans:Ronit vogt sionov,Danae Tsavdaridou,Muna Aqawi,Batya Zaks,Doron steinberg and Miriam Shanish , Sionov et al BMC Oral Health ( 2021)

58. CONCLUSION Understanding the stages of development and various structures in enamel, their variations can help us to diagnose, evaluate and go ahead with a suitable treatment plan 58

59. BIBLIOGRAPHY Orban’s oral histology & embryology-GS Kumar Shafer’s text book of oral pathology –Shafer, Hine, Levi Oral pathology-J.V. Soames 3rd edition Oral and Maxillofacial Pathology – Neville,Damm,Allen,Chi Ten Cate’s oral histology-Antonio Nancy Essentials of oral biology – Maji Jose Sturdevant’s art & science of operative dentistry- Harald O Heyman Operative dentistry- Marzouk Grossman’s Endodontic practice- B.suresh chandra 59 Tooth mousse containing casein phosphopeptide -amorphous calcium phosphate prevents biofilm formation of streptococcus mutans:Ronit vogt sionov,Danae Tsavdaridou,Muna Aqawi,Batya Zaks,Doron steinberg and Miriam Shanish , Sionov et al BMC Oral Health ( 2021)

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