Enamel.pptx

Enamel is the hardest tissue and outer covering of tooth. The presentation consists of physical ,chemical properties , structure , developmental stages of enamel, age changes , clinical implications, and defects in enamel. Learning about enamel will enhance the basic knowledge of new dental aspirants about dentistry.

1. ENAMEL DR. SARGAM R. PARATE , 1 st year pg DEPARTMENT OF CONSERVATIVE DENTISTRY AND ENDODONTICS . BHABHA COLLEGE OF DENTAL SCIENCES , BHOPAL.

2. INTRODUCTION PHYSICAL PROPERTIES CHEMICAL PROPERTIES  STRUCTURE OF ENAMEL DEVELOPMENT OF ENAMEL AGE CHANGES IN ENAMEL CLINICAL IMPLICATIONS DEFECTS IN ENAMEL EPITHETIAL ENAMEL ORGAN AMELOGENESIS LIFE CYCLE OF AMELOBLASTS CONTENTS

3. INTRODUCTION Enamel is the hardest substance in the human body . Highly mineralized structure present as the outer most covering of the crown. Epithelial derived hard tissue ,formed by ameloblasts which cannot reform itself . Origin - Ectodermal Non-vital , acellular , avascular.

4. Modulus of elasticity – Higher Hardness – 296 KHN Specific gravity -2.8 Density – 2.8-3.0 gm/sq.cm Non –electrical conductive material (Insulator at RTM) Brittle Translucent tissue Colour : Yellowish white – grayish white Thickness varies Semi-permeable membrane PHYSICAL PROPERTIES

5. CHEMICAL PROPERTIES

6. FIG : Structure of Hydroxyapatite crystal

7. STRUCTURE OF ENAMEL Enamel lamellae Enamel tufts Dentinoenamel Junction Enamel spindles. Enamel rods Incremental lines Hunter – Schreger bands Gnarled enamel Surface structures Enamel cuticle

8. ENAMEL RODS Enamel consists of enamel rods, prisms or interprismatic sheaths. No.of rods : 5 million – Mand lateral incisor 12 million – Max first molar Torturous course from DEJ to outer surface Length is greater than thickness – oblique direction Dimensions : Diameter – 4 um Breadth – 5 um Length – 9 um Fig : Enamel rod

9. SUBMICROSCOPIC STRUCTURE Fig : KEYHOLE SHAPED STRUCTURE

10. ULTRASTRUCTURE Fig : CRYSTAL ORIENTATION SHOWING ENAMEL BODY AND TAIL Fig : ULTRASTRICTURE OF ENAMEL ROD

11. DIRECTION OF ENAMEL RODS Directions of rods : Right angle to the dentin surface. Horizontal – cervical part of deciduous teeth. Oblique –middle third of the crown Vertical – cusp tips Fig : Direction of enamel rods

12. CLINICAL SIGNIFICANCE Unsupported enamel rods should not be left at cavity margins – soon break and produce leakage. Bacteria lodge in spaces -initiation of secondary dental caries. Uneven dissolution of enamel rods to get pitted and irregular surface increases mechanical bonding with enamel in composites and pit-fissure sealants. Beveling - increase surface area – more no. of enamel rods exposed – more retention. Fig: Unsupported and supported enamel

13. INCREMENTAL LINES OF RETZIUS Ground section : Brownish bands Represents incremental deposition of enamel i.e. successive apposition during formation of enamel layers. Longitudinal section – surrounds tip of the dentin Transverse section – concentric circles. Directions : C ervically – Run obliquely DEJ-Surface – deviate occlusally Fig : Incremental lines of Retzius

14. CLINICAL SIGNIFICANCE Lines become prominent during carious attack. Reflect variations in structure and mineralization during growth. Helps in chronological mapping of dental development.

15. STRIATIONS Dark transverse lines seen crossing the enamel giving striated appearance to enamel rods. Represents daily increments of growth during enamel formation. Rate of enamel formation : 4 um Fig: Cross-striations of Enamel rod

16. H UNTER-SCHREGER BANDS Alternating dark and light bands seen in longitudinal section under oblique reflected light. Optical phenomenon caused due to change in direction of enamel rods. Found in inner 2/3 rd of enamel starting from DEJ. Prisms when cut : Longitudinally – Dark bands – Diazones Transversely - light bands - Parazones Angle b/w parazones and diazones – 40 degrees. Fig : Hunter- schreger bands

17. GNARLED ENAMEL Optical appearance near the dentin ,in the region of cusps / incisal edge , bundles of rods seem to interwine more irregularly when seen in cut section . FIG: Gnarled enamel

18. SURFACE STRUCTURES PRISMLESS ENAMEL PERIKYMATA ENAMEL ROD ENDS PITS CAPS ENAMEL BROCHS CRACKS NEO-NATAL LINE Fig : Different surface structures of enamel

19. PRISMLESS ENAMEL Structure less layer of enamel . 30 um thick Seen in 70% permanent and all deciduous teeth. Commonly seen – cervical areas least seen - cusp tips Fig : A. Prism less enamel , B. Prismatic enamel

20. PERIKYMATA Transverse wave like grooves. External manifestation of Striae of Retzius . Parallel to each other and to CEJ. CEJ- 30 perikymata /mm occlusal / incisal edge – 10 perikymata /mm Absent - occlusal part of primary teeth present – postnatal cervical areas. Fig: P erikymata

21. ENAMEL ROD ENDS Circular depressions Shallowest – cervical region Deepest – incisal / occlusal edges CLINICAL SIGNIFICANCE : Contribute to adherence of plaque which result to caries attack Fig : Enamel rod ends

22. PITS Small depressions on enamel surface. Diameter – 1-1.5 um Represent ends of ameloblasts ENAMEL CAPS Small elevations on enamel surface. Diameter – 10-15 um Caused due to enamel deposition on non- mineralizable debris. ENAMEL BROCHS Large enamel elevations . Diameter - > 10-15 um

23. CRACKS Narrow fissure-like structures seen on all surfaces. Outer edges of enamel lamellae . Disappear on decalcification. Right angle to DEJ. Fig: Cracks on enamel surface

24. NEONATAL LINE OR RING Accentuated incremental line of Retzius . Boundary b/w pre-natal and post-natal enamel. Result of abrupt change in the nutrition of newborn infant. Usually seen in deciduous teeth and permanent first molars. Fig: Neo-natal line

25. ENAMEL CUTICLE Nasmyth’s membrane / primary enamel cuticle , delicate membrane covers entire crown of newly erupted tooth , soon removed by mastication. S ecreted after epithelial enamel organ retracts from cervical region during tooth formation. Function: protects the enamel surface from resorptive activity of adjacent vascular tissue. Fig : Enamel cuticle

26. ENAMEL LAMALLAE Thin leaf-like hypocalcified structures. Extend from enamel surface – DEJ Develops in planes of tension during enamel maturation . Best visualized – Transverse section CLINICAL SIGNIFICANCE – Can act as pathways for caries producing bacteria. Fig: B. Enamel lamellae

27. TYPES OF LAMALLAE

28. ENAMEL TUFTS Arise at DEJ – enamel to about 1/5 th -1/3 rd of its thickness. Consists of hypocalcified enamel rods and interprismatic substances. Consists of highest enamel protein concentration. According to TENCATES , Develop due to abrupt change in the direction of group of rods that arise from DEJ. Best visualized – Transverse section Fig : Enamel tufts

29. DENTINOENAMEL JUNCTION DEJ is scalloped with convexity directed towards dentin. Also k/as Amelo -dentinal junction. Fig : Dentinoenamel junction

30. CLINICAL SIGNIFICANCE Scalloping increases the surface area of enamel. Lateral spread of dental caries. Stress distribution and resist enamel crack propagation. In some pathological condition DEJ becomes flat and enamel get chipped off easily. D entinogenesis imperfecta Ehler-Danlos Syndrome Fig : Dentinoenamel junction

31. ENAMEL SPINDLES Thickened odontoblastic processes passing across DEJ to enamel. Appears dark in transmitted light when seen in ground section. Commonly seen – cusp region (crowding of odontoblast occur) Best visualized – longitudinal section CLINICAL SIGNIFICANCE : Sudden sensitivity occurs during cavity preparation as bur reaches DEJ Fig : Enamel Spindles

32. DEVELOPMENT OF ENAMEL

33. EPITHELIAL ENAMEL ORGAN Enamel organ , also known as the dental organ, is a cellular aggregation seen in a developing tooth. Function : F ormation of enamel Initiation of   dentin  formation , E stablishment of the shape of a tooth's  crown Establishment of the DEJ. Originate from stratified epithelium of primitive oral cavity. Fig : Enamel organ

34. EPITHELIAL ENAMEL ORGAN CONSISTS OF FOUR LAYERS : Outer enamel epithelium Stellate reticulum Stratum intermedium Inner enamel epithelium Fig : Epithelial Enamel Organ

35. In Early stages of development of enamel organ ,OEE has single layer of cuboidal cells , separated from dental sac by delicate basement membrane. P rior to formation of hard tissue , regular arrangement of OEE is maintained only at cervical parts of enamel organ. At highest convexity of organ , OEE cells are irregular in shape During enamel formation ,OEE cells develop villi, cytoplasmic vesicles and mitochondria for active transport of materials. Forms the middle part of enamel organ. Star shaped , with long processes reaching all directions from central body. Connected to each other and to stratum intermedium by desmosomes. Function : act as buffer against physical forces that might distort developing DEJ. Reduced in thickness after first layer of dentin is laid. OUTER ENAMEL EPITHETIUM (OEE) STELLATE RETICULUM

36. INNER ENAMEL EPITHELIUM (IEE) STRATUM INTERMEDIUM Situated between stellate reticulum and inner enamel epithelium. Flat to cuboid in shape , arranged in 1-3 layers. Connected to each other and to neighbouring cells by desmosomes . Function : believed , role in production of enamel itself through control of fluid diffusion in and out of ameloblasts S how mitotic division even after cells of IEE cease to divide. Derived from basal cell layer of oral epithelium. Columnar shape. Differentiate into ameloblasts to produce enamel matrix. Fig : showing OEE &IEE

37. CERVICAL LOOP   Location on an enamel organ in a  developing tooth where the outer enamel epithelium and the inner enamel epithelium join . During root formation the inner layers of epithelium disappear and only the basal layers are left creating  Hertwig's epithelial root sheath  (HERS). FIG : Cervical Loop

38. LIFE CYCLE OF AMELOBLAST According to Function :

39. Fig: Life cycle of Ameloblast

40. MORPHOGENIC STAGE Stage determine morphology of the crown and DEJ. Cells are short and columnar Large oval nuclei -fill the cell body. Golgi apparatus and centrioles -proximal end of cells mitochondria –dispersed in cytoplasm During ameloblast differentiation terminal bars appear , migrating the mitochondria to basal region of cell. IEE is separated from C.T of dental papilla by delicate basal lamina. Fig: Morphogenic Stage

41. ORGANIZING STAGE IEE interact with adjacent C.T which differentiate into odontoblasts. Change in the appearance of IEE cells occur- longer , nucleus free –zone at distal ends . Reversal of polarity – migration of G olgi apparatus and centrioles from proximal ends to distal ends. Clear cell free zone b/w IEE and dental papilla disappear , due to elongation of epithelial cells towards papilla. Epithelial cells come in close contact with C.T of pulp differentiate into odontoblasts. Fig : Organizing Stage

42. Pre-ameloblast secrete proteins- play role in epithelial mesenchymal interaction. Terminal phase – formation of dentin by odontoblasts begins. When dentin forms , original source of nourishment of ameloblast cuts off – then supplied by capillaries . Fig : Organizing Stage

43. FORMATIVE STAGE Ameloblast enter formative stage after first layer of dentin is formed. Presence of dentin necessary for the beginning of enamel matrix formation. D uring formation of enamel matrix : Ameloblast –retain same length and arrangement. Cytoplasmic inclusion and organelles – change in organization and number. Earliest change –development of blunt cell processes on ameloblast , which penetrate basal lamina and enter predentin . Fig : Formative Stage

44. MATURATIVE STAGE Enamel maturation occurs after most of the thickness of enamel matrix is formed in occlusal / incisal area. At cervical area the enamel matrix formation is still progressing. Stratum intermedium cells –lose cuboidal shape and regular arrangement , converts into spindle shape. Ameloblasts – reduced in length and attached to enamel matrix. They display microvilli at distal extremities . Cytoplasmic vacuoles contains materials resembling enamel matrix. These structures i ndicate resorptive function of these cells. Fig : Maturative Stage

45. PROTECTIVE STAGE When enamel is fully developed , fully calcified – ameloblast is present as well-defined layer and cease to get differentiated from startum intermedium and O EE . Cells form stratified epithelial covering of enamel k/as Reduced enamel epithelium. Function : protecting mature enamel by separating from C.T until tooth erupts. If C.T comes in contact with enamel , anomalies develop .Enamel may either get resorbed or may get covered by cementum . Fig: Reduced enamel epithelium

46. DESMOLYTIC STAGE REE proliferates and induce atrophy of C.T separating it from OEE , so that fusion of two epithelia occur. Epithelial cells elaborates enzymes – capable of destroying C.T fibers by desmolysis . Premature degeneration of REE may prevent eruption of tooth. Fig : Fusion of OEE & IEE

47. AMELOGENESIS Enamel formation. Begins at Late bell stage of tooth development. Formation begins as soon as IEE &OEE differentiate.

48. UNDER ELECTRON MICROSCOPY

49. Fig : Stages of Amelogenesis

50. PRESECRETORY STAGE MORPHOGENIC PHASE : Shape of crown is determined. Low columnar cells with centrally located nucleus and poorly developed Golgi bodies, mitochondria are scattered throughout cell. First junctional complex develop ( ameloblasts near St. intermedium ) DIFFERENCIATION PHASE: Cells of IEE become tall columnar and nucleus shifts towards St. intermedium. Increase in RER and Golgi bodies shift distally. Second junctional complex develop(b/w tome’s process towards enamel) Development of tome’s processes occur.

51. FORMATION OF TOME’S PROCESSES Fig : Formation of Tome’s Processes

52. SECRETORY STAGE

53. ENAMEL FORMATION

54. Fig : Enamel Formation

55. MATURATION STAGE Before tooth erupts in the oral cavity, enamel hardens by the process of maturation. Takes place at the expense of enamel fluid and matrix proteins. During this stage ameloblats are called pre-secretory cells (secrete min amount of ameloblastin and amelogenin )

56. MINERALIZATION

57. Fig : Immediate partial mineralization

58. FIG: Mineralization in molar from occlusal to cervical region Fig : Maturation stage of mineralization

59. ATTRITION Wear facets seen in older people Loss of vertical dimension of crown and flattening of proximal contour. DISCOLOURATION Teeth darken with age. Addition of organic material / deepening of dentin colour . PERMEABILITY Teeth become less permeable. With age pores diminishes as crystals acquire more ions. MODIFICATION OF SURFACE Generalized loss of enamel rods. Slower flattening of perikymata later disappear completely.

60. CLINICAL IMPLICATIONS

61. DENTAL CARIES Destruction of enamel surface with acid, lead to the dissolution of enamel matrix, following carious attack. Caries preferentially attack cores of rods and more permeable striae of Retzius – promote lateral spread of caries and undermining adjacent enamel. Fig : Dental caries

62. FLOURIDATION Incorporation of fluoride ions make hydroxyapatite crystals more resistant to carious attack. Decreases rate of demineralization. Increases rate of remineralisation. Fig : Fluoride Application

63. ACID ETCHING TECHNIQUE Removes plaque , debris and thin layer of enamel. By dissolving minerals in enamel, etchants can remove outer 10 um of enamel surface, and makes a porous layer of 5-50 um deep into enamel. Increases porosity through dissolution of crystals. Helps in mechanical bonding of composites to enamel surface. Fig : Acid etching technique

64. BLEACHING Lightening of colour of tooth through the application of chemical agent helps in oxidizing the organic pigmentation of enamel. Fig : Bleaching of teeth

65. DEFECTS IN ENAMEL GENETIC Amelogenesis Imperfecta H ypoplastic (Type 1) Hypomaturation (Type 2) Hypocalcified (Type 3) NON –GENETIC Dental caries Attrition Abrasion Abfraction Erosion Localised non-hereditary enamel hypoplasia Localised non-hereditary enamel hypo calcification. Fluorosis

66. SR.NO DISEASE DEFECT CLINICAL FEATURE PICTURE 1. AMELOGENESIS IMPERFECTA Defect in gene encoding enamel matrix protein. Type 1- Hypo plastic AI Defect in formation of matrix protein Ameloblast fail to lay down sufficient matrix Enamel – pitted, grooved, thin ,hard translucent Small teeth with open contacts. Type 2-Hypomaturation AI Defect in maturation stage. Enamel softer and chips off easily. Mottled brown -yellow white Type 3-Hypocalcified AI Defect in calcification stage. Most common Enamel – normal thickness, easily lost by attrition. Dull , lustrous, honey colored , stains easily. GENETIC DEFECT

67. SR.NO DISEASE DEFECT PICTURE 1. Dental caries Demineralization of inorganic part and destruction of organic substance . 2. Attrition Loss of tooth structure from direct frictional forces. 3. Abrasion Mechanical wear other than mastication 4. Abfraction Caused by forces placed on teeth during biting, eating, chewing . NON-GENETIC DEFECT IN ENAMEL

68. SR.NO DISEASE DEFECT PICTURE 5. Erosion Dissolution of mineralized tooth structure by chemical process. 6. Localized non hereditary enamel hypoplasia Defect in ameloblasts during formation stage. 7. Localized non hereditary enamel hypo calcification Defect in mineralization stage. 8. Fluorosis Hypo mineralization of enamel caused due to excessive ingestion of fluoride during enamel formation.