Enamel

The presentation discusses about tooth enamel in detail including its formation, characteristics, structure and histological features along with its clinical considerations. It is well supported with diagrams for better understanding of the text.
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1. ENAMEL Made By: Dr. Akshat Sachdeva MDS Ist Year Dept. of Conservative Dentistry and Endodontics Sudha Rustagi College of Dental Sciences & Research

2. INTRODUCTION Hardest calcified tissue in the human body that covers the anatomic crown of the tooth. Only ectodermal derivative of the tooth. Varies in thickness in different areas. Thicker at incisal and occlusal areas and becomes progressively thinner until it terminates at CEJ.

3. Enamel Dentin Pulp Chamber Pulp Canal Periodontal Fibers Cementum Fig. 1 : Showing supporting structures of tooth Source: Sturdevant’s Art and Science of Operative Dentistry

4. DEVELOPMENT OF ENAMEL The enamel organ consists of 4 distinct layers : Inner and outer enamel epithelium are separated by a large mass of cells differentiated into two distinct layers. L ayer that is close to the inner enamel epithelium consists of two or three rows of flat polyhedral cells called stratum intermedium . The other layer, which is more loosely arranged , constitutes stellate reticulum . Outer Enamel Epithelium Stellate Reticulum Stratum Intermedium Inner Enamel Epithelium

5. OUTER ENAMEL EPITHELIUM C onsists of a single layer of cuboid cells , separated from the surrounding connective tissue by a delicate basement membrane. C ells of the outer enamel epithelium become irregular in shape a t the highest convexity of the enamel organ. During enamel formation, cells of the outer enamel epithelium develop villi and cytoplasmic vesicles and large numbers of mitochondria .

6. STELLATE RETICULUM C ells in this layer are star shaped with long processes reaching in all directions from a central body. C onnected with each other and with the cells of the outer enamel epithelium and the stratum intermedium by desmosomes . S tellate reticulum is noticeably reduced in thickness when the first layers of dentin are laid down.

7. STRATUM INTERMEDIUM Cells are flat to cuboidal in shape and are arranged in one to three layers. C onnected with each other and with the neighboring cells of stellate reticulum and inner enamel epithelium by desmosomes . Tonofibrils are found in the cytoplasm . C ells in this layer show mitotic division even after the cells of inner enamel epithelium cease to divide.

8. INNER ENAMEL EPITHELIUM C ells of inner enamel epithelium are derived from the basal cell layer of oral epithelium. T hese cells assume a columnar form and differentiate into ameloblasts that produce the enamel matrix. C ell differentiation occurs earlier in the region of incisal edge or cusps than in the area of cervical loop.

9. 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 .

10. LIFE CYCLE OF AMELOBLAST According to function, the life span of cells can be divided into six stages : Morphogenic . Organizing. Formative. Maturative . Protective. Desmolytic .

11. MORPHOGENIC STAGE The cells are short and columnar , with large oval nuclei that almost fill the cell body . The ameloblasts before differentiation interact with mesenchymal cells and determine shape of the DEJ and the crown. Golgi apparatus and the centrioles are located in the proximal end of the cell , whereas the mitochondria are evenly dispersed throughout the cytoplasm.

12. ORGANIZING STAGE Inner enamel epithelium interacts with the adjacent connective tissue cells, which differentiate into odontoblasts . Cells of inner enamel epithelium become longer, and nucleus-free zones at distal ends of the cells become almost as long as the proximal parts containing nuclei. Staining methods reveal presence of acidophil granules in proximal part of the cell .

13. Epithelial cells come into close contact with connective tissue cells of the pulp, which differentiate into odontoblasts . Formation of dentin by odontoblasts begins during terminal phase of the organizing stage. When dentin forms , it cuts off ameloblasts from their original source of nourishment, and from then on they are supplied by capillaries that surround the outer enamel epithelium.

14. Source: Essentials of Oral Biology by Maji Jose

15. FORMATIVE STAGE Ameloblasts enter this stage after the first layer of dentin has been formed. Presence of dentin is necessary for the beginning of enamel matrix formation. During formation of enamel matrix, ameloblasts retain approximately the same length and arrangement. Earliest apparent change to appear is the development of blunt cell processes on ameloblast surfaces, which penetrate the basal lamina and enter predentin .

16. MATURATIVE STAGE Enamel maturation i.e. full mineralization occurs after most of the thickness of the enamel matrix has been formed in the occlusal or incisal area . During enamel maturation, the ameloblasts are slightly reduced in length and are closely attached to enamel matrix. Ameloblasts display microvilli at their distal extremities , and cytoplasmic vacuoles containing material resembling enamel matrix are present.

17. PROTECTIVE STAGE When the enamel has completely developed and has fully calcified, the ameloblasts cease to be arranged in a well-defined layer. Cell layers then form a stratified epithelial covering of the enamel , the so-called reduced enamel epithelium , which functions to protect the mature enamel by separating it from connective tissue until the tooth erupts. Anomalies may develop if connective tissue comes in contact with the enamel .

18. DESMOLYTIC STAGE Reduced enamel epithelium proliferates and seems to induce atrophy of the connective tissue. It has been suggested that epithelial cells elaborate enzymes that are able to destroy connective tissue fibers by desmolysis . Premature degeneration of the reduced enamel epithelium may prevent the eruption of a tooth.

19. Source: Essentials of Oral Biology by Maji Jose

20. AMELOGENESIS T wo processes are involved in the development of enamel : Organic matrix formation. Mineralization.

21. ENAMEL MATRIX FORMATION Ameloblasts begin their secretory activity when a small amount of dentin has been laid down. A meloblasts lose their projections separating them from predentin . I slands of enamel matrix are deposited along the predentin . A thin, continuous layer of enamel is formed along the dentin.

22. Amelogenin is the major component of enamel matrix proteins . Amelogenins have been shown to form minute nanospheres between which enamel crystals form . A bsence of amelogenin has been found to result in the formation of hypoplastic teeth . Ameloblastin and enamelin are the other important proteins of the enamel matrix. A new protein, amelotin is suggested to help in enamel formation.

23. DEVELOPMENT OF TOMES’ PROCESS P rojections of ameloblasts into the enamel matrix have been named Tomes’ process . T hey contain typical secretion granules as well as rough endoplasmic reticulum and mitochondria. Tomes’ process is partially separated from cell body by an incomplete septa formed by microfilaments and tonofilaments .

24. Ameloblasts over maturing enamel are considerably shorter than the ameloblasts over incompletely formed enamel. C hanges occurring in the ameloblasts prior to the onset of maturation process are called transition stage . During this stage: Ameloblasts reduce in height E namel secretion stops completely and Process of amelogenin removal starts . Ameloblasts attach to the basal lamina by hemidesmosomes .

25. MINERALIZATION OF ENAMEL MATRIX Mineralization of the enamel matrix takes place in two stages . In the first stage, an immediate partial mineralization occurs in the matrix segments. F irst mineral is in the form of crystalline apatite . S tudies have shown that the initial mineral is octacalcium phosphate , which may act as a template for hydroxyapatite.

26. Second stage or maturation , is characterized by the gradual completion of mineralization. Maturation process starts from height of the crown and progresses cervically . The rate of formation of enamel is 4 μm /day . Organic matrix gradually becomes thinned and more widely spaced to make room for the growing crystals. Ameloblasts undergo apoptosis after formation of enamel, hence enamel formation does not occur later on while formation of other hard tissues continues throughout life.

27. PHYSICAL CHARACTERISTICS Enamel forms a protective covering of variable thickness over the entire surface of the crown. C olor of enamel – covered crown ranges from yellowish white to grayish white . C olor is determined by differences in the translucency of enamel. Yellowish teeth have a thin, translucent enamel through which the yellow color of the dentin is visible and grayish teeth have a more opaque enamel.

28. Thickest over the cusps and incisal edges and thinnest at the cervical margins. Attains a maximum thickness of about 2 to 2.5 mm on the cusps of molars and premolars. S pecific gravity of enamel is 2.8 . It has been found that enamel can act like a semipermeable membrane , permitting complete or partial passage of certain molecules.

29. CHEMICAL CHARACTERISTICS ENAMEL Inorganic Content (96%) Organic content + water (4%) Proteins Amelogenins Nonamelogenins (90%) (10%) Amelogenins are low molecular weight proteins and are rich in proline , histidine , glutamine and leucine . Nonamelogenins are high molecular weight proteins and are rich in glycine, aspartic acid and serine.

30. Inorganic material of enamel is hydroxyapatite . C rystals of hydroxyapatite are hexagonal in cross-section. Average concentrations(%) of three major constituents namely oxygen , calcium and phosphorus , are 43.4, 36.6, and 17.7 respectively . M inor constituents together account for 2.3%, of which sodium carbon and magnesium are the principal constituents.

31. STRUCTURE E namel is composed of enamel rods or prisms, rod sheath and an interprismatic substance . E namel rods normally have a clear crystalline appearance, permitting light to pass through them . In cross-sections of human enamel , many rods resemble fish scales .

32. ULTRASTRUCTURE A more common pattern is a keyhole or paddle-shaped prism in human enamel. R ods measure about 5 μm in breadth and 9 μm in length. Each enamel rod is built up of segments separated by dark lines that give it a striated appearance . S triations are suggested to be due to a diurnal rhythm in the enamel formation and that in these areas rods show variation in composition .

33. Source: Manual of Oral Histology and Oral Pathology by Maji Jose

34. HUNTER – SCHREGER BANDS Alternating dark and light strips of varying widths. Occur due to abrupt change in direction of enamel rods. Prisms cut longitudinally to produce dark bands are called parazones , while those cut transversely to produce light bands are called diazones . A ngle between parazones and diazones is about 40 degrees .

35. Source: Manual of Oral Histology and Oral Pathology by Maji Jose

36. INCREMENTAL LINES OF RETZIUS Appear as brownish bands in ground sections of enamel. Illustrate the incremental pattern of enamel , i.e. the successive apposition of layers of enamel during formation of the crown. I ncremental lines of Retzius appear as concentric circles . Reflect variations in structure and mineralization of enamel.

37. Source: Manual of Oral Histology and Oral Pathology by Maji Jose

38. GNARLED ENAMEL Arrangement of enamel rods becomes more complicated in the region of cusps and incisal edges. Enamel rods become more irregular and intertwine with each other especially near the DEJ. This creates an optical appearance called as gnarled enamel .

39. Source: Manual of Oral Histology and Oral Pathology by Maji Jose

40. SURFACE STRUCTURES Structure less layer of enamel, called prismless enamel has been described in 70% of permanent teeth and all deciduous teeth. Found least often over the cusp tips and most commonly toward the cervical areas of the enamel surface. In this layer, the apatite crystals are parallel to one another and perpendicular to the striae of Retzius .

41. Perikymata are transverse, wave-like grooves , believed to be the external manifestations of the striae of Retzius . They are continuous around a tooth with a fairly regular course and usually lie parallel to each other and to the CEJ. Pits of about 1–1.5 μm in diameter and small elevations of about 10–15 μm called enamel caps are seen on the irregular enamel surface. Larger enamel elevations are termed enamel brochs .

42. NEONATAL LINE Prominent incremental line separating prenatal and postnatal enamel. Prenatal enamel usually is better developed than the postnatal enamel. Fetus develops in a well-protected environment with an adequate supply of all the essential materials. Found to be more frequently absent in permanent first molars of boys than girls.

43. Source: Manual of Oral Histology and Oral Pathology by Maji Jose

44. ENAMEL CUTICLE Primary enamel cuticle or Nasmyth’s membrane covers the entire crown of newly erupted tooth but is probably soon removed by mastication. Erupted enamel is covered by a pellicle , a precipitate of salivary proteins. Within a day or two after pellicle formation, it becomes colonized by microorganisms to form bacterial plaque .

45. ENAMEL LAMELLAE Leaf like structures extending from outer surface of enamel towards dentin. Three types of lamellae are seen: Type A : Composed of poorly calcified enamel rods. Restricted to enamel. Type B : Consists of degenerated cells and may extend into dentin. Type C : Filled with organic matter derived from saliva and maybe extended into dentin.

46. ENAMEL TUFTS Ribbon like structures extending from DEJ into enamel. Resemble tufts of grass when viewed in ground sections . Consist of hypocalcified enamel rods and interprismatic substance. Extend in the direction of long axis of the crown.

47. Source: Manual of Oral Histology and Oral Pathology by Maji Jose

48. ENAMEL SPINDLE Odontoblastic processes crossing DEJ and extending to the enamel. Appear as dark spindle shaped structures. In ground sections of dried teeth, the organic content of the spindles disintegrates and is replaced by air, and the spaces appear dark in transmitted light . Found mainly in cusp tip region.

49. Source: Manual of Oral Histology and Oral Pathology by Maji Jose

50. DENTINO-ENAMEL JUNCTION A ppears as a scalloped line with convexity directed towards dentin. C rystals of dentin and enamel mix with each other . M ore pronounced in the occlusal area, where masticatory stresses are greater.

51. AGE CHANGES Most apparent age change in enamel is attrition or wear of the occlusal surfaces and proximal contact points as a result of mastication. This is evidenced by a loss of vertical dimension of the crown and by flattening of the proximal contour. It has been seen that facial and lingual surfaces loose their structure rapidly than do proximal surfaces, and anterior teeth loose their structure more rapidly than do posterior teeth.

52. Tooth Darkening : Teeth appear to darken with age . Darkening may be caused by deepening of dentin color seen through the progressively thinning layer of translucent enamel . Permeability : Enamel becomes less permeable with advancing age. Decrease in permeability is caused due to increase in the size of the crystals which in turn decreases the pores between them causing a reduction in permeability.

53. CLINICAL CONSIDERATIONS C ourse of the enamel rods is of importance in cavity preparations . During cavity preparation, it is important that unsupported enamel rods are not left at the cavity margins because they would soon break and produce leakage. Bacteria would lodge in these spaces thus inducing secondary dental caries .

54. Deep enamel fissures predispose teeth to caries. Caries penetrate the floor of fissures rapidly because the enamel in these areas is very thin . Eventually, an area of dentin becomes carious because the entrance to the cavity is minute. Careful examination is necessary to discover such cavities because most enamel fissures are minute.

55. TETRACYCLINE STAINING Discoloration of teeth due to tetracycline may occur if therapeutic regimens are taken either during pregnancy or following childbirth. F orms a complex with calcium ions in the surface of hydroxyapatite crystals. Usually avoided during pregnancy or till the child completes 8 years.

56. ECTOPIC ENAMEL Also called as enamel pearl or enameloma . P resence of enamel in unusual locations , mainly the tooth root . U sually develops on roots of maxillary permanent molars. M ost incidental findings require no therapy . Meticulous oral hygiene should be maintained to prevent localized loss of periodontal support.

57. CLINICAL CONSIDERATIONS The principal expressions of pathologic amelogenesis are: Hypoplasia occurs when matrix formation is affected and is manifested as pitting, furrowing, or even total absence of the enamel . Hypocalcification results when maturation is lacking or incomplete and can be seen in the form of opaque or chalky areas on normally contoured enamel surfaces. C auses of such defective enamel formation can be generally classified as systemic, local, or genetic.

58. If drinking water contains fluoride in excess of 1.5 parts per million , chronic endemic fluorosis may occur as a result of continuous use throughout the period of amelogenesis . It is important to urge substitution of water with levels of fluoride (about 1 part per million) well below the threshold for fluorosis. Teeth most frequently affected are incisors , canines and first molars.

59. A small amount of fluoride (about 1 to 1.2 parts per million ) reduces susceptibility to dental caries without causing mottling. If an injury occurs in the formative stage of enamel development, hypoplasia of the enamel will result. An injury during the maturation stage will cause a deficiency in calcification .

60. AMELOGENESIS IMPERFECTA Structural defect of tooth enamel. Also called as: Hereditary enamel dysplasia. Hereditary brown enamel. Hereditary brown opalescent teeth. Prevalence of this condition has been estimated to range from 1 in 718 to 1 in 14,000, depending on the population studied.

61. Classification of amelogenesis imperfecta (AI) according to Witkop (1989 ): Type – I: Hypoplastic . Type – II: Hypomaturation . Type – III: Hypocalcified . Type – IV: Hypomaturation-hypoplastic with taurodontism . Hypoplastic AI represents 60–73% of all cases, hypomaturation AI represents 20–40%, and hypocalcification AI represents 7%.

62. Modified Classification of AI:

63. Etiology of AI is related to the alteration of genes involved in the process of formation and maturation of the enamel. Defective gene has been found to be closely linked to the locus DXS85 at Xp22 . This also has been identified as the general location of the human gene for amelogenin , the principal protein in developing enamel.

64. Hypoplastic AI is characterized by: Thin enamel possessing yellowish-brown color. Glossy square-shaped crown. Lack of contact between adjacent teeth. Flat occlusal surfaces of posterior teeth due to attrition. Radiographically , there is a presence of thin radiopaque layer of enamel with normal radiodensity . Histologically, defect in the enamel matrix formation is seen.

65. Hypoplastic AI

66. Hypocalcified form of AI is characterized by: Softer enamel which wears down rapidly. Pigmented dark brown colored enamel. Radiographically , thickness of enamel is normal but radiodensity of enamel is less than that of dentin. Histologically , defects of matrix structure and mineralization is seen.

67. Hypocalcified AI

68. Hypomaturation form of AI is characterized by: Thickness of enamel is harder than hypocalcified type and may crack away from the crown. Mottled‑colored cloudy white/yellow/brown/snow capped. Radiographically , radiodensity of enamel is similar to that of dentin. Histologically, alterations in enamel rod and rod sheath structures had been noted.

69. Hypomaturation AI

70. There is no specific treatment for the condition. M ain objectives of treatment include preserving patient's remaining dentition, and to treat and preserve the patient's occlusal vertical height. Esthetic issues should be considered since the color of tooth crown is yellow from exposure of dentin due to enamel loss. Factors to be considered in deciding treatment options include classification and severity of AI, the patient's social history, clinical findings etc.

71. Full-coverage crowns can be used to compensate for the abraded enamel in adults. Aesthetics may be addressed via placement of composite or porcelain veneers . P atient's oral hygiene and diet should be controlled as they play an important role in the success of retaining future restorations . Teeth may have to be extracted in worst cases and implants or dentures can be considered for replacement.

72. ENAMEL HYPOPLASIA I ncomplete or defective formation of the organic enamel matrix of teeth . Hereditary type Environmental factors - Usually involves both deciduous - Involves either dentition and permanent dentition. and sometimes even a single tooth. - Generally affects only enamel. - Both enamel and dentin affected to some degree.

73. In mild environmental hypoplasia, there may be only a few small grooves, pits, or fissures on the enamel surface. If the condition is more severe, the enamel may exhibit rows of deep pits arranged horizontally across the surface of the tooth.

74. HEREDITARY ENAMEL HYPOPLASIA Genetic conditions exhibiting enamel defects: Treacher Collins Syndrome. Congenital erythropoietic porphyria. Ectodermal dysplasia. Epidermolysis bullosa . Tuberous sclerosis . DiGeorge syndrome Kenny- Caffrey syndrome.

75. Hypoplasia results only if the injury occurs during the time the teeth are developing, or more specifically, during the formative stage of enamel development. Different factors may give rise to the condition which include: Nutritional deficiency (vitamins A, C, and D ). Congenital syphilis (Hutchinson’s teeth/mulberry molars). Local infection or trauma (Turner’s hypoplasia). Ingestion of chemicals (chiefly fluoride called mottled enamel). I diopathic causes. Treatment includes veneers for teeth affected by the condition.

76. MOTTLED ENAMEL Occurs due to intake of fluoride-containing drinking water causing disturbance of ameloblasts during the formative stage. W ide range of severity exists in the appearance of mottled teeth: Questionable changes characterized by occasional white flecking or spotting of the enamel.

77. M ild changes manifested by white opaque areas involving more of the tooth surface. M oderate and severe changes show pitting and brownish staining of the tooth surface.

78. C orroded appearance of the teeth. T eeth which are moderately or severely affected may show a tendency for wear and even fracture of the enamel . Treatment : Bleaching of the affected teeth with an agent such as hydrogen peroxide is frequently effective. P rocedure must be carried out periodically as the teeth continue to stain.

79. EFFECT OF ACID ETCHING Acid etching of the enamel surface has become an important technique in clinical practice . Enamel surface is etched with an acid to remove the smear layer on enamel that was created during cavity preparation, making the relatively smooth enamel surface pitted and irregular . When a composite resin is placed on this irregular surface, it can achieve mechanical bonding with the enamel .

80. Depending on the crystal orientation to the surface, three types of etching patterns are produced. The most common is type I , characterized by preferential removal of rods. In type II pattern, the interrod crystals are preferentially removed .

81. Occurring less frequently is type III , which is irregular and indiscriminate. Phenomenon of acid etchants producing differing surface patterns is still debatable. M ost commonly held view is that the etching pattern depends on crystal orientation .

82. ENAMEL RENAL GINGIVAL SYNDROME First described by MacGibbon in 1972. Extremely rare disorder characterized by an autosomal recessive pattern featuring: Severe enamel hypoplasia. Intrapulpal calcification. Failed tooth eruption. Nephrocalcinosis . Suggestive cause: Mutation in gene FAM20A .

83. CONCLUSION Enamel is the hardest calcified tissue in the human body that covers anatomic crown of the tooth . Cells responsible for enamel formation are the ameloblasts . Enamel is an important structural entity and its protection is of utmost importance. Aspire to inspire before you expire!

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