Enamel clinical aspect sagar hiwale


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Enamel clinical aspect sagar hiwale

  2. 2.  STRUCTURE OF ENAMEL- CLINICAL IMPORTANCE  CLINICAL CONSIDERATIONS  ENAMEL DEFECTS  Carious defects 1. Incipient caries 2. Arrested caries  Non carious defects 1. Developmental defects: 2. Systemic conditions affecting enamel 3. Regressive defects:  Discolorations  Age changes and clinical consideration  CLINICAL IMPLICATIONS  Fluoridation  Acid etching  Enamel microabrasion  Enamel macroabrasion  CONCLUSION  REFRENCES
  3. 3. MINERAL CONTENT  Enamel is the hardest tissue in the human body. Its mineral portion is approximately 96% of its weight,the rest is organic components and water.  The mineral elements include hydroxyapatite crystals, approximately 0.03μm to 0.2 μm, surrounded by a thin film of firmly bound water. CLINICAL SIGNIFICANCE:-  Poorly mineralized enamel –more white  More mineralized –more translucent.
  4. 4. DIRECTION OF RODS • The rods are oriented at right angles to the dentin surface. • In the cervical & central parts of the crown of a permanent teeth, they are approximately horizontal. • Near the incisal edge or tip of cusps they change gradually to an increasingly oblique direction until they are almost vertical in the region of the edge or tip of the cusps. • CLINICAL SIGNIFICANCE:- • Follow the direction of enamel RODS during cavity preparation so that enamel margins are supported. 4
  6. 6. • If the discs are cut in an oblique plane, the bundles of rods seem to interwine more irregularly. • Its optical appearance of enamel is called gnarled enamel. • CLINICAL SIGNIFICANCE:- • This enamel is not subject to cleavage as regular enamel. • This enamel does not yield readily to pressure of hand cutting instruments.
  7. 7. HUNTER-SHREGAR BANDS  Site: Anterior tooth- Incisal surface  Posterior tooth- Cervical region  Importance: Distribute and dissipate impact forces.
  8. 8. ENAMEL TUFTS  These projections arise in Dentine and extend into enamel in the direction of long axis of crown, hence may play a role in spread of caries.
  9. 9. ENAMEL LAMELLAE  Contains mostly organic material which is WEAK AREA, therefore predisposes tooth to entry of bacteria ,hence dental caries..
  10. 10. Perikymata :-  Transverse wave like grooves appear to be theTransverse wave like grooves appear to be the external manifestations ofexternal manifestations of striae of retziusstriae of retzius..  Continuous around the tooth and parallel to eachContinuous around the tooth and parallel to each other and to the CEJ.other and to the CEJ.  Seen in freshly erupted teeth or in tooth which isSeen in freshly erupted teeth or in tooth which is not subjected to abrasive forces.not subjected to abrasive forces.  Average ofAverage of 30 perikymata/mm30 perikymata/mm in cervical regionin cervical region andand 10/mm10/mm in occlusal region.in occlusal region. These may contribute to adherance of plaque material which results in caries.
  11. 11. Perikymata
  12. 12. NASMYTH’S MEMBRANE  Covers newly erupted tooth.  Membrane replaced by pellicle.  Microbes invade pellicle to form plaque. ENAMEL PEARLS  Occasionally found on root surface towards cervical margin.  Importance: Predisposed to plaque accumulation following gingival recession.
  13. 13.  They – act as bacterial/ food traps thickness of enamel predispose tooth to caries. Fissure
  15. 15.  Dental caries Definition: dental caries is defined as a multifactorial , transmissible ,infectious oral disease caused primarily by the complex interaction of cariogenic oral flora with fermentable dietary carbohydrates on the tooth surface over time. Sturdevant 6th edition
  16. 16.  Demineralization occurs as follows
  17. 17.  Definition White opaque chalky spots observed when the tooth surface is desiccated are termed as incipient caries Sturdevant 4th edition  Radiographically seen as faint radiolucency Chalky white spot
  18. 18.  Definition: Caries which becomes static or stationary and doesn't show any tendency for further progression  Clinically intact ,discolored ( black or brown spots ) ARRESTED CARIES
  19. 19.  Translucent zone  Dark zone  Body of the lesion  Surface zone
  20. 20. For an ideal enamel wall , following are the Noy’s structural requirements- 1) The enamel wall must rest on sound dentine and all carious dentine must be removed
  21. 21. 2)Enamel which forms cavosurface angle must have their inner ends resting on sound dentin
  22. 22. 3) The rods which form cavosurface angle must be supported on sound dentine and their outer ends must be covered by restorative material (possibly by giving a bevel)
  23. 23. 4) Cavosurface angle must be beveled so that the margins will not be exposed to injury in condensing restorative material against it.
  24. 24. 1)Amelogenesis Imperfecta- Hereditary defect of enamel Ectodermal disturbance  Genes causing Amelogenesis Imperfecta: • AMELX (5% cases) • ENAM (most cases) • MMP20 • KLK
  25. 25. o Defective matrix formation. o Enamel has not formed to full normal thickness Hypoplastic type Hypocalcified type o Enamel is so soft that it can be removed by a prophylaxis instrument. o Defective mineralization of formed matrix Hypomaturation type o Immature Enamel crystals o Defective enamel can be pierced by an explorer point under firm pressure
  26. 26. 1) Small teeth with short root 2) Open contact General features of Amelogenesis Imperfecta
  27. 27. 3) Discoloration ranging from yellow to dark brown. 4)Thin enamel 5)Enamel could look wrinkled 6)Delay in eruption 7)Occlusal surfaces and incisal edges severely abraded 8)Sensitivity
  28. 28. 1. Enamel may be totally absent 2. Appear as thin layer, chiefly over the tips of the cusps and the interproximal surfaces. 3. Same radiodensity as dentin , it become difficult to differentiate between two Radiographic features
  29. 29. Treatment 1)Full veneering 2)Selective odontotomy esthetically reshaping the teeth.
  30. 30. II)Enamel Hypoplasia  Incomplete or defective formation of the organic matrix Causes: 1.Nutritional defect 2.Exanthametous diseases 3.Congenital syphilis 4.Ingestion of fluoride
  31. 31. 1) Hutchinsons incisors (screw driver shaped central incisors) 2) Mulberry molars (small globular masses of enamel on occlusal surface) Hypoplasia due to syphilis
  32. 32. Treatment •Selective odontotomy and esthetic reshaping of the tooth enamel •Metallic restorations •Bleaching
  33. 33.  Tetracycline Generalized type of intrinsic stain  When the tetracycline is administered during the time of enamel formation it forms a complex chelating compound with the organic and inorganic components of the enamel. The created compound is very stable.  Discoloration depends upon:  Dosage  Length of time over which administration occurred  Form of tetracycline
  34. 34.  According to Moffitt:  Critical period for tetracycline induced discoloration in deciduous dentition • 4 months in utero to 3 months postpartum (maxillary and mandibular incisors) • 5 months in utero to 9 months postpartum (maxillary and mandibular canines)  In permanent dentition • 3-5 months postpartum to 7 yrs of age
  35. 35.  Discoloration varies from yellow –orange to dark blue  Drugs: Chlortetracycline –grayish stains Minocycline –grayish discoloration Oxytetracycline –yellow stains
  36. 36.  Treatment Conservative methods: I. Bleaching I. Microabrasion II. Macroabrasion III. Veneering
  37. 37.  Fluorosis Generalized intrinsic stain  Chronic ingestion of flouride ions interfers with ameloblast function during formative stage of tooth development and disturb their activity
  38. 38.  Clinical features 1) Mild changes • White flecking or spotting of enamel 2)Moderate to severe changes •Brown staining of surface •Pitting •Tendency of enamel to fracture
  39. 39.  Treatment Conservative methods: I. Bleaching I. Microabrasion II. Macroabrasion III. Veneering
  40. 40. Discoloration: Can occur due to Extrinsic factors: 1. Tobacco/tea stains 2. Poor oral hygiene 3. Food colors 4. Gingival bleeding 5. Existing restorations 6. Chromogenic bacteria Intrinsic factors: 1. Caries. 2. Fluorosis. 3. Tetracycline and other drugs. 4. Age changes. 5. Non vital teeth 6. Internal resorption. 7. Hereditary disorders.
  42. 42.  EXTRINSIC DISCOLORATIONS  Avoidance of the foods and beverages that cause stains  Using proper tooth brushing and flossing techniques  Professional tooth cleaning: Some extrinsic stains may be removed with ultrasonic cleaning , enamel microabrasion, enamel macroabrasion  INTRINSIC DISCOLORATIONS  Bleaching  Enamel microabrasion  Enamel macroabrasion  Veneering
  43. 43.  Definition: Surface tooth structure loss resulting from direct frictional forces between contacting teeth . (Marzouk 1st edi)  Types of Attrition 1.Occluding surface attrition 2.Proximal surface attrition  Causes 1. Tooth to tooth contact 2.Parafunctional mandibular movements
  44. 44.  Clinical features 1. Sensitivity 2. Flattening of incisal and occlusal surface 3. Flattening of inclined planes 4. Flattening of proximal contact areas 5. Facet formation 6. Reverse cusp 7. Loss of vertical dimension of teeth 8. Decay at occluding areas 9. Angular chelitis 10.Cheek bite 11.Temporo mandibular problems Flattening of incisal
  45. 45.  Treatment 1. Para functional activities should be controlled with protecting occlusal splints. 2. Endodontic therapy for pulpally involved teeth 3. Occlusal equilibration, by selective grinding of tooth surfaces 4. Restorative modalities(only metallic restoration)
  46. 46. Abrasion Definition: Surface loss of tooth structure resulting from direct friction forces between teeth and external objects, or from frictional forces between contacting teeth components in the presence of an abrasive medium. Causes 1. Improper use of tooth brush 2. Improper use of tooth pick and dental floss 3. Habitual opening of bobby pins with teeth. 4. Use of abrasive dentifrices Marzouk 1st edition
  47. 47.  Clinical features 1. Linear in outline(following path of brush bristles) 2. Angular peripheries 3. Notching of central incisors 4. Wedge shaped ditch on proximal exposed root surface
  48. 48.  Treatment 1. Diagnosing the cause 2. Removing the causative factor(habits) 3. Desensitizing exposed dentin(if tooth is sensitive) 4. Restorative treatment
  49. 49.  Definition Loss of tooth structure resulting from chemico- mechanical acts in the absence of specific microorganisms Marzouk 1st edition  Causes 1. Ingested acid(lemon and citrus fruits) 2. Chronic vomiting 3. Frequent regurgitation  Rate of erosion is 1micron per day Erosion
  50. 50.  Clinical features 1. Shallow, broad, smooth ,highly polished, scooped out depression on the enamel surface adjacent to cementoenameljunction 2. Confined to gingival third of labial surface
  51. 51.  Treatment 1. Complete analysis of diet, chronic vomiting, environmental factors should be performed 2. Restorative treatment (tooth colored material can be used with minimal or no tooth preparation)
  52. 52.  Abfraction Definition: Strong eccentric occlusal force resulting in microfractures at the cervical area of tooth causing wedge shaped defects Sturdevant 6th edition Causes  Heavy force in eccentric occlusion Clinical feature  Wedge shape defect  Defect has smooth surface Treatment  Restoration
  53. 53. Age changes & Clinical considerations •Attrition is seen in aged people. •Wear facets are common. •Decrease in vertical dimension and flattening of proximal contours. •Color changes with age. •Permeability decreases. •Caries incidence is less in aged people. •Surface composition: more amount of fluoride and localized increase in nitrogen.
  54. 54. Fluoridation  It decreases the solubility of enamel  It acts in the following way: I. Forms fluoroapatite which is less soluble than hydroxyapatite II. Inhibits demineralization III.Enhances remineralization IV.Inhibits bacterial metabolism
  55. 55. Acid etching  ACID ETCHING TECHNIQUE- Buonocore in 1955  Micromechanical bonding b/w enamel and resin based restorative material. Mode of action-  Increases the porosity of exposed surfaces by dissolution of crystals - creates a micro porous layer from 5 to 50 µm deep
  56. 56. Three etching patterns predominate:- (Preferential removal of rods) TYPE II TYPE III (Junction b/w type 1 n type 2) (Preferential dissolution of prism core) TYPE I
  57. 57.  Enamel etching transforms the smooth enamel surface into an irregular surface  Etched enamel has high surface energy (72 dynescm) allow resin to wet the tooth surface better when resin penetrates into micro porosities and polymerized to forms resin tags
  58. 58. Resin tags interlocked with the surface irregularities created by etching which form mechanical bond to enamel.  Bond strength:16-20Mpa
  59. 59.  Originally recommended 60 secs using 37% phosphoric acid.  Currently,etching time for most etching gel is 15 sec  Aprismatic enamel requires double the etching time required by prismatic Etching time
  60. 60. Involves the surface dissolution of enamel by acid along with the abrasiveness of the pumice to remove superficial stains or defects Commercially developed system for enamel microabrasion. [PREMA (Premier enamel micro abrasion) Enamel microabrasion In 1984 Mc Closkey reported this technique In1986 Croll and cavanaugh modified this technique
  61. 61.  PREMA contains a reduced concentration of hydrochloric acid (approx 11%)+ silicon carbide particles in a water soluble gel paste.  Mode of action 1. Physical removal of stained outer enamel layer by stripping action of acid and abrasive action of pumice 2. The etching action removes interprismatic substance and changes light refraction characteristics 3. There is oxidation of some pigments
  62. 62. Procedure
  63. 63.  Removal of localized superficial white spots and other surface stains or defects is called macroabrasion Sturdevant 6th edition  12 fluted composite finishing bur or fine grit finishing diamond in a high speed handpiece is used Macro abrasion
  64. 64. Procedure
  65. 65. CONCLUSION Enamel is an important structural entity of the tooth hence its protection is utmost important. Its function is to form a resistant covering of the teeth, rendering them suitable for mastication.
  66. 66.  Marzouk : Operative Dentistry, First Edition  Orban :Oral Histology and Embryology,Tenth Edition  Oral pathology SHAFER’S  Sturdevant :Art and Science of Operative Dentistry, Fifth and sixth Edition  Ten Cates: Oral Histology , Seventh Edition  Enamel microabrasion,theodore p croll