dental caries classifications, histopathology

dental caries classifications, histopathology

1. Dental caries – part 2 Contents Classification Histopathology 1

2. 2 CLASSIFICATION:

3. According to location: Primary caries Caries of pit and fissure origin Caries of enamel smooth surface origin Backward caries Forward caries Residual caries Root surface caries Secondary (recurrent) caries 3

4. 4 According to extent: a. Incipient (reversible) caries b. Cavitated (irreversible) caries

5. 5 According to hard tissue affected: a. Enamel b. Dentin c. Cementum   Others: Primary caries & secondary caries Nursing caries Radiation caries Rampant caries

6. 6 ACCORDING TO LOCATION: Primary caries: Primary caries is the original carious lesion of the tooth. Accordingly 3 morphologic types of primary caries are evident in clinical observations. Type I – pit & fissure and occlusal surfaces. Type II – Smooth surfaces of which there are 2 variants interproximal and cervical / gingival. Root surface caries.

7. 7 These caries can form in the regions of pits and fissures Usually resulting from imperfect coalescence of the developmental enamel lobes. Such caries are not so clinically noticeable until the forces of mastication fracture the increasing amount of unsupported enamel . Type I / Pit and fissure caries :

8. 8 Limited to the – Occlusal surfaces of molars and premolars - Buccal pits of molars - Lingual surfaces of maxillary anterior teeth Poor self cleansing features Usually occurs before smooth surface caries Clinically - Black or brown in color - Slightly soft consistency - “Catch” the tip of a fine explorer

9. Caries of enamel smooth surface origin: 9 Smooth surface caries does not begin as an enamel defect, but rather in a smooth area of the enamel surface that is habitually unclean and is thereby continually or usually covered by plaque.

10. Progression 10

11. 11 Forward caries: Forward caries is wherever the caries cone in enamel is larger or atleast the same size as in dentine.

12. Backward caries: 12 When the spread of caries along the DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the junction and is termed as backward caries.

13. Recurrent caries (secondary caries): 13 It occurs at the junction of a restoration and the tooth and may progress, under the restoration. It is termed as recurrent caries. This condition usually indicates that microleakage is present- -due to poor cavity preparation, -faulty restoration or a combination of these factors .

14. Root surface caries: 14 These kind of caries originate in the dentinal root portion of a tooth. It is predominantly found in the dentitions of older age groups with significant gingival recession and exposed root surfaces. It initiates on the surface of mineralized dentin and cementum which have greater organic content. For this reason, bacterial flora causing root caries is also different from flora causing smooth surface caries.

15. Linear enamel caries : 15 This is an atypical form of dental caries called linear enamel caries. The lesions predominate on the labial surfaces of the anterior maxillary teeth on the region of the neonatal line. Lesion is crescent shape Increase caries susceptibility of posterior teeth. Recent evidence suggests that neonatal line forms due to transient hypocalcemia , a normal feature of the neonatal period

16. Odontoclasia : 16 Variant of linear enamel caries Results in gross destruction of the labial surfaces of incisor teeth Cause may be an inherent structural defect

17. EARLY CHILDHOOD CARIES 17

18. Early childhood caries “A suddenly appearing, widespread, rapid burrowing type of caries, resulting in early involvement of the pulp and affecting those teeth usually regarded as immune to ordinary decay.” - Massler A complex disease involving maxillary primary incisors within a month after eruption and spread rapidly to involve other primary teeth. -Davies (1988) 18

19. CLASSIFICATION 19

20. NURSING CARIES A unique pattern of dental decay in young children due to prolonged and improper nursing/feeding habit. -Winter et al, 1966 20

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22. CLINICAL FEATURES 22

23. Mandibular anterior teeth are usually spared because of: Protection by tongue Cleansing action of saliva due to presence of the orifice of the duct of sublingual glands very close to lower incisors. 23

24. PROGRESSION OF THE LESION 24

25. NURSING CARIES RAMPANT CARIES 25

26. NURSING CARIES RAMPANT CARIES 26

27. 27 Complication of radiation therapy of oral cancer lesion Radiation induced xerostomia produces caries conducive environment Carious lesion develops as early as 3 months after onset of xerostomia May be caused by other factors like salivary gland tumors, autoimmune diseases, prolong illness Radiation caries:

28. Adolescent caries: 28 Acute caries attack at 11-18 years of age Lesion in teeth and surfaces that are relatively immune to caries Small opening in enamel with extensive undermining Rapid clinical course Little or no secondary dentin formation

29. Arrested caries: 29 Caries which becomes static or stationary and does not show any tendency for progression Both dentitions are affected Lesion appears as large open cavity with lack of food retention Superficially softened and decalcified dentin gets burnished and has brown stained polished appearance - “Eburnation of dentin

30. 30 Senile Caries Caries activity that spurts up during the old age. They are located exclusively on the root surfaces of the teeth. Also seen in association with partial denture clasps. Causes: gingival recession, decreased salivary secretion, poor oral hygiene.  

31. Occult Caries / Hidden Caries 31 Not clinically diagnosed, but detected only on radiograph. Seen in persons with low caries index suggestive of increased fluoride exposure. Also called as fluoride bombs or fluoride syndrome

32. CERVICAL BURNOUT 32

33. 33 G.V.Black’s Classification   Class-I: - Caries on the occlusal surfaces of molars and premolars - Occlusal 2/3 of the buccal and lingual surfaces of molars - Lingual surfaces of the anterior teeth Class-II: - lesions found on the proximal surfaces of molars and premolars Class-III: - lesions found on the proximal surfaces of anterior teeth, but do not involve the incisal angle

34. 34 Class-IV: - lesions found on the proximal surfaces of anterior teeth and involving incisal angle Class-V: - lesions found on the gingival third of the facial and lingual surfaces of anterior and posterior teeth. Class-VI: - were not included in Black’s classification - Proposed by Siomon - Lesions on the incisal edge and cusp tips of the teeth  

35. 35 ACCORDING TO EXTENT

36. 36 ICDAS classification

37. Root caries (New in ICDAS II) E = Excluded root surfaces (no gingival recession) 0 = Sound (no caries or restoration) 1 = Non- cavitated carious root surface— soft or leathery 2 = Non- cavitated carious root surface— hard and glossy 3 = Cavitated (greater than 0.5mm in depth) carious root surface— soft or leathery 4 = Cavitated (greater than 0.5mm in depth) carious root surface—hard and gloss 6 = Extensive cavity: an extensive cavity involves at least half of a tooth surface and possibly reaching the pulp. 7 = Filled root with no caries 37

38. 9 = Used for the following conditions 97 = Tooth extracted because of caries (tooth surfaces will be coded 97) 98 = Tooth extracted for reasons other than caries (all tooth surfaces coded 98) 99 = Unerupted (tooth surfaces coded 99) 38

39. The shared vision for the International Caries Detection and Assessment System is now that: it employs an evidence-based and preventively oriented approach, is a detection and assessment system classifying stages of the caries process, is for use in dental education, clinical practice, research and public health, provides all stakeholders with a common caries language, has evolved to comprise a number of approved, compatible ‘formats’, supports decision-making at both individual and public health levels and has generated the International Caries Classification and Management System, to enable improved long-term caries outcomes. 39

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46. HISTOPATHOLOGY 46

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49. Knowledge Of macroscopic features: detection & diagnosis of caries Of shape of lesion: cavity preparation Characteristics: Chronic disease Not self-limiting Cavity formation subclinical Total destruction Light microscopy Enamel lesion Mineral loss (signs, symptoms) visible Time Electron microscopy 49

50. Dental Caries Enamel Caries Dentin Caries Cementum Caries (Root caries) Smooth surface caries Pit and fissure caries 50

51. Speed of lesion formation Incipient caries to clinical caries: 18 ± 6 months Peak rate for incidence of caries: 2-4 yrs ( avg 3yrs) after eruption Poor oral hygiene, excess sucrose: 3 weeks Radiation induced Xerostomia: 3 months Occlusal caries require less time than smooth surface 51

52. Basic structure of enamel 52

53. Estimating mineral loss Clinical considerations Refractive indices of Hydroxyapatite, water and air Histological considerations Microradiography Polarized light microscopy 53

54. ENAMEL CARIES MACROSCOPIC FEATURES: White spot lesion Opaque, chalky white Surface features-SEM ( Thylstrup , 1994) : Deepened & irregular Tomes processes pits Irregular cracks & fissures Widened intercrystalline spaces Fractures of perikymata edges Microcavities 54

55. Brown spot lesion Sites Occlusal surfaces: Fissure morphology ( Newbrun , 1989) Starts at both sides of fissure wall 55

56. MICROSCOPIC FEATURES: Triangular/wedge in shape Divided into 4 zones Can be viewed in Plain transmitted light Polarized light-clearer picture 56

57. Histological features of early enamel caries 57 Loss of inter-rod substance prominent enamel-rods Appearance of transverse striations of enamel rods due to segmental demineralization Accentuation of incremental striae of Retzius

58. H/F of Advanced enamel caries 58 Classified on the basis of pore volume and mounting media used Zone 1 – Translucent zone Zone 2 – Dark zone Zone 3 – Body of lesion Zone 4 – Surface zone These zones are from the dentin towards the outer enamel surface

59. ZONE 1: TRANSLUSCENT ZONE At the advancing front- 5 -100 µm Seen with quinoline Pore volume: 1% Not always present, sometimes near lateral part 59

60. ZONE 2: THE DARK ZONE More constant feature-90-95% lesions Pore volume -2-4% Why is it called dark zone? 2 theories for small pores 60

61. ZONE 3: THE BODY OF THE LESION Largest zone Pore vol : 5% at periphery, 25% in centre Appears translucent in quinoline and dark with water Striae of retzius well marked old./chronic lesions: bands of well mineralized tissue Bacteria in between prisms (rods) 61

62. ZONE 4: THE SURFACE ZONE 20-50 µm Pore vol : 1% Negatively birefringence in water Importance: serves as barrier to bacterial invasion 62

63. Smooth surface caries The earliest manifestation of incipient enamel caries is the appearance of an area of decalcification , beneath the dental plaque, which resembles a smooth chalky white area. There is loss of interprismatic substance, with increased prominence and roughening of the ends of the enamel rods. White spot lesion 63

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65. Accentuation of incremental striae of Retzius . As deeper layers of enamel are involved it forms a cone shaped lesion with the apex toward the DEJ and the base toward the surface of the tooth. Eventual loss of continuity of enamel surface –feels rough to explorer tip. 65

66. Pit and fissure caries Fissures are diverse in shape and size Carious lesion starts at both side of fissure rather than at the base, penetrating nearly perpendicular to the DEJ. Lesion is cone-shaped with base towards dentine and apex towards enamel surface 66

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68. Progression of enamel lesion Caries dissolution along the rods Highest degree of tissue porosity is along “Central Traverse” Oldest part-along CT, lesion spreads laterally along the surface 68

69. Central defects of crystals-hollow hexagons As dissolution increases, disorganization of crystal arrangement, invasion of bacteria 69

70. Ultrastructural changes in enamel caries Destruction of crystals at borders & within the prism Arcade like defects bounded by rows of resistant crystals- “caries crystals” More dissolution in heads and less in tails 70

71. Remineralization/arrest Enamel most susceptible to caries during & after eruption 1 st molar:12-14 months 2 nd molar:14-18 months Premolars:1-2 months-less prone {Backer-Dirks (1966)} 71

72. Mechanism of arrest of non- cavitated lesions: Maintains original crystalline framework Etched crystallites serve as nucleating agents Wear & polishing of the partly dissolved external surface-regain of surface hardness Remineralized area: brown or black spots Mechanism Cavitated lesions can also be arrested with proper plaque control ( thylstrup ) New mechanism of remineralization : CPP-ACP 72

73. Clinical significance of enamel caries 73

74. CARIES OF DENTIN Begins with the natural spread of the process along the DEJ and rapid involvement of the dentinal tubules. The dentinal tubules act as tracts leading to the pulp (path for micro-organisms). Caries advances more rapidly as dentin provides much less resistance to acid attack . Early Dentinal Changes: -initial penetration of the dentin by caries  dentinal sclerosis, -calcification of dentinal tubules and sealing off from further penetration by micro-organisms, -more prominent in slow chronic caries. Dentinal sclerosis 74

75. DENTINAL CARIES Progression of enamel caries to dentin: 5.4% from 11 – 22 yrs ( Mejare et al, 1999) MACROSCOPIC CHANGES: Lateral spread along DEJ Cone shaped-apex towards the pulp Affected dentin-Brown or black in colour 75

76. MICROSCOPIC CHANGES: (mechanism) Caries advancement proceeds through 3 stages Acids demineralize the dentin Organic matter degenerates Loss of structural integrity & bacterial invasion 1 st mild stimuli –defense reaction of dentin-tubular sclerosis/TRANSPARENT ZONE Dentin demineralization-when lesion reaches DEJ Arrest of caries Cavitation of dentin-bacterial invasion 76

77. 77 Zone of Decomposed dentin Zone of Bacterial invasion Zone of Demineralisation Zone of Dentinal sclerosis Zone of Fatty degeneration Retreating Odontoblastic process INFECTED DENTIN AFFECTED DENTIN Dentinal caries

78. Behind the transparent sclerotic zone, decalcification of dentin appears. In the earliest stages, when only few tubules are involved, microorganisms may be found penetrating the tubules  Pioneer Bacteria. 78

79. This initial decalcification involves the walls allowing them to distend as the tubules are packed with microorganisms. Each tubule is seen to be packed with pure forms of bacteria, eg ., one tubule packed with coccal forms the other tubule with bacilli. 79

80. As the microorganisms proceed further they are distanced from the carbohydrates substrate that was needed for the initiation of the caries. Thus the high protein content of dentin must favour the growth of the microorganisms. Therefore proteolytic organisms might appear to predominate in the deeper caries of dentin while acidophilic forms are more prominent in early caries. 80

81. Advanced Dentinal Changes ; -decalcification of walls, confluence of the dentinal tubules, tiny “liquefaction foci”, described by Miller are formed by the focal coalescing and breakdown of dentinal tubules. These are ovoid areas of destruction parallel to the course of the tubules which filled with necrotic debris and increase in size by expanding. The adjacent tubules are distorted and their course is bent due to this expansion. 81

82. The destruction of dentin by decalcification and then proteolysis occurs in numerous focal areas- leading to a necrotic mass of dentin of a leathery consistency. Clefts present in the carious dentin that extends at right angles to the dentinal tubules, accounts for the peeling off of dentin in layers while excavating. 82

83. Shape of the lesion is triangular with the apex towards the pulp and the base towards the enamel. Zone 1; Zone of Fatty Degeneration of Tome’s Fibers,(next to pulp) -due to degeneration of the odontoblastic process. This occurs before sclerotic dentin is formed and makes the tubules impermeable. Zone 2; Zone of dentinal sclerosis, -deposition of Ca salts in the tubules. Zone 3; Zone of decalcification of dentin Zone 4; Zone of bacterial invasion Zone 5; Zone of decomposed dentin due to acids and enzymes. 83

84. ZONE OF FATTY DEGENERATION: Of the Tomes fibres -stained by Sudan red Importance: Fat contributes to impermeability of dentinal tubules Maybe a predisposing factor favouring sclerosis Innermost layer of dentinal caries towards pulp Due to deposition of fatty tissue in odontoblastic processes Seen usually in rapidly progressing caries No crystals or bacteria in lumen of tubules Intertubular dentin  normal 84

85. ZONE OF TUBULAR SCLEROSIS: Reaction of vital dentinal tubules & pulp Seals off tubules to further penetration by bacteria Mineralization process-2 types Hydroxyapatite crystals & large rhomboidal crystals ( whitlockite ) Transluscent appearance- transluscent /transparent dentin As the microorganisms cause destruction to dentin, initially there is an attempt to stop the advancement of caries by depositing the minerals. There is a deposition of mineral in intertubular dentin. Zone is called “transparent zone” Odontoblasts also start depositing dentin. At the periphery of sclerotic dentin, dead tracts are present. 85

86. ZONE OF BACTERIAL INVASION Initially tubules with single type of bacteria Liquefaction foci-beadings, varicosities, moth-eaten, rosaries Decalcification is by bacterial acid diffusion Very narrow zone, softer than normal dentin Further loss of minerals from inter tubular dentin Large crystals within lumen of dentinal tubules 86

87. ZONE OF DEMINERALIZATION Narrow zone Occlusion of tubules Softer than normal dentin Few microorganisms in the tubules – “pioneer bacteria” 87

88. 88 Zone of Decomposed Dentin / Infected Dentin Outermost zone, large scale destruction of dentin Foci of Miller join together Areas of dentin decomposition, occur perpendicular to dentinal tubules  “Transverse Clefts” Mechanism of formation of Clefts - not known May follow course of incremental lines or May result from coalescence of liquefaction of adjacent tubules Also may rise by extensive proteolytic activity along interconnecting lateral branches of odontoblastic processes Bacteria shift from dentinal tubules to the peri & inter tubular dentin

89. Zone of Decalcification with Bacterial Invasion / Turbid Dentin Initially only few tubules are involved & micro-orgs also less These are acidogenic , pioneer bacteria (initiators), present long before lesion is clinically detected Bacteria multiply within tubules & are seen in advancing front of lesion Walls of tubules are thin & when micro-orgs penetrate, they cause irregularities/distensions of walls  ROSARY BEAD appearance Later, bacteria have proteolytic activity, areas of proteolysis appear as spaces containing necrotic material & bacteria These areas  “Liquefaction Foci of Miller”. These areas vary in number & are parallel to dentinal tubules 89

90. TO SUMMARIZE: 90

91. Other features In slowly advancing lesions Sclerotic dentin-very hard, shiny Hypermineralized – radioopaque In moderately advancing lesions Dead tracts Reparative/reactionary dentin Pulp stones In rapidly advancing lesions Abscess, necrosis of pulp 91

92. Zones of dentin (sturdevant) ZONES OF DENTIN: Zone 1: normal dentin Zone 2: subtransparent dentin Zone 3: transparent dentin Zone 4: turbid dentin Zone 5: infected dentin AFFECTED DENTIN INFECTED DENTIN Caries detector – basic fuschin / 1% acid red ( Fusayama , 1979) 92

93. Secondary / Reactionary dentin 93 Protective mechanism to protect pulp Develops as a result of localized, non-specific irritation to odontoblasts Hyper mineralized,less number of dentinal tubules having irregular & torturous course

94. ROOT CARIES Occurs in older individuals where root/cementum is exposed Microorganisms penetrate along the clefts, sharpey’s fibres Delamination occurs along incremental lines Brush like appearance Radioopaque surface layer seen Dentinal tubular reactions 94

95. Root Caries Root caries as defined by HAZEN, is a soft, progressive lesion that is found anywhere on the root surface that has lost its connective tissue attachment and is exposed to the environment. -the root surface must be exposed to the oral environment before caries can develop here. -Plaque and micro-organisms are essential for the cause and progression of the lesion, mostly Actinomyces , -micro-organisms invade the cementum either along the Sharpey’s fibers or between the bundles of fibers. 95

96. 96 -spread laterally, since cementum is formed in concentric layers. -after decalcification of cementum, destruction of matrix occurs similar to dentin with ultimate softening and destruction of this tissue. -invasion of micro-organisms into the dentinal tunbules , finally leading to pulp involvement. -the rate is slower due to fewer dentinal tubules than crown area

97. 97 Histopathology: Outer surface of cementum – hyper mineralized, thus more caries resistant Resistance due to Reprecipitation of minerals from within Precipitation of minerals from Plaque Clefts formed, through which bacteria penetrate & cause tooth structure destruction Penetration occurs along course of Sharpey's fibers Once cementum completely exposed & destroyed, underlying dentin is involved

98. A tooth surface without caries. The first signs of demineralization. The enamel surface has broken down. A filling has been made but the demineralization has not been stopped. The demineralization proceeds and undermines the tooth. The tooth has fractured. 98

99. Conclusion : Dental caries should be considered as a consequence of ecologically driven imbalances of oral microbial biofilms. An appreciation of ecological principles will enable a more holistic approach to be taken in caries control. A better understanding of the process of biofilm formation ,its genetic regulation is necessary to the development of novel strategies for oral disease prevention and control. 99

100. Conclusion : Among the multifactorial etiology of dental caries diet plays an important role in the occurrence of dental caries. This seminar intended to provide an overview of the evidence for an association between diet and dental caries which has already been established and documented by a series of studies. But the information available regarding the association of diet and dental caries under the Indian context and the effect of rapid changes in urbanization and economic development on the Indian diet is sparse and needs further research. 100

101. Conclusion : The way ahead should be considered under 2 aspects: 1. The extrapolation of the data to the India diet and conditions. 2. The task of diet changes which requires lifestyle changes that would be challenging to bring about and thus should be an important focus area for dental public health programs/ approaches in any setting for different age groups and populations. 101

102. References : Cariology – Newbrun . Murray J.J. et al. The prevention of oral disease. 4 th Ed. Shafer. A textbook of Oral Pathology. 4 th Ed. S.S.Hiremath.Textbook of Preventive & Community Dentistry. Per Axelsson . Diagnosis and Risk Prediction of Dental Caries. 2000, Quintessence Publishing Co. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 102

103. References : T.W. Cutress et al. Effects of fluoride-supplemented sucrose on experimental dental caries and dental plaque ph. Adv Dent Res 9(1):14-20, February, 1995 . Lingström P, van Houte J, Kashket SFood starches and dental caries. Crit Rev Oral Biol Med. 2000;11(3):366-80 . Brian A. et al . Sugar Consumption and Caries Risk:A Systematic Review. Journal of Dental Education . October 2001. Volume 65, No.10 103

104. References : Gordon Nikiforuk . Understanding Dental Caries.Karger Publishers. D.T.Zero . Sugars- The Arch Criminal? Caries Res 2004;38:277-285 . Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6 th edition , 2004, Pearson Prentice Hall.. Carole A. Palmer, Diet and Nutrition in Oral Health.Julie Levin Alexander, 2003. 104

105. References : Marsh P. Dental plaque as a biofilm and a microbial community-implications for health and disease. BMC Oral Health 2006,6:S14. Thomas H.J et al .Managing the complexity of a dynamic biofilm. JADA, 2006;Vol.137;10s-15s. Scheie A.A &Peterson F.C.The Biofilm concept:consequences for future prophylaxis of oral diseases? Crit Rev Oral Biol Med 15(1):4-12 (2004) 105

106. Questions asked in NTRUHS examination : Balanced diet in prevention of dental caries – 20 M – APR 2015 Early childhood caries – 7 M – 2011 Diet counselling – 2011 and 2013 for 7M and 20M Cariogenecity – 2003 Rampant caries – 2003 Bacteriological role in caries – 2002 Diet for healthy teeth – 2001 Genetics and dental caries- 2001. 106

107. Newbrun stated that “ the dentist of future will still have to treat caries, but unquestionably the emphasis will be on early diagnosis and preventive intervention.” Times change and we change with time ”. Thank you 107