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Dental Caries

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Ramkumar Adhikari

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Dental Caries

  1. 1. PRESENTED BY: RAM KUMAR ADHIKARI B.D.S. 4th BATCH (3rd YEAR) KDCTH
  2. 2. CONTENTS  Introduction of dental caries.  Pre disposing factors of dental caries.  Different types of dental caries.  Diagnosis of dental caries.  Prevention of dental caries.
  3. 3. INTRODUCTION OF DENTAL CARIES • 'Caries' is Latin for 'rot' or ‘decay’. • Dental caries means rotten or decayed teeth. • Caries is the noun which names the disease. • Carious is the adjective, not 'a caries’, 'a carious area' or 'an area of caries'. • Benjamin Franklin stated that “ hot things, sharp things, sweet things, cold things, all rot the teeth and make them look like old things”.
  4. 4. HISTORICAL BACKGROUND • Dental caries is considered as a ‘disease of modern civilization’. • Prehistoric man rarely suffered from tooth destruction. • Pre Neolithic periods(12,000 BC ) anthropological studies revealed that dolicocephalic skulls did not exhibit dental caries.
  5. 5. HISTORICAL BACKGROUND (contd.) • Neolithic periods(12,000 to 3000 BC) skulls from brachycephalic man showed carious teeth. • Caries in prehistoric man(3000 to 750 BC). • Pithecanthropus- earliest known ancestors, there was no evidence of dental caries. • Evidence of caries was found in skulls of prehistoric race who lived in central Europe about 15,000 yrs ago.
  6. 6. DEFINITION • According to WHO- Dental caries is a microbial multifactorial disease of calcified tissue of teeth, characterized by demineralization of the inorganic portion and destruction of organic content. MICROBIOLOGY 1. Bacteria involved : • Streptococci e.g. mutans, sobrinus • Lactobacilli e.g. acidophilus 2. Possibly associated bacteria : • Steptococci e.g. mitis • Actinomyces e.g. viscosus
  7. 7. CARIOGENIC PROPERTIES OF MICROORGANISM • They are able to produce acid rapidly from fermentable carbohydrates (acidogenic). • They thrive under acid conditions (aciduric). • Produce extracellular and intracellular polysaccharides which contribute to the plaque matrix; intracellular polysaccharides can be used for energy production and converted to acid when sugars are not available
  8. 8. VARIOUS FACTORS INFLUENCING THE PROGRESSION OF CARIES • Bacteria in dental plaque • Substrate such as a fermentable carbohydrate (dietary sugars) • A susceptible tooth surface • Time
  9. 9. ROLE OF PLAQUE • Plaque is an adhesive layer which deposits on the surface of the tooth and has colonies of bacteria. • It prevents the escape of acid into the saliva. • It protects acid from buffering action of saliva due to its diffusion limiting properties. • In 2weeks the plaque is mature but there are considerable site-to-site variations in its composition. Each site can be considered as unique and these local variations may explain why lesions progress in some sites but not others in the same mouth.
  10. 10. ROLE OF PLAQUE (contd.) In the upper picture, a disclosing agent reveals the plaque, while in the lower picture the plaque has been removed. White spot lesions are visible on the canines, but not on other tooth surfaces, although plaque is present.
  11. 11. ROLE OF CARBOHYDRATE • Caries prevalence is low in populations adhering to a primitive way of living and a diet of local products with little sugar. • A drastic increase in caries is invariably seen when these population “improve "their standard of living and adopt a modern “civilized "diet with high sugar content. • A strong correlation between caries development and sugar consumption. • Refined carbohydrates are more caries producing than crude carbohydrates. • Bacteria +Sugars +Teeth → Organic acids → Caries
  12. 12. ROLE OF CARBOHYDRATE (contd.) More availability of substrate for bacteria More chances of CARIES Diffusion in plaque due to low molecular weight Acid formation •Aspartic acid •Butyric acid •Glutamic acid Demineralization of teeth CARBOHYDRATE Synthesis of polysaccharide •Glucan from glucose •Levan from fructose •Dextran from sucrose Holding the plaque over the tooth surface CARIES
  13. 13. ROLE OF CARBOHYDRATE (contd.) • The carbohydrate rapidly diffuse in the plaque and fermented to form acids there. So, pH at the surface of tooth falls below critical level causing rapid demineralization of enamel. • The plaque remains acidic for some time, taking 30–60 min to return to its normal pH in the region of 7. • The curve drawn for pH during carbohydrate diet is termed as Stephan’s curve.
  14. 14. ROLE OF CARBOHYDRATE (contd.) The shaded area represents the risk of carious attack to the tooth surface: this area is larger in a patient with extensive caries. Stephan’s curve.
  15. 15. A SUSCEPTIBLE TOOTH SURFACE • Surface enamel is more resistant to caries than subsurface enamel. • Surface enamel has high mineral content as fluoride, zinc, lead and iron. • Hypoplastic enamel, deep narrow occlusal fissures, buccal or lingual pits predispose tooth to develop caries. Enamel hypoplasia Occlusal pits and fissures
  16. 16. A SUSCEPTIBLE TOOTH SURFACE (contd.) • Attrition at occlusal surface causes lesser chance of caries. • Rotated, malaligned, out of positioned, teeth are difficult to clean and favour the development of caries. • Under normal conditions, the tooth is continually bathed in saliva. It is capable of remineralizing the early carious lesion because it is supersaturated with Ca and P. • When salivary buffering capacity has been lost, a low Ph environment is encouraged and persists for longer duration causing demineralization of enamel.
  17. 17. TIME 1. It is evident that the mere existence of the three factors operating together does not result in instantaneous mineral loss. 2. Therefore a fourth circle is often added to stress the time dimension taken for dental caries to develop.
  18. 18. Microorganisms Host & tooth Substrate Time Caries The four circle diagrammatically represent the parameters involved in the carious process. All four factors must be acting concurrently (overlapping of the circles) for caries to occur.
  19. 19. OTHER FACTORS • Age • Sex • Geography • Race • Economics status • Nutrition • Health status
  20. 20. Schematic illustration of the determinants of the caries process. Those that act at the tooth surface level are found in the inner circle, while the more distant determinants are found in the outer circle. (Adapted from Fejerskov and manii, 1990)
  21. 21. THEORIES OF CARIES FORMATION • Early theories: The legend of the worm • Endogenous theories: Humoral theories Vital theories • Exogenous theories: Chemical (acid) theory Parasitic (septic) theory Chemicoparasitic (acidogenic) theory Proteolytic theory Proteolysis chelation theory Sucrose chelation theory • Other theories: Sulfatase theory Autoimmune theory
  22. 22. THEORIES OF CARIES FORMATION(contd.) There is no universally accepted opinion of the etiology of dental caries. Various theories have been proposed from time to time to study the caries formation. EARLY THEORIES OF CARIES ETIOLOGY The legend of the worm theory:- • Earliest reference of tooth decay and toothache came from the ancient Sumerian text known as ‘the legend of the worm’. • In Japanese the word for dental caries is ‘mush – ha (mushi – room; ha – tooth), meaning hollow tooth. • The same terminology is employed by the Chinese; the word for hollow tooth is ‘chung Choo’.
  23. 23. The legend of the worm (contd.) • The early history of India, Egypt and the writing of Homer and popular lore also make reference to the worm as the cause of toothache. • Remedy for toothache –mix beer, plant known as Salkilbir and oil together and put it on the tooth. • Fumigation devices continued to be used in England late 19th century. • An interesting therapeutic method applied by the Chinese about 2700 BC for the treatment of various disease including dental tissues was acupuncture.
  24. 24. ENDOGENOUS THEORIES A. Humoral Theory: Greek physicians advanced the humoral theory of disease. The ancient Greeks considered that a persons physical and mental constitution was determined by the relative proportions of the four elemental fluids of the body which correspond to the four humors, • Blood Sanguine • Phlegm Phlegmatic • Black bile Melancholic • Yellow bile Choleric Hippocrates, ‘the father of medicine’, while favoring the concept of humoral pathology also referred to the accumulated debris around teeth and to their corroding action. He also stated that stagnation of juices in the teeth was the cause of toothache.
  25. 25. ENDOGENOUS THEORIES (contd.) B. Vital Theory: A vital theory of tooth decay was advanced towards the end of the 18th century, which postulated that tooth decay originated, like bone gangrene form within the tooth itself.
  26. 26. EXOGENOUS THEORIES A. Chemical (Acid) theory: • In the 17th and 18th centuries paralleling new insights into chemistry, there emerged the concept that teeth are destroyed by acids formed in the oral cavity. • Robertson proposed that dental decay was caused by acid formed by fermentation of food particles around teeth. • Since fermentation was at this considered to be a strictly non- vital process, the possibility that microorganisms were involved was not, as yet recognized.
  27. 27. EXOGENOUS THEORIES (contd.) B. Parasitic or Septic Theory In 1843 – filamentous parasites are removed from carious cavities. Dental caries was thought to develop as a result of the infiltration and decomposition of the enamel cuticle, the inter prismatic substance of enamel and finally dentin.
  28. 28. EXOGENOUS THEORIES (contd.) C. Miller’s Chemicoparasitic Theory (Acidogenic theory)-1884 Theory states that caries is caused by acids produced by microorganisms of the mouth. Miller was student of Koch and his extensive studies of the oral micro flora and its relationships to caries were greatly influenced by Koch and other scientists of the day. Form Koch he learned to isolate, stain and identify bacteria.
  29. 29. Miller’s Chemicoparasitic Theory (Acidogenic theory) -contd. • At this time, Pasteur had discovered that the process of conversion of sucrose to lactic acid is mediated by micro organisms. • This enabled Miller to assign to oral microorganisms the rule of acid formation and thus assigned a chemical role to flora which is the basis of his Chemicoparasitic theory of dental caries. • He published the results of his studies in 1882. He formulated the hypotheisis in which he stated: Dental decay is a chemico parasitic process consisting of two stages, entitled text “Die Mikroorganismen der Mundhohle”.
  30. 30. Miller’s Chemicoparasitic Theory (Acidogenic theory) -contd. •The decalcification of enamel results in its total destruction. Decalcification of dentin, as a preliminary stage, followed by dissolution of the softened residue. •The acid which affects this primary decalcification is derived from the fermentation of starches and sugar lodged in the retaining centers of the teeth.
  31. 31. EXOGENOUS THEORIES (contd.) D.The Proteolytic Theory-1956 • Mature enamel is more highly mineralized tissue. The human tooth contains about 1.5% to 2% organic material, of which 0.3% to 0.4% is protein i.e. glycoprotein. • According to the PROTEOLYTIC THEORY, the organic component is most vulnerable and is attacked by hydrolytic enzymes of microorganisms. This precedes the loss of the inorganic phase. • Gottlieb (1944) stated that the initial action was due to proteolytic enzymes which attacks the lamellae, rod sheaths, tufts and walls of the dentinal tubules. • He suggested that a coccus, probably Staphylococcus aureus, causative organisms of dental caries.
  32. 32. The Proteolytic Theory (contd.) • According to Gottlieb, acid alone produces chalky enamel but i.e. not true caries. His ideas were based on the observations of histological specimens and the similarity between carious enamel and enamel whose organic components were stained with silver nitrate. • There has been no bacteriological confirmation between staphylococcus pyogenes and caries. • Gottlieb stated that yellow pigmentation was characteristic of caries and is due to pigment produced by proteolytic organisms.
  33. 33. The Proteolytic Theory (contd.) Conclusion • It is not an universally accepted theory as there is no satisfactory evidence to support that the initial attack on enamel is proteolytic. • Caries can occur in the absence of proteolytic organism. • Proteolysis may occur in the advanced carious lesion but not in initiation of caries.
  34. 34. EXOGENOUS THEORIES (contd.) E. Proteolysis Chelation Theory • Originated by Schatz & Martin • This theory considers dental caries to be a simultaneous microbial degradation of the organic components of enamel by proteolysis and the dissolution of the minerals of the tooth by the process known as chelation. • The breakdown products of the organic components of enamel (keratin, citrates, mucopolysaccharide, lipids) may have chelating properties and can dissolve the minerals in enamel. • Chelates is a complex compound of ion(ca) and two or more groups. • The proteolysis-chelation theory states that inorganic and organic portions of enamel are attacked simultaneously and it occur independent of pH of the medium.
  35. 35. Proteolysis Chelation Theory (contd.) This theory is also not universally accepted as it cannot explain the following facts: Increased caries incidence with increased sugar intake. Increased caries activity with increased lactobacillus count. Decreased caries incidence following topical or systemic administration of fluoride.
  36. 36. EXOGENOUS THEORIES (contd.) E. Sucrose Chelation Theory • Proposed by Eggers-Lura (1967) • Theory suggests that sucrose itself cause dissolution of enamel by forming unionized calcium saccharates.
  37. 37. OTHER THEORIES A.Auto-immunity theory In this theory, it is suggested that 'forbidden clones' of lymphocytes attack target cells (odontoblast) rendering the tooth vulnerable to caries attack.
  38. 38. Distribution of dental caries according to tooth surface:- Occlusal > Interproximal >Buccal Caries Susceptibility Individual teeth According to Brekhus(1931) Teeth % Upper and lower 1st molar 95% Upper and lower 2nd molar 75% Upper 2nd bicuspids 45% Upper 1st bicuspids 35% Lower 2nd bicuspids 35% Upper central and lateral incisors 30% Upper canine and lower 1st premolar 10% Lower anterior teeth 3%
  39. 39. CLINICAL RISK ASSIGNMENT FOR CARIES A patient is at high risk for the development of new cavitated lesions if: 1. High mutans streptococci (MS) counts are found. Bacteriologic testing MS should be done if:  The patient has one or more medical health history risk factors.  The patient has undergone antimicrobial therapy  The patient presents with new incipient lesion  The patient is undergoing orthodontic care  The patient’s treatment plan calls for extensive restorative dental work 2. Any two of the following factors are present: – Two or more active carious lesions – Large number of restorations – Poor dietary habits – Low salivary flow
  40. 40. CLASSIFICATION OF DENTAL CARIES 1.CLINICAL CLASSIFICATION • According to the stage of lesion progression: 1. Non cavitated lesion 2. Cavity • According to the severity of the disease: 1. Acute caries (active) 2. Chronic caries (slowly progression) 3. Stabilized caries (arrested) • According to clinical manifestation: 1. White spot lesion macula caroisa 2. Superficial caries caries superficialis 3. Medium caries caries media 4. Deep caries caries profunda 5. Secondary caries caries secundaria
  41. 41. CLASSIFICATION OF DENTAL CARIES (contd.) 2. ANATOMICAL According to anatomical depth of the defect: 1. Enamel caries 2. Dentin caries 3. Cementum caries According to location of the lesion: 1. Coronal caries 2. Occlusal surfaces 3. Smooth surfaces 4. Approximal surfaces 5. Root caries According to intensively of caries within the dentition: 1. Single lesion 2. Multiple lesions 3. Systemic destruction
  42. 42. CLASSIFICATION OF DENTAL CARIES (contd.) According to the stage of lesion progression 1.Non cavitated lesion Initial form of caries development in which there is whitish discoloration of the surface of the tooth occur and there is no cavity developed. 1.CLINICAL MANIFESTATION A white spot lesion at the entrance to the fissure on a molar.
  43. 43. CLASSIFICATION OF DENTAL CARIES (contd.) 2. Cavitated lesion The progression of white spotty lesion leads to the formation of the cavitated lesion which may be minimally or maximally extended from the tooth surface to inward direction (towards pulp).
  44. 44. CLASSIFICATION OF DENTAL CARIES (contd.) According to the severity of the disease: 1. Acute caries (active) • It is a form of dental caries which runs a rapid clinical course. • It is usually occurs in children and younger individual having larger dentinal tubules without sclerosis which facilitate faster spread of caries. • The opening of the lesion is usually naarrow which prevents entry of salivary buffer to neutralize acid formed by fermentation. • Pain is usually present in acute caries with pulp involvement.
  45. 45. CLASSIFICATION OF DENTAL CARIES (contd.) RAMPANT CARIES • It is acute fulminating type of caries that involves multiple teeth in multiple surfaces. • This caries involves those teeth surfaces that are considered immune to caries • A caries increment of ten or more new carious lesions over a period of about one year is characteristic of rampant caries. • This occurs in about 4-8 years for deciduous teeth but in 11-19 years for permanent teeth. Rampant caries in adult Rampant caries in 10 year adult boy
  46. 46. NURSING BOTTLE CARIES (Baby bottle syndrome) • It is a form of rampant caries affecting the deciduous dentition, most commonly the four anterior. • It occurs due to prolonged use of nursing bottle containing milk or sweetened juice, breastfeeding or sweetened pacifiers as an aid for sleeping after one year of age. • Caries rapidly develops, so after some time only root stumps remain in mouth at the place of carious teeth. • Mandibular anterior teeth are protected by tongue and continuously cleansed with saliva, so usually not affected. CLASSIFICATION OF DENTAL CARIES (contd.)
  47. 47. 2.Chronic caries (slowly progression) • It is a slow progressing dental caries usually affecting adult patients. • The opening of the cavity is wide, causing less retention of plaque and more entry of salivary buffer. • As the process is slow, there is sclerosis of dentine and formation of reparative dentine to protect the pulp. • The carious dentine is stained deep brown. • Pulp involvement is a late feature and pain is usually not evident in chronic dental caries. CLASSIFICATION OF DENTAL CARIES (contd.)
  48. 48. CLASSIFICATION OF DENTAL CARIES (contd.) 3. Stabilized caries (arrested) • Carious lesion, whose progression is ceased due to cleansing action of toothbrush, mastication and saliva, because of the wide opening of the lesion. • Affected dentine is burnished and becomes brown, hard and polished (termed as eburtion of dentine) An arrested carious lesion in the lower first premolar. The lesion was well into dentine, but the tissue was hard and shiny.
  49. 49. CLASSIFICATION OF DENTAL CARIES (contd.) According to clinical manifestation: 1. White spot lesion macula caroisa • The earliest visible sign of enamel caries is the ‘white spot lesion’. • The active lesion is matt and feels rough if a sharp probe is gently drawn across it.
  50. 50. 2. Superficial caries (Caries of superficialis) • At a superficial caries the area of destruction of enamel is determined without violation of enamel – dentine connection and without changes in a dentine. • There is destruction of enamel – dentine connection at progress of process, and there is the next stage of carious process. CLASSIFICATION OF DENTAL CARIES (contd.)
  51. 51. 3. Middle caries (Caries of media) A middle caries is characterized three areas which appear at research of cut of tooth in a light microscope: 1st – to disintegration and demineralization; 2nd – transparent and to the intact dentine; 3d – reparative dentine and changes in pulp of tooth. CLASSIFICATION OF DENTAL CARIES (contd.)
  52. 52. 4.Deep caries (Caries of profunda) • At research of cut of tooth with a deep carious cavity in a light microscope appear, as well as at a middle caries, three areas: • 1st – to disintegration and demineralization; • 2nd – transparent and to the intact dentine; • 3d – reparative dentine and changes in pulp of tooth. • It should be noted that at a deep caries more expressed changes appear in pulp of tooth, than at the middle depth of cavity both in hard fabrics of tooth and in pulp of tooth. • In a vascular-nervous bunch changes have likeness with sharp inflammation, up to complete disintegration of axial cylinders of nervous fibres. CLASSIFICATION OF DENTAL CARIES (contd.)
  53. 53. 5. Secondary caries caries secundaria • Secondary caries occurs at the junction of a restoration and the tooth and may progress under the restoration. • It is often termed recurrent caries. • This condition usually indicates that micro leakage is present, along with other conducive to caries CLASSIFICATION OF DENTAL CARIES (contd.)
  54. 54. 2. ANATOMICAL According to anatomical depth of the defect: 1. Enamel caries • Four zones can be identified. • The lesion has a conical shape with apex facing the dentine. 1. Translucent zone 2. Dark zone 3. Body of the lesion 4. Surface zone CLASSIFICATION OF DENTAL CARIES (contd.) 1. Translucent zone 2. Dark zone 3. Body of the lesion 4. Surface zone
  55. 55. Enamel caries (contd.) Surface (a) appears to be intact. Body of lesion (b) shows enhancement of striae of Retzius. Dark zone (c) surrounds body of lesion while translucent zone (d) is evident over entire advancing front of lesion.
  56. 56. a. Translucent Zone • The deepest zone is the translucent zone and represents the advancing front of the enamel lesion. • The name refers to its structure less appearance when perfused with quinoline solution and examined with polarized light. • In this zone, the pores or voids form along the enamel prism (rod) boundaries, presumably because of the ease of hydrogen ion penetration during the carious process. • When these boundary area voids are filled with quinoline solution, which has the same refractive index as enamel, the features of the area disappear. • The pore volume of the translucent zone of enamel caries is 1%, 10 times greater than normal enamel. Enamel caries (contd.)
  57. 57. b. Dark Zone • The next deepest zone is known as the dark zone because it does not transmit polarized light. • This light blockage is caused by the presence of many tiny pores too small to absorb quinoline. • These smaller air- or vapor-filled pores make the region opaque. • The total pore volume is 2% to 4%. • There is some speculation that the dark zone is not really a stage in the sequence of the breakdown of enamel; rather, the dark zone may be formed by deposition of ions into an area previously only containing large pores. Enamel caries (contd.)
  58. 58. Dark Zone(contd.) • It must be remembered that caries is an episodic disease with alternating phases of demineralization and remineralization. • There is also a loss of crystalline structure in the dark zone, suggestive of the process of demineralization and remineralization. • The size of the dark zone is probably an indication of the amount of remineralization that has recently occurred. Enamel caries (contd.)
  59. 59. Enamel caries (contd.) c.Body of the Lesion • The body of the lesion is the largest portion of the incipient lesion while in a demineralizing phase. • It has the largest pore volume, varying from 5% at the periphery to 25% at the center. • The striae of Retzius are well marked in the body of the lesion, indicating preferential mineral dissolution along these areas of relatively higher porosity.
  60. 60. Body of lesion (contd.) • The first penetration of caries enters the enamel surface via the striae of Retzius. The interprismatic areas and these cross-striations provide access to the rod (prism) cores, which are then preferentially attacked. • Bacteria may be present in this zone if the pore size is large enough to permit their entry. • Studies using transmission electron microscopy (TEM) and scanning electron microscopy (SEM) demonstrate the presence of bacteria invading between the enamel rods (prisms) in the body zone. Enamel caries (contd.)
  61. 61. d.Surface Zone • The surface zone is relatively unaffected by the caries attack. • It has a lower pore volume than the body of the lesion (less than 5%) and a radiopacity comparable to unaffected adjacent enamel. • The surface of normal enamel is hypermineralize by contact with saliva and has a greater concentration of fluoride ion than the immediately subjacent enamel. • It has been hypothesized that hypermineralization and increased fluoride content of the superficial enamel are responsible for the relative immunity of the enamel surface. • However, removal of the hypermineralized surface by polishing fails to prevent the reformation of a typical, well-mineralized surface over the carious lesion. Enamel caries (contd.)
  62. 62. Surface Zone (contd.) • Thus, the intact surface over incipient caries is a phenomenon of the caries demineralization process rather than any special characteristics of the superficial enamel. • Nevertheless, the importance of the intact surface cannot be overemphasized, because it serves as a barrier to bacterial invasion. • As the enamel lesion progresses, conical-shaped defects in the surface zone can be seen by SEM. • These are probably the first sites where bacteria can gain entry into a carious lesion. • Arresting the caries process at this stage results in a hard surface that may at times be rough, though cleanable Enamel caries (contd.)
  63. 63. According to anatomical depth of the defect 2. Dentin caries  In cross section dentin caries is V shaped with base at dentino- enamel junction and apex toward pulp.  Five different zones have been described in carious dentin. The zones are most clearly distinguished in slowly advancing lesions.  In rapidly progressing caries, the difference between the zones becomes less distinct. Different zones in dentinal caries are: 1. Normal dentin 2. Subtransparent dentin 3. Transparent dentin 4. Turbid dentin 5. Infected dentin
  64. 64. Dentin caries (contd.) Zones of Dentinal Caries. 5 4 3 2 1 Observing from the pulpal side at the advancing edge of carious lesion following different zones can be seen. ZONE 1 Zone of fatty degeneration of Tomes’ fibers ZONE 2 Zone of dentinal sclerosis/Subtransparent dentin ZONE 3 Zone of decalcification/Transparent dentin ZONE 4 Zone of bacterial invasion/Turbid dentin ZONE 5 Zone of decomposed dentin/Infected dentine
  65. 65. Dentin caries (contd.) Zones of Dentinal Caries. Caries advancement in dentin proceeds through three changes: a. weak organic acids demineralize the dentin; b. the organic material of the dentin, particularly collagen, degenerates and dissolves; and c. the loss of structural integrity is followed by invasion of bacteria.
  66. 66. Zone 1: Normal Dentin. •The deepest area is normal dentin, which has tubules with odontoblastic processes that are smooth, and no crystals are in the lumens. •The inter tubular dentin is normal. •No bacteria are in the tubules. •Stimulation of the dentin (e.g.by osmotic gradient [from applied sucrose or salt], a bur, a dragging instrument, or desiccation from heat or air)- produces a sharp pain. Dentin caries (contd.)
  67. 67. Zone 2: Subtransparent Dentin/ Zone of sclerosis • Zone of demineralization of the intertubular dentin and initial formation of very fine crystals of calcium salt in the tubule lumen. • Damage to the odontoblastic process is evident however no bacteria are found in the zone. • Stimulation of the dentin produces pain, and the dentin is capable of remineralization. Dentin caries (contd.)
  68. 68. Zone 3: Transparent Dentin/ Zone of Decalcification without Bacterial Invasion • Zone of carious dentin that is softer than normal dentin and shows further loss of mineral from the inter-tubular dentin and many large crystals in the lumen of the dentinal tubules. • Stimulation of this region produces pain. • No bacteria are present. • The collagen cross-linking remains intact in this zone. • The intact collagen can serve as a template for remineralization of the intertubular dentin. • This region remains capable of self-repair if the pulp is vital. Dentin caries (contd.)
  69. 69. Zone 4: Turbid Dentin/ Zone of Decalcification with Bacterial Invasion Zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules, which are filled with bacteria. There is very little mineral present and the collagen in this zone is irreversibly denatured. The dentin in this zone will not self-repair. This zone cannot be remineralized and must be removed before restoration. Dentin caries (contd.)
  70. 70. Dentin caries (contd.) Decalcified section of carious dentine showing dentinal tubules penetrated by deeply staining bacteria. In places the tubules appear to have been pushed apart by aggregations of bacteria called liquefaction foci.
  71. 71. Dentin caries (contd.) Decalcified section of carious dentine showing tubules penetrated by bacteria. The tissue appears to have split at right angles to the tubules along the incremental lines of growth. These splits are called transverse clefts.
  72. 72. Zone 5: Infected Dentin. • The outermost zone • Infected dentin consists of decomposed dentin. • There is no recognizable structure to the dentin and collagen and mineral seem to be absent. • Great numbers of bacteria are dispersed in this granular material. • Removal of infected dentin is essential to sound, successful restorative procedures as well as prevention of spreading the infection. Dentin caries (contd.)
  73. 73. INFECTED AND AFFECTED DENTINE Dentin caries (contd.) INFECTED DENTINE AFFECTED DENTINE Infected dentin has bacteria present Affected dentin has no bacteria Collagen is irreversibly denatured. Collagen is reversibly denatured Not remineralizable and must be removed Remineralizable, and should be preserved Zones 4 (turbid zone) and 5 (infected dentine) Zones 2 (subtransparent dentin) and 3 (transparent dentin) In chronic (slow) caries, infected dentin usually is discolored & because the bacterial front is close to the discoloration front, it is advisable in caries removal to remove all discolored dentin unless judged to be within 0.5 mm of the pulp. In acute (rapid) caries the discoloration is very slight & the bacterial front is well behind the discoloration front, some discolored dentin may be left, although any "clinically remarkable“ discoloration should be removed.
  74. 74. GV Black Classified Carious Lesions into 6 types based on their location: • Class I • Class II • Class III • Class IV • Class V • Class VI Classification of Dental Caries (contd.)
  75. 75. Class I Caries All pit-and-fissure caries are Class I, and they are assigned to three groups, as follows. Caries on the occlusal surface of premolars and molars Caries on Occlusal Two Thirds of the Facial and Lingual Surfaces of Molars. Caries on the lingual surface of maxillary incisors GV Black Classification of Dental Caries (contd.)
  76. 76. Class II Caries Caries on the proximal surfaces of posterior teeth are Class II. GV Black Classification of Dental Caries (contd.)
  77. 77. Class III Caries Caries on the proximal surfaces of anterior teeth that do not involve the incisal angle are Class III GV Black Classification of Dental Caries (contd.)
  78. 78. Class IV Caries Caries on the proximal surfaces of anterior teeth that do involve the incisal edge are Class IV. GV Black Classification of Dental Caries (contd.)
  79. 79. Class V Caries Caries on the gingival third of the facial or lingual surfaces of all teeth (except pit and fissure lesions) are Class V. GV Black Classification of Dental Caries (contd.)
  80. 80. Class VI Caries Restorations on the incisal edge of anterior teeth or the occlusal cusp heights of posterior teeth are Class VI. GV Black Classification of Dental Caries (contd.)
  81. 81. WHO classification The shape and the depth of the carious lesion can be scored on a 4 point scale: D1-Clinically detectable enamel lesions with intact (non-cavitated) surfaces. D2-Clinically detectable cavities limited to enamel. D3-Clinically detectable lesions in dentin (with and without cavitation of dentin). D4–Lesions into the pulp. Classification of Dental Caries (contd.)
  82. 82. Professor Nigel Pitts. The ‘iceberg of dental caries’. Diagnostic thresholds used in epidemiology and practice. In epidemiological surveys the iceberg ‘floats’ at the D3 threshold (cavity in dentine). Most lesions arrestable by preventive care are hidden below the water. If patients who only present with D1 and D2 lesions are described as ‘caries-free’ by epidemiologists.
  83. 83. Caries Diagnosis Diagnosis: The use of scientific or clinical methods to establish the cause and nature of person’s illness or injury and the subsequent functional impairment caused by the pathology.- Tabers Cyclopedic dictionary Objective: 1. To identify patients with lesions that require surgical (restorative) treatment. 2. To identify patients with lesions that require non- surgical (preventive) treatment. 3. To identify patients who are at high risk for developing carious lesions.
  84. 84. Diagnosis is important for three reasons: • It forms the basis for a treatment decision. Active lesions require some form of active management whereas arrested lesions do not. • Informing the patient. The patient is central to the management of the carious process. It is the patient who will control the process, not the professional. The dentist’s role is to inform the patient whether any action is required. • Advising health service planners. Epidemiological surveys inform the politicians who commission them of the state of health and disease of the population. These surveys should assist them to direct money appropriately. Caries Diagnosis WHY IS DIAGNOSIS IMPORTANT?
  85. 85. Diagnostic Methods 1. Identification of subsurface demineralization (inspection, radiography, dye uptake methods). 2. Bacterial testing. 3. Assessing environmental conditions (pH, salivary flow, salivary buffering). Caries Diagnosis (contd.)
  86. 86. A patient is at high risk for the development of new cavitated lesions if: 1. High mutans streptococci (MS) counts are found. Bacteriologic testing MS should be done if:  The patient has one or more medical health history risk factors.  The patient has undergone antimicrobial therapy  The patient presents with new incipient lesion  The patient is undergoing orthodontic care  The patient’s treatment plan calls for extensive restorative dental work 2. Any two of the following factors are present: – Two or more active carious lesions – Large number of restorations – Poor dietary habits – Low salivary flow CLINICAL RISK ASSIGNMENT FOR CARIES
  87. 87. Assessment Tools: 1- Patient History. 2- Clinical Examination. 3- Nutritional Analysis. 4- Salivary Analysis. 5- Radiographic Assessment. Caries Diagnosis (contd.)
  88. 88. Assessment Tools 1- Patient History – Caries Risk Indicators Caries Diagnosis (contd.) Factors High Risk Characteristics Age less than 18, older than 65 Socioeconomic lower Status Medications Reduced Salivation Fluoride History Lack of Fluoride during tooth development Dietary Habits high intake of carbohydrate, tobacco and alcohol Genetic Predisposition Family of history of disease General Health Debilitation and decreased ability to self- care
  89. 89. Assessment Tools 1- Patient History – Caries Risk Indicators Caries Diagnosis (contd.) A past history of caries experience is the best predictor of future caries activity
  90. 90. Assessment Tools 2- Clinical Examination:  Salivary function.  Plaque accumulation.  Inflammation of soft tissues.  Poor oral hygiene.  Cavitated lesions .  Existing restorations. Caries Diagnosis (contd.) Risk of Caries Development
  91. 91. Assessment Tools 3- Nutritional Analysis Frequent exposure to sucrose increases the likelihood of plaque development by the more cariogenic MS organisms. Caries Diagnosis (contd.)
  92. 92. Assessment Tools 4- Salivary Analysis: Secretion Rate: Caries Diagnosis (contd.) High level of salivary flow: cariostatic effect Xerostomia or dry mouth: favorable environment for caries development
  93. 93. Assessment Tools 4- Salivary Analysis  Secretion Rate.  Buffering Capacity.  Number of MS and Lactobacilli: Caries Diagnosis (contd.) High S.mutans count high risk Low S.mutans count low risk
  94. 94. Assessment Tools 4- Salivary Analysis Patient Check-Up kit from GC Caries Diagnosis (contd.)
  95. 95. Assessment Tools 5- Radiographic Assessment • Although radiographs may show caries that is not visible clinically. • The minimal depth of a detectable lesion on a radiograph is about 500 lam. • Although radiographs tend to underestimate the histologic extent of a carious lesion, approximately 60% of teeth with radiographic proximal lesions in the outer half of dentin are likely to be noncavitated. • Thus, many lesions evident radiographically are not cavitated and should be remineralized rather than restored. Caries Diagnosis (contd.)
  96. 96. Caries Diagnosis (contd.) Medical History Factors Associated With Increased Caries Risk
  97. 97. Caries Diagnosis for Pits and Fissures 1-U.S. Public Health Service criteria USPHS : 1. Softening at the base of the P&F. 2. Opacity surrounding the P&F. 3. Softening of enamel that may be flaked away. 2- Technical Tools. Caries Diagnosis (contd.)
  98. 98. Caries Diagnosis for Pits and Fissures  Cavitation at the base of a pit or fissure sometimes can be detected tactilely as softness or by binding of the explorer tip.  However, mechanical binding of an explorer in the pits or fissures may be due to noncarious causes, such as the shape of the fissure, sharpness of the explorer, or force of application.  Thus, explorer tip binding is not by itself a sufficient indication to make a caries diagnosis. Caries Diagnosis (contd.)
  99. 99. Caries Diagnosis for Pits and Fissures Caries Diagnosis (contd.)
  100. 100. Caries Diagnosis for Pits and Fissures Caries Diagnosis (contd.) The use of sharp dental explorer noncavitated incipient lesions could become cavitated Cavitated means that extensive enamel demineralization has lead to destruction of the walls of the pit or fissure and bacterial invasion has occurred. Demineralization of the underlying dentin is usually extensive by the time the cavitation has occurred.
  101. 101. Caries Diagnosis for Pits and Fissures Pits & Fissure Caries Treatment Decision Making Noncavitated (caries-free): • No radiolucency below occlusal enamel • Deep grooves may be present • Superficial staining may be present in grooves • Mechanical binding of explorer may occur Cavitated (diseased): • Chalkiness of enamel on walls and base of pit or fissure • Softening at the base of a pit or fissure • Brown-gray discoloration under enamel adjacent to pit or fissure • Radiolucency below occlusal enamel Caries Diagnosis (contd.)
  102. 102. Caries Diagnosis (contd.) The following feature indicate that the caries may be arrested:  White or brown spot lesions with shiny surface If a cavitated lesion exists in a pit or fissure, it must be restored. If the pit or fissure is not cavitated but at risk, then it should be sealed. The pits and fissures of molar teeth in children should be sealed routinely as soon as possible after eruption. Pits and fissures in adults should be sealed if the adult is found to have multiple active lesions or found to be at high risk. Caries Diagnosis for Pits and Fissures
  103. 103. Caries Diagnosis for Smooth Surfaces • Bitewing radiographs are the most typical method for evaluation of the proximal smooth surfaces for evidence of demineralization because these areas usually are not readily assessed visually or tactilely. • An early lesion is detectable radiographically as a localized decrease in the density of the enamel immediately below the proximal contact, resulting in a radiolucent area on the radiograph. • Proximal radiolucencies detectable on bite-wing radiographs should be examined clinically because many are not associated with cavitation of the surface and are not conclusive evidence for restorative treatment. Caries Diagnosis (contd.)
  104. 104. Caries Diagnosis for Smooth Surfaces Proximal Caries Treatment Decision Making Non cavitated: • Surface intact; use of an explorer to judge surface must be done with caution because excessive force can cause penetration of intact surface over demineralized enamel • Opacity of proximal enamel may be present • Radiolucency may be present • Marginal ridge is not discolored • Opaque area may be seen in enamel by translumination Cavitated: • Surface broken, detectable visually or tactilely; temporary mechanical separation of the teeth may aid diagnosis • Marginal ridge may be discolored • Opaque area in dentin on translumination • Radiolucency is present Caries Diagnosis (contd.)
  105. 105. Caries Diagnosis for Smooth Surfaces The following indicate that the lesion is arrested: Caries Diagnosis (contd.) Cavitated lesion, often dark brown, with hard dentin at their bases, the lesions are not plaque covered and are often remote from gingival margin. Shiny white or brown lesion, often well exposed due to recession, the lesion are not plaque covered.
  106. 106. Tactile examination (careful!) • A sharp, curved probe (Briault) can be used gently to try to determine whether an approximal lesion is cavitated, but if this instrument or a scaler is used in a heavy-handed manner, it can actually cause cavitation. Caries Diagnosis (contd.) Caries Diagnosis for Smooth Surfaces- Approximal surfaces
  107. 107. Caries Diagnosis for Smooth Surfaces Bitewing radiographs • The bitewing radiograph is of paramount importance in the diagnosis of the approximal carious lesion, although it should be remembered that the technique is relatively insensitive as it is not able to detect early subsurface demineralization. • In this technique the central beam of X-rays is positioned to pass at right angles to the long axis of the tooth, and tangentially through the contact area. • The film is positioned in a film holder on the lingual side of the posterior teeth. • The patient then closes the teeth together on the film holder. • A beam-aiming device on the holder guides the position of the tube. • This directs the beam at right angles to the film and the contact areas of the teeth. Caries Diagnosis (contd.)
  108. 108. Caries Diagnosis for Smooth Surfaces Caries Diagnosis (contd.) A bitewing radiograph is being taken. The film is held lingually by a film holder and the patient closes together on a part of this holder. A beam-aiming device helps the operator position the tube so that the beam is directed at right angles to the film.
  109. 109. Caries Diagnosis for Smooth Surfaces Caries Diagnosis (contd.) Diagrammatic representations of caries on bitewing radiographs. Appearances graded 0–2 are unlikely to be cavitated, while grade 4 will almost certainly be cavitated. The problem comes with grade 3 which may or may not be cavitated
  110. 110. Caries Diagnosis for Smooth Surfaces Transmitted light • Transmitted light can also be of considerable assistance in the diagnosis of approximal caries. • This technique consists of shining light through the contact point. • A carious lesion has a lowered index of light transmission and therefore appears as a dark shadow that follows the outline of the decay through the dentine. Caries Diagnosis (contd.) A mirror view of the palatal aspect of the upper anterior teeth. Lesions are visible mesially and distally on the upper right central incisor.
  111. 111. Caries Diagnosis for Smooth Surfaces FIBEROPTIC TRANSILLUMINATION: • Carious lesion have lowered index of light transmission, when teeth are examined with the fiberoptic light source, caries appears as a dark shadow • After drying the tooth, a fiberoptic probe can be placed in the buccal or lingual embrassures directly beneath the contact area between two adjacent teeth. • If caries is present , dark shadow is seen beneath the marginal ridge Advantage  Non invasive  No radiation hazard  No permanent record Fiberoptic Transillumination is used in the area where there is Difficulty in placing probe Caries Diagnosis (contd.)
  112. 112. Caries Diagnosis (contd.) FIBEROPTIC TRANSILLUMINATION Caries Diagnosis for Smooth Surfaces Proximal Caries Use of a fibreoptic light in the diagnosis of approximal caries
  113. 113. Caries Diagnosis (contd.) Digital Imaging Fiber-Optic Transillumination (DIFOTI) The DIFOTI (Electro-Optical Sciences Inc.) uses white light, a CCD camera, and computer-controlled image acquisition and analysis to detect caries
  114. 114. Caries Diagnosis for Smooth Surfaces Tooth separation • One further technique to assist with the diagnosis of approximal caries is the use of tooth separation. • A small round elastic is forced between the contact points using a special pair of applicating forceps. • After a few days the teeth are separated. The dentist can now feel, very gently, with a probe to detect whether a cavity is present. • Alternatively, a little elastomer impression material can be injected between the teeth. • After a few minutes the set material can be removed with a probe and the impression examined to see whether there is a cavity. Caries Diagnosis (contd.)
  115. 115. Caries Diagnosis for Smooth Surfaces Tooth separation Caries Diagnosis (contd.) (a) Orthodontic separator is placed between the canine and first premolar. (b) Separation achieved 48 hours later. Note it is not possible to see the distal surface of the canine clearly. (c) Taking an elastomer impression of the contact area. (d) Elastomer impression of the contact area showing no cavitation on the distal aspect of the canine; a restoration is not needed.
  116. 116. Caries Diagnosis for Root Surfaces Active lesions are close to gingival margin and plaque covered. Soft and leathery in consistency. Visual white – yellow – light brown – dark brown. Tactile Soft (easily penetrated) – hard. Rate of progression Slow (due to remineralization &exposure to saliva and fluoride). Rapid (due to rapid progression in dentin). Caries Diagnosis (contd.) Arrested lesions are: Often some distance from gingival margin and not covered with plaque. As hard as surrounding root surface.
  117. 117. Detection with chemical dyes Caries Diagnosis (contd.) •Dyes are a diagnostic aid for detecting caries in questionable areas (i.e., for locating soft dentin that is presumably infected). •Fusayama introduced a technique in 1972 that used a basic fuchsin red stain to aid in differentiating layers of carious dentin. •Because of potential carcinogenicity, basic fuchsin was replaced by another dye, acid red 52, which showed equal effectiveness. •Studies show dye stains are about 85% effective in detecting all caries in a tooth. •Clinical removal of caries without the aid of a dye is 70% effective
  118. 118. Detection with chemical dyes Caries Diagnosis (contd.) A, Prepared tooth before adding caries indicator. B, The tooth is treated with a 1% acid red 52 solution for 10 seconds. C, After rinsing with water for 10 seconds, some tooth structure shows discoloration. The stain indicates decalcified dentin. If the stained tooth structure is soft and appears carious, it should be removed. D, After removal of soft, carious tooth structure, some harder, less stained tooth remains, giving a pink appearance to some areas of this tooth. This healthy, stained tooth structure should not be removed.
  119. 119. Caries Activity Tests: Salivary Bacteria. Plaque Index. Diet. Salivary Analysis. Caries Diagnosis (contd.)
  120. 120. Goal • To reduce the number of cariogenic bacteria. • To limit tooth demineralization. Caries Prevention
  121. 121. Preventive methods include • Limiting pathogen growth and metabolism. • Increasing the resistance of the tooth surface to demineralization Caries Prevention
  122. 122. A. General Health. B. Fluoride Exposure. C. Immunization. D. Salivary Function. E. Antimicrobial Agents. F. Diet. G. Oral Hygiene. H. Xylitol Gums. I. Pit and Fissure Sealants. J. Restorations. Caries Prevention
  123. 123. A. General Health Declining health... Decreased patient’s immunologic system... Increased risk for caries... Need for increased preventive measures. Caries Prevention Patients should be examined for:
  124. 124. B. Fluoride Exposure Fluoride in trace amounts increases the resistance of tooth structure to demineralization 1- Fluoride ions enhances the precipitation of fluoroapatite from Ca and PO4 ions into the tooth structure, which is more acid resistant 2- Allows the remineralization of incipient non cavitated lesions 3- Fluoride has an antimicrobial acitivity Caries Prevention
  125. 125. B. Fluoride Exposure Caries Prevention Route Method of Delivery Conc. Systemic Public Water Supply 1 ppm More than 10ppm...fluorosis Topical (self-application) Low dose / High frequency rinses (0.05% NaF daily) 225 ppm Individual patients at home High dose / Low frequency rinses (0.2% NaF weekly) 900 ppm Supervised rinses in public schools Fluoridated Dentifrices (daily) 1000 ppm Topical (professional application) Acidulated phosphate fluoride gel (annually or semiannually) 12,3000 ppm Most effective and least objectionable Sodium Fluoride sol. (2%) 20,000 ppm Stannous Fluoride sol.(8%) 80,000 ppm Bitter metallic taste, staining Fluoride Varnish Higher uptake, but lower dosage
  126. 126. C. Immunization ? Potential Side Effects Safety Cost Caries Prevention
  127. 127. D. Salivary Functioning Role of Saliva: - Washing away food. - Buffering capacity. - Lubricant. - Remineralization. - Antimicrobial. Caries Prevention
  128. 128. Role of Saliva: - Washing away food. - Buffering capacity. - Lubricant. - Remineralization. - Antimicrobial. Caries Prevention Salivary stimulants •Gums •Paraffin waxes •Saliva subsitutes (Sialgen) D. Salivary Functioning
  129. 129. E. Antimicrobial Agents Caries Prevention Agent Mechanism of Action Persistence in the Mouth Side Effects Chlorohexidine Antiseptic; prevents bacterial adherence long Bitter taste, stains teeth and tongue brown, mucosal irritation
  130. 130. F. Diet Dietary Sucrose Increase MS colonization in plaque Increase caries potential of plaque Prolonged decline in pH Caries Prevention
  131. 131. Dietary Counselling  To identify the sources of sucroses and acidic foodstuffs  To reduce the frequency of their ingestion Caries Prevention F. Diet
  132. 132. G. Oral Hygiene Plaque Free Surfaces: Do Not Decay Caries Prevention Mechanical Plaque Removal Topical Antibiotics Does not engender the risk of infection with opportunistic organisms Long term use predisposes the patient to infection with antibiotic resistant pathogens (Candida Albicans)
  133. 133. G. Oral Hygiene Plaque Free Surfaces: Do Not Decay Caries Prevention Flossing Brushing Rinsing
  134. 134. H. Xylitol Gums  Natural sugar obtained from birch trees  MS cannot ferment xylitol  Xylitol reduces the MS by altering their metabolic pathways Caries Prevention
  135. 135. I. Pit & Fissure Sealants A preventive method for P & F caries 1- Mechanical filling of the P & F with resin 2- MS cannot reach P & F 3- Easier cleaning of P & F during mastication and brushing Caries Prevention
  136. 136. Advantages 1. Prevent caries in newly erupted teeth 2. Arrest incipient caries 3. Prevent bacterial growth in sealed fissures 4. Prevent infection of other sites Caries Prevention
  137. 137. Caries Treatment In the Past Drill and Fill Approach In the Present Early Detection and Remineralization In the Future?
  138. 138. Refrences Sturduvant’s Art And Science Of Operative Dentistry, Fifth Edition Chap. 3; Pg: 102- 130 Essential Of Dental Caries, Third Edition , Oxford University Press Fundamental of Operative Dentistry, Second Edition, Quintessence publishing co. Tooth-Colored Restoratives Principles and Techniques, Ninth edition, BC Decker Inc Clinical Text on Oral Pathology, Ruchir Tripathi

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