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Dental caries


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Dental caries: History, Etiology, Histopathogenesis and Clinical types

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Dental caries

  1. 1. Dental CariesHistory, Etiology, Histopathogenesis andClinical types
  2. 2. ―HOT things sharp things, sweet things, cold things, all things rotthe teeth and make them look like old things‖.
  3. 3. CONTENTS Introduction Definition Classification Epidemiology Etiology – earlier concepts Current concepts of caries etiology Clinical characteristics of caries Histopathology of caries References
  4. 4. INTRODUCTION―Rot or decay‖ pre-historic period, prevalence modern times
  5. 5. History
  6. 6.  History :•An image from 1300s (A.D.) England depicting a dentist extracting a tooth withforceps.
  7. 7. • Archaeological evidence shows that dental caries is an ancient disease.• Skulls supposedly dating from a million years ago through the neolithicperiod show signs of caries, excepting those from the Paleolithic andMesolithic ages.• The increase of caries during the neolithic period may beattributed to the increase of plant foods containing carbohydrates.
  8. 8. • Neolithic period : hole in a tooth torelieve an abscess in 5½ minutes.
  9. 9.  A Sumerian text from 5000 BC describes a "tooth worm" as the causeof caries. Evidence of this belief has also been found in India, Egypt, Japan, andChina. Unearthed ancient skulls show evidence of primitive dental work. In Pakistan, teeth dating from around 5500 BC to 7000 BC shownearly perfect holes from primitive dental drills References to caries are found in the writings of Homer and Guy deChauliac.
  10. 10.  The Ebers Papyrus, an Egyptian textfrom 1550 BC, mentions diseases ofteeth. During the Sargonid dynasty ofAssyria during 626 BC to 668,writings from the kings physicianspecify the need to extract a toothdue to spreading inflammation.
  11. 11.  Consumption of cooked foods : smallincrease in caries prevalence. The Greco-Roman civilization, in addition to the Egyptian, had treatmentsfor pain resulting from caries.
  12. 12.  Rate of caries : low through the Bronze and Iron ages, butsharply increased during the Medieval age. Periodic increase : caries prevalence : small 1000 AD
  13. 13.  Treatment consisted mainly of herbal remediesand charms, but sometimes also includedbloodletting. The barber surgeons of the time providedservices that included tooth extractions.
  14. 14. › Learning their training from apprenticeships, thesehealth providers were quite successful in endingtooth pain and likely prevented systemic spread› of infections in many cases.› Among Roman Catholics, prayers to SaintApollonia, the patroness of dentistry, were meant toheal pain derived from tooth infection.
  15. 15. › There is also evidence of caries increase inNorth American Indians after contact withcolonizing Europeans.› Before colonization,› North American Indians subsisted on hunter-gatherer diets, but afterwards there was agreater reliance on maize agriculture, whichmade these groups more susceptible to caries.
  16. 16.  By the Enlightenment,the belief that a "tooth worm" caused caries was nolonger accepted in the medical community. Pierre Fauchard, known as the father of moderndentistry,was one of the first to reject the idea worms causedtooth decay and noted that sugar was detrimental tothe teeth and gingiva.
  17. 17.  In 1850, another sharp increase in the prevalence of cariesoccurred and is believed to be a result of widespread diet changes. Prior to this time,cervical caries was the most frequent type of caries,but increased availability of sugar cane, refined flour,bread, and sweetened tea corresponded with a greaternumber of pit and fissure caries.
  18. 18.  In the 1890s, W.D. Miller conducted aseries of studies that led him to propose anexplanation for dental caries that wasinfluential for current theories.
  19. 19.  He found that bacteria inhabited the mouth and that they produced acidswhich dissolved tooth structures when in the presence of fermentablecarbohydrates.
  20. 20. › This explanation is known as thechemoparasitic caries theory.› Millers contribution, along with the researchon plaque by G.V. Black and J.L. Williams,served as the foundation for the currentexplanation of the etiology of caries.
  21. 21. Definition and ClassificationClassifications
  22. 22. According to Sturdevant:Dental caries is a infectious microbiologic disease of the teeth that results in localizeddissolution and destruction of calcified tissuesAccording to WHO:It is defined as localized post eruptive pathological process of external origin involvingsoftening of the hard tooth tissue and proceeding to the formation of cavity.According to Shafer, Hine,Levy:It is defined it as a ―microbial disease of the calcified tissues of theteeth, characterized by demineralization of the inorganic portion and destruction ofthe organic substance of the tooth.
  23. 23.  G V Black‘s classificationClass I lesions : All pit-and-fissure restorations are Class I,and they are assigned to three groups, as follows.They usually have three locations:the occlusal surfaces of molars and premolarsthe occlusal two thirds of the buccal and lingual surfaces of molars andthe lingual surfaces of anterior teeth.
  24. 24. Class II Lesions: Restorations on the proximal surfaces of posterior teeth areClass II.
  25. 25. Class III lesions : are found on proximal surfaces of anteriorteeth that do not involve or necessitate removal of the incisal angle.
  26. 26. Class IV: Class IV Restorations. Restorations on the proximalsurfaces of anterior teeth that do involve the incisal edgeare Class IV.
  27. 27. Class V Restorations: Restorations on the gingival third of the facial orlingual surfaces of all teeth (except pit-and-fissure lesions) are Class V.
  28. 28. Class VI Restorations: Restorations on the incisal edge ofanterior teeth or the occlusal cusp heights of posterior teethare Class VI.They usually start in a traumatic or a formative defect.
  29. 29. According to Sturdevents:He has classified dental caries mainly according to 3 criterion:– Location.– Extent.– Rate.
  30. 30. According to Location: Primary caries. Caries of Pit & Fissure origin. Caries of enamel smooth surface origin. Backward caries. Forward caries. Residual caries. Root surface caries. Secondary (recurrent) caries.
  31. 31. › According to Extent: Incipient caries (reversible). Cavitated caries (irreversible).› According to Rate (speed) of caries spread: Acute (rampant) caries. Chronic (slow or arrested) caries.
  32. 32. Mount G. J.(1997)classified dental caries based on site and size.A) Site Site 1: includes lesions on pit & fissures of posterior teeth, buccalgrooves of mandibular molars, palatal grooves of maxillary molars& erosion lesions on incisal edges Site 2: includes lesions in contact areas of posterior and anteriors. Site 3: includes lesions originating in gingival third of all teeth
  33. 33. B) Size Size 0: small and early enough to be remineralized lesion with onlyresidual stain Size 1: (mild) includes lesions which have passed just beyondremineralization Size 2: (moderate) includes larger lesions, with adequate tooth structureto support restoration Size 3: (enlarged) includes lesions in which tooth structure & restorationare susceptible to fracture Size 4: (severe) includes lesions which have destroyed a major portionof tooth structure
  34. 34.  Classification according to Mc Ghee Superficial caries- surface of enamel affected Simple caries – penetration into DEJ Deep seated caries – cavity of sufficient depth Caries with almost exposed pulp – large well defined cavity Caries with pulp involvement Caries with perforation laterally or through the floor of the pulp Loss of crown of the tooth from caries Caries of remaining root
  35. 35. WHO ClassificationIn this classification the shape and depth of the caries lesion scored on afour point scaleD1. clinically detectable enamel lesions with intact (non cavitated) surfacesD2. Clinically detectable cavities limited to enamelD3. Clinically detectable cavities in dentinD4. Lesions extending into the pulp
  36. 36. Etiology of Caries
  37. 37. › Etiology : complex problem complicated by many indirect factors thatobscure the direct or indirect causes.› No universally accepted opinion : etiology› Numerous references on dental caries including early theories haveattempted to explain its etiology.
  38. 38. › The oral cavity houses more than 250 microbial species.› Unlike oral epithelium, the epithelium of the tooth does not shed and toothmorphology has many areas inaccessible to physiological clearance mechanisms.› Thus, a tooth becomes an ideal place for the stubborn adherence for many ofthese species.› This colonization occurs as a string of methodical adhesion, succession,andprogression.
  39. 39. Usha C, Sathyanarayanan R. 2009› Host• Enamel crystal structure• Enamel mineral• Saliva quality• Saliva quantity• Immune response• Host behaviour• Host attitudes› Environment• Plaque quantity& quality• Enzymes• Minerals• Bacterial substrate• Socioeconomics
  40. 40. › Organisms that are capable of adhesion adhere to the salivary pellicle onthe tooth and form a convenient arena for the subsequent aggregation ofother organisms that are incapable of initial adhesion.› These are all endogenous / host microorganisms, not external infectiousagents. In fact, this natural colonization of the tooth prevents any invasionby an exogenous organism by way of colonization resistance
  41. 41. › There are three major hypotheses for the etiology of dental caries:› the specific plaque hypothesis› the nonspecific plaque hypothesis› the ecological plaque hypothesis› The specific plaque hypothesis has proposed that only a few specificspecies, such as Streptococcus mutans and Streptococcus sobrinus, areactively involved in the disease.
  42. 42. › On the other hand, the nonspecific plaque hypothesis› maintains that caries : outcome of the overall activity ofthe total plaque microflora, which is comprised of many bacterialspecies.› The ecological plaque hypothesis suggests› caries is a result of a shift in the balance of the residentmicroflora driven by changes in local environmental conditions.
  43. 43. › S. mutans, e.g., species of Veillonella, Lactobacillus, Bifidobacterium,Propionibacterium, low-pH non-S. mutans streptococci, Actinomyces, andAtopobium, also may play an important role in caries production.› Actinomyces spp. And non-S. mutans streptococci may be involvedin the initiation of the disease.
  44. 44. › However, many theories have evolved through years of investigation andobservation;› the acidogenic theory› the proteolytic theory› proteolysis-chelation theory, are among many which have stood the test oftime.
  45. 45. Theories of formation of caries:Early theoiresThe legend of worms: The earliest reference to tooth decay is from ancientsumerian text – LEGEND OF WORMS Given in 5000 b.c Stated that worms are responsible for causation ofcaries
  46. 46. Endogeneous theories: Also called humoral theory Proposed by Greek physicians Stated that caries produced by internal action of acids and corroding humors Imbalance in humorsVital theory› Tooth was thought to be source of problem and caries started from within tooth
  47. 47. Exogenous theories Chemical theory: Parmly in 1820 Stated that dental decay affected externally Unidentified chymal agent is responsible
  48. 48.  Parasitic theory: Theory proposed by Erdl First to relate microorganisms as causative agent is Erdl in 1843 Fincus, in 1847, a German physician attributed dental caries to‗DENTICOLAE‘ Generic name proposed to decay related organisms Theory stated that living micro organisms caused the disintegration in bothenamel and dentin
  49. 49. Septic theory: Proposed by Underwood and Miller :1880 Acid capable of causing decalcification of was actually produced bybacteria , which feeds on organic fibrils of dentinChemico-parasitic theory: Also called acidogenic theory Proposed by Willought D Miller in 1884 Stated that dental decay is a chemico-parasitic process
  50. 50.  Two stages : decalcification of tooth substance dissolution of softened residue This theory is the back bone of current knowledge of understandingetiology of dental caries Theory has been accepted
  51. 51.  Draw backs in theory: Prediliction of certain specific sites on a tooth Why some populations are caries free ? Doesnt explain phenomenon of arrested caries Theory implicates the study of role of carbohydrates, microorganisms, acids and dental plaque
  52. 52. Proteolytic theory: Although the evidence for the so called acidogenic theory is considerable, analternative explanation is the proteolytic theory. Bodecker , in 1878, demonstrated – certain enamel structures are made upof organic material such as enamel lamellae and enamel rod sheaths Serves as a path way for entry of micro organisms Pincus , in 1948, 1949 proposed that nasmyths membrane and other enamelproteins or mucoproteins yielding sulfuric acid upon hydrolysis
  53. 53. Preoteolysis Chelation theory› This theory proposed by Schatz et al (1955)› Simultaneous microbial degradation of the organic components(hence, proteolysis) and the dissolution of the minerals of the tooth by theprocess known as chelation.› A chelate results from combining an inorganic metal ion withat least two electron-rich functional groups in a singleorganic molecule.
  54. 54.  It considers dental caries to be a bacterial destruction of teethwhere the initial attack is essentially on the organic components of enamel. The breakdown products of this organic matter have chelating properties andthereby dissolve the minerals in enamel.
  55. 55.  This results in the formation of substances which may form solublechelates with the mineralized component of the tooth and thereby decalcifythe enamel at a neutral or even alkaline pH. Enamel also contains other organic components besides keratin, such asmucopolysaccharides, lipid and citrate, which may be susceptible tobacterial attack and act as chelators.
  56. 56. Sucrose chelation theory Egglers-Lura (1967) proposed that sucrose itself, and not the acid derivedfrom it, can cause dissolution of enamel by forming an ionized calciumsaccharate. The theory is that calcium saccharates and calcium complexingintermediaries require inorganic phosphate, which is subsequentlyremoved from the enamel by phosphorylating enzymes.
  57. 57. Auto immune theory It suggests that few odontoblasts cells at some specific sites within thepulp of few specific teeth are damaged by the autoimmune mechanisms. For this reason, the defence capacity and integrity of overlying enamel anddentin in those specific areas are compromised and they can be thepotential sites for caries development.
  58. 58. Role of plaque as etiologic factor Soft, translucent and tenaciously adherent materialaccumulating on the surface of teeth is commonly called as plaque 90% contains bacteria and its byproducts Adherence of micro organisms : Few specialized microorganisms primarily streptococci adhere onto thetooth surfaces Bacteria contains receptors Adhere to even other filamentous and spiral bacteria forming colonies
  59. 59. Plaque communities and habitats : Dorsum of tongue : S.salivarius Teeth : S.sanguis and S.mitisHabitat Predominant speciesMucosa S.mitis, sanguis, salivariusTongue S.salivarius, mutans and sanguisTeeth (non carious) S.sanguis
  60. 60. › Acids : initially decalcify the enamel have a pH: 5.5 to 5.2 or less and areformed in the plaque material,› which has been described as an organic nitrogenous mass ofmicroorganisms firmly attached to the tooth structure
  61. 61. Role of carbohydrates : Cariogenic carbohydrates are dietary in origin Cariogenicity varies with : frequency of ingestion, physical form, chemical composition, routes of administration and presence of other food constituents Sticky solid carbohydrates are more cariogenic They in detergent foods are less damaging
  62. 62.  Ones which are rapidly cleared by saliva are less cariogenic Plaque organisms produce little acid from the sugar alcohols sorbitol ormannitol.› The acids involved in the initiation of the caries process are normalmetabolic by-products of the microorganisms and are generated by themetabolism of carbohydrates.
  63. 63.  Carbohydrates fed entirely by stomach tube or intravenously are notcariogenic Meals high in fat, protein and salt reduce retentiveness of carbohydrates Refined pure carbohydrates are more cariogenic Bacteria + sugar + teeth – organic acids = caries
  64. 64. Role of micro organisms :Type of caries MicroorganismsPit and fissure Mutans, sanguis, lactobacillus, actinomycesSmooth surface Mutans , salivariusRoot surface A.viscosus, naesulundi, S.mutans and sanguisType of caries Microorganisms
  65. 65. Streptococcus mutans : First isolated by CLARKE in 1924 Catalase –ve , gram +ve cocci Cariogenic strains contain lysogenic bacteriophage Serotypes a to h Polymerize glucose and fructose moieties of sucrose to glucans andfructans
  66. 66.  Extra cellular polymers Homopolymers of glucans – dextran and mutan are synthesized byS.mutans Mutan- important constituent of plaque, less soluble and resistant to acidattack Fructans are highly soluble , degraded by plaque bacteria
  67. 67. Lactobacilli : Gram +ve non spore forming rods Acidogenic and aciduric Produce lactic acidOral actinomyces : Gram +ve filamentous organisms A.naesulundi and viscosus – facultative anaerobes A. Israeli and odontolyticus – strict anaerobes
  68. 68. Role of acids : Exact mechanism is not known Probably occurs due to enzyme breakdown of sugars Acids formed are chiefly lactic acid and butyric acid Monosaccharides and disaccharides – greatest fall in pH
  69. 69. Current concepts in etiology of caries :Three primary factors: the host,the microbial florathe substrate.a fourth factor — the time — must be considered in any discussion of theetiology of caries.In other words,Caries requires a susceptible host,a cariogenic flora anda suitable substrate that must be presentfor a sufficient length of time.
  70. 70. Host factors and components Tooth compositionmorphologic characteristicsposition Saliva compositionphquantityantibacterial factorsquantity and viscosity Diet physical factors (quality of diet)local factors carbohydrate, vitamin andfluorine content Systemic conditions
  71. 71. › Tooth› Most vulnerable to proximal caries during first 2 years following eruption.› Continuous increase in incidence of proximal caries in adolescent patientconcurrent with a comparative decrease in incidence of occlusal caries.› Saliva is another host factor : critical to process.› It mechanically cleans teeth and clears carbohydrates and acids from plaque.
  72. 72. › Neutralizes plaque acids, thuspH and diffusion gradient for calcium and phosphate.› As these two minerals return to tooth, remineralization occurs incombination with fluoride.› Acquired pellicle is an acellular film that covers tooth surface and allowsoral bacteria to adhere to tooth.
  73. 73. › Dietary factors› Diet is another important component in carious process.› Diet of highly cariogenic carbohydrates is metabolized readily by plaquebacteria to produce acids.› Acids diffuse into enamel as minerals diffuse out from tooth, leading tocavitation.
  74. 74. › It is not only composition of diet that is of concern but also frequency of‗‗sugar‘‘ challenge.› If sufficient time between acid challenges occurs, demineralization can bereversed, with resultant neutralization
  75. 75. › Bacterial process (agent factors)› Acquired pellicle is an acellular film thatcovers tooth surface and allows oral bacteriato adhere to tooth.› Bacteria in dental plaque are diverse, butsome species are implicated morespecifically.
  76. 76. › Two main groups of acidogenic bacteria havebeen identified:S mutans and Lactobacillus.› Actinomyces isrealli has been isolated frompartially erupted teeth with white spot lesions.
  77. 77. Microflora of dental caries› Pit and fissure caries:› S mutans, S sanguis, other streptococci Lactobacillus, actinomyces.› Smooth surface caries: S mutans, S salivarius› Root caries: A viscus, A naeslundi,› other filamentus rods, streptococci species.› Deep lesions: lactobacillus, A viscus, A naeslundii,› other filamentus rods, S mutans, bacillus, Rothia,› propionibacterium, Arachnia, Eubacterium.
  78. 78. Acc to Orland and by Fitzgerald, Jordan, and Achard› Dental caries will not occur in absence of microorganisms.› Animals did not develop caries even when fed a high-carbohydratediet.› Caries did develop in these animals when they were inoculated withmicroorganisms from caries-active animals and then fed cariogenicdiets.
  79. 79. › They can produce acid to decalcify toothAciduricstreptococci, lactobacilli,diphtheroids, yeasts, staphylococci, and certainstrains of sarcinae.S mutans: major and mostvirulent of caries-producingorganisms.• Acids that initiallydecalcify the enamelhave a pH of 5.5 to5.2 or less and areformed in plaque,
  80. 80. › Loesche› Conducted an review of literature regarding etiology of caries.› Stated that aciduricity appears to be most consistent attribute of S. mutansand is associated with cariogenicity.› S. sobrinus may be more important in smooth-surface decay and associatedwith rampant caries.› Concluded thatS.mutans, S sobrinus, and lactobacilli are human odontopathogens.
  81. 81. He also stated that› aciduricity : most consistent attribute of S. mutans and is associated with itscariogenicity.› Also observed that,› Other aciduric species such as S. sobrinus may be more important in› smooth-surface decay and are perhaps associated with› rampant caries.
  82. 82. › Acids caries process are normal metabolic by-products of microorganisms› Which are generated by metabolism of carbohydrates.› Outer surface of enamel is more resistant to demineralization by acid thanis deeper portion of enamel,the greatest amount of demineralization occurs 10 to 15 μm beneath theenamel surface.
  83. 83. Saliva› which is supersaturated with calcium and phosphate and has acid-bufferingcapability,› diffuses into plaque› neutralizes acids and repairs enamel.› Time required for remineralization is determined by : age of plaque, nature of carbohydrate consumed, presence or absence of fluoride.
  84. 84. Acc to Llory et al., 1972. Despite the continuous flow of saliva,Dental plaque can accumulate at a rapid rate of (10-20 mg/day) in theabsence of oral hygiene procedures but the rate of plaque accumulationappears to be even more rapid in patients with xerostomia› Dental plaque developed for 12 hours or less, enamel demineralizationresulting from a single exposure to sucrose will be remineralized by within10 minutes.
  85. 85. › 4 hours are required for enamel repair resulting from a exposure to sucrosein presence of dental plaque that is 48 hours old.
  86. 86. › Fluoride enhances rate of remineralization of enamel by saliva, also forms of a fluorhydroxyapatite, which increases resistance of enamel to acid attack.
  87. 87. › Caries may be considered as a continuous dynamic process.› Involving repeating periods of demineralization by organic acids ofmicrobial origin and subsequent remineralization by salivary components(or therapeutic agents),› but in which overall oral environment is imbalanced towarddemineralization.
  88. 88. Socioeconomic status low socioeconomic status has an impact on carious process. caries rate among individuals living below poverty level is higher. Lack of access to care among poor exacerbates condition because dentalcaries is more likely to remain untreated.
  89. 89.  Barriers to dental care may include :I. limited incomeII. lack of value placed on dental healthIII. lack of knowledge of oral care,IV. and transportation limitations.
  90. 90. Window of infectivity: Caufield 1993› 7-31 months: Teeth erupt› Provide virgin habitat for bacteria.› Second window of infectivity.(Krass 1967, Edrman 1975)› 6-12 yrs: Permanent teeth erupt.› Provide new habitat for bacteria
  91. 91. Caries progression› Time for progression from incipient caries to clinical caries (cavitation) onsmooth surfaces is estimated to be 18 months+/- 6 months .› Peak rates : 3 years after eruption of tooth. (incidence)› Poor oral hygiene and frequent exposures to sucrose can produce incipientlesions in as little as 3 weeks.› Caries development in healthy individuals is usually slow in comparison tocompromised persons
  92. 92. › Radiation induced xerostomia (drymouth) can lead to cariesdevelopment in as little as 3 monthsfrom onset of radiation.
  93. 93. Histopathology of caries
  94. 94. Caries of enamel› In pits and fissures, it spreads in triangular pattern with base towards DEJand apex towards surface.› Microscopically 4 zones are are seena) Translucent zone:b) Dark zonec) Body of lesiond) Surface zone
  95. 95.  The translucent zone is the advancingfront of the caries. i.e the innermost zone longitudinal sections and when the teethare examined in a clearing agent havingrefractive index similar to that of enamelsuch as quinoline or balsam. The preferential removal of inorganicsalts is evident whereas evidence oforganic material removal is not seen inthe translucent zone.
  96. 96. The Dark Zone Zone immediately above the translucent zone Appears dark Exhibits approximately 6% loss of minerals perunit volume of enamel. It shows a +ve birefringence in polarized lightwhile normal enamel has negativebirefringence.
  97. 97. The Body of Lesion Occupies major portion of the lesion Area of max demineralization The body of the lesion is positivelybirefringent. This is the largest zone whichexhibits enhanced striae of Retzius.
  98. 98. The surface layer Itis approximately 20-100 um thick Thinner in active lesion and Thicker in inactive ones. Partial demineralization = 10%mineral loss takes place in this layer. Char‘ feature : broadening of prismsheaths.Surface layer
  99. 99.  The surface layer is approximately 20-100 um thick it is thinner in activelesion and thicker in inactive ones. Partial demineralization equivalent to10% mineral loss takes place in thislayer. The characteristic feature of this layeris the broadening of prism sheaths.
  100. 100. Stages of Progression of Occlusal caries: Natural lesions present itself as underminingthe enamelFinal outcome:Necrosis andperiapicalinflamatoryreactions
  101. 101. Caries of dentin When the carious lesion haspenetrated the enamel, it spreads laterally along the dentinoenamel junction, undermining theenamel. The pattern of invasion is depicted ascone shaped lesion with its base atthe dentino-enamel junction and apextowards the pulp.
  102. 102.  The histopathology of dentinal caries has been studied extensively. Thepathological changes have been divided into various zones :A. Zone of fatty degeneration of tomes fibers
  103. 103. A. Zone of dentinal sclerosis or hypermineralizationcharacterized by deposition of calcium salts in dentinaltubulesB.C. Zone of decalcification of dentin, a narrowzone, preceding bacterial invasionD. Zone of bacterial invasion of decalcified but intact dentinE. Zone of decomposed dentinBacterial invasion of dentinTotal destruction of dentinby caries (necrosis)
  104. 104. Ekstrand et al,19911: Reactive dentin2: Sclerotic dentin3:Zone of demineralization4:Zone of bacterial invasion5: Peripheral rod direction
  105. 105.  According to sturdavent‘s Normal dentin: deepest area is normal dentin, which has tubules with odontoblasticprocesses and no crystals are in the lumen Sub transparent dentin: zone of demineralization of intertubular dentin initial formationof very fine crystals, damage to odontoblast process is evident, no bacteria is found Transparent dentin: zone of carious dentin that is softer than normal dentin, further lossof minerals from intertubular dentin, many large crystals are present in the tubulelumen. Stimulation of this region produces pain. No bacteria present Turbid dentin: zone of bacterial invasion widening and distortion of dentinaltubules, which are filled with bacteria. Very little mineral present and collagen in thiszone is irreversibly denatured
  106. 106.  Infected dentin : outermost zone, consists of decomposed dentin that isteeming with bacteria great number of bacteria present. Collagen and mineral absent
  107. 107.  Caries of Cementum The cemental caries is usually seen where thereis gingival recession and the oral hygiene ispoor. Clinically, The lesions appear as saucer shaped cavities. The micro organisms involved in rootcaries, chiefly actinomyces, appear to invadecementum either along Sharpeys fibers orbetween bundles of fibers comparable toinvasion along dentinal tubules.
  108. 108. › The dentin involvement of cemental caries is similar to that of dentininvolvement in coronal caries.› As was noted in coronal dentin, there may be sclerotic response, eitherpartially or completely, occluding the tubules with mineral crystals.
  109. 109. Pit and Fissure caries The pits and fissures of newly eruptedteeth are colonized by bacteria Bacterial plug Large variations in the microflora found inpits and fissures G+ve cocci, S.sangius are commonlyfound in pits and fissures of newly eruptedteeth S.mutants- carious pits and fissures
  110. 110.  Long narrow orifice prevents visiual and tactile examination Pit and fissure caries expands as it penetrates into the enamel Entry site- smaller Actual vision- bigger- making clinical diagnosis difficult Occlusal enamel rods bend down and terminate on the dentin- affects agreater area of DEJ Cross section- ‗inverted V‘
  111. 111. Smooth surface caries Less favorable site for plague attachment, plaque develops on smooth surfaces near gingiva or under contacts Provide extra shelter Lesions have a broad area of origin and a conical or pointed extension Path of ingress- parallel to the enamel rods Cross section- ‗V shape‘ with a wide area of origin,apex towards DEJ
  112. 112. Root caries Cementum is rougher than enamel and readilyallow deposition of plaque Cementum is relatively thin and provides littleresistance to caries Root caries have less well defined margins U shaped in cross section Progress more rapidly due to lack of enamelcovering Commonly seen in older persons with gingivalrecession
  113. 113. Acute Dental Caries Runs a rapid clinical course Early pulp involvement Commonly seen in children and young adults Large dentinal tubules- show no sclerosis Process is so rapid that there is little time for deposition of reparativedentin
  114. 114.  Initial entrance- small Rapid spread of the process at DEJ Saliva dose not easily penetrate Acid accumulated in the cavity Dentin is stained light yellow Pain is an common feature
  115. 115. Rampant caries Characterized by sudden, rapid, almostuncontrollable destruction of teeth. Affecting surfaces of teeth that are relatively cariesfree, usually proximal cervical surfaces of themandibular incisors. A caries incriment in 10 or more new carious lesionsover a period of about 1 year. Most often observed in primary dentition and in teenage. Diatery factors affecting oral substrate and oral floraand physiological factors affecting saliva aresignificant.
  116. 116. Nursing bottle caries Also called nursing caries, baby bottle syndrome, bottlemouth syndrome Affects deciduous dentition Causes – usage of nursing bottle containing milk or milkformula, fruit juice or sweetened water, breast feeding, sugaror honey sweetened pacifiers Clinically- widespread destruction of decidious teeth Commonly involves four maxillary incisors followed bymolars and then cuspids Severe- only root stumps remain Mandibular incisors usually escape – covered and protectedby the tongue
  117. 117. Adolescent caries Two chronological ages when acute rapidly progressing caries are seen 4 – 8years and 11 – 18 years Acute caries attack in the later stage is termed as adolescent caries Seen in teeth or surfaces that are relatively immune to caries Small opening in enamel, extensive undermining Little time for the formation of reparative dentin Important to detect caries at an early stage for preventing it
  118. 118. Chronic caries Progress slowly Tends to involve pulp much later than acute caries Common in adults Entrance to the caries larger Less food retention Greater access to saliva Allows formation of dentinal sclerosis and deposition of secondary dentin Carious dentin stained deep brown Cavity is a shallower one , minimum softening of dentin Little undermining of enamel, and moderate lateral spread of caries at the dej Pain is not a common feature due to secondary dentin deposition
  119. 119. Recurrent caries› Immediate vicinity of restoration› Inadequate extension of restoration or poor adaptation› Favours retention of debris› Renewed caries follows a same pattern as primarycaries
  120. 120. › Reccurent caries might occur if all the carious dentin is not removed Besicin 1943 studied the fate of bacteria sealled in dentinal tubules and foundthat lactobacilli die out while streotococci persisted.
  121. 121. Arrested caries Caries which are static or stationary , doesnot show tendency for caries progression Both deciduous and permanent dentitionare affected Occurs mostly in caries of occlusalsurfaces Large open cavity, lack of food retention
  122. 122.  Supeficially softenedand decalcified dentinis graduallyburnished- eburnationof dentin Sclerosis andsecondary dentinformation occur Another form of arrested caries- seen onthe proximal surfaces in which adjacentapproximating tooth is extracted
  123. 123.  Brown stained area just below the contact point of thetooth Very early caries which in many cases are arrested afterextraction, thus forming a self cleanseable area
  124. 124.  Muhler studied the effects of topical application of stannous fluorideon caries and gave few acquired characteristics Presence of brown pigmentation Change from a soft to hard texture Change from chalkie whiteness to brown No increase in the size of the lesion No further progression of the lesion as long as the pigmentation remained Also stated that ―smaller the size of the lesion at the time of initialapplication of fluorides , greater are the chances of caries arrest‖
  125. 125. Radiation caries Development of rampant caries in patientsundergoing radiation therapy of head and neck arecalled rampant caries Del regato, observed the effects of xerostomia wasa complication of radiation caries in1939 Besides xerostomia an increase in viscosity and pHof saliva also effects
  126. 126.  Frank in 1961, salivary gland system and saliva secretion is of fundamentalimportance in maintaining a carious free teeth Consequence of irradiation- 3 forms of caries formed Given by Frank and Baden in 1965 and 1970 respectively 1sttype-• char‘caries type lesion, completely encircling the tooth• Amputation of the crown is seen• Sometimes extension to labial buccal and lingual surface
  127. 127.  2ndtype-• Brown to black discolouration of the crown• Occlusal and incisal surface wear away 3rd type-• Begins as a spot depression, spreads from incisal or occlusal surfaces tolabial buccal or lingual surfaces• Enamel shell is destroyed and coronal dentin is disintegrated leaving areduced, irregular, discoloured stump
  128. 128. Forward and backward caries Considered as a graphical representation of pathway ofcaries progression First component to be involved is interprismatic enamel Disintegrating substances passing through these leads toundermining of enamel prisms Resultant carious surface in enamel is cone shape both inpit and fissure caries and smooth surface caries First component to be involved in the dentin is theprotoplasmic extensionwith in the dentinal tubules These extensions are spaced widely near dej butnareclosely spaced near pulp
  129. 129.  Caries cone in dentin have apex towards the pulpal surface and base ofthe cone towards dej Where ever the caries cone is larger in enamel or atleast the size of thedentin is called forward caries SCarious process in dentin progresses in a much faster rate than enamel Caries spread laterally creating undermined enamel In addition decay attack from dentinal surface This is termed as backward caries