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Pathogenesis of dental caries


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Pathogenesis of Dental Caries

Pathogenesis of dental caries

  1. 1. Pathogenesis ofDental Caries Ujwal Gautam 431, BDS 2009 College of Dental Surgery, BPKIHS
  2. 2. SUGAR + TEETH + MICRO-ORGANISMS ORGANIC ACID Caries Caries Tetralogy, Newbrun, 1982
  3. 3. Dental Caries Dental Caries is an irreversiblemicrobial disease of the calcifiedtissues of the teeth, characterizedby de-mineralisation of inorganicportion and destruction of organicsubstance of the tooth, which oftenleads to cavitation.Shafer‘s Textbook of Oral Pathology, 6th edition
  4. 4.  Can remineralisation explain the reversibility? Caries initiation is due to demineralisation of inorganic component and destruction of organic component. Which occurs first? Does cavitation necessarily involve in the carious process?
  5. 5. Role of Carbohydrates• Carbohydrate caries content in diet incidence suggested by; HopeWood House Study, Sullivan and Harris- 1958, Harris-1963 Vipeholm Study, Gustaffson et al, 1954 Patient with Hereditary Fructose Intolerance have less chance of developing caries, Newbrun- 1969
  6. 6. Role of CarbohydratesFermentable Carbohydrates CARIOGENIC BACTERIA acid
  7. 7. Role of CarbohydratesCariogenicity of Carbohydrates determined by:Sticky, solid Carbohydrate more cariogenic than liquidMono or di- saccharides more cariogenic than poly saccharideIncreased frequency of diet has more chance of cariogenicityIn-between diets increase the chance of caries Sucrose is more cariogenic than fructose While Xylitol, sorbitol and Sachharin are found to be non- cariogenic.
  8. 8. Role of CarbohydratesCariogenicity of Starch???• Starch are very slowly diffused into the diet and they also require extra cellular amylase to become hydrolysed before they can be assimilated and metabolised by plaque bacteria.
  9. 9. Role of Carbohydrates• Role of Salivary Carbohydrates??? »NO EFFECT as they are bound to proteins and are not available for microbial degradation
  10. 10. Role of microorganisms Antoni Van Leeuwenhock (1632-1723)indicated the presence of microorganisms in the scrappings obtained from the carious lesion of tooth surface Erdl, in 1843, first associated filamentousmicroorganisms to caries on a causative basis ___ Parasitic Theory
  11. 11. Evidence for role of microorganisms: – Oral organisms can demineralise tooth enamel in vitro and produce lesions similar to the naturally occurring dental caries; Miller, 1889 – Streptococcus mutans is invariably isolated from carious lesions in the teeth of British patients; Clark, 1924 – certain bacteria with acidogenic potential can be isolated and identified from the carious lesions; Florestano, 1942
  12. 12. • S. mutans : development of early carious lesions in enamel• Lactobacilli : associated with dentinal caries• Actinomyces : associated with root surface caries• Vellionella: possibly anti-cariogenic
  13. 13. • Catalase -ve, gram +ve, facultative anaerobic cocci • Grow as convex colonies in mitis salivarius bacitracin agarCariogenicity due to: • Aciduric, can survive at pH as low as 4.2 • Present in large number in saliva • Can adhere to acquired pellicle thus facilitating plaque formation • Can adhere and grow even in hard and smooth tooth surfaces • Homofermentive; lactic acid being the major productRole of S. mutans: a) Lactic acid production b) Formation of adhesive plaques c) Production of fermentable sugars
  14. 14. Sucrose glucose + fructose invertase Glucosyl Fructosyl transferase transferase enzymesproduced by S. mutans glucans fructans Promote reservoir accumulation for of plaque fermentable sugars for oral bacteria
  15. 15. • gram +ve, non spore forming rods • grow best in microaerophilic condition • grows in rogosa agar (low pH suppresses others) acidogenic + aciduric Possibility as Secondary invaders due to their acidophilic naturePredominant site of attack are deep fissures and deep dentinal lesions
  16. 16. Role of acid― caries is caused by acid formed by fermentation of food particles around the teeth‖Robertson, 1835___Chemical (acid) theory
  17. 17. Role of acid ―.. dental caries is caused by acid produced by microorganismsfrom the fermentation of dietary carbohydrates‖ W. D. Miller, 1889 _____ Miller’s Chemicoparasitic TheoryChemical Theory Parasitic Theory  most accepted & backbone of current knowledge and understanding of etiology of Dental caries
  18. 18. Role of acid ACID CAUSE DISSOLUTION OF THE HYDROXYAPATITE CRYSTALS OF THE ENAMEL FOLLOWED BY DENTINE (Demineralisation)• Major degradation product of carbohydrates; Lactic acid Butyric acid Resulting from anaerobic catabolism
  19. 19. Role of acid mere presence of acid is of less significance‗acidic saliva causes tooth decay‘Localisation of acid upon tooth surface holding mechanism = Dental Plaque
  20. 20. Role of Dental Plaque Miller ruled out • Plaque is the soft, non role of Plaque in mineralised, thin Carious process and transparent film regarded it as a predominently consisting of protective layer over the enamel micro organisms suspended in salivary mucins and extracellular bacterial G. V. Black, 1889, associated Dental polysaccharides. Plaque with caries • Initiation of Plaque is with and described it as formation of acquired a separate identity pellicle from salivary glycoproteins which later Bibby described the harbors organisms such as S. nature of plaque, sanguis, A. viscous, A. its role in caries naeslundii, Veillonellae aka and adherence on pioneering organisms tooth surface • S. mutans appears in due course
  21. 21. Plaque Hypotheses TheoriesNon-Specific Plaque Hypothesis purports thecaries disease is an outcome of the overallactivity of the total plaque microflora andnot a specific organism.Specific Plaque Hypothesis proposes that amongthe diverse collection of bacteriaencompassing the plaque microflora, only a fewspecies of bacteria are involved in thedisease. The plaque per se is not pathogenic,but the presence of pathogenic species withinthe plaque causes dental caries.
  22. 22.  Harbors the cariogenic bacteria on tooth surface Acid production on plaque-tooth interface through fermentation of carbohydrates Localisation of acid thus produced Prevents the diffusion of acid Restrict the buffering action of saliva
  23. 23. Buffering capacity of Saliva » Bicarbonate » Urea » Arginine-rich proteins ** Sellman, 1949 found that total amount of acidrequired to reduce the salivary pH is always greater for saliva from caries resistant persons• Initiation of caries occurs at pH 5.2 - 5.5; At 5.5 pH, saliva ceases to be saturated with calcium and phosphate leading to the dissolution of inorganic components of tooth  CRITICAL pH
  24. 24. describes the changes in pH ocurring within dental plaquewhen it is subjected to a carbohydrate diet
  25. 25. Homeostasis at normal pHSaliva is supersaturated with respect to enamel Sali Ca+aPRP va Ca+statherin [Ca] [PO4] [Ca] [PO4] Enamel Ca10(PO4)6OH2
  26. 26. DemineralizationDietary CHO + biofilm = lactic acid; diffusion into enamel = local pH drop Sal [Ca] Ca+aPRP iva Ca+statherin [PO ] 4 [Ca] [PO4] [Ca] [PO4] to exit saliva CHO + CHO CHO [H ] [H+] [H+] Enamel [H+] Enamel [H+] solubility increases Ca10(PO4)6OH2
  27. 27. pH at enamel‗plaque-tooth interface‘  demineralization less than 5.5 process beginsloss of calcium and phosphates from the surface and subsurface enamel, creating a white spot lesion. 1st detectable evidence of Enamel demineralisation frank cavitation if the bacterial plaque is not regularly removed from the tooth surface.
  28. 28. RemineralizationSaliva flow clears CHO; salivary HCO3 returns pH to normal Sal[Ca] iva 3] statherin Ca+aPRP[PO4] [HCO CHOmove into [Ca] [PO4] [Ca] [PO4]enamel [HCO3] [HCO3] CHOEnamel Enamelbecomeslesssoluble Ca10(PO4)6OH2
  29. 29. demineralization process is reversible provided that the acidogenic properties of the biofilm are neutralized. Buffering capacity of salivaIf dietary carbohydrates are removed / pH = 7  REMINERALISATION occurs Once the pH returns to higher than the critical point, demineralization isarrested and minerals can be added back to the partially dissolved enamel crystallites.
  30. 30. Alternating cycles ofDemineralisation & Remineralisation • Net loss – Subsurface demineralization – New caries – Progression of old lesions • Net gain - remineralization of existing lesions
  31. 31. Remineralization, a conservative alternative to conventional caries removal and dental restoration• natural process for repairing subsurface non-cavitated carious lesions caused by organic acids created by bacterial metabolism of fermentable carbohydrates.• Fluoride ions in the presence of calcium and phosphate promote remineralization by building a new surface on existing crystal remnants in subsurface demineralized lesions thus favoring the formation of the more favored fluorapatite crystal in the enamel.
  32. 32. Dental cariesRobert H Selwitz, DDS, Amid I Ismail, DrPH and Nigel B Pitts, BDS The Lancet Volume 369, Issue 9555, Pages 51-59 (January 2007) DOI: 10.1016/S0140-6736(07)60031-2Diagram of thecaries process asregular flux ofdemineralisation(destruction) andremineralisation(repair); Adapted fromKidd and Joyston-Bechal,199749 Copyright © 2007 Elsevier Ltd Terms and Conditions
  33. 33. Caries, a Proteolytic processProteolytic enzymes liberated by cariogenic bacteria destruction of the organic matrix detachment of inorganic crystals from one another collapse of whole structure CAVITATION. Gottlieb (1994) and Gottlieb, Diamond and Applebaum (1946) _______ Proteolytic theory
  34. 34. however,• Proteolytic bacteria are rare in oral cavity• No explanation for role of carbohydrates, acid, etc in dental caries• Carious lesions cannot be reproduced in vitro by the proteolytic mechanisms• Gnotobiotic studies: caries can occur in absence of proteolytic organisms.• Enamel is largely inorganic. So, the caries initiation from proteolytic activity is less likelyTHOUGH ITS ROLE IN CARIES PROGRESSION CANNOT BE RULED OUT
  35. 35. CARIES = acidogenic + proteolytic, a possibility? ______ Manley and Hardwick (1951)Both type of organisms can be present, eachfunctioning independently.Possible mechanisms; microorganisms invade enamel lamellae, attack enamel and involve dentine before clinical evidence of caries. Alteration in enamel prior to invasion by micro organisms through decalcification
  36. 36. Proteolytic Chelation theoryProteolytic breakdown of organic portion of enamel Proteolytic breakdown products + acquired pellicle + food debris = chelating agent CHELATION  -vely charged chelating agent releases +vely charged Calcium ions from enamel/dentine Dissolution of inorganic component of tooth _______ Schatz et al, 1955
  37. 37. Factors that influence Dental Caries (Workshop on Dental Caries mechanisms & Control Techniques, University of Michigan, 1947)Host factors ComponentsA. Tooth 1. Composition 2. Morphologic characteristics 3. PositionB. Saliva 1. Composition a. Inorganic b. Organic 2. pH 3. Quantity 4. Viscosity 5. Antibacterial factorsC. Diet 1. Physical factors a. Quality of Diet 2. Local factors a. Carbohydrate content b. Vitamin content c. Fluorine contentD. Systemic conditions
  38. 38. Histological Changes
  39. 39. Pit and Fissure cariesDue to Poor self-cleansing/ developmental faults of tooth Early lesions appear black/ brown; feel soft and ‗catch‘ Region bordering the lesion appear opaque bluish white Caries follow the direction of enamel rods and thus form cone shaped lesion with base at DEJ Undermining occurs through lateral spread at DEJ May penetrate into dentine through dentinal tubules
  40. 40. Smooth surface cariesEarliest change is the appearance of whitechalky spot which is due to the loss ofinterprismatic substance of enamel Earliest microscopic change involves accentuation of striae of Retzius and Perikymata Appears as well demarcated faint opacity or yellow/brown pigmentation with adsorption of exogenous materials by porous region With progression, forms a cone shaped lesion with base towards the tooth surface Eventual loss of enamel leads to roughening and superficial decalcification
  41. 41. Longitudinal ground sections reveal 4 zones Translucent zone advancing front of enamel lesion appears structureless after imbibition with quinolone in transmitted light pore volume 1% compared to 0.1% of sound enamel no evidence of protein loss Dark zone usually present as a dark brown zone in the transmitted light due to excessive demineralisation shows birefringence with sound enamel after imbibition with quinolone in polarised light, so called positive zone contains 2-4% pore volume Body of Lesion area of greatest demineralisation polarised light shows pore volume of 5% near periphery and 25% in the centre region appears translucent when examined in quinolone under transmitted light shows birefringence with sound enamel after imbibition with water Surface zone partial dimeneralisation of 1- 10% pore volume less than 5% of the spaces negative birefringence of surface region with water imbibition positive birefringence of porous subsurfaceregion
  42. 42. Dentinal Caries• Defense reaction of pulpo-dentinal complex – Sclerotic dentine – Reactionary dentine formation – Sealing of dead tracts• Carious destruction – Demineralisation – Proteolysis
  43. 43. Early dentinal changes: Deposition of fat globules Sclerosis of dentinal tubules Decalcification of wall of dentinal tubules  Pioneer bacteria Microbial invasion: Proteolytic, AcidogenicAdvanced Dentinal Changes: Decalcification and confluence of dentinal tubules Thickening of sheath of Neuman Increase in diameter of Dentinal tubules with lodging of microorganisms Formation of Liquifaction foci Acidogenic and proteolytic activity Formation of transverse clefts Caries progression with apex pulpally and base towards enamel
  44. 44. Zones in advancing lesion ofdentinal caries:i. Zone of fatty degeneration of Tomes‘ fibresii.Zone of dentinal sclerosisiii.Zone of decalcification of Dentineiv.Zone of bacterial invasionv. Zone of decomposed dentine
  45. 45. Root Caries• Initiates on mineralised cementum and dentin surfaces which have greater organic component than enamel tissue• On buccal or lingual surface of tooth• Dental plaque and microbial invasion important aspect• Decalcification of cementum follows destruction of remaining matrix
  46. 46. Arrested caries• No tendency for further progression• Exclusively in occlusal surface• Large open cavity in which the superficially softened and decalcified dentine is burnished to a brown, polished hard surface.
  47. 47. ORAL HEALTH CONSEQUENCES• apical periodontitis• periapical abscess• osteomyelitis of the jaw
  48. 48. Pathogenesis of Dental Caries  Fermentation of dietary sugars by Oral micro- organisms  De-mineralisation  Re-mineralisation  Further demineralisation and Cavitation  Initiation / Formation of Caries
  49. 49. Dental Caries is a multifactorial diseaseHistopathologist  stages of lesion viewed microscopically.Chemist  interrelationship beetween pH, mineral flux and solubility at tooth-saliva interfaceMicrobiologist  interaction involving oral bacteria and dental tissue Current concept of caries etiology impliesinterplay of host, microbial floras, substrate and time as the principle factors
  50. 50. References• Shafer, Hine, Levy; Shafer‘s Textbook of Oral Pathology; 6th Ed.; Elsevier; 2009• Shobha Tandon; Textbook of Pedodontics; 2nd Ed.; Paras Medical Publisher• M. W. Roberts, J. T. Wright; The Dyanamic Process of Demineralisation and Remineralisation; Dimensions of Dental Hygiene. July 2009; 7(7): 16, 18, 20-21• J.D.B. Featherstone; The Continuum of Dental Caries— Evidence for a Dynamic Disease Process; Journal of Dental Research; July 2004 Vol.83 no. suppl 1• M. Hurlbutt, B. Novy, D. Young; Dental Caries: A pH- mediated disease; CDHA Journal – Winter 2010• Alexander V. Zavgorodniy, Ramin Rohanizadeh, Michael V. Swain, Ultrastructure of dentine carious lesions, Archives of Oral Biology, Volume 53, Issue 2, February 2008, Pages 124-132, ISSN 0003-9969, 10.1016/j.archoralbio.2007.08.007. ( 03996907001999)