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Dental caries
The document discusses dental caries as an irreversible microbial process, covering definitions, classifications, and mechanisms of demineralization and remineralization. It explores the role of diet, bacteria, and the microbiology involved, especially focusing on Streptococcus mutans as a primary causative agent. Furthermore, various theories regarding dental caries development and the physiological zones affected are detailed.
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Dental caries
- 1. VS MIGHTY TOOTH INVISIBLE STRAINS GOODMORNING!Dr. Ram
- 2. DENTAL CARIES - Anirreversible microbial process…. Dr. Ram
- 3. •INTRODUCTION •DEFINITION •REMINERALISATION AND DEMINERALISATION •CLASSIFICATIONOF DENTAL CARIES •ZONES OF ENAMEL CARIES •ZONES OF DENTAL CARIES •MICROBIOLOGY OF THE DENTAL CARIES •THEORIES OF DENTAL CARIES CONTENTS I’M READY… Dr. Ram
- 4. •IMMUNOLOGY OF DENTALCARIES •GENERAL CLINICAL FEATURES •DIAGNOSIS •CARIES ACTIVITY TESTS •MANAGEMENT AND TREATMENT •RECENT UPDATES WHERE I’M I NOW? Dr. Ram
- 5. • COMMON REASONFOR TOOTH LOSS. •Disease of Civilization- Due to habits & Diet. •TRANSMISSIBLE DISEASE. •WINDOW OF INFECTION MATERNAL CARIES LEVEL DIETARY SUCROSE LEVELS INTRODUCTION Dr. Ram
- 6. Simple caries can… ? nextDr. Ram
- 7. DEFINITION OF DENTALCARIESDEFINITION OF DENTAL CARIES MISTAKE?? Dr. Ram
- 8. •REMINERALISATION AND DEMINERALISATIONOF DENTAL CARIES PLAQUE FORMATION ( NATURAL , PHYSIOLOGICAL PROCESS) BACTERIA----------CARBOHYDRATES---------SUCROSE----------PH-BELOW -5 DEMINERALISATION REMINERALISATION Saliva neutralizes the acid, ph increased and minerals may be gained. Dr. Ram
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- 10. The cumulative processof de and remineralisation leads to net loss of minerals. DENTAL CARIES Dr. Ram
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- 17. Pit & FissureCaries Bluish Discoloration Dr. Ram
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- 20. Secondary / RecurrentCaries Dr. Ram
- 21. ETIOLOGY OF DENTALCARIESETIOLOGY OF DENTAL CARIES Dr. Ram
- 22. Factors responsible forcarbohydrates to be cariogenic 1.Physical nature- Sticky, solid carbohydrates, REFINED. 2. Chemical nature- glucose, galactose, sucrose, lactose & starch. 3. Route of intake- tube/IV line don’t contribute to caries 4. Clearance rate- salivation causes less caries & vice versa 5. Frequency of intake- INTAKE, caries incidence is more Dr. Ram
- 23. Other components ofdiet Primitive man – unrefined, fibrous diet which cleaned teeth automatically, caries’ incidence Modern man – soft diet with refined sugars, caries’ incidence Dr. Ram
- 24. Fat & proteinstaken with sugars prevent attachment of carbohydrates to tooth surface Dr. Ram
- 25. PLAQUE AND MICROBIES OF DENTAL CARIES Andtheir types Dr. Ram
- 26. ACQUIRED PELLICLE 1st layer ofglycoprotein deposited on teeth 30 mins after brushing. Doesn’t contain micro-orgs, but gets colonized with bacteria-forming plaque. Derived from saliva. Dr. Ram
- 27. PLAQUE AND TYPES –Is a white, tenacious substance/deposit on tooth surface which contains glycoproteins derived from saliva. – Also contains, micro-orgs, desquamated epithelial cells, Ca, Ph, etc – Causes dental caries & periodontal disease – Formed from structure called “acquired pellicle” Dr. Ram
- 28. •Acidogenic bacteria-dental caries •Proteolyticbacteria-periodontal disease BACTERIA Pioneer / primary bacteria – initiate caries S.mutans (smooth surface caries) Lactobacillus acidophilus (pit & fissure caries) Actinomyces (root surface caries) Invaders / secondary bacteria Staphylococcus, VeillonellaeDr. Ram
- 29. •MICROBIOLOGY OF THEDENTAL CARIES •STREPTOCOCCOUS •ACTINOMYCES •LACTOBACILLI Dr. Ram
- 30. S.m, S.sang Lacto. Actinomyce. Sm, S salivaries A.v Acti. N S.M S.sang LA. SP ACT. SP FILAMENTOUS ROD SHAPED Dr. Ram
- 31. S.MUTANS •Most common, smoothsurface caries producing org Both acidogenic & aciduric. •Attachment to tooth by Glucans dextrans synthesis from dietary sucrose by polymerization. •Synthesized by enzyme present in mutans’ cell wall – Glycosyl transferase.( GT) Dr. Ram
- 32. sucrose stored bymutans, released when required to cause caries. •Mutans thickness of plaque – hampers diffusion of salivary bi-carbonates into plaque, risk of caries. Dr. Ram
- 33. Stephan’s curve Critical pH– 5.5 Resting pH in caries active ppl – 5.8 In caries immune ppl – 6.5 Graph showing behavior of pH in caries active & immune ppl, after a 10% glucose rinse SALIVA IMMUNE ACTIVE CARBOHYDRATE DIET Dr. Ram
- 34. SALIVA Flow rate: FR, caries & vice versa Buffering capacity: BC, caries & vice versa Amount of salivary secretion: , then caries Dr. Ram
- 35. COMPONENTS OF SALIVA •Bicarbonates(salivary buffers), diffuse into plaque, acid •Anti-bacterials like lactoferrin, lysosome, thiocynate, etc, present in saliva. •Ig A in saliva, prevents attachment of bacteria on tooth surface Ions Ca, P help in remineralization. •Salivary urea & bicarbonate rate of glycolysis I.e, glucose metabolism is faster, so, contact time of teeth with carbohydrates is reduced Dr. Ram
- 36. THEORIES OF DENTALCARIES 1) EARLY THEORIES: WORMS 2) ENDOGENOUS THEORY - HUMORAL - VITAL - STAGNATION 3) EXOGENOUS THEORIES -CHEMICAL THEORY -PARASITIC/SEPTIC THEORY -CHEMICO-PARASITIC THEORY ( MILLER’S/ ACIDOGENIC) THEORY -PROTEOLYTIC THEOTY -PROTEOLYTIC CHELATION THEORY -COMBINED ACIDIOGENIC AND PROTEOLYTIC THEORY Dr. Ram
- 37. OTHER THEORIES -SULFATES THEORY -COMPLEXINGAND PHOSPHORYLATING THEORY -SUCROSE CHELATING THEORY -AUTOIMMUNE THEORY -GENETIC THEORY -CELLULOSE THEORY -CARIES SURVILLENCE THEORY Dr. Ram
- 38. • ACIDOGENIC THEORY –Miller 1890, most accepted. – “Acids formed due to the fermentation of dietary carbohydrates by oral bacteria leads to progressive decalcification of tooth structure with subsequent disintegration of organic matrix” – He isolated micro-orgs from his experiments & stated that many were involved in the carious process. TOOTH PLAQUE BACTERIA SUGAR ACIDS TOOTH DECAY Dr. Ram
- 39. – 4 importantfactors which can influence process of tooth destruction in process of dental caries • Dietary carbohydrates, micro-organisms, acid, plaque. Dr. Ram
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- 41. PELLICLE FORMATION COLONIZATION OFS. MUTANS AFTER 0-4 HRS 4-24 HRS MANY MICROBIAL COLONIES ARE FORMED WITH IN IT. PLAQUE FORMATION S.MUTANTS DOMINATION CONVERSION OF CARBOHYDRATES INTO SUGARS ( SUCROSE) RELEASE OF ACID (LACTIC ACID )Dr. Ram
- 42. • LIMITATIONS – Didnot explain sub-surface demineralization – Failed to justify rampant caries – Did not explain caries in impacted tooth Dr. Ram
- 43. Proteolytic theory • “Formation of DC is essentially a proteolytic process. Bacteria present produce hydrolytic substances/enzymes & cause proteolysis leading to dissolution of organic substances” • His view micro-orgs don’t cause decalcification but dissolution of organic substances present in the tooth. Micro orgs entered enamel through enamel lamellae & caused dissolution. Dr. Ram
- 44. • Limitations – Thecarious lesion couldn’t be reproduced in vitro by the proteolytic mechanism. – Proteolytic bacteria are very uncommon in the oral cavity. – This theory cant explain the role of sucrose, pH and fluoride in DC Dr. Ram
- 45. Proteolytic Chelation theory •Chelate formation- citrate, lactate • During DC, proteolytic breakdown of organic portion of enamel matrix takes place first. • Following this, chelating agent is formed by combination of proteolytic breakdown products, acquired pellicle, food debris, etc. – Ex of chelating agent: citrate, lactate, etc Dr. Ram
- 46. •Even this theoryfailed to explain about sugar or acid production Dr. Ram
- 47. Autoimmune theory • Fewodontoblast cells at specific sites within pulp of specific teeth are damaged by autoimmune mechanism • Due to this the defense capacity & integrity of of enamel and dentin in those specific areas are compromised and act as potential sites for caries development in future Dr. Ram
- 48. DENTAL CARIES •ZONES OFENAMEL CARIES •ZONES OF DENTAL CARIES Dr. Ram
- 49. •ZONES OF ENAMELCARIES E N A M E L -ZONE- 1 -ZONE-2 -ZONE-4 -ZONE-5 TRANSLUCENT ZONE DARK ZONE BODY OF THE LESION SURFACE ZONEDr. Ram
- 50. ENAMEL CARIES (PIT AND FISSURE) 1 2 3 4 . Inner most zone Advancing end Birefringence – polarised light Max demineralised area 40 microns thickness Dr. Ram
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- 54. •ZONES OF DENTINALCARIES Enamel DEJ Dentin E-D- ACIDS- DEMINERALIZATION ZONE-1- Fatty degeneration (T D F) ZONE-2- Dentinal sclerosis ZONE-3- Demineralization ZONE-4- Bacterial invasion/ Turbid Dentin ZONE-5- Decomposed dentin Dr. Ram
- 55. DECALCIFIED STRUCTURE OFDENTAL CARIES 5 4 3DEMINERLIZED ZONE (WITHOUT BACTERIAL INVASION) ROSARY BEAD APPEARENCE Dr. Ram
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- 57. ZONE-2- DENTINAL SCLEROSIS ZONE-1- (F D T D F) •ADVANCING END NEAR PULPAL SURFACE •DEPOSITION OF FAT GLOBULES AT THE ODONTOBLASTIC PROCESS ZONE-1- Fatty degeneration (T D F) ZONE-2- Dentinal sclerosis ZONE-3- Demineralization ZONE-4- Bacterial invasion ZONE-5- Decomposed dentin Dr. Ram
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- 59. Expansion & FusionOf Tubules- Liquefaction Foci Dr. Ram
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- 61. Caries in DentinalTubules Dr. Ram
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- 63. Bacteria wins thebattle! Thank you!Dr. Ram