etiology of dental caries
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Etiology of Dental Caries. Dr.Rai Tariq Masood. Early Theories. Worm Theory Humour Theory Parasitic Theory Vital Theory Chemical Theory Chemo-parasitic Theory Proteolytic Theory Proteolysis- Chelation Theory. Current Concepts of Caries Etiology. Keyes Circles

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etiology of dental caries

Etiology of Dental Caries

Dr.Rai Tariq Masood

early theories
Early Theories
  • Worm Theory
  • Humour Theory
  • Parasitic Theory
  • Vital Theory
  • Chemical Theory
  • Chemo-parasitic Theory
  • Proteolytic Theory
  • Proteolysis-Chelation Theory
current concepts of caries etiology
Current Concepts of Caries Etiology

Keyes Circles

  • Caries is multi-factorial disease comprising of four factors
  • Susceptible Tooth Surface
  • Micro-organism
  • Diet (Sucrose)
  • Appropriate time

Each one of them is of equal importance in aetiology of caries

classification based on morphology
Classification Based on Morphology
  • Occlusal Caries ( Pit & Fissure Caries)
  • Smooth Surface Caries

Buccal & Lingual Caries

Proximal Caries

classification based on severity progression
Classification Based on Severity & Progression
  • Rampant Caries
  • Early Childhood Caries ( Baby Bottle Tooth Decay)
  • Radiation Caries
classification based on part of tooth involved
Classification Based on Part of Tooth Involved
  • Enamel Caries
  • Dentinal Caries
  • Cemental Caries
classification based on activity
Classification Based on Activity
  • Primary Caries
  • Secondary Caries
  • Residual Caries
  • Arrested Caries
clinical manifestations of caries process
Clinical Manifestations of Caries Process

1-Early Changes

  • First time demineralization of enamel when PH falls below 5.2 – 5.5
  • Demineralization can not be detected clinically
2 white spot lesion
2- White Spot Lesion
  • First visible clinical presentation
  • Caused by sub-surface enamel demineralization
  • Surface is intact
  • It may or may not progress to frank cavitation
3 hidden or occult caries
3- Hidden or Occult Caries
  • Calcium and Phosphate moves from subsurface to the surface.
  • Calcium and Phosphate along with fluoride from saliva precipitate on effected surface enamel.
  • It will occlude the pores that limits demineralization of surface enamel.
  • Hence intact surface enamel and caries in subsurface level.
  • Not clinically visible.
4 frank cavitation
4- Frank Cavitation
  • Sub-surface carious lesion increases in dimensions.
  • Collapse of surface layer
  • Cavitation
  • More plaque accumulation so rapid tooth destruction.
  • It takes 18 (+- 6 months) to progress from white lesion to cavitation.
5 arrested caries
5- Arrested Caries
  • Carious lesion can become arrested at any stage.
  • If the causal factors are changed or protective factors are increased.
  • Example :Proximal Carious lesion and if adjacent tooth is lost then it becomes self cleansing.
micro biology of dental caries
Micro-Biology of Dental Caries

Streptococcus Mutans

  • Ability to stick to tooth surfaces
  • Ability to produce lactic acid
  • Resist the acidogenic environment
  • Produce intracellular polysaccharide

Streptococcus Sobrinus

Lactobacillus

formation o f plaque
Formation of Plaque
  • Adherence of bacteria to pellicle or enamel surface.
  • Adhesion between bacteria by polysaccharide chains
  • Subsequent growth of bacteria
risk factors protective factors
Risk Factors/Protective Factors
  • Total oral Bacterial population
  • Tooth Morphology
  • Salivary secretion rate
  • Intake of carbohydrates
  • Oral Hygiene Habits
  • Use of Fluorides
role of saliva in caries
Role of Saliva in Caries
  • Also called Liquid Enamel because of high mineral content
  • Cleansing Action
  • Buffering Capacity
  • Antibacterial Action by Lysozyme,Lactoperoxidase,hemoprotein enzyme (Prevents bacterial colonization)
  • Saturated with Calcium and Phosphate
  • Most prominent antibody in saliva IGA.
  • Proteins like statherin protects hydroxyapetitecrystals.
slide20

Flow rate: Role of saliva, with respect to caries, is in the removal of bacterial and debris. Average un-stimulated flow rate is 0.3 ml/minute and amount prior to swallowing 0.9-1.2 ml

  • Quantity: Normal is 700-800 ml/day. Less leads to rampant caries as seen in Xerostomia.
  • Viscosity: Thick saliva associated with high caries but not confirmed.
  • pH: Depends on bicarbonate content.Saliva may be slightly acidic as it is secreted at unstimulated flow rates but may reach PH of 7.8 at high flow rates.
buffering action
Buffering Action
  • Bicarbonates are most important buffers
  • It reacts with acid and release weak carbonic acid.
  • Carbonic acid is rapidly decomposed into water and carbon dioxide.
  • So acid is completely removed.
  • When there is excess sucrose intake,intense acid production will breakdown the buffers.
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