Transcript Etiology of Dental Caries

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
• Caries is multi-factorial disease comprising of
four factors
1. Susceptible Tooth Surface
2. Micro-organism
3. Diet (Sucrose)
4. Appropriate time
Each one of them is of equal importance in
aetiology of caries
Classification Based on Morphology
• Occlusal Caries ( Pit & Fissure Caries)
• Smooth Surface Caries
Buccal & Lingual Caries
Proximal Caries
Classification Based on Severity &
Progression
• Rampant Caries
• Early Childhood Caries ( Baby Bottle Tooth
Decay)
• Radiation Caries
Classification Based on Part of Tooth
Involved
• Enamel Caries
• Dentinal Caries
• Cemental Caries
Classification Based on Activity
•
•
•
•
Primary Caries
Secondary Caries
Residual Caries
Arrested Caries
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
• 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
• 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
• 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
• 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
•
•
•
•
Streptococcus Mutans
Ability to stick to tooth surfaces
Ability to produce lactic acid
Resist the acidogenic environment
Produce intracellular polysaccharide
Streptococcus Sobrinus
Lactobacillus
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
•
•
•
•
•
•
Total oral Bacterial population
Tooth Morphology
Salivary secretion rate
Intake of carbohydrates
Oral Hygiene Habits
Use of Fluorides
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 hydroxyapetite crystals.
• 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
• 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.
Thank you