Dental caries ppt
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  • 1. DENTAL CARIES RUBAB HAIDER RABIA IQBAL
  • 2. DENTAL CARIES
    • --Progressive bacterial damage to teeth exposed to saliva.
    • --one of the most major causes of all diseases and major cause of tooth loss.
    • --ultimate effect-to breakdown enamel and dentin and open a path for bacteria to reach pulp.
    • Consequences-inflammation of pulp and periapical tissues.
  • 3. AETIOLOGY
    • Four major factors involved in etiology:-
    • Cariogenic bacteria
    • Bacterial plaque
    • Susceptible tooth surface
    • Fermentable bacterial substrate (sugar)
  • 4.  
  • 5. Bacteriology of Dental Caries
    • Major organisms responsible for caries are:-
    • Strep mutans
    • Lactobacilli
    • Other strains of streptocooci
  • 6. Cariogenic prop of strep mutans
    • Produces lactic acid from sucrose
    • Can live at ph as low as 4.2
    • Forms large amounts of extracellular,sticky,insoluble glucan plaque matrix.
    • Adheres to pellicle and contributes to plaque formation.
  • 7. BACTERIAL PLAQUE
    • Adherent deposit on the teeth.
    • BIOFILM-consists of viscous phase formed from bacteria and extracellular polysaccharide matrices.
    • In stagnation areas,plaque bacteria can form acid from sugars over long periods to attcack tooth surfaces.
    • Production of high acid concentration contributes to low ph.
  • 8. SUCROSE
    • Colonisation by cariogenic bacteria is highly dependant on sucrose content of diet.
    • In absence of sucrose-S mutans cannot be made to colonise the mouth.
    • Severe reduction in dietary sucrose-causes S mutans to decline in number or disappear from the plaque.
    • Frequent feeds of small quantities are more cariogenic.
  • 9. CARIES SPREAD TO ENAMEL
    • Acids formed by bacterial fermentation from dietary sugars leads to a pH fall in the plaque which dissolve tooth enamel, initiating the development of carious lesions.
    • The progression of demineralization in enamel continues to the point where dissolution of hydroxyapatite exeeds remineralization.
    • Bacteria cant invade enamel until demineralization provides them pathways to enter.
  • 10. CARIES SPREAD TO DENTIN
    • Non bacterial pre-cavitation,acid softening of the matrix.
    • Migration of bacteria along the tubules.
    • Distortion of tubules
    • Breakdown of intervening matrix forming liquefaction foci.
    • Progressive disintegration of remaining matrix
  • 11. PULPAL RESPONSE
    • Pulpal tissue subjacent to deep caries lesions often shows the presence of chronic inflammation, including lymphocytes, macrophages and plasma cells.
    • Formation of tertiary dentin is usually visible on the pulpal aspect and the increase in dentin thickness.
  • 12.  
  • 13. CLINICAL Symptoms and Signs Caries initially involves only the enamel and produces no symptoms. A cavity that invades the dentin causes pain , first when hot, cold, or sweet foods or beverages contact the involved tooth, and later with chewing or percussion . Pain can be intense and persistent when the pulp is severely involved
  • 14. CLINICAL
    • Direct inspection
    • Sometimes use of x-rays or special testing instruments
    • Routine, frequent (q 6 to 12 mo) clinical evaluation identifies early caries at a time when minimal intervention prevents its progression. A thin probe, sometimes special dyes, and transillumination by fiberoptic lights are used, frequently supplemented by new devices that detect caries by changes in electrical conductivity or laser reflectivity. However, x-rays are still important for detecting caries, determining the depth of involvement, and identifying caries under existing restorations
    SIGNIFICANSE
  • 15. CLINICAL SIGNIFICANCE
    • Pulp involvement?
    • Reversible or irreversible pulpitis?
    • Spread?
  • 16. Consequences of Dental Caries
    • Possible facial cellulitis requiring hospitalization
    • Impaired language development
    • Reduced self-esteem
    • Possible systemic illness for children with special health care needs
  • 17. Consequences of Dental Caries
  • 18. ORAL HEALTH CONSEQUENCES
    • apical periodontitis,
    • periapical abscess,
    • cellulitis,
    • and osteomyelitis of the jaw
  • 19. Spread from maxillary teeth
    • may cause purulent sinusitis,
    • meningitis,
    • brain abscess,
    • orbital cellulitis,
    • and cavernous sinus thrombosis.
  • 20. Spread from mandibular teeth may cause
    • Spread from mandibular teeth may cause
    • Ludwig's angina,
    • parapharyngeal abscess,
    • mediastinitis, pericarditis,
    • empyema, and jugular thrombophlebitis.