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Dental caries ppt


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Dental caries ppt

  2. 2. DENTAL CARIES <ul><li>--Progressive bacterial damage to teeth exposed to saliva. </li></ul><ul><li>--one of the most major causes of all diseases and major cause of tooth loss. </li></ul><ul><li>--ultimate effect-to breakdown enamel and dentin and open a path for bacteria to reach pulp. </li></ul><ul><li>Consequences-inflammation of pulp and periapical tissues. </li></ul>
  3. 3. AETIOLOGY <ul><li>Four major factors involved in etiology:- </li></ul><ul><li>Cariogenic bacteria </li></ul><ul><li>Bacterial plaque </li></ul><ul><li>Susceptible tooth surface </li></ul><ul><li>Fermentable bacterial substrate (sugar) </li></ul>
  4. 5. Bacteriology of Dental Caries <ul><li>Major organisms responsible for caries are:- </li></ul><ul><li>Strep mutans </li></ul><ul><li>Lactobacilli </li></ul><ul><li>Other strains of streptocooci </li></ul>
  5. 6. Cariogenic prop of strep mutans <ul><li>Produces lactic acid from sucrose </li></ul><ul><li>Can live at ph as low as 4.2 </li></ul><ul><li>Forms large amounts of extracellular,sticky,insoluble glucan plaque matrix. </li></ul><ul><li>Adheres to pellicle and contributes to plaque formation. </li></ul>
  6. 7. BACTERIAL PLAQUE <ul><li>Adherent deposit on the teeth. </li></ul><ul><li>BIOFILM-consists of viscous phase formed from bacteria and extracellular polysaccharide matrices. </li></ul><ul><li>In stagnation areas,plaque bacteria can form acid from sugars over long periods to attcack tooth surfaces. </li></ul><ul><li>Production of high acid concentration contributes to low ph. </li></ul>
  7. 8. SUCROSE <ul><li>Colonisation by cariogenic bacteria is highly dependant on sucrose content of diet. </li></ul><ul><li>In absence of sucrose-S mutans cannot be made to colonise the mouth. </li></ul><ul><li>Severe reduction in dietary sucrose-causes S mutans to decline in number or disappear from the plaque. </li></ul><ul><li>Frequent feeds of small quantities are more cariogenic. </li></ul>
  8. 9. CARIES SPREAD TO ENAMEL <ul><li>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. </li></ul><ul><li>The progression of demineralization in enamel continues to the point where dissolution of hydroxyapatite exeeds remineralization. </li></ul><ul><li>Bacteria cant invade enamel until demineralization provides them pathways to enter. </li></ul>
  9. 10. CARIES SPREAD TO DENTIN <ul><li>Non bacterial pre-cavitation,acid softening of the matrix. </li></ul><ul><li>Migration of bacteria along the tubules. </li></ul><ul><li>Distortion of tubules </li></ul><ul><li>Breakdown of intervening matrix forming liquefaction foci. </li></ul><ul><li>Progressive disintegration of remaining matrix </li></ul>
  10. 11. PULPAL RESPONSE <ul><li>Pulpal tissue subjacent to deep caries lesions often shows the presence of chronic inflammation, including lymphocytes, macrophages and plasma cells. </li></ul><ul><li>Formation of tertiary dentin is usually visible on the pulpal aspect and the increase in dentin thickness. </li></ul>
  11. 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
  12. 14. CLINICAL <ul><li>Direct inspection </li></ul><ul><li>Sometimes use of x-rays or special testing instruments </li></ul><ul><li>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 </li></ul>SIGNIFICANSE
  13. 15. CLINICAL SIGNIFICANCE <ul><li>Pulp involvement? </li></ul><ul><li>Reversible or irreversible pulpitis? </li></ul><ul><li>Spread? </li></ul>
  14. 16. Consequences of Dental Caries <ul><li>Possible facial cellulitis requiring hospitalization </li></ul><ul><li>Impaired language development </li></ul><ul><li>Reduced self-esteem </li></ul><ul><li>Possible systemic illness for children with special health care needs </li></ul>
  15. 17. Consequences of Dental Caries
  16. 18. ORAL HEALTH CONSEQUENCES <ul><li>apical periodontitis, </li></ul><ul><li>periapical abscess, </li></ul><ul><li>cellulitis, </li></ul><ul><li>and osteomyelitis of the jaw </li></ul>
  17. 19. Spread from maxillary teeth <ul><li>may cause purulent sinusitis, </li></ul><ul><li>meningitis, </li></ul><ul><li>brain abscess, </li></ul><ul><li>orbital cellulitis, </li></ul><ul><li>and cavernous sinus thrombosis. </li></ul>
  18. 20. Spread from mandibular teeth may cause <ul><li>Spread from mandibular teeth may cause </li></ul><ul><li>Ludwig's angina, </li></ul><ul><li>parapharyngeal abscess, </li></ul><ul><li>mediastinitis, pericarditis, </li></ul><ul><li>empyema, and jugular thrombophlebitis. </li></ul>