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  1. 1. Pathobiology of Caries DENT 5301 Introduction to Oral Biology Dr. Joel Rudney
  2. 2. Major concepts <ul><li>Caries is a process, not a disease </li></ul><ul><ul><li>Driven by biofilm, but initiated by the host </li></ul></ul><ul><ul><li>Closely linked to specific microenvironments </li></ul></ul><ul><li>The process is dynamic and reversible </li></ul><ul><ul><li>Oral ecological shifts are normal and cyclical </li></ul></ul><ul><li>Many factors influence the outcome </li></ul><ul><ul><li>Microbes are necessary, but not sufficient </li></ul></ul>
  3. 3. Understanding the process <ul><li>Enamel is a unique hard tissue </li></ul><ul><li>Enamel is 95% mineralized </li></ul><ul><ul><li>Minimal protein content </li></ul></ul><ul><li>Enamel is acellular and non-vital </li></ul><ul><ul><li>Cannot repair itself </li></ul></ul><ul><li>Enamel is permeable </li></ul><ul><ul><li>Water and small molecules </li></ul></ul><ul><li>Enamel is in dynamic chemical equilibrium with the oral environment </li></ul><ul><li>Enamel caries is primarily a chemical process </li></ul>
  4. 4. Equilibrium at normal pH Saliva is supersaturated with respect to enamel Saliva Enamel Ca 10 (PO 4 ) 6 OH 2 [Ca] [PO 4 ] [Ca] [PO 4 ] Ca+statherin Ca+aPRP
  5. 5. Demineralization Saliva Enamel Ca 10 (PO 4 ) 6 OH 2 [Ca] [PO 4 ] [Ca] [PO 4 ] Ca+statherin Ca+aPRP Dietary CHO + biofilm = lactic acid; diffusion into enamel = local pH drop Enamel solubility increases [Ca] [PO 4 ] exit to saliva CHO CHO CHO [H + ] [H + ] [H + ] [H + ] [H + ]
  6. 6. Remineralization Saliva Enamel Ca 10 (PO 4 ) 6 OH 2 [Ca] [PO 4 ] [Ca] [PO 4 ] statherin Ca+aPRP Saliva flow clears CHO; salivary HCO 3 returns pH to normal Enamel becomes less soluble [Ca] [PO 4 ] move into enamel CHO CHO [HCO 3 ] [HCO 3 ] [HCO 3 ]
  7. 7. Alternating cycles of de/re-min <ul><li>Break even - sound enamel or arrested caries </li></ul><ul><li>Net loss </li></ul><ul><ul><li>Subsurface demineralization </li></ul></ul><ul><ul><li>New caries </li></ul></ul><ul><ul><li>Progression of old lesions </li></ul></ul><ul><li>Net gain - remineralization of existing lesions </li></ul>
  8. 8. Enamel caries <ul><li>Begins as discrete lesions in the enamel of specific sites (reservoirs) </li></ul><ul><li>Occlusal pits and fissures of Interproximal contacts </li></ul><ul><li>molars and premolars between adjacent teeth (usually posterior) </li></ul><ul><li>Caries risk varies greatly between tooth sites </li></ul><ul><li>Micro-environments account for this variation </li></ul>
  9. 9. Enamel caries <ul><li>White spot lesions </li></ul><ul><li>Intact surface </li></ul><ul><li>Subsurface </li></ul><ul><li>demineralization </li></ul><ul><li>Advanced enamel caries </li></ul><ul><li>Intact surface </li></ul><ul><li>“ Sticky” fissures </li></ul><ul><li>Visible in radiographs </li></ul><ul><li>Dentin defensive reaction </li></ul>Enamel caries can be remineralized peri343/WsptPrev02/wspt7.htm
  10. 10. Dentinal caries <ul><li>Cavitation </li></ul><ul><li>Demineralization + proteolysis </li></ul><ul><li>Bacteria move down tubules </li></ul><ul><li>Pulpal involvement </li></ul><ul><li>Major damage if unchecked </li></ul>Can be arrested, but generally must be restored Love et al. Infect. Immun. 68:1359
  11. 11. Risk factors The initiation and progression of caries is the outcome of interaction between: <ul><li>Microbial factors </li></ul><ul><li>Host factors </li></ul><ul><li>Behavioral/dietary/environmental factors </li></ul><ul><li>Institutional factors </li></ul>
  12. 12. Cariogenicity of microbes <ul><li>Streptococcus mutans/sobrinus </li></ul><ul><ul><li>Major source of demineralization </li></ul></ul><ul><ul><li>Cariogenic properties </li></ul></ul><ul><ul><ul><li>Highly acidogenic </li></ul></ul></ul><ul><ul><ul><li>Highly aciduric </li></ul></ul></ul><ul><ul><ul><li>Extracellular polysaccharide </li></ul></ul></ul><ul><ul><ul><li>from sucrose - insoluble </li></ul></ul></ul><ul><ul><ul><li>Adheres to pellicle </li></ul></ul></ul><ul><ul><ul><ul><li>So do most oral strep </li></ul></ul></ul></ul><ul><ul><ul><li>Transmisible - mother/caregiver to child </li></ul></ul></ul><ul><ul><ul><ul><li>So are all oral bacteria </li></ul></ul></ul></ul><ul><ul><li>Microcolonies - localized zones of high acidity in protected sites </li></ul></ul><ul><ul><ul><li>Occlusal pits and fissures; interproximal contacts </li></ul></ul></ul>
  13. 13. Microbes as risk factors <ul><li>Necessary, but not sufficient </li></ul><ul><li>High S. mutans levels in saliva/plaque increase risk </li></ul><ul><ul><li>Longitudinal studies </li></ul></ul><ul><ul><ul><li>Most people who get new lesions will have “high” levels BUT </li></ul></ul></ul><ul><ul><ul><li>Many people with “high” levels won’t get new lesions </li></ul></ul></ul><ul><li>The majority of oral streptococci belong to non-mutans species </li></ul><ul><ul><li>S. mutans is a minority streptococcus - not a good competitor </li></ul></ul><ul><ul><li>High % of acidogenic/aciduric non-mutans = increased risk? </li></ul></ul><ul><ul><li>Low % of acidogenic/aciduric non-mutans = decreased risk? </li></ul></ul><ul><li>Other species may moderate risk </li></ul><ul><ul><li>Are high levels of Veillonella related to lower lactate levels? </li></ul></ul>
  14. 14. Antimicrobial strategies <ul><li>Targeted attacks on mutans streptococci </li></ul><ul><ul><li>Fundamental concept - S. mutans is the main demineralizer </li></ul></ul><ul><ul><li>Caries vaccines - results not impressive </li></ul></ul><ul><ul><ul><li>Secretory immune system (S-IgA) is tolerant of oral microbes </li></ul></ul></ul><ul><ul><li>Topical antibodies - results not impressive </li></ul></ul><ul><ul><li>NEW Antimicrobial peptides combines w/ S. mutans pheromones </li></ul></ul><ul><li>Broad-spectrum attempts to eliminate/limit biofilm </li></ul><ul><ul><li>Allows for the possibility of other acidogenic species </li></ul></ul><ul><ul><li>Systemic antibiotics (fungal overgrowth) </li></ul></ul><ul><ul><li>Chlorhexidine rinses or varnishes (recolonization from reservoirs) </li></ul></ul><ul><ul><li>NEW Antimicrobial peptides (a “natural” defense system) </li></ul></ul><ul><ul><li>NEW Quorum sensing inhibitors </li></ul></ul><ul><li>Replacement with “probiotics”, natural or genetically engineered </li></ul><ul><li>All approaches have limitations, possible risks </li></ul>
  15. 15. Host factors - teeth <ul><li>Genetics (twin studies) </li></ul><ul><ul><li>Occlusal morphology </li></ul></ul><ul><ul><ul><li>Predisposing </li></ul></ul></ul><ul><ul><ul><ul><li>Complexity (e.g. buccal pits) </li></ul></ul></ul></ul><ul><ul><ul><li>Simplicity may be protective </li></ul></ul></ul><ul><li>Environment (diet, prevention) </li></ul><ul><ul><li>Resistance to demineralization </li></ul></ul><ul><ul><li>Replacement ions in hydroxyapatite </li></ul></ul><ul><ul><ul><li>Fluoride, strontium - protective </li></ul></ul></ul><ul><ul><ul><li>Selenium - predisposing </li></ul></ul></ul>
  16. 16. Host factors - no saliva <ul><li>Saliva is an important regulator of the caries process </li></ul><ul><ul><li>Xerostomia due to radiation therapy or Sjogren’s syndrome </li></ul></ul><ul><ul><ul><li>Very high S. mutans levels + rampant caries </li></ul></ul></ul><ul><ul><ul><li>Decay in unusual sites in multiple teeth </li></ul></ul></ul> © Eastman Dental Institute
  17. 17. Host factors - normal saliva <ul><li>What is the effect of individual variation in saliva? </li></ul><ul><li>Variation in flow rate </li></ul><ul><ul><li>High flow rate - protective; low (normal) flow rate - predisposing </li></ul></ul><ul><ul><li>Not considered a major risk factor by itself </li></ul></ul><ul><li>Variation in salivary buffering capacity (HCO 3 ) </li></ul><ul><ul><li>High HCO 3 - protective; Low HCO 3 - predisposing </li></ul></ul><ul><ul><li>Not considered a major risk factor by itself </li></ul></ul><ul><li>Variation in antimicrobial protein concentrations </li></ul><ul><ul><li>S-IgA , peroxidase , lysozyme , lactoferrin and others </li></ul></ul><ul><ul><li>Expectation: High [ ] - protective; Low [ ] - predisposing </li></ul></ul><ul><ul><li>Studies results are inconsistent, sometimes contradictory </li></ul></ul>
  18. 18. Diet and behavior <ul><li>Sucrose and refined CHO - predisposing </li></ul><ul><ul><li>Archeological and historical evidence define major changes </li></ul></ul><ul><ul><li>Effect of smaller fluctuations more difficult to measure </li></ul></ul><ul><li>Intraoral plaque pH studies of cariogenicity </li></ul><ul><ul><li>Hard cheeses - protective BUT NOT HEART-HEALTHY </li></ul></ul><ul><ul><li>Artificial sweeteners (xylitol) - protective </li></ul></ul><ul><ul><li>The Happy Tooth logo in Europe - plaque pH ≥ 5.7 </li></ul></ul><ul><li>“ Stickiness” - resistance to clearance - how long does pH stay low? </li></ul><ul><li>Frequency of intake - how many demineraliztion episodes/day </li></ul><ul><ul><li>The extremes of Vipeholm </li></ul></ul><ul><ul><li>The reality of shifting dietary patterns </li></ul></ul><ul><li>Oral hygiene (F - products), dental visits, parental oversight </li></ul>
  19. 19. “ Social demineralization” <ul><li>Affecting caries prevalence at the population level </li></ul><ul><li>Institutional “remineralizing” factors </li></ul><ul><ul><li>Public health programs - water fluoridation and sealants </li></ul></ul><ul><ul><li>Research on prevention - NIDCR, IADR, and ADA </li></ul></ul><ul><ul><li>Dental education and outreach - dental insurance </li></ul></ul><ul><ul><li>Corporate introduction of fluoride oral health products </li></ul></ul><ul><ul><li>Dramatic declines in caries prevalence during the ‘80s </li></ul></ul><ul><li>Institutional “demineralizing” factors </li></ul><ul><ul><li>Lifestyle change - high frequency use of high CHO foods </li></ul></ul><ul><ul><li>Mass-marketing of junk foods - the school budget dilemma </li></ul></ul><ul><ul><li>Budget cuts - decreases in prevention, access to care </li></ul></ul><ul><ul><li>Will this be a decade of demineralization? </li></ul></ul>$