1. Pathobiology of Caries
DENT 5301
Introduction to Oral Biology
Dr. Joel Rudney

2. Major concepts Caries is a process, not a disease
Driven by biofilm, but initiated by the host
Closely linked to specific microenvironments
The process is dynamic and reversible
Oral ecological shifts are normal and cyclical
Many factors influence the outcome
Microbes are necessary, but not sufficient

3. Understanding the process
Enamel is a unique hard tissue
Enamel is 95% mineralized
Minimal protein content
Enamel is acellular and non-vital
Cannot repair itself
Enamel is permeable
Water and small molecules
Enamel is in dynamic chemical equilibrium with the oral environment
Enamel caries is primarily a chemical process

4. Equilibrium at normal pH
Saliva is supersaturated with respect to enamel
Saliva
Ca+aPRP
Ca+statherin
[Ca] [PO4]
[Ca] [PO4]
Enamel
Ca10(PO4)6OH2

5. Demineralization Ca+aPRP Ca+statherin [Ca] [PO4] [Ca] [PO4]
Dietary CHO + biofilm = lactic acid; diffusion into enamel = local pH drop
Saliva
Ca+aPRP
[Ca]
[PO4]
exit to
saliva
Ca+statherin
[Ca] [PO4]
[Ca] [PO4]
CHO
CHO
[H+]
CHO
[H+]
[H+]
Enamel
[H+]
Enamel
solubility
increases
[H+]
Ca10(PO4)6OH2

6. Remineralization Ca+aPRP statherin [Ca] [PO4] [Ca] [PO4] Ca10(PO4)6OH2
Saliva flow clears CHO; salivary HCO3 returns pH to normal
Saliva
[Ca]
[PO4]
move into
enamel
Ca+aPRP
statherin
[HCO3]
CHO
[Ca] [PO4]
[Ca] [PO4]
[HCO3]
[HCO3]
CHO
Enamel
Enamel
becomes
less
soluble
Ca10(PO4)6OH2

7. Alternating cycles of de/re-min
Break even - sound enamel or arrested caries
Net loss
Subsurface demineralization
New caries
Progression of old lesions
Net gain - remineralization of existing lesions

8. Enamel caries
Begins as discrete lesions in the enamel of specific sites (reservoirs)
Occlusal pits and fissures of Interproximal contacts
molars and premolars between adjacent teeth (usually posterior)
Caries risk varies greatly between tooth sites
Micro-environments account for this variation

9. Enamel caries Enamel caries can be remineralized White spot lesions
peri343/WsptPrev02/wspt7.htm
White spot lesions
Intact surface
Subsurface
demineralization
Advanced enamel caries
Intact surface
“Sticky” fissures
Visible in radiographs
Dentin defensive reaction
Enamel caries can be remineralized

10. Dentinal caries Can be arrested, but generally must be restored
Love et al. Infect. Immun. 68:1359
Cavitation
Demineralization + proteolysis
Bacteria move down tubules
Pulpal involvement
Major damage if unchecked
Can be arrested, but generally
must be restored

11. Risk factors
The initiation and progression of caries is the outcome of interaction between:
Microbial factors
Host factors
Behavioral/dietary/environmental factors
Institutional factors

12. Cariogenicity of microbes
Streptococcus mutans/sobrinus
Major source of demineralization
Cariogenic properties
Highly acidogenic
Highly aciduric
Extracellular polysaccharide
from sucrose - insoluble
Adheres to pellicle
So do most oral strep
Transmisible - mother/caregiver to child
So are all oral bacteria
Microcolonies - localized zones of high acidity in protected sites
Occlusal pits and fissures; interproximal contacts

13. Microbes as risk factors
Necessary, but not sufficient
High S. mutans levels in saliva/plaque increase risk
Longitudinal studies
Most people who get new lesions will have “high” levels BUT
Many people with “high” levels won’t get new lesions
The majority of oral streptococci belong to non-mutans species
S. mutans is a minority streptococcus - not a good competitor
High % of acidogenic/aciduric non-mutans = increased risk?
Low % of acidogenic/aciduric non-mutans = decreased risk?
Other species may moderate risk
Are high levels of Veillonella related to lower lactate levels?

14. Antimicrobial strategies
Targeted attacks on mutans streptococci
Fundamental concept - S. mutans is the main demineralizer
Caries vaccines - results not impressive
Secretory immune system (S-IgA) is tolerant of oral microbes
Topical antibodies - results not impressive
NEW Antimicrobial peptides combines w/ S. mutans pheromones
Broad-spectrum attempts to eliminate/limit biofilm
Allows for the possibility of other acidogenic species
Systemic antibiotics (fungal overgrowth)
Chlorhexidine rinses or varnishes (recolonization from reservoirs)
NEW Antimicrobial peptides (a “natural” defense system)
NEW Quorum sensing inhibitors
Replacement with “probiotics”, natural or genetically engineered
All approaches have limitations, possible risks

15. Host factors - teeth Genetics (twin studies) Occlusal morphology
Predisposing
Complexity (e.g. buccal pits)
Simplicity may be protective
Environment (diet, prevention)
Resistance to demineralization
Replacement ions in hydroxyapatite
Fluoride, strontium - protective
Selenium - predisposing

16. Host factors - no saliva
Saliva is an important regulator of the caries process
Xerostomia due to radiation therapy or Sjogren’s syndrome
Very high S. mutans levels + rampant caries
Decay in unusual sites in multiple teeth
© Eastman Dental Institute

17. Host factors - normal saliva
What is the effect of individual variation in saliva?
Variation in flow rate
High flow rate - protective; low (normal) flow rate - predisposing
Not considered a major risk factor by itself
Variation in salivary buffering capacity (HCO3)
High HCO3 - protective; Low HCO3 - predisposing
Variation in antimicrobial protein concentrations
S-IgA, peroxidase, lysozyme, lactoferrin and others
Expectation: High [ ] - protective; Low [ ] - predisposing
Studies results are inconsistent, sometimes contradictory

18. Diet and behavior Sucrose and refined CHO - predisposing
Archeological and historical evidence define major changes
Effect of smaller fluctuations more difficult to measure
Intraoral plaque pH studies of cariogenicity
Hard cheeses - protective BUT NOT HEART-HEALTHY
Artificial sweeteners (xylitol) - protective
The Happy Tooth logo in Europe - plaque pH ≥ 5.7
“Stickiness” - resistance to clearance - how long does pH stay low?
Frequency of intake - how many demineraliztion episodes/day
The extremes of Vipeholm
The reality of shifting dietary patterns
Oral hygiene (F- products), dental visits, parental oversight

19. “Social demineralization”
Affecting caries prevalence at the population level
Institutional “remineralizing” factors
Public health programs - water fluoridation and sealants
Research on prevention - NIDCR, IADR, and ADA
Dental education and outreach - dental insurance
Corporate introduction of fluoride oral health products
Dramatic declines in caries prevalence during the ‘80s
Institutional “demineralizing” factors
Lifestyle change - high frequency use of high CHO foods
Mass-marketing of junk foods - the school budget dilemma
Budget cuts - decreases in prevention, access to care
Will this be a decade of demineralization? $