Pathogenesis of Dental Caries

1. Pathogenesis of
Dental Caries
Ujwal Gautam
431, BDS 2009
College of Dental Surgery, BPKIHS

2. SUGAR + TEETH + MICRO-ORGANISMS
ORGANIC ACID
Caries
Caries Tetralogy, Newbrun, 1982

4. Dental Caries
Dental Caries is an irreversible
microbial disease of the calcified
tissues of the teeth, characterized
by de-mineralisation of inorganic
portion and destruction of organic
substance of the tooth, which often
leads to cavitation.
Shafer‘s Textbook of Oral Pathology, 6th edition

5.  Can remineralisation explain
the reversibility?
 Caries initiation is due to
demineralisation of inorganic
component and destruction of
organic component. Which occurs
first?
 Does cavitation necessarily
involve in the carious process?

6. Role of Carbohydrates
• Carbohydrate caries
content in diet incidence
suggested by;
HopeWood House Study, Sullivan and
Harris- 1958, Harris-1963
Vipeholm Study, Gustaffson et al, 1954
Patient with Hereditary Fructose
Intolerance have less chance of
developing caries, Newbrun- 1969

7. Role of Carbohydrates
Fermentable Carbohydrates
CARIOGENIC
BACTERIA
acid

8. Role of Carbohydrates
Cariogenicity of Carbohydrates determined by:
Sticky, solid Carbohydrate more cariogenic
than liquid
Mono or di- saccharides more cariogenic
than poly saccharide
Increased frequency of diet has more chance
of cariogenicity
In-between diets increase the chance of
caries
 Sucrose is more cariogenic than
fructose
 While Xylitol, sorbitol and Sachharin
are found to be non- cariogenic.

9. Role of Carbohydrates
Cariogenicity of Starch???
• Starch are very slowly diffused
into the diet and they also
require extra cellular amylase
to become hydrolysed before
they can be assimilated and
metabolised by plaque bacteria.

10. Role of Carbohydrates
• Role of Salivary Carbohydrates???
»NO EFFECT
as they are bound to
proteins and are not
available for microbial
degradation

11. Role of microorganisms
Antoni Van Leeuwenhock (1632-1723)
indicated the presence of microorganisms
in the scrappings obtained from the
carious lesion of tooth surface
Erdl, in 1843, first
associated filamentous
microorganisms to caries on a
causative basis
___ Parasitic Theory

12. Evidence for role of microorganisms:
– Oral organisms can demineralise tooth
enamel in vitro and produce lesions
similar to the naturally occurring dental
caries; Miller, 1889
– Streptococcus mutans is invariably
isolated from carious lesions in the
teeth of British patients; Clark, 1924
– certain bacteria with acidogenic
potential can be isolated and identified
from the carious lesions; Florestano,
1942

13. • S. mutans : development of early carious
lesions in enamel
• Lactobacilli : associated with dentinal
caries
• Actinomyces : associated with root surface
caries
• Vellionella: possibly anti-cariogenic

14. • Catalase -ve, gram +ve, facultative
anaerobic cocci
• Grow as convex colonies in mitis
salivarius bacitracin agar
Cariogenicity due to:
• Aciduric, can survive at pH as low as 4.2
• Present in large number in saliva
• Can adhere to acquired pellicle thus facilitating
plaque formation
• Can adhere and grow even in hard and smooth tooth
surfaces
• Homofermentive; lactic acid being the major
product
Role of S. mutans:
a) Lactic acid production
b) Formation of adhesive plaques
c) Production of fermentable sugars

15. Sucrose glucose + fructose
invertase
Glucosyl Fructosyl
transferase transferase
enzymes
produced by
S. mutans
glucans fructans
Promote reservoir
accumulation for
of plaque fermentable
sugars for
oral
bacteria

16. • gram +ve, non spore forming rods
• grow best in microaerophilic
condition
• grows in rogosa agar (low pH
suppresses others)
acidogenic + aciduric
Possibility as Secondary invaders due to
their acidophilic nature
Predominant site of attack are deep fissures
and deep dentinal lesions

17. Role of acid
―..dental caries is caused by acid
formed by fermentation of food
particles around the teeth‖
Robertson, 1835___Chemical (acid) theory

18. Role of acid
―.. dental caries is caused by
acid produced by microorganisms
from the fermentation of dietary
carbohydrates‖
W. D. Miller, 1889 _____ Miller’s
Chemicoparasitic Theory
Chemical Theory
Parasitic Theory
 most accepted & backbone of current
knowledge and understanding of etiology
of Dental caries

19. Role of acid
ACID CAUSE DISSOLUTION OF THE
HYDROXYAPATITE CRYSTALS OF THE
ENAMEL FOLLOWED BY DENTINE
(Demineralisation)
• Major degradation product of carbohydrates;
Lactic acid
Butyric acid
Resulting from anaerobic catabolism

20. Role of acid
mere presence of acid is of less
significance
‗acidic saliva causes tooth decay‘
Localisation of acid upon tooth surface
holding mechanism = Dental Plaque

21. Role of Dental Plaque
 Miller ruled out • Plaque is the soft, non
role of Plaque in mineralised, thin
Carious process and transparent film
regarded it as a predominently consisting of
protective layer
over the enamel micro organisms suspended in
salivary mucins and
extracellular bacterial
 G. V. Black, 1889,
associated Dental polysaccharides.
Plaque with caries • Initiation of Plaque is with
and described it as formation of acquired
a separate identity pellicle from salivary
glycoproteins which later
 Bibby described the harbors organisms such as S.
nature of plaque, sanguis, A. viscous, A.
its role in caries naeslundii, Veillonellae aka
and adherence on pioneering organisms
tooth surface • S. mutans appears in due
course

22. Plaque Hypotheses Theories
Non-Specific Plaque Hypothesis purports the
caries disease is an outcome of the overall
activity of the total plaque microflora and
not a specific organism.
Specific Plaque Hypothesis proposes that among
the diverse collection of bacteria
encompassing the plaque microflora, only a few
species of bacteria are involved in the
disease. The plaque per se is not pathogenic,
but the presence of pathogenic species within
the plaque causes dental caries.

23.  Harbors the cariogenic bacteria
on tooth surface
 Acid production on plaque-tooth
interface through fermentation of
carbohydrates
 Localisation of acid thus
produced
 Prevents the diffusion of acid
 Restrict the buffering action of
saliva

24. Buffering capacity of Saliva
» Bicarbonate
» Urea
» Arginine-rich proteins
** Sellman, 1949 found that total amount of acid
required to reduce the salivary pH is always greater
for saliva from caries resistant persons
• Initiation of caries occurs at pH 5.2 -
5.5;
At 5.5 pH, saliva ceases to be
saturated with calcium and phosphate
leading to the dissolution of inorganic
components of tooth  CRITICAL pH

25. describes the changes in pH ocurring within dental plaque
when it is subjected to a carbohydrate diet

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

27. Demineralization
Dietary CHO + biofilm = lactic acid; diffusion into enamel = local pH drop
Sal [Ca]
Ca+aPRP
iva
Ca+statherin [PO ] 4
[Ca] [PO4]
[Ca] [PO4] to
exit
saliva
CHO +
CHO CHO [H ]
[H+]
[H+]
Enamel [H+] Enamel
[H+] solubility
increases
Ca10(PO4)6OH2

28. pH at enamel
‗plaque-tooth interface‘  demineralization
less than 5.5 process begins
loss of calcium and phosphates from the surface and
subsurface enamel, creating a
white spot lesion.
1st detectable evidence of
Enamel demineralisation
frank cavitation if the
bacterial plaque is not
regularly removed from the
tooth surface.

29. Remineralization
Saliva flow clears CHO; salivary HCO3 returns pH to normal
Sal
[Ca]
iva 3]
statherin Ca+aPRP
[PO4] [HCO CHO
move into [Ca] [PO4]
[Ca] [PO4]
enamel [HCO3] [HCO3] CHO
Enamel Enamel
becomes
less
soluble Ca10(PO4)6OH2

30. demineralization process is reversible
provided that the
acidogenic properties of the biofilm are
neutralized.
Buffering capacity of saliva
If dietary carbohydrates are removed / pH
= 7  REMINERALISATION occurs
Once the pH returns to higher than the
critical point, demineralization is
arrested and minerals can be added back to
the partially dissolved enamel
crystallites.

31. Alternating cycles of
Demineralisation & Remineralisation
• Net loss
– Subsurface demineralization
– New caries
– Progression of old lesions
• Net gain - remineralization of existing
lesions

32. Remineralization, a conservative alternative
to conventional caries removal and dental
restoration
• natural process for repairing
subsurface non-cavitated carious
lesions caused by organic acids
created by bacterial metabolism of
fermentable carbohydrates.
• Fluoride ions in the presence of
calcium and phosphate promote
remineralization by building a new
surface on existing crystal remnants
in subsurface demineralized lesions
thus favoring the formation of the
more favored fluorapatite crystal in
the enamel.

33. Dental caries
Robert H Selwitz, DDS, Amid I
Ismail, DrPH and Nigel B
Pitts, BDS
The Lancet
Volume 369, Issue 9555,
Pages 51-59 (January
2007)
DOI: 10.1016/S0140-6736(07)60031-2
Diagram of the
caries process as
regular flux of
demineralisation
(destruction) and
remineralisation
(repair); Adapted from
Kidd and Joyston-Bechal,
199749
Copyright © 2007 Elsevier Ltd Terms and Conditions

34. Caries, a Proteolytic
process
Proteolytic enzymes liberated by cariogenic
bacteria
destruction of the organic matrix
detachment of inorganic crystals from one
another
collapse of whole structure
CAVITATION.
Gottlieb (1994) and Gottlieb, Diamond and Applebaum (1946)
_______ Proteolytic theory

35. however,
• Proteolytic bacteria are rare in oral cavity
• No explanation for role of carbohydrates,
acid, etc in dental caries
• Carious lesions cannot be reproduced in vitro
by the proteolytic mechanisms
• Gnotobiotic studies: caries can occur in
absence of proteolytic organisms.
• Enamel is largely inorganic. So, the caries
initiation from proteolytic activity is less
likely
THOUGH ITS ROLE IN CARIES PROGRESSION CANNOT BE
RULED OUT

36. CARIES = acidogenic + proteolytic,
a possibility?
______ Manley and Hardwick (1951)
Both type of organisms can be present, each
functioning independently.
Possible mechanisms;
 microorganisms invade enamel lamellae,
attack enamel and involve dentine before
clinical evidence of caries.
 Alteration in enamel prior to invasion by
micro organisms through decalcification

37. Proteolytic Chelation theory
Proteolytic breakdown of organic portion
of enamel
Proteolytic breakdown products +
acquired pellicle + food debris =
chelating agent
CHELATION  -vely charged chelating
agent releases +vely charged Calcium
ions from enamel/dentine
Dissolution of inorganic component of
tooth
_______ Schatz et al, 1955

38. Factors that influence Dental Caries
(Workshop on Dental Caries mechanisms & Control Techniques,
University of Michigan, 1947)
Host factors Components
A. Tooth 1. Composition
2. Morphologic
characteristics
3. Position
B. Saliva 1. Composition
a. Inorganic
b. Organic
2. pH
3. Quantity
4. Viscosity
5. Antibacterial factors
C. Diet 1. Physical factors
a. Quality of Diet
2. Local factors
a. Carbohydrate content
b. Vitamin content
c. Fluorine content
D. Systemic conditions

39. Histological Changes

40. Pit and Fissure caries
Due to Poor self-cleansing/ developmental faults of tooth
Early lesions appear black/ brown;
feel soft and ‗catch‘
Region bordering the lesion appear
opaque bluish white
Caries follow the direction of enamel
rods and thus form cone shaped lesion
with base at DEJ
Undermining occurs through lateral
spread at DEJ
May penetrate into dentine through
dentinal tubules

41. Smooth surface caries
Earliest change is the appearance of white
chalky spot which is due to the loss of
interprismatic substance of enamel
Earliest microscopic change involves
accentuation of striae of Retzius and
Perikymata
Appears as well demarcated faint opacity or
yellow/brown pigmentation with adsorption of
exogenous materials by porous region
With progression, forms a cone shaped
lesion with base towards the tooth surface
Eventual loss of enamel leads to
roughening and superficial
decalcification

42. Longitudinal ground sections reveal 4 zones
Translucent zone
advancing front of enamel lesion
appears structureless after imbibition with quinolone
in transmitted light
pore volume 1% compared to 0.1% of sound enamel
no evidence of protein loss
Dark zone
usually present as a dark brown zone in the
transmitted light due to excessive
demineralisation
shows birefringence with sound enamel after imbibition
with quinolone in polarised light, so called
positive zone
contains 2-4% pore volume
Body of Lesion
area of greatest demineralisation
polarised light shows pore volume of 5% near periphery
and 25% in the centre region
appears translucent when examined in quinolone under
transmitted light
shows birefringence with sound enamel after imbibition
with water
Surface zone
partial dimeneralisation of 1- 10%
pore volume less than 5% of the spaces
negative birefringence of surface region with water
imbibition
positive birefringence of porous subsurfaceregion

44. Dentinal Caries
• Defense reaction of
pulpo-dentinal complex
– Sclerotic dentine
– Reactionary dentine formation
– Sealing of dead tracts
• Carious destruction
– Demineralisation
– Proteolysis

45. Early dentinal changes:
 Deposition of fat globules
 Sclerosis of dentinal tubules
 Decalcification of wall of dentinal tubules 
Pioneer bacteria
 Microbial invasion: Proteolytic, Acidogenic
Advanced Dentinal Changes:
 Decalcification and confluence of dentinal
tubules
 Thickening of sheath of Neuman
 Increase in diameter of Dentinal tubules with
lodging of microorganisms
 Formation of Liquifaction foci
 Acidogenic and proteolytic activity
 Formation of transverse clefts
 Caries progression with apex pulpally and
base towards enamel

46. Zones in advancing lesion of
dentinal caries:
i. Zone of fatty degeneration of Tomes‘
fibres
ii.Zone of dentinal sclerosis
iii.Zone of decalcification of Dentine
iv.Zone of bacterial invasion
v. Zone of decomposed dentine

47. Root Caries
• Initiates on mineralised cementum
and dentin surfaces which have
greater organic component than
enamel tissue
• On buccal or lingual surface of
tooth
• Dental plaque and microbial
invasion important aspect
• Decalcification of cementum
follows destruction of remaining
matrix

48. Arrested caries
• No tendency for further
progression
• Exclusively in occlusal surface
• Large open cavity in which the
superficially softened and
decalcified dentine is
burnished to a brown, polished
hard surface.

49. ORAL HEALTH CONSEQUENCES
• apical periodontitis
• periapical abscess
• osteomyelitis of
the jaw

50. Pathogenesis of Dental
Caries
 Fermentation of dietary
sugars by Oral micro-
organisms
 De-mineralisation
 Re-mineralisation
 Further demineralisation
and Cavitation
 Initiation / Formation of
Caries

51. Dental Caries is a multifactorial
disease
Histopathologist  stages of lesion
viewed microscopically.
Chemist  interrelationship beetween pH,
mineral flux and solubility at
tooth-saliva interface
Microbiologist  interaction involving
oral bacteria and dental tissue
Current concept of caries etiology implies
interplay of host, microbial floras, substrate
and time as the principle factors

52. References
• Shafer, Hine, Levy; Shafer‘s Textbook of Oral
Pathology; 6th Ed.; Elsevier; 2009
• Shobha Tandon; Textbook of Pedodontics; 2nd Ed.;
Paras Medical Publisher
• M. W. Roberts, J. T. Wright; The Dyanamic Process of
Demineralisation and Remineralisation; Dimensions of
Dental Hygiene. July 2009; 7(7): 16, 18, 20-21
• J.D.B. Featherstone; The Continuum of Dental Caries—
Evidence for a Dynamic Disease Process; Journal of
Dental Research; July 2004 Vol.83 no. suppl 1
• M. Hurlbutt, B. Novy, D. Young; Dental Caries: A pH-
mediated disease; CDHA Journal – Winter 2010
• Alexander V. Zavgorodniy, Ramin Rohanizadeh, Michael
V. Swain, Ultrastructure of dentine carious lesions,
Archives of Oral Biology, Volume 53, Issue 2,
February 2008, Pages 124-132, ISSN 0003-9969,
10.1016/j.archoralbio.2007.08.007.
(http://www.sciencedirect.com/science/article/pii/S00
03996907001999)