This document discusses the etiology and pathogenesis of dental caries. It begins by defining dental caries and exploring early theories of its causes. It then examines the role of microorganisms like streptococcus mutans and lactobacilli in producing acid through fermentation of carbohydrates. Key factors in the development of caries are said to be the interaction between oral microbes, carbohydrate substrates in the diet, and the acid they produce. The document also notes the influence of host factors like teeth, saliva, and individual susceptibility on caries development.

1. By Dr Ajish M Saji
Deparment of Oral Pathology
Malabar Dental College
Edappal

2.  Introduction
 Etiology
 Role of micro organisms
 Current concepts of caries etiology
 Pathophysiology
 Conclusion
 References

3.  Definition-
 Word caries is derived from the Latin word
‘rot’ or ‘decay’.
3

4.  Race
 Age
 Gender
 Familial

5.  Early theories
◦ Legend of worms.
◦ Endogenous theories.
◦ Chemical theory.
◦ Parasitic theory.
5

6.  Earliest reference – Sumerian text ‘Legend of
worms’.
 Dated back 5000 BC – excavated-Euphrates
valley of the lower Mesopotamian area.
 Homer-worms as the cause of toothache.
6

7.  Humoral theory by Greek physicians-
imbalance in humors resulted in disease.
 Hippocrates, Celsus, Galen and Avicenna-the
Vital theory of tooth decay
7

8.  Parmly in 1820-‘chymal agent’ responsible
for caries.
 Supported by Robinson in 1835-acid formed
by fermentation of food particles around the
teeth.
8

9.  Erdl in 1843-filamentous organisms.
 Ficnus in 1847 -‘denticolae’ .
 Leber and Rottenstein-purely chemical
process.
9

10.  Clark, Tomes and Magitot-bacteria-
exogenous source of the acids.
 Underwood and Milles in 1880-septic theory.
10

11.  By Willoughby D Miller.
 Theory – Caries is caused by acids produced
by microorganisms of mouth.
 Dental decay is a chemoparasitic process
consisting of two stages.
◦ Preliminary stage.
◦ Subsequent stage.
11

12.  Assigned an essential role to three factors in
the caries process:
◦ The oral microorganisms in acid production and
proteolysis.
◦ The carbohydrate substrate.
◦ The acid which causes dissolution of tooth
minerals.
12

13.  Unable to explain,
◦ The predilection of specific sites on a tooth to
dental caries.
◦ The initiation of smooth surface caries.
◦ Why some population are caries free and the
phenomenon of arrested caries.
13

14.  Cariogenic carbohydrate are dietary in origin.
 Salivary carbohydrates-proteins, and other
compounds and are not readily available for
microbial degradation.
 Cariogenicity of dietary carbohydates varies
with…
14

15.  Sticky, solid carbohydrate are more caries
producing.
 Carbohydrate in detergent foods less
damaging than in soft retentive foods

16.  Polysaccharides-less easily fermented by
plaque bacteria than monosaccharides and
disaccharides.
 Meals high in fat, protein or salt reduce the
oral retentiveness of carbohydrates.
 Refined pure carbohydrates are more caries
producing.
16

17.  Lactobacilli.
 Veillonella.
 Oral actinomyces.
 Oral streptococci – S .mutans, S .sanguis, S
.salivaris, S .mitior.
17

18.  Gram positive facultative anaerobic
bacteria.
 Rod shaped, non-spore forming.
 Usually straight, although they can form
spiral or coccobacillary forms under certain
conditions.
 Often found in pairs of varying length

22.  Are mainly responsible for caries PROGRESSION
 Appear during the first year of a child’s life
 Are present in high numbers in:
 Isolation – selective agar medium – Rogosa –
suppresses growth of other organisms by its low
pH.

23.  Number increases if mutans streptococci start
to colonize the oral cavity- favorable acid
environment.
 In children- coronal caries
 In adults-root caries and in deep dentinal
caries associated with pulpitis.

24.  Preferentially settle in niches with a low pH-value
and in the vicinity of plaque accumulation.
 Do not adhere to tooth surfaces on their own
account, but need retention niches such as:

25.  Significant correlation b/t carious lesions and the
lactobacilli count in both children and adults.
 The higher the DMF index, the higher the
lactobacillus count.
 The larger the size of the carious lesion, the
more lactobacilli present
 A high lactobacilli count is an indicator of high
sugar intake

26.  Have the capacity to produce acids and an
ability to grow and survive in an acidic
environment.
 Have a fermentative metabolism.
 2 metabolic types exist:
◦ Homolactic fermentation.
◦ Heterolactic fermentation.

27.  Homofermentative lactobacillus-Embden-
Meyerhof pathway
 Heterofermentative lactobacillus-
Phosphoketolase pathway
 Both metabolic pathways result in the
acidification of the environment

30.  Gram +ve, filamentous.
 Include – A. naeslundii, A. viscosus –
facultative anaerobes.
 A. isralii, A. odontolyticus – anaerobes.
30

31.  Gram –ve cocci .
 Found in plaque
 Lack key enzymes involved in glycolysis and
hexose monophosphate shunt – therefore do
not utilize sugars as an energy source.
 It utilizes lactic acid by converting it to
propionic and other weak acids.
31

32.  Most important species found in the oral
cavity include – S. mutans, S. sanguis, S.
mitior, S. salivarious, S. milleri.
32

33.  First isolated in 1924 by Clarke and termed S.
mutans.
 Gram +ve cocci forming short to medium
chains.
 S. mutans can be selectively cultured in mitis
salivarius agar containing 20% sucrose and
0.2% units/ml of bacitracin.
33

36.  S. mutans synthesizes insoluble
polysaccharides from sucrose, it is
homofermentative and is more aciduric.
 Cariogenic strains of S. mutans contain
lysogenic bacteriophage.

37.  Based on nucleic acid base content and
hybridization, S. mutans have been divided
into 5 genotypes as S. mutans, S. rattus, S.
sobrinus, S. cricetus, S. ferus.
 S. mutans and sobrinus commonly found in
plaque.
 S. mutans strains divided into 8 serotypes
designated ‘a’ through ‘h’.
37

38.  Clark named this organism ‘‘mutans’’
because of the observed changes in cell
shape depending on growth condition.
 Two major types of S. mutans adhesins
mediate the attachment: cell-surface proteins
and sucrose-derived glucans.

39.  There are more than 60 proteins responsible
for cell envelope biogenesis, including 5
penicillin-binding proteins, 3 ABC
transporters,10 glycosyltransferases, and 6
autolysins.
 Four types of autolysins were found in
UA159-muramidase, amidase 2, an endolysin
and the LrgB family protein.

40.  Most important substrate to involve S.
mutans in caries is disaccharide sucrose.
 Sucrose metabolized by S. mutans results in
production of lactic acid.
 S. mutans polymerize glucose and fructose to
synthesize glucans and fructans.

41.  Glucans more significant-promote
accumulation of S. mutans on teeth.
 Hypopolymers of glucans-dextran and mutan
are synthesized by S. mutans

42.  Enzymes that synthesize glucans and fructans
are glucosyl and fructosyltransferases.
 Lipoteichoic acid-extracellualr polymer in S.
mutans.
 S. mutans store amylopectin.
 S. mutans possess invertase-hydrolyze
sucrose intracellularly to free glucose and
fructose.

43.  Galactose -Leloir and tagatose 6-phosphate
pathway.
 The newly identified gene clusters is one
responsible for the synthesis and degradation
of starch (SMU.1535–1541) that includes
pullulanase.

45.  Acid tolerance of S. mutans -presence of a
membrane-bound, acid-stable, proton-
translocating F0F1 ATPase-maintain the
intracellular pH at 7.5.
 Some oral streptococci use the arginine
deiminase pathway to survive a decrease in
environmental pH.

46.  Three types of solute transporting ATPases
are present: P-type, F-type, and ABC-type.
 The P-type ATPases -transport of calcium
and potassium, as well as bacterial resistance
to the toxic metals copper and cadmium.

47.  Virulence factors-adhesins, glucan-producing
and -binding exoenzymes, proteases and
cytokine-stimulating molecules.

48.  Occurs primarily in occlusal fissures.
 α hemolytic streptococcus species, formerly
called s.b.e, first isolated from patients with
subacute bacterial endocarditis.
 Sucrose containing media as small, firm
colonies and form extra cellular
polysaccharides in sucrose broth.

49.  Found in tongue, throat and saliva. Found
less in dental plaque.
 Produce water soluble polymer of fructose
called levan.

50.  Commonly isolated bacteria.
 Produces soft, round and black-brown
colonies on mitis salivarius agar.

51.  Acid production occurs through enzymatic
breakdown of the sugar. Acids formed are
lactic acid and butyric acid.
 Plaque holds the acid to the tooth surface for
a long period of time.

52.  It is the soft, nonmineralized, bacterial
deposit which forms on teeth and dental
prostheses that are not adequately cleaned.
 Aciduric and acidogenic streptococci and
lactobacilli are numerous in plaque.

53.  Pathogenecity of plaque depend on their microbial
composition in quantitative & qualitative terms & upon
availability of dietary sugars.
 Formation of dental plaque require 2 types of specific
bacterial adherent interactions,
◦ Bacteria attach selectively to acquired pellicle.
◦ Bacteria accumulate via specific adhesive & cohesive interaction
involving components of plaque matrix & direct bacterial cell
contact.

54.  In dental plaque 3 basic group of
microorganisms predominate-streptococci,
actinomyces and veilonella.
 Of all these S. mutans considered chief
etiologic agent in human caries today.

55.  Theory – organic or protein elements of tooth
are the initial pathway of invasion by
microorganisms.
 Enamel lamellae as pathways for organisms in
the progress of dental caries.

56.  No satisfactory evidence to support the claim
that the initial attack on enamel is proteolytic.
 Gnotobiotic studies :- Caries can occur in the
absence of proteolytic organisms.
 Conclusion :- Proteolysis in the initiation of
dental caries is likely to be of no significance,
but its role in the progression of the more
advanced carious lesions cannot be ruled out.

57.  Theory- Simultaneous microbial degradation
of the organic components and the
dissolution of the minerals of the tooth by
the process known as chelation (Schatz
1955).
 Effects of chelation:-
◦ Independent of the pH of the medium.
◦ Removal of metallic ions such as calcium from a
biologic calcium-phosphorous system may occur at
a neutral or even alkaline pH.

58.  Egglers – Lura (1967) proposed that sucrose
itself, and not the acid derived from it, can
cause dissolution of enamel by forming an
ionized calcium saccharate.
 Calcium saccharates and calcium complexing
intermediaries require inorganic phosphate,
which is subsequently removed from the
enamel by phosphorylating enzymes.

59.  Etiology
 An interplay of three principal factors is
responsible,
 Host (teeth and saliva)
 Microorganisms in the form of dental plaque
 Substrate (diet)

60. Food
Time
Bacteria
Tooth Caries
Individual Susceptibility

62.  Teeth
 Composition: Deficiency in fluorine, zinc, lead
and iron-increased caries.
 Morphological characteristics: Deep, narrow
occlusal fissures, and lingual and buccal pits.
As teeth get worn (attrition), caries declines.

63.  Position:
 The interdental areas.
 Malalignment of the teeth-crowding,
abnormal spacing, etc. can increase the
susceptibility to caries.

64.  Saliva
 Saliva has a cleansing effect on the teeth.
Normally, 700–800 ml of saliva is secreted
per day.
 Caries activity increases as the viscosity of
the saliva increases.
 The quantity as well as composition, pH,
viscosity and buffering capacity of the saliva
plays a role in dental caries.

65.  Quantity: Reduced salivary secretion as found
in xerostomia and salivary gland aplasia gives
rise to increased caries activity.
 Composition: Inorganic—fluoride, chloride,
sodium, magnesium, potassium, iron,
calcium and phosphorus are inversely related
to caries.
 Organic—ammonia retards plaque formation
and neutralizes the acid.

66.  pH: A neutral or alkaline pH can neutralize
acids formed by the action of microorganisms
on carbohydrate food substances.
 Antibacterial factors: Saliva contains enzymes
such as lactoperoxidase, lysozyme,
lactoferrin and immunoglobulin (Ig)A, which
can inhibit plaque bacteria.

67.  Hydrogen carbonate- main buffer
component.
 Lysozyme-bacteriolysis-disrupting bacterial
cell wall.
 Lactoferrin- interfere bacterial growth.
 Lactoperoxidase-inhibit glucose metabolism.

68.  Vitorino-large amounts of phosphoproteins-
more remineralization.

69.  Dental plaque is a thin, tenacious microbial
film that forms on the tooth surfaces.
 The dental plaque holds the acids-close
contact with the tooth surfaces –prevents…

70.  Vitamins A, D, K, B complex (B6), calcium,
phosphorus, fluorine, amino acids such as
lysine and fats have an inhibitory effect on
dental caries.

71.  Drifting of the teeth in the edentulous space.
 Malalignment of the teeth.
 Gingival recession, abrasion and abfraction
defects at the neck of the tooth increase root
caries.

72.  Selenium in the soil increases the formation
of caries while molybdenum and vanadium
decrease it.
 A high temperature is associated with a lower
prevalence of caries.

73.  A low socioeconomic and literacy status is
associated with caries.
 Urbanization is linked to an increased
incidence of caries.
 Caries is more common in childhood and
adolescence, and after 60 years of age, when
the incidence of root caries is higher.
 Females develop caries more often than
males.

74.  Non-vegetarians develop caries more often
than vegetarians.
 Availability/access to a health care facility can
affect utilization of health care services.
 Lack of oral health insurance promotes oral
neglect and increases disease levels.

75.  Microbial acid production in plaque.
 Stephan et al. - patients who exhibited various
degrees of caries activity.
 The pH readings were obtained prior to rinsing
for 2 min with a 10% glucose solution and at
intervals thereafter until the pH returned to its
original value.
 There was a rapid pH drop, indicating that the
glucose was instantaneously converted to acid
products, mainly lactic acid, to overwhelm the
available salivary buffering capacity.

77.  (i) Protective role of saliva.
 The saliva contains pH rise factors such as
urea and a tetrapeptide called sialin which
contains lysine and arginine.
 The hydrolysis of these basic compounds by
certain members of the plaque flora liberates
ammonia, causing the pH to rise.

78.  Saliva contains certain proline-rich proteins
and tyrosine-rich peptide, called statherin-
delays both the onset and rate of
precipitation of calcium phosphate salts from
supersaturated solutions.
 The maintenance of the supersaturated state
of these ions provides a constant and
powerful remineralizing mechanism on those
surfaces that are bathed by saliva.

79.  Salivary proteins or glycoproteins such as
lysozyme, lactoperoxidase, lactoferrin, and
high-molecular weight agglutinins possess
antibacterial activity.
 They are present at relatively constant levels,
exhibit broad-spectrum activity, and lack any
aspects of immunological memory.
 Organisms which colonize the oral surfaces
apparently are resistant to these proteins.

80.  S. mutans and S. sobrinus are minimally
affected by lysozyme and they are routinely
found in human plaque.
 S. cricetus and S. rattus bind lysozyme at
significantly faster rates and are inhibited by
1% of the dosage that is required to inhibit S.
mutans and S. sobrinus.

81.  (ii) Critical pH.
 The pH at which this demineralization begins
is known as the critical pH and is in the
vicinity of pH 5.0 to 5.5.
 pH at which the hydroxyapatite of the tooth
acts as a buffer.

82.  (iii) Demineralization-remineralization.
 The early enamel lesion-subsurface
demineralization.
 The predecessor of this lesion is a
histologically undetectable chemical lesion
caused by the diffusion into the enamel of
undissociated lactic and possibly acetic acids
produced by plaque microbes during a
nutrient pulse.

83.  At some distance below the enamel surface
these acids dissociate and react with the
hydroxyapatite of the enamel crystals to form
soluble calcium and phosphate products.
 As these ions diffuse outward, some of them
may reprecipitate as calcium phosphate salts
in the surface layer, so as to create a
histologically sound outer layer overlying a
porous subsurface structure.

84.  Whenever a fermentable dietary substrate
diffuses into the plaque and is converted to
acid end products, some degree of
subsurface demineralization occurs.
 Then, between meals, the pH in the plaque
returns to neutrality and calcium and
phosphate ions in the plaque, driven by the
supersaturated concentration gradient,
diffuse into the lesion, promoting
remineralization .

85.  These demineralization-remineralization cycles
can be documented in the incipient lesion as
characteristic zones that reflect large
hydroxyapatite crystals due to remineralization
(dark zone) and small hydroxyapatite crystals
due to demineralization (translucent zone).
 Demineralization which progresses to cavitation
occurs if the frequency and magnitude of acid
production overwhelm the repair process.

86.  Dental caries, otherwise known as tooth
decay, is one of the most prevalent chronic
diseases of people worldwide; individuals are
susceptible to this disease throughout their
lifetime.
 Risk for caries includes physical, biological,
environmental, behavioural, and lifestyle-
related factors.

87.  R Rajendran ,B Shivapadasundaram ,Shafer’s
Textbook Of Oral Pathology ,Elsevier ,Fifth
Edition.
 NASEEM SHAH, NCMH Background Papers-
Burden of Disease in India, Oral and dental
diseases: Causes, prevention and treatment
strategies.
 WALTER J. LOESCHE, MICROBIOLOGICAL
REVIEWS, Dec. 1986, p. 353-380 Vol. 50, No.
4, Role of Streptococcus mutans in Human
Dental Decay.

88.  Dragana Ajdic et al, PNAS October 29, 2002
vol. 99 no. 22, Genome sequence of
Streptococcus mutans UA159, a cariogenic
dental pathogen.
 Dental clinics of North America, Current
concepts in cariology, July 2010, Vol 54,
No:3.