Pathophysiology of caries and pulpal reactions to caries

© Ramaiah University of Applied Sciences
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Faculty of Dental Sciences

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Pathophysiology Of Caries And
Pulpal Reactions To Caries
Presented :Dr. Arbiya Anjum S
Moderator :Dr. Poornima Ramesh

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CONTENTS
• Introduction
• Theories
• Etiology
• Histological
Characteristics Of
Dentinal Caries
• Dead Tracts
• Sclerotic Dentin
• Dentinal Reactions To
Caries
• Dentinal zones of caries
• Enamel zones of caries
• Pulpal reactions to
caries
• Dentinal permeability
• Inflammatory response
• Reparative dentin
formation
• Conclusion
• References

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Dental Caries
• Caries in Latin ‘rot’ or ‘decay’ and from ancient Irish ara chrinn
• Is an irreversible microbial disease of the calcified tissues of the
teeth, characterized by demineralization of the inorganic portion and
destruction of the organic substance of the tooth, which leads to
cavitations. (Shafer'S Textbook Of Oral Pathology 6Th Edition)
• Is an infectious microbiologic disease of teeth that results in localized
dissolution and destruction of the calcified tissues. (Sturdevant's Art and Science of
Operative Dentistry)

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EARLY THEORIES
The Legend of
worms
5000 BC, from
Mesopotamian
area caused by
worm that drank
blood of teeth
Chemical Theory
1819, by Parmly,
unidentified
chemical
agent,stated that
caries began on
enamel surface
where food
putrefied
Endogenous
Theory
1843,proposed by
Erdl , filamentous
parasite in
plaque,termed as
“Denticolae”
Parasitic Theory
1) Humoral
Theory
4 Humors of
body –
blood,phlegm,
black & yellow
bile
2) Vital Theory
Tooth decay
originated like
bone gangrene,
from within the
tooth itself

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Exogenous theories
Miller’s Chemico - Parasitic Theory
• Theory: Caries is caused by acids produced by microorganisms
of the mouth
• Two stages:
1. Decalcification of enamel and dentin(preliminary stage)
2. Dissolution of the softened residue(subsequent stage)
• Limitations of Miller’s Theory
Predilection
of specific
sites on a
tooth
Phenomenon
of arrested
caries
Why some
populations
are caries
free?
Initiation of
smooth
surface caries

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Proteolytic Theory
• Theory: Organic or protein elements of a tooth are the initial
pathway of invasion by microorganism
• Enamel lamella are pathways for organisms in the progress of
dental caries
• Gottlieb and Gottlieb, Diamond and Applebaum: “Caries is
essentially a proteolytic process: microorganisms invade
organic pathways and destroy them in their advance. Acid
formation accompanied proteolysis”
• Drawbacks: No satisfactory evidence to support the claim that
the initial attack on enamel is proteolysis

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• Gnotobiotic studies: caries can occur in the absence of
proteolytic organism
• 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

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Proteolysis-Chelation Theory
• Theory: Simultaneous microbial degradation of the organic
components and the dissolution of the minerals of the tooth by the
process known as chelation(Schatz et al 1955)
• Chelation: A process involving the complexing of a metallic ion to a
substance through a covalent bond which results in a highly
stable,poorly dissociated or weakly ionized compound
• Removal of metallic ions such as calcium from a biologic calcium-
phosphorus system may occur at a neutral or even alkaline pH
• The proteolysis-chelation theory resolves the argument as to
whether initial attack of dental caries is on the organic or inorganic
portion of enamel by stating that both may be attacked
simultaneously

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P athophysiology of Dental Caries , G eorg Conrads et al, 2018
Presence of
acidogenic-
aciduric bacteria
and their ability
to attach to the
pellicle coated
tooth
surface,directly
or indirectly
(Conrads et al)
Environmental
conditions
favours
multiplication
and metabolism
of the species &
access to low-
molecular sugars
and low redox
potential
High sugar and
low oxygen
leads to rapid
fermentation
and acid
production
Common Principles Of Etiology Of Caries

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Current concepts of caries etiology
• Dental caries a multi factorial disease an interplay of 3 primary
factors:
1. Host (saliva and teeth)
2. Cariogenic biofilm(microorganisms)
3. Fermentable carbohydrates(substrate)
4. Time as inevitable fourth factor
(Modified from Keyes PH, Jordan HV: Factors influencing initiation, transmission and inhibition of dental caries. In Harris RJ,
editor: Mechanisms of hard tissue destruction, New York, 1963, Academic Press.)

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Tooth habitats
The smooth enamel surfaces immediately gingival to the
proximal contacts and in the gingival third of the facial
and lingual surfaces of the clinical crown
Pit and fissures
Sub gingival caries
Sturdavent 7th edition

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Saliva
• Nature’s Anticaries Agent
Names Action
Effects on Plaque Biofilm
Community
SALIVARY ENZYMES
Amylase Cleaves—1,4 glucoside bonds Increases availability of
oligosaccharides
Lactoperoxidase Catalyzes hydrogen peroxide–
mediated oxidation; adsorbs to
hydroxyapatite in active form
Lethal to many organisms:
suppresses plaque formation on
tooth surfaces
Lysozyme Lyses cells by degradation of
cell walls, releasing
peptidoglycans; binds to
hydroxyapatite in active
conformation
Lethal to many organisms;
peptidoglycans activate
complement; suppresses plaque
formation on tooth surfaces
Lipases Hydrolysis of triglycerides to free
fatty acids and partial glycerides
Free fatty acids inhibit
attachment and growth of some
organisms
NON-ENZYME PROTEINS
Lactoferrin Ties up free iron Inhibits growth of some iron-
dependent microbes
Secretory immunoglobulin
A(IgA) (smaller amounts of
IgM, IgG)
Agglutination of bacteria inhibits
bacterial enzymes
Reduces numbers in saliva by
precipitation; slows bacterial
growth
Glycoproteins (mucins) Agglutination of bacteria Reduces numbers in saliva by
precipitation

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functions
Quality
Viscosity

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Cariogenic biofilm
• Dental plaque -the soft, tenacious film
accumulating on the surface of teeth
• Biofilm -by-products, extracellular
matrix, and water
• The accumulation of biofilm on teeth
is a highly organized and ordered
sequence of events
From Welch JL, Rossetti BJ, Riekem
CW, et al: Biogeography of a human oral microbiome at the micron scale, Proc Natl Acad Sci USA
9;113(6):E791–E800, 2016. doi:10.1073/pnas.1522149113)

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From Xiao J, Klein MI, Falsetta ML, et al: The exopolysaccharide matrix modulates the interaction between 3D architecture and
virulence of a mixed-species oral bioilm, PLoS Pathog8(4):e1002623, 2012.
Sturdavent 7th ed

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• The bacteria most responsible for dental cavities are the Mutans
streptococci
• Only a few specific species of bacteria are believed to cause dental
caries Streptococcus mutans and Lactobacillus species among them
• They produce high levels of lactic acid following fermentation of
dietary sugars, and are resistant to the adverse effects of low pH
• As the cementum of root surfaces is more easily demineralized than
enamel surfaces, a wider variety of bacteria can cause root caries
including Lactobacillus acidophilus, Actinomyces spp., Nocardia spp.,
and Streptococcus mutans
Bacteria

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Lactobacilli
• Gram positive, non spore forming rods,‘Secondary invader’
• Homofermentative-L. casei and L. acidophilus
• Heterofermentative- L. fermentum and L. brevis
• It is both acidogenic and aciduric. Multiply in low pH of plaque
and carious lesions
• ‘universal etiology’ questioned -amount of acid formed
compared to others

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Oral Actinomyces
• Gram positive, filamentous organism
• A.naeslundi and A.viscosus- facultative anaerobes
• A.israelii and A.odontolyticus-strict anaerobes
• A.viscosus predominant flora of plaque overlying root lesion
however it is also found on sound root surfaces

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Streptococcus Mutans
• First isolated 1924 Clarke
• Catalase negative, gram positive cocci forming
short to medium chains
• Cariogenic stains contain lysogenic bacteriophage
• 5 genotype: S.mutans, S.rattus, S.sobrinus,
S.cricetus, S.ferus
• Eight sterotypes: ‘a’ through ‘h’

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Metabolism
• Most important substrate in carious process is disaccharide
sucrose
• Energy utilization via glycolytic pathway leads to lactic acid
production and degradation of sucrose to free glucose and
fructose by invertase
• Ability to form adhesive plaque explains specific dependence on
sucrose
• Polymerizing glucose and fructose moieties of sucrose to glucans
and fructans. Enzymes synthesis is glucosyl- and
fructosyltransferases

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• Electron microscopic view of plaque reveals 2 types:
Globular component- water soluble
Fibrillar component – water insoluble glucan
• Lipoteichoic acid a highly negatively charged contribute to
adhesion of bacteria
• Significant invertase activity hydrolyze sucrose to free
glucose and fructose

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Approximate proportional distribution
of predominant cultivable flora of four
oral habitats. (Redrawn from Morhart R, Fitzgerald R: Composition and
ecology of the oral flora. In Menaker L, editor: The biologic basis of dental caries, New York,
1980, Harper & Row.)
(Ahydrogen-ion concentration associated with dental caries activity, J Dent Res 23:257, 1944. , adapted
and redrawn from Stephan RM: Intra-oral )
Sturdavent 7th ed

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Oral Habitats
Sturdavent 7th edition

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The micro-environmental conditions in the habitats associated with host health are
generally aerobic, near neutrality in pH, and positive in oxidation-reduction potential.
Significant micro-environmental changes are associated with caries and periodontal
disease The changes are the result of the plaque community metabolism
.
Habitat Predominant Species Environmental Conditions within Plaque
Mucosa S. mitis Aerobic
S. sanguis pH approximately 7
S. salivarius Oxidation-reduction potential positive
Tongue S. salivarius Aerobic
S. mutans pH approximately 7
S. sanguis Oxidation-reduction potential positive
Teeth (non-carious) S. sanguis Aerobic
pH 5.5
Oxidation-reduction negative
Gingival crevice Fusobacterium Anaerobic
Spirochaeta pH variable
Actinomyces Oxidation-reduction very negative
Veillonella
Enamel caries S. mutans Anaerobic
pH <5.5
Dentin caries S. mutans Anaerobic
Lactobacillus pH <5.5
Root caries Actinomyces Anaerobic
pH <5.5

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Diet
Chemical nature of diet
• Type of carbohydrate
• Frequency of intake
• Contact time
• Calcium ,vitamin B &D
deficiency
• Higher levels of selenium
• Fluoride content
• Phosphates, molybdenum
and vanadium
Physical nature of diet
• Coarse and fibrous food
• Refined and sticky
starchy food

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Role of heredity
Genetic
modifications in
dental enamel,
immune response,
genetic regulation of
salivary function and
inherited alterations
in sugar metabolism
Senpuku et al (1998)
and Acton et al
(1999) have
correlated specific
HLA-DR types with
binding S.
Mutans antigens
and S.
Mutans colonization
Acton concluded
that ‘genes within
MHC modulate the
level of oral
cariogenic
organisms’
Bachrach and young
(1927) -showed that
the monozygotic
twins had a more
similar caries
incidence than
dizygotic twins and
that different-sex
dizygotic twins had
the greatest
variance
Mariani et al (1994)-
HLA-DR3- increased
enamel defects and
HLA-DR5, 7 -
reduced frequency
of enamel defects

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Role of immunity
Salivary IgA and GCF immunoglobulins (IgG, IgM and IgA) along with neutrophil leukocytes
and macrophages - prevention of dental caries
Immune response exerted by the gingival crevicular immune system is more potent
compared to the salivary immune mechanism
Salivary IgA - prevents S. mutans from adhering to the tooth surface,The IgG antibodies acting
as opsonins, facilitate phagocytosis and the death of S. mutans by the action of macrophages
and neutrophil leukocytes

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Time
When acid
challenges occur
repeatedly, the
eventual collapse
of enough enamel
crystals and
subsequently rods
will result in
surface
breakdown
This means that in
all mouths there is
continual
demineralization
and
remineralization of
enamel; therefore,
an individual is
never free of
dental caries
This may take
from months to
years, depending
on the intensity
and frequency of
the acid attack
The process of
enamel
demineralization
and
remineralization is
constantly cycling
between net loss
and gain of
mineral
It is only when the
balance leans
towards net loss
that clinically
identifiable signs
of the process
become apparent

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Role of carbohydrates
• Etiology of dental caries:
Bacteria + sugars + teeth organic acids caries
• Early studies by Miller showed teeth incubated in mixtures of
saliva and bread/sugar, decalcification occurred.
• No effect when meat or fat was used instead, cane sugar and
cooked starches produced acid, but little acid was formed
when raw starch was used.

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• Cariogenicity of dietary carbohydrate varies:
1. Frequency of ingestion
2. Physical form
3. Chemical composition
4. Route of administration
5. Other food constituents
• Glucose/sucrose via stomach tube or IV – No decay.
• Meals high in fat, protein or salt reduce oral retentiveness of
carbohydrate.

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Carious Dentin
3.→Infected carious dentin
2.→Affected Carious Dentin
1.→ Normal Dentin
3. = Bacteria Filling the tubules
Granular material in intertubular dentin
Little mineral , lacks cross banding of collagen
2. = Loss of mineral in intertubular and peritubular dentin
Many crystals in lumen of tubules
Dentin appears transparent Sturdevant- 7th Edition

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• Progression of caries in dentin is different from that in
overlying enamel
• Much more organic material in dentin, possesses microscopic
tubules - provide freeway for ingress of acids and egress of
mineral
Histological characteristics of dentinal caries
• The dentino-enamel junction has least resistance to
caries attack and allows rapid lateral spreading once
caries has penetrated enamel
Dentinal caries - v- shaped in cross section

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Dead Tracts
• Represent Empty Tubules Filled with
air
• Due to → Degeneration of
odontoblastic process (caries,
erosion, attrition etc)
• Initial step in fomation of sclerotic
dentin
• Black in transmitted light, WHITE IN
REFLECTED LIGHT
• Odontoblastic degeneration -Areas
of narrow pulp horns ↓ sensitivity
Orban’s- 12th edition

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Sclerotic Dentin
Reactive sclerosis
Deposition of Apatite Crystals &
Collagen in Dentinal Tubules.
• Blocking of tubules- Defensive reaction.
• Filled with H. A - Obliteration of Lumen- Peritubular Dentin.
• Refractive indices are equalized- Transparent

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SCLEROTIC DENTIN
• Fracture toughness
reduced
• Reduced Permeability
• Prolonged pulp vitality
• Resistant to Caries

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Tertiary dentin
• In response to dental caries, there may be production of more dentin toward the
direction of the pulp
• Protect the pulp for as long as possible from the advancing bacteria
• As more tertiary dentin is produced, the size of the pulp decreases
• If the odontoblasts survive long enough to react to the dental caries, then the
dentin produced is called "reactionary" dentin
• If the odontoblasts are killed, the dentin produced is called "reparative" dentin

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Dentinal Reaction To Caries
Sturdevant- 5th Edition
Slowly advancing
lesion
Moderate-
intensity attack
Severe,rapidly
advancing caries
Repair of demineralized
dentin by apposition of
peritubular dentin and
remineralization of
intertubular dentin
Results in bacterial
invasion of the dentin
Overpowers
dentinal defences
Sclerotic dentin
formation occurs ahead
of demineralization
“Dead tracts” formation
takes place
Results in
infection,abscess
and death of pulp
Function of sclerotic
dentin is to wall off
lesion by sealing
tubules
Replacement
odontoblasts
Reparative dentin on
the affected portion of
pulp chamber wall.
Reaction to a long-term, low-
level acid demineralization,
associated with slowly
advancing lesion
Reaction to a moderate –
intensity attack
Reaction to severe, rapidly
advancing caries

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Enamel zones
Translucent zone
Deepest zone , Structureless appearance, Pores or
voids form along the enamel prism, Pore volume
is 1%, 10times greater than normal enamel
Dark zone
Does not transit polarized light , Total pore
volume is 2 to 4 % ,periphery to 25% at the center
Body of the lesion
Largest portion of the incipient lesion while in a
demineralizing phase, Has largest pore volume
Surface zone -Unaffected by caries,Lower pore
volume than the body of the lesion
A, From Silverstone LM, et al. editors: Dental caries, London and Basingstoke, 1981, Macmillan, Ltd. Reproduced with permission of Palgrave Macmillan. B,
Courtesy Dr. Masatoshi Ando

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Stuurdavent 7th edition, Darling AI: The pathology and prevention of caries, Br Dent J 107:287–302, 1959

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Zones Of Dentinal Caries
Caries advancement proceeds through 3 changes :
Weak organic acid demineralize the
dentin
Organic material (collagen)
degenerates and dissolves
Loss of structural integrity → bacterial
invasion
Sturdevant- 5th Edition

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5.Reactive dentin
non specific defense reaction
of the pulp to injury
4.Zone of destruction
filled with masses of destroyed
dentin tissue, bacteria and their
metabolic products
3 Zone of bacterial invasion
increase number of destroyed
dentinal tubules
2 Dark Zone
increased loss of minerals
in the dentin
1. sclerotic zone
(translucent zone)
A demarcation zone
which separates an
affected tissue from
sound dentin

43
Carious dentin
Infected or outer
carious dentin
Affected or inner
carious dentin
INFECTED DENTIN AFFECTED DENTIN
Soft and demineralized dentin
teeming with bacteria
Demineralized dentin, not yet
invaded by bacteria
Collagen is irreversibly denatured Collagen cross linking remains
Cannot remineralize Can act as template for
remineralization
Soft necrotic tissue followed by
leathery dentin which flakes away
with an instrument
Discolored and softer than normal
dentin that doesn’t flake easily
Dyes : 0.5% basic Fushin in
propylene glycol stains only
irreversibly denatured collagen
Does not stain with caries
detecting dye

44
Faculty of Dental Sciences©M. S. Ramaiah University of Applied Sciences
44
Histology of carious tissue, modified from Innes et al
and Ogawa et al
P athophysiology of Dental Caries , G eorg Conrads et al

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Pulpal reactions to caries
Pulpal Responses to Caries and Dental Repair
A.J. Smith School of Dentistry, University of
Birmingham, UK caries research
Decrease in
dentin
permeability
Tertiary Dentin
Formation
Inflammatory
and immune
reactions

46
Decrease in dentin permeability
Pashley, E. L., Talman, R., Horner, J. A., & Pashley, D. H. (1991). Permeability of normal versus carious dentin. Dental Traumatology, 7(5), 207–211.
Increase the deposition
of mineral crystals in
intratubular dentin
Narrowing the dentinal
tubules
Decrease in dentin
permeability
Channels of
diffusion – Dentinal
tubules
More no of tubules
per unit area
towards pulpal side
as compared to
peripheral dentin
Fluid permeation is
proportional to
Tubule diameter
and number
Permiation of
coronal dentin >
radicular dentin
(fogel hm et al)
Clinical importance
– Dentin beneath a
deep cavity
preparation is more
permeable than
dentin underlying a
shallow cavity

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Tertiary dentin formation
• Not the most effective pulpally mediated defense
• The resultant dentin character is highly dependent on the stimulus
• Mild carious lesion - odontoblasts activate to elaborate the organic
matrix of dentin, similar in morphology to physiologic dentin and
may only be apparent due to a change in the direction of the new
dentinal tubules
• In aggressive carious lesion- repopulation of the disrupted
odontoblast layer with differentiating progenitors, forming
reparative dentin, its morphology can range from organized tubular
dentin to more disorganized irregular fibrodentin
Acidic byproducts of
the carious process
Degrade the
dentin matrix
Liberate bioactive
molecules
sequestered during
dentinogenesis
Reassume their
role indentin
formation

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Inflammatory And Immune Reactions
• Early inflammatory response - focal accumulation of chronic
inflammatory cells
• It is mediated;Initially by odontoblasts; the most peripheral cell in
the pulp, and encounter foreign antigens first & later by dendritic
cells, which are responsible for antigen presentation and stimulation
of T lymphocytes
• In the most advanced phase of carious destruction, the immune
response is accompanied by immuno-pathologic destruction of
pulpal tissue

49
Initially- inflammatory reaction within the pulp and subsequent
reactions will depend on the degree of healing that takes
place and on repair reactions , tertiary dentinogenesis
modifies permeability
The latter permeability may profoundly affect the degree and
extent of pulpal inflammatory responses to caries [Reeves
and Stanley, 1966; Bergenholtz, 1990]
Pulpal inflammation may be observed even at the earliest
stages of enamel caries [Brännström and Lind, 1965] when
the response is likely to be low grade and chronic in nature
A less pronounced cariogenic injury to the dentine-pulp
complex was recent-ly observed on precavitated enamel
lesions [Bjørndal etal., 1998] showing only changes in the
subodontoblastic region
Moreover, arrested enamel lesions had no similar
disorganisation, which indicates the reversible nature of the
response

50
• Two distinct populations of dendritic cells:
•CD11c+ found in the pulp/dentin border and subjacent
to pits and fissures.
•F4/80+ concentrated in the perivascular spaces in the
subodontoblastic zone and inner pulp
• Odontoblasts play a role in the humoral immune response to
caries
• Immunoglobulin(Ig)G, IgM, and IgA have been localized in
the cytoplasm and cell processes of odontoblasts in human
carious dentin, suggesting that these cells actively transport
antibodies to theinfection front

51
Conclusion
Overall, a carious lesion should be regarded
as a dynamic process
Its progression does not only depend on the bacterial
infiltration and the local environment, but also on the
host pulp response

52
https://www.youtube.com/watch?v=PP1GiWVorPQ

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References
• Shafer's textbook of oral pathology 6th edition
• Sturdevant's art and science of operative dentistry 6th and 7th
edition 2019
• Orban’s- 12th edition
• P athophysiology of dental caries , G eorg conrads
• Modified from keyes ph, jordan hv: factors influencing initiation,
transmission and inhibition of dental caries. In harris rj,
editor: mechanisms of hard tissue destruction, new york, 1963,
academic press

54
• Redrawn from morhart r, fitzgerald r: composition and ecology of
the oral flora. In menaker l, editor: the biologic basis of dental
caries, new york, 1980, harper & row
• Pathogenesis of pulpitis resulting from dental caries, j endod. 7;52
trowbridge et al
• Pulpal responses to caries and dental repair A.J. Smith school of
dentistry, university of birmingham, UK caries research
• Pashley, E. L., Talman, R., Horner, J. A., & Pashley, D. H. (1991).
Permeability of normal versus carious dentin. Dental traumatology,
7(5), 207–211
• A hydrogen-ion concentration associated with dental caries
activity, j dent res 23:257, 1944
• Approximate proportional distribution of predominant cultivable
lora of ive oral habitats.(From Simón-Soro Á, Tomás I, Cabrera-
Rubio R, et al: Microbial geography of the oral cavity, J Dent
Res92:616, 2013

55
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