Dental caries /certified fixed orthodontic courses by Indian dental academy

Dental Caries

INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
www.indiandentalacademy.com

Contents
 Introduction
 History
 Definitions
 Epidemiology
 Classification
 Carious process
 Concepts of caries development


 Plaque
 Host factors-tooth ,saliva
 Substrate
 Socioeconomic factors
 Summary
 References


Introduction
 Dental caries is the most common chronic
disease (5 billion people worldwide)

 It is costly in terms of time and work hours lost,
money spent. In addition the expense incurred
in education of health professional required to
cope with this disease in terms of prevention,
treatment and oral rehabilitation.


HISTORY
 Aristotle, Hippocrates and Shakespeare have all
written on dental caries in their writings.
 Some theories put forward are the Worm theory,
Vital theory etc.
 L. S. Parmly (1819)-first contributed to current
understanding of caries mechanism
 Emil Magitot experimented using Pasteur
findings. He produced artificial carious lesions in
extracted teeth.


 W.D.Miller (1890) Chemo parasitic theory.
 Gottlieb (1941) – Proteolysis theory.
 Schatz & Martin(1955) –Proteolysis chelation
theory.


Definitions
 Dental caries is a microbial disease of the
calcified tissues, characterized by
demineralization of the inorganic portion and
destruction of organic portion of the tooth.
(Shafer)
 Dental caries is an infectious microbiologic
disease of the teeth that results in localized
dissolution and destruction of the calcified
tissues. (Sturdevant)

 Dental caries is defined as a progressive,
irreversible multifactorial in nature affecting the
calcified tissues of teeth, characterized by
demineralization of the inorganic portion and
destruction of organic portion of the tooth.
(Soben peter)


EPIDEMIOLOGY
 Prehistoric man skulls-very infrequent caries.
attributed to rough coarse nature of food
consumed.
 Exposure to processed foods, refined
carbohydrates, soft drinks and snacks has been
shown to increase the frequency of caries.


Epidemiology
 Decline in caries prevalence in developed
countries.
 Increasing prevalence of caries in less developed
countries.
 Polarization of caries


 Most common epidemiologic measure of caries
is evaluation of measure of permanent teeth that
are diseased, missing or filled (DMF)
 Either reported as no of teeth (DMFT) or no of
surfaces (DMFS) affected.
 A cumulative index.
 But over-estimates the prevalence of caries.


Geographical differences
 More remote areas of world with less access to
refined foods shows decreased incidence of
caries.
 Caries often rightly called Disease of the
civilization


Family differences
 More caries rate seen in siblings of individuals
with high caries rates & less incidence seen in
siblings of caries immune individuals.
 Children of high caries incident parents shows
higher caries incidence.
 Attributed mainly to genetic factors such as
tooth morphology, salivary flow rate and also to
dietary habits and oral hygiene habits of the
family.


Gender
 Girls show high caries incidence than boys of
same age till early teens.
 Attributed to earlier eruption of teeth in girls
because of early growth spurt.
 Significant as teeth are maximally susceptible to
caries immediately after eruption.


Age
 Even at age six around 20% of the children have
caries incidence in their permanent dentition.
 Most frequently involved is the first permanent
molar (six yr molar)


Caries susceptibility in permanent
dentition
 Sites ranked in decreasing order of occurrence
1) Fissure of the molars
2) Mesial & distal surface of first molars.
3) Mesial surface of second molars & distal surface of
second premolars.
4) Mesial & distal surface of maxillary first premolars
5) Distal surface of canines & Mesial surface of
mandibular first premolars
6) Approximal surface of maxillary incisors

CLASSIFICATION
I. STURDEVANT
Based on - Location
- Extent
- Rate of progression


According to location:
a. Primary caries
b. Caries of pit and fissure origin
c. Caries of enamel smooth surface origin
d. Backward caries
e. Forward caries
f. Residual caries
g. Root surface caries
h. Secondary (recurrent) caries

 According to extent:
a. Incipient (reversible) caries
b. Cavitated (irreversible) caries

 According to rate of progression:
a. Acute (rampant) caries
b. Chronic (slow or arrested) caries


II. DCNA:
According to tooth type:
a. Deciduous (A-T)
b. Permanent (1-32)
According to anatomic site
a. Pit and fissure caries
b. Smooth surface caries- inter proximal, cervical
c. Root surface caries

According to hard tissue affected:
a. Enamel
b. Dentin
c. Cementum Others:
a. Primary caries & secondary caries
b. Nursing caries
c. Radiation caries
d. Rampant caries


III.GORDAN
Based on
1. Morphology (anatomical site )

2. Dynamics (severity and rate of
progression)
3. Chronology (age patterns)


 According to morphology:
a. Occlusal pit and fissure and smooth
surface caries
b. Root caries
c. Linear enamel caries (Odontoclasia)

 According to rate of progression:
a. Rampant caries
b. Incipient caries
c. Arrested caries
d. Recurrent caries
e. Xerostomia induced caries (radiation caries)


Black’s classification of tooth
preparation
 Class-I: - caries on the occlusal surfaces of
molars and premolars
- occlusal 2/3 of the buccal and lingual
surfaces of molars
- lingual surfaces of the anterior teeth.
 Class II- restorations on proximal surfaces of
posterior teeth.
 Class III- restorations on anterior teeth that do
not involve the incisal angles.


 Class IV- Restorations on anterior teeth that
involve the incisal angles.
 Class V- Restorations on all gingival third of
facial or lingual surfaces of all teeth (except pit
and fissure lesions)
 Class VI- restorations on incisal edge of anterior
teeth or the occlusal cusp heights of posterior
teeth.
proposed by Siomon


1. Simple caries: one
surface is involved

2. Compound caries:
two surfaces are
involved

3. Complex caries: three
or more surfaces are
involved


WHO classification
 The shape and the depth of the carious lesion
can be scored on a 4 point scale
 D1 -Clinically detectable enamel lesions with
intact (non cavitated) surfaces
 D2 -Clinically detectable cavities limited to
enamel
 D 3 -Clinically detectable lesions in dentin (with
and without cavitation of dentin)
 D 4 – Lesions into the pulp.

Mounts classification
 According to site and size of the lesion
 Site 1- pits,fissures and enamel defects on
occlusal surfaces of posterior teeth or other
smooth surfaces, such as cingula pits on anterior
teeth.
 Site 2- Approximal enamel immediately below
contact areas with adjacent teeth
 Site 3- the cervical third of the crown or
following gingival recession, the exposed root
surface.

According to the size
 Size 1- Minimal involvement of the dentin but
beyond treatment by remineralization alone.
 Size 2- moderate involvement of dentin.
following cavity preparation, remaining enamel
is sound, well supported by dentin and unlikely
to fail under normal occlusal load.


 Size 3- enlarged beyond moderate. Remaining
tooth structure is weakened to the extent that
cusps or incisal edges are split or likely to fail if
left exposed to occlusal or incisal load. The
cavity needs to be further designed to provide
support and protection to the remaining tooth
structure.
 Size 4- extensive caries with bulk loss of tooth
structure.


Classification of root caries
Grade I ( Incipient)
 Surface texture: Soft, can be penetrated with a Dental
Explorer
 No surface defect

 Pigmentation: variable; Light tan to brown

Grade II (shallow)
 Surface texture: Soft, irregular, rough can be
penetrated with a Dental Explorer
 Surface defect (<0.5mm in depth)


 Grade III (Cavitation)
 Surface texture: Soft, can be penetrated with a Dental
Explorer
 Surface defect: Cavitation present (> 0.5mm in
depth): no pulpal involvement

 Grade IV (pulpal)

 Deeply penetrating lesion with pulpal or root canal
involvement.

From Billings (1986)

Ekstrand classification
 Three criteria used in the classification
 Visual, Radiographic and Histological
examinations

Caries research1998;32;247-254

Visual examination
0 –No or slight change in enamel translucency after
prolonged air drying(>5 sec)
1 –Opacity (white) hardly visible on the wet surface but
distinctly on the wet surface after air drying.
1 a- Opacity (brown) hardly visible on the wet surface but
distinctly on the wet surface after air drying.
2- Opacity (white) distinctly visible without air drying.
2a- Opacity (brown) distinctly visible without air drying.
3 –Localized enamel breakdown in opaque or discoloured
enamel and /or greyish discolouration from underlying
dentin.
4- Cavitation in opaque or discoloured enamel exposing the
underlying dentin.


Radiographic examination
0- No radioluscency visible
1- Radioluscency visible in the enamel
2- Radioluscency visible in the dentin but
restricted to the outer third of the dentin
3- Radioluscency extending to middle third of the
dentin
4- Radioluscency in the pulpal third of the dentin


Histological examination
0- No enamel demineralization or a narrow surface zone
of opacity (edge phenomenon)
1- Enamel demineralization limited to outer 50% of
enamel layer
2- Demineralization involving between 50% of the enamel
and1/3rd of dentin
3- Demineralization involving middle1/3rd of dentin
4- Demineralization involving inner 1/3rd of dentin


PIT AND FISSURE CARIES
 Limited to the – occlusal surfaces of
molars and premolars
- buccal pits of molars
- lingual surfaces of
maxillary anterior teeth
 Poor self cleansing features
 Usually occurs before smooth surface caries
 Clinically - black or brown in
color
- slightly soft consistency
- “catch” the tip of a fine
explorer
 Adjacent enamel appears bluish white
 “Internal Caries”

Smooth Surface Caries
 Develops on - proximal surfaces of the teeth
- gingival third of the buccal and
lingual surfaces (cervical caries)

 Preceded by the formation of dental plaque.

 Usually initiate just below the contact point.

 Clinically- initially as faint white opacity or yellow
brown pigmented area.

 Adjacent enamel appears bluish white.


Cervical Caries
 Appears as crescent shaped lesion.
 May extend proximally.

 Almost always an open cavity.

 Lack of oral hygiene on the part of patient.


Backward Caries
 Lateral spread of the lesion along the DEJ
exceeds the caries in the contiguous
enamel, caries extends into this enamel
from the junction.


Forward Caries
 Caries cone in enamel is larger or at least
the same size as that in dentin


Residual Caries
 Caries that remains in a completed cavity
preparation
 Not acceptable if - present at DEJ

- prepared enamel wall




Root Surface Caries
 In old age patients
 Initiates at the surface of a mineralized
dentin and Cementum which have greater
organic content
 Usually have rapid clinical course


Recurrent (secondary) caries:
 Occurs at the junction of the
restoration and the
cavosurface of the enamel
 May extend beneath the
restoration
 Indicates unusual
susceptibility to caries attack,
poor cavity preparation,
defective restoration.
 Also indicates presence of
microleakage.


Incipient (reversible) caries:
 First evidence of caries activity
in enamel
 Clinically as white opaque
region
 Subsurface demineralization
has occurred but no cavitation
 May take up extrinsic stains
 May undergo remineralization-
called as “caries reversibility”
or “consolidation” of early
enamel carious lesion


Cavitated (irreversible) caries:
 Lesion that has
advanced into dentin
with broken surface
 Remineralization is not
possible
 Treatment include cavity
preparation and
restoring with suitable
material.


Linear enamel caries
(odontoclasia):
 Atypical form of dental
caries in primary dentition
 Lesion predominates on the
labial surface of the
maxillary anterior teeth in
the region of neonatal zone
 Lesion is crescent shape
 Increase caries susceptibility
of posterior teeth.


 Odontoclasia:
- variant of linear enamel caries
- results in gross destruction of the
labial surfaces of incisor teeth
- cause may be an inherent
structural defect


Acute dental caries:
 Rapid clinical course resulting in early
pulp involvement
 Frequently in children and young adults

 Entry of lesion remains small while rapid
spread along the DEJ
 Clinically appears light yellow in colour

 Pain is often present


Chronic dental caries
 Common in adults
 Large entrance of the lesion

 Dentin is stained deep brown

 Moderate lateral spread of caries at DEJ

 Pain is not a common clinical finding.

 Slowly progressive lesion that involves
pulp much later


Rampant caries:
 Sudden and rapid onset and
almost uncontrollable
destruction of teeth
 Involves teeth that are
ordinarily caries free
(mandibular incisors)
 Ten or more new
increments of carious lesion
in one year


Nursing Bottle (Infancy or Soother)
Caries
 Rapidly progressing caries
affecting primary dentition usually
during first 2 years of life
 4 maxillary anterior are affected
first
 If unchecked, maxillary and
mandibular molars may also get
involved
 Lower anterior are spared
(characteristic feature)


Adolescent caries:
 Acute caries attack at 11-18
years of age
 Lesion in teeth and surfaces
that are relatively immune to
caries
 Small opening in enamel with
extensive undermining
 Rapid clinical course
 Little or no secondary dentin
formation


Arrested caries:
 Caries which becomes static or
stationary and does not show any
tendency for progression
 Almost exclusively occurs on
occlusal surfaces
 Both dentitions are affected
 Lesion appears as large open cavity
with lack of food retention
 Superficially softened and
decalcified dentin gets burnished
and has brown stained polished
appearance
“Eburnation of dentin”


Xerostomia induced caries (radiation
caries)
 Complication of radiation
therapy of oral cancer lesion
 Radiation induced
xerostomia produces caries
conducive environment
 Carious lesion develops as
early as 3 months after onset
of xerostomia
 May be caused by other
factors like salivary gland
tumors, autoimmune
diseases, prolong illness

Senile Caries
 Caries activity that spurts up during the
old age.
 They are located exclusively on the root
surfaces of the teeth.
 Also seen in association with partial
denture clasps.
 Causes: gingival recession, decreased
salivary secretion, poor oral hygiene.


Occult Caries / Hidden Caries
 Not clinically diagnosed, but detected
only on radiograph.
 Seen in persons with low caries index
suggestive of increased fluoride exposure.
 Also called as fluoride bombs or fluoride
syndrome


ETIOLOGICAL THEORIES
Early theories

Endogenous theories

Exogenous theories


EARLY THEORIES
1. The Legend of the Worm:


ENDOGENOUS THEORY
Humoral Theory
“dental caries is produced by internal
action of acrid and corroding humors”

Vital Theory
“tooth decay originated, like bone
gangrene, from within the tooth itself”


EXOGENOUS THEORY
Chemical (Acid) theory:
“ teeth are destroyed by acids formed in the
oral cavity ”

Parasitic (Septic) theory:
“ microorganisms are associated with
carious process ”


Acidogenic Theory
 Proposed by W.B.Miller 1890, most accepted
 “Acids formed due to the fermentation of dietary
carbohydrates by oral bacteria leads to progressive
decalcification of tooth structure with subsequent
disintegration of organic matrix.”
 He isolated micro-organisms from his experiments &
stated that many were involved in the carious process.
 3 important factors which can influence process of
tooth destruction in process of dental caries:
Dietary carbohydrates, micro-organisms and acid


 Limitations

 Did not explain sub-surface
demineralization
 Failed to justify rampant caries
 Did not explain caries in impacted
tooth
 Phenomenon of arrested caries is
not explained
 Smooth surface caries is not
accounted in this theory


Proteolytic Theory
 Proposed by Glottlieb in 1941.
 “formation of dental caries is essentially proteolytic
process. Bacteria present produce hydrolytic enzymes
and cause proteolysis leading to the dissolution of
organic substance.”
 Microorganisms invade the organic substance first.
 He did admit that, acid formation accompanied the
proteolysis.
 Yellow pigmentation of dental caries is because of
pigment production by proteolytic organism.
 Caries is initiated at slightly alkaline pH.

Limitations:
 In vitro studied didn’t prove the proteolytic
process of caries.
 Proteolytic bacteria are uncommon in oral
cavity.
 Didn’t explain about the role of sucrose, pH
and fluoride in dental caries.
 Protein content of enamel is 0.6%. So,
initiation of caries by proteolytic process is
questionable.


Proteolytic-chelation Theory
 Proposed by Schwatz in 1955.
 Stated that two processes are involved in caries –
proteolysis & chelation.
 Chelation is a process involving complexing of ions into
a complexing substance by covalent bond which results
in a highly stable, poorly dissociated and weekly ionized
compound called chelate.
 Bacterial attack on enamel is initiated by keratolytic
microorganisms.
 Eg: citrates, lactates
 Chelates are always –ve.


Limitations:
 Fails to make a mention of sugar and acid
production.
 Scientists proved that chelates are weak and
can not cause de calcification.
 Schwatz said, carbohydrates does not cause
acid production but it stimulates proteolysis,
which is not true.
 Lactobacillus in dental caries is because of
chelation and said that microorganisms are not
involved in caries.

Sucrose Chelation Theory
 If there is a very high concentration of sucrose
in mouth of a caries active individual, there can
be formation of complexes like calcium
saccharates, calcium complexing
intermediaries, etc by action of
phosphorylating enzymes

 These complexes cause release of Ca, P ions
from enamel and result in DC

 Limitations
 Sucrose readily gets metabolized to form acids,
hardly any scope for formation of calcium
saccharates, etc.
 Very high levels of pH required for formation of
Calcium saccharates, which is no achievable in
the oral cavity


Autoimmune Theory
 Few odontoblast cells at specific sites within
pulp of specific teeth are damaged by
autoimmune mechanism
 Due to this the defense capacity & integrity of of
enamel and dentin in those specific areas are
compromised and act as potential sites for caries
development in future


Sulfatase Theory
 Proposed by Pincus in 1951.
 Bacterial sulfatases hydrolyses the mucoitin
sulfate of enamel and chondroitin sulfate of
dentin producing sulfuric acid that in turn
causes decalcification.
 Limitation:
Sulfated polysacharide in enamel is very
small and not readily accessible as a substrate
for enzymatic degradation. So, this is highly
unlikely hypothisis for the degragation of
tooth enamel.

Levine’s theory
 Proposed by Levine in 1977.
 Established chemical relationship between enamel,
plaque and factors which favors the movement of
minerals between them.
 Also called as “SEW – SAW” mechanism.
 Said enamel demineralization and remineralization is a
continuous process.
 Movement of ions between enamel and plaque occurs in
both direction which depend upon
- plaque ph
- calcium and phosphate ions at the interface
- fluoride ion concentration


CURRENT CONCEPTS IN CARIES ETIOLOGY

Cariogenic
Keyes 1960 bacteria (dental
plaque)

Traditional
concept
Host factors: Diet:
Tooth Fermentable
Saliva carbohydrate


Newbrun’s concept


Characters
of caries Fejerskhov and Manji 1990
Social class

Modern
Flow rate
concept Education
Saliva Composition
Income
Buffer

Microbial Fluoride
species Biofilm Tooth
Biological Genetic
determinants Time
Composition
Diet Sugar
Behavior
Frequency Attitude

Socio-
economical factors Knowledge

TEETH
 Morphology:
 Accentuated pits and fissures
 Enamel hypoplasia
 Mottled enamel
 Bucco-lingual width of carious teeth
 Position:
 Malpositioned teeth
 Rotated teeth


3. Composition:
 Surface vs subsurface enamel


DIET
 Carbohydrate is a cariogenic diet
Cariogenicity is based on
1. Physical nature
2. Chemical nature
3. Mode of intake
4. Clearance rate
5. Frequency of intake
6. Other dietary factors


PLAQUE AND
MICROORGANISMS
PLAQUE:
 The concept about dental plaque was first
proposed by Williams in 1897
 Consist of

- salivary component- mucin
- desquamated epithelial cells
- microorganisms
- calcium and phosphate


To produce caries, micro organisms should
have following properties:
1. Should be acedogenic.
2. Should be aceduric.
3. Should posses attachment mechanism.
4. Should have the capacity to store
sucrose.
5. Should be able to synthesize
extracellular glucans.


1. Pioneer / primary bacteria – initiate caries
 S.mutans (smooth surface caries)

 Lactobacillus acidophilus (pit & fissure
caries)
 Actinomyces (root surface caries)

2. Invaders / secondary bacteria
 Staphylococcus, Veillonellae


Streptococci mutans:
 Chief etiological agent in dental caries disease
1. it can produce low pH (acidogenic)
2. it can survive in low pH (acidouric)
3. utilize sucrose at a faster rate than other
bacteria
4. can metabolize sucrose to synthesize glucan
and fructan ( attachment mechanism )
5. it can store intracellular glycogen amylopectin type
polysaccharides that act as a reservoir of substrate and
prolongs its metabolic activity


Other Bacteria
 Lactobacillus acidophilus
 Found in carious dentin & saliva of persons with high
caries activity
 Release lactic acid
 Actinomyces
 Found esp. in root caries
 Acidogenic
 Attachment to tooth by glycoprotein called Lectin


Acids produced are
a) Lactic acid
b) Acetic acid
c) Butyric acid
d) Propionic acid

e) Traces of formic acid
 Lactic acid is the strongest acid


Plaque pH:
 Critical pH- 5.5
 Caries active, pH- 5 to 5.5
 Caries immune, pH- 6.8

STEPHEN’S CURVE


Concept of critical pH
 pH at which any particular saliva ceases to be
saturated with calcium and phosphorus ions is
referred to as critical pH.
 Below this value the inorganic constituents
dissolve .
 With conc. of H+ ions, more phosphate ions
leave the solid apatite phase.
 Above this pH the remineralization takes place


STEPHAN CURVE

Approximately twenty minutes after ingestion of sucrose, and once the supply of
fermentable nutrients is exhausted, the bacterial will cease to produce acids and the
plaque pH will gradually return to a slightly alkaline resting level.


MINOR FACTORS
I. SALIVA:
1. Flow rate
2. Viscosity
3. Buffering capacity
4. Amount of saliva

Components of saliva:
 Bicarbonates
 Anti-bacterial agents
 Ig-A
 Salivary urea and bicarbonates


II. Dietary factor
 Diet containing Phosphates decreases caries
 Proteins & fat also prevents or decreases caries, as they
prevent attachment of carbohydrates to tooth
 Trace elements of Vanadium & Molybdenum decreases caries
 Selenium increases risk of caries
 Vitamin A & B are important in formation of hard tissues.
Thus if they are deficient, hypoplasia of teeth is seen, teeth
more prone to caries
 Fibrous food help in cleansing of teeth, removal of lodged
food

III. Hereditary factors:


HISTOPATHOLOGY
Important for:
1. Research purpose
2. To know the changes taking place in dental
caries
 Not important for diagnosis.
Studied under:
 Light microscope
 Electron microscope
 Polarized microscope


Histological Features of early
enamel caries
 Loss of inter-rod substance
 prominent enamel-rods
 Appearance of transverse
striations of enamel rods due
to segmental demineralization
 Accentuation of incremental
striae of Retzius

Preferential loss of Interprismatic
Substance


Histological Features of Advanced enamel caries
Classified on the basis of pore volume and
mounting media used
 Zone 1 – Translucent zone
 Zone 2 – Dark zone
 Zone 3 – Body of lesion
 Zone 4 – Surface zone
 These zones are from the dentin towards the outer enamel
surface


NORMAL ENAMEL

DEJ

SURFACE LAYER

BODY OF THE LESION

DARK ZONE

TRANSLUSCENTZONE


Translucent Zone
 Is deepest & forms advancing front of lesion
 Not seen always, seen in 50% of cases. When
seen, appear clear due to mounting media
which enters these big pores making them look
clear/bright
 Pore volume is 1%, which is more than normal
(0.1%)
 Zone cant be easily identified clinically /
radiographically


Dark zone / positive zone
 Dark zone as mounting media cant penetrate this zone.
Positive zone as it is always present
 Pore volume – 2-4%. 2 types of pores seen here  large
& small
 Initially only large pores, later change to micro-pores.
This change mainly due to demineralization occurring in
deeper areas which release ions & there is
remineralization of superficial areas
 This zone is narrower in rapidly advancing caries &
wider in slowly advancing caries


Dark zone / positive zone


Body of the lesion
 Largest zone, between dark & surface zone
 Greater amount of demineralization taking place.
Pore size – 5-25%
 5% variation is near periphery, 25% at center
 Prominent striae of Retzius due to
demineralization of inorganic minerals
 Contains apatite crystals larger than that found
in normal enamel


Body of the lesion


Surface Zone
Quite intact, appears radio-opaque

 Unaffected despite subsurface

demineralization; may be due to:
 surface remineralization by

salivary ions

 More amount of fluoride


Dentinal Caries
 Once lesion spreads to DEJ, there is lateral

spread of caries

 Surface enamel gets unsupported enamel

rods  enamel #  greater cavitation

 Zones of dentinal caries.

 Zones start from pulpal side towards

dentinal side


1. Zone of Fatty Degeneration of Tomes’ process

2. Zone of Sclerosis

3. Zone of Decalcification without Bacterial

Invasion

4. Zone of Decalcification with Bacterial Invasion

5. Zone of Decomposed Dentin / Infected dentin


DENTINAL CARIES

Zone of
Decomposed Zone of
dentin Dentinal Retreating
Zone of Zone of Odontoblastic
sclerosis Fatty
Bacterial process
invasion Zone of degener
Demineralisation ation

INFECTED DENTIN AFFECTED DENTIN

Fatty Degeneration of Tomes’
Process
 Innermost layer of dentinal caries towards pulp
 Due to deposition of fatty tissue in odontoblastic
processes
 Seen usually in rapidly progressing caries
 No crystals or bacteria in lumen of tubules
 Intertubular dentin  normal


Zone of Sclerosis/Sub-Transparent
Dentin
 As the microorganisms cause destruction to dentin,
initially there is an attempt to stop the
advancement of caries by depositing the minerals.
 There is a deposition of mineral in intertubular
dentin.
 Zone is called “transparent zone”
 Odontoblasts are also start depositing dentin.
 At the periphery of sclerotic dentin, dead tracts are
present.


Zone of Decalcification without
Bacterial Invasion / Transparent
Dentin
 Decalcification is by bacterial acid diffusion
 Very narrow zone, softer than normal dentin
 Further loss of minerals from inter tubular dentin
 Large crystals within lumen of dentinal tubules


Zone of Decalcification with
Bacterial Invasion / Turbid Dentin
 Initially only few tubules are involved & micro-orgs also
less
 These are acidogenic, pioneer bacteria (initiators),
present long before lesion is clinically detected
 Bacteria multiply within tubules & are seen in advancing
front of lesion


 Walls of tubules are thin & when micro-orgs
penetrate, they cause irregularities/distensions
of walls  ROSARY BEAD appearance
 Later, bacteria have proteolytic activity, areas of
proteolysis appear as spaces containing necrotic
material & bacteria
 These areas  “Liquefaction Foci of Miller”.
 These areas vary in number & are parallel to
dentinal tubules


Zone of Decomposed Dentin /
Infected Dentin
 Outermost zone, large scale

destruction of dentin

 Foci of Miller join together

 Areas of dentin decomposition,

occur perpendicular to dentinal

tubules  “Transverse Clefts”


 Mechanism of formation of Clefts - not known
 May follow course of incremental lines or
 May result from coalescence of liquefaction of
adjacent tubules
 Also may rise by extensive proteolytic activity along
interconnecting lateral branches of odontoblastic
processes
 Bacteria shift from dentinal tubules to the peri & inter
tubular dentin


Secondary / Reactionary dentin

 Protective mechanism to protect pulp

 Develops as a result of localized, non-specific irritation

to odontoblasts

 Hyper mineralized, less number of dentinal tubules

having irregular & torturous course


Root Caries / Cemental Caries
Histopathology:
 Outer surface of
cementum – hyper
mineralized, thus more
caries resistant
 Resistance due to
 Reprecipitation of
minerals from within
 Precipitation of
minerals from Plaque


 Clefts formed, through which bacteria
penetrate & cause tooth structure
destruction
 Penetration occurs along course of
Sharpey's fibers
 Once cementum completely exposed &
destroyed, underlying dentin is involved


Microorganisms found in various
types of carious lesions
Pit and fissures S.mutans,
S.sanguis,lactobacillus
sp.actinomyces
Smooth surface caries S.mutans, S.salivarius

Root caries Actinomyces viscosus,
A.naeslundii, s.mutans,
s.sanguis,s.salivarius
Deep dentinal caries Lactobacillus sp,
Actinomyces viscosus,
A.naeslundii

Human longitudinal interventional
studies
1) Vipeholm studies-Gustaffson et al 1954
2) Turku sugar studies-Schenin, Makinen 1975
3) Hereditary fructose intolerance-Newbrun 1969
4) Hopewood house-Sullivan & Harris
5) Von der Fehr et al(1970) and Loe et al(1972)


Vipeholm studies-Gustaffson et al
1954
 Five yr interventional study by Gustaffson et al
on 436 inmates in a mental institution in
Vipeholm district hospital, Sweden.
 It was done to determine the relation between
caries and sugar consumption
 The experimental design divided inmates into 7
groups.


Experimental groups
1) Control group-low sugar diet only at meals
2) Sucrose group-high sugar mostly in drinks with
meals
3) Bread group-received sugar intake half or equal
to normal in sweetened bread at meals
4) Caramel group-22 sticky candies in two
portions at meals or 4 portions between meals.


5) 8 toffee group-8 toffees in two portions at
meals or 4 portions between meals
6) 24 toffee group-24 toffees at their pleasure
throughout the day
7) Chocolate group-given milk chocolates in 4
portions between meals.


Conclusions
 Consumption of sugar is associated with only
slight increase in caries incidence if ingestion is
limited to meal times(4 times a day)
 In subjects with poor oral hygiene, consumption
of sugar both b/w meals & at meals is associated
with marked increase in caries incidence
 Caries activity subsides once sugar rich foods are
withdrawn from diet


 In subjects with poor oral hygiene, caries
develops despite avoidance of sugar.
 Increase in caries activity varies widely between
individuals


Turku sugar studies-Schenin,
Makinen 1975
 Done in Turku, Finland (1972-1974)
 Done to study effect of dental caries in almost
total substitution of sucrose with fructose or
xylitol.
 125 young adults divided into 3 groups.
 Sucrose -35,fructose -38, xylitol-52
 Evaluated by two standardized bitewing
radiographs on each side of mouth

 Results –dramatic reduction in caries prevalence
was seen after two yrs of xylitol consumption.
 Fructose was as cariogenic as sucrose in 1st 12
months but became less cariogenic at end of 24
months.


Turku sugar studies
7
Sucrose
Fructose
6 Xylitol

5

4

3

2

1

0
0 2 4 6 8 10 12 14 16
www.indiandentalacademy.com 18 20 22 24 Month

Hopewood house-Sullivan & Harris
 Study was done on institutionalized children aged 3-14
yrs residing at Hopewood house, Bowral, New South
Wales, Australia.
 The main feature was absence of meat and rigid
restriction of refined carbohydrates. The meals were
supplemented by vitamin concentrates and occasional
serving of nuts and honey.
 At end of 10 yr period, DMFT index score was 1.1 just
10% of the score of other state schools in Australia.


 As the children grew older and moved out of
Hopewood house,they no longer adhered to the
original diet and there was a steep increase in
DMFT index again.
 Thus this study demonstrated that dental caries
can be reduced by restricted diet even in absence
of beneficial effects of fluoride and unfavorable
oral hygiene.
 But the resistance is not permanent.


PREVENTION OF DENTAL
CARIES

“An ounce of prevention is worth a
pound of dental cure”.
-Old Dental Public Health Proverb


AIMS OF PREVENTION

 AIMS OF PREVENTION (Sturdevant):

1. Limiting pathogen growth & metabolism

2. Increasing resistance of tooth surface to demineralization

3. Caries control methods which include operative

procedures

CLASSIFICATION OF METHODS FOR
PREVENTION
 According to SHAFER:


CHEMICAL MEASURES

 Substances which alter tooth surface/structure
 Fluorine
 Bis-biguanides

 Silver nitrate

 Zinc chloride & potassium ferrocyanide

 Interfere with carbohydrate degradation
through enzymatic alterations
 Vitamin K
 Sarcoside

 Interfere with bacterial growth & metabolism
 Urea & ammonium compounds

 Chlorophylls

 Nitrofurans

 Penicillins

 Other antibiotics

 Caries vaccine

 Ozone technology


Mechanism Of Action Of Fluorides
 Increased enamel resistance/reduction in enamel
solubility
 Formation of fluorapatite

 Increased rate of post eruptive maturation
 Deposition of minerals in hypomineralized areas

 Remineralization of incipient lesions
 Enhances remineralization rate
 Larger crystals are formed

 Inhibition of demineralization
 Well formed surface layer also seen

 Interference with plaque microorganisms
 High conc-bacteriocidal
 Low concentration-bacteriostatic
 Enzymatic interference-enolase, protein-extruding
ATPase, sugar transport

 Modification in tooth morphology
 Smaller, shallow fissures


NUTRITIONAL MEASURES

 Diet counseling

 restriction of refined carbohydrates

 Phosphated diets

 Calcium phosphate rich diet.

 Sugar substitutes

 Non-caloric sweeteners-aspartame, saccharine

MECHANICAL MEASURES
 Dental prophylaxis
 Tooth brushing
 Mouth rinsing
 Dental floss
 Oral irrigators
 Detergent foods
 Chewing gum
 Pit & fissure sealants
 Preventive resin restorations

Summary
 Dental caries is an oral infection.
 Dental caries has a multi-factorial causation involving
the interaction of host factors (tooth surface, saliva,
acquired pellicle), diet, and dental plaque (biofilm).
 Besides these other modifying factors like
socioeconomic status and behavioral patterns also
greatly influence the caries process in a complex
manner.
 A good understanding of the caries process can help in
formulation of better diagnosis,prevention and
treatment of dental caries.


References
1) Sturdevant's Art and Science of Operative
Dentistry-5th edition
2) Cariology Ernest Newbrun- 3rd edition
3) Diagnosis & Risk prediction of dental caries-
Per Axelsson.
4) The biologic basis of dental caries-Lewis
Menaker
5) Essentials of Preventive and Community
dentistry- Soben Peter -2nd edition

Dental caries /certified fixed orthodontic courses by Indian dental academy

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