GOOD MORNING

GOOD MORNING
DENTAL CARIES
DENTAL CARIES
 INTRODUCTION
 PREVALENCE OF DENTAL CARIES.

 HISTORY OF DENTAL CARIES

 THEORIES OF DENTAL CARIES

a)Early theories

b)Modern theories
 ETIOLOGY OF DENTAL CARIES
 LOCAL FACTORS AFFECTING CARIES.
 CLINICAL CHARACTERISTICS OF LESIONS.
 CLINICAL CLASSIFICATION OF DENTAL
CARIES.
 HISTOPATHOLOGICAL FEATURES OF
CARIOUS LESIONS:
ENAMEL CARIES.
DENTINAL CARIES
CEMENTAL CARIES.
 PREVENTION OF DENTAL CARIES.
 CONCLUSION.
 REFERENCES
 DENTAL CARIES
LATIN MEANING– DRY ROT
MEANING SLOW
DISINTEGRATION THAT MAY
AFFECT ANY OF THE BIOLOGICAL
HARD TISSUE AS A RESULT OF
BACTERIAL ACTION.
• SHAFER:

DEFINED AS THE MICROBIAL

DISEASE OF THE CALCIFIED
TISSUES OF THE
TEETH,CHARACTERISED BY
DEMINERALISATION OF THE
INORGANIC PORTION AND
DESTRUCTION OF THE ORGANIC
SUBSTANCE OF THE TOOTH.
 PREVALENCE OF DENTAL CARIES:

 More prevalent in modern man in highly industrialised

society.
 INTERDEPARTMENTAL COMMITTEE ON NUTRITION AND
NATIONAL DEFENCE(ICNND)and
WHO studies:
Lowest – Asia &African countries.(0.5 – 1.7DMFT)
Low to moderate—Malaysia, Thailand, Burma,
Vietnam, China,
India &New guinea (4.5DMFT).
High caries– Newzealand,Brazil,Australia & Argentina.
(5.6DMFT)
Highest– American & Other western countries s.(12-18
DMFT).
 HISTORY OF DENTAL
CARIES
 PREHISTORIC AGE:
DENTAL CARIES - A DISEASE OF
MODERN CIVILIZATION.

 ANTHROPOLOGICAL STUDIES :
SKULLS OF DOLICOCEPHALIC
MEN FROM PRENEOLITHIC
PERIOD - NO DENTAL CARIES.

SKULLS OF BRACHYCEPHALIC
MEN OF NEOLITHIC PERIOD -
CONTAINED CARIOUS TOOTH.
 MODERN SOCIETIES:
TODAY DENTAL
CARIES IS VIRTUALLY A UNIVERSAL
DISEASE AS CIVILIZATION HAS
PENETRATED TO ALMOST ALL AREAS
OF THE WORLD.
THE CHANGE IN DIET THAT IS
ESSENTIALLY PRIMITIVE TO ONE
CHARACTERISTIC OF HIGHLY
INDUSTRIALIZED SOCIETY INDICATES
THAT MODERN CIVILISATION AND
INCREASED DENTAL CARIES ARE IN
CONSTANT ASSOCIATION.
 THEORIES OF DENTAL
CARIES
 EARLY THEORIES:
LEGEND OF WORMS-HOMER:
Earliest reference to tooth decay
discovered around 5000bc on a clay tablet
excavated from the mesopotamian area.
Idea of this theory was that caries
is caused by worms was universal as evident
from the writings of Homer.
 ENDOGENOUS THEORY-GALEN:
Humoral theory advocated by greek
physician-proposed that dental caries was caused
by the internal action of acids and corroding
humors.
4 HUMORS:Blood
Phlegm
Yellow bile
Black bile.
HIPPOCRATES supported this theory and added that
accumulation of debris& stagnation of juices over
the teeth caused toothache.
 CHEMICAL THEORY-PARMLY:

Dental decay affected

externally not internally and that an
unidentified “chymal agent” was
responsible for caries.
ROBERTSON in 1835: dental
decay was caused by acid formed by
fermentation of food particles.
 PARASITIC THEORY-FICNUS:
Ficnus in 1847 attributed dental caries
to “denticolae” for decay producing
microorganisms.
LEBER&ROSENSTEIN-DENTAL
CARIES is purely chemical process and
microorganisms continued the disintegration.
UNDERWOOD&MILLES 1880-
explained that acid capable of causing
decalcification was actually produced by bacteria
feeding on organic fibrils of dentin.
 MODERN THEORIES:
1) Acidogenic theory –Miller.
bacteria+sugars+teethorganic
acidscaries
Role of carbohydrates.
Role of microorganisms.
Role of acids.
 LIMITATIONS OF MILLERS THEORY:
1)Unable to explain the prediliction of
specific sites on a tooth to dental caries
and the initiation of smooth surfaces was
not accounted.
2)Does not explain why some populations
are caries free and phenomena of
arrested caries.
3)Caries of partially erupted teeth was not
explained.
4)One accepted phenomena that carious
dentin if left under a filling continues to
decay remain unsolved.
 PROTEOLYTIC THEORY(GOTTLIEB-1944)
Gottlieb believed that instead of decalcification
of inorganic part as suggested in Millers theory,the
initial action is due to proteolytic enzymes attacking
the lamellae,rod sheaths,tufts and walls of the
tubules etc ie.. All organic components.
Once the inorganic part is set free, after
the dissolution of organic part,the salts are
dissolved subsequently by acidogenic bacteria.
According to go Gottlieb staphylococcal
species are said to play vital role in initiating
proteolytic activity.
Limitations of proteolytic theory:
1)Enamel is a highly mineralised tissue. Though
enamel contains 1.0%to 1.5% organic matrix out
of which 0.6% is protein,initiation of caries with
breakdown of this small % of protein is highly
questionable.
2)Till date loss of enamel by proteolysis is not
proved experimentally.
3)sulphatases of gram –ve bacilli,considered to
dissolve mucotin sulfate of enamel are not found
in abundance.
4)enzyme systems capable of attacking keratin
have also not been demonstrated
 PROTEOLYSIS-CHELATION
THEORY(SCHATZ et al-1955):
This theory described that there
is simultaneous microbial degradation
of organic component by proteolysis
and the dissolution of inorganic part by
the process of chelation.

CHELATE=compounds that are

able to bind metallic ions such as
Ca,Fe,Cu,Zn etc by valence bonds.
 Limitations Proteolysis-chelation theory:
1)Since enamel contains a very little amount
of organic component,could its dissolution
produce sufficient amount of chelates to
disintegrate the rest of inorganic enamel is
doubtful.
2)although chelation is an accepted biological
phenomenon,its role in caries initiation is
yet to be established.
3)breakdown of organic portion by
proteolysis in initiating caries lack
experimental evidence.
 4)Levins theory (1977):
a)pH of plaque.
b)calcium &phosphate
ion conc at the interface.
c)fluoride ion
concentration.
 5)Bandlish theory:
L.K.BANDLISH
emphasized more on attrition
and its role in caries etiology.
According to him oral
fluids protect enamel by
providing a protective covering
on the enamel surface.
 ETIOLOGY OF
DENTAL CARIES
 SUSCEPTIBLE
TOOTH SURFACE:
1.)Morphology of tooth:
Presence
of deep narrow
occlusal
fissures or buccal or
lingual pits.

Conversely,in case of
attrition,inclined
planes
become relatively
plane and prevent
food lodgement.
VARIATION OF PITS AND FISSURES.
2)POSITION OF TOOTH IN THE ARCH:
Malaligned(buccally/lingually placed)
Out of position
Rotations.
CHEMICAL COMPOSITION OF TOOTH:
 No difference in chemical composition of
carious &sound enamel in contents of calcium,
phosphorus, magnesium and carbon.(Sathish
chandra).
Significant difference in fluoride content.
ENAMEL—410 ppm
CARIOUS ENAMEL—139ppm.
DENTIN—873ppm
CARIOUS DENTIN—223ppm.
 Surface enamel more resistant to caries than
subsurface
enamel.
 FACTORS RESPONSIBLE AS FAR AS
DIET&DENTAL CARIES ARE
CONCERNED:
1. Particle size& roughness of diet.
2. Palatability of diet.
3. Eating&drinking pattern after and
within diet.
4. Retention and clearance of food.
5. Age at which diet is offered.
ETIOLOGICAL AGENTS OF CARIES:
Pathogenic bacterial plaque.
 It is defined as soft deposits that form the
biofilm adhering to the tooth surface or other
hard surfaces in the oral cavity including
removable and fixed restorations.
(CARRANZA).
 Bacteria are the major component of plaque
—2x1011 bacteria/gm.
 COMPOSITION OF PLAQUE

 ORGANIC  INORGANIC
PORTION PORTION

GLYCOPROTEINS CALCIUM
POLYSACCHARIDE PHOSPHORUS&
PROTEINS TRACE ELEMENTS:
LIPIDS SODIUM
POTASSIUM
FLUORIDE.
FORMATION OF DENTAL PELLICLE
 Pellicle appears as 3 different structures:
1) subsurface component-
dendritic configuration.
2) surface component.
3) supra surface portion-
scalloped appearance.
 Non-specific plaque hypothesis
 Specific plaque hypothesis.

plaque is considered to be
pathogenic only when the signs
of disease are present.
 MICROORGANISMS:
Three groups are largely responsible for caries process i.e.
a. Streptococcus group
 S-mutans
 S-sangius
 S-mitor
 S-Salivaris
 S-Milleri
Actinomycotic group
 A – Israli
 A – Viscous
 A – Naeslundi
Lactobacillus acidophilic group
 STREPTOCOCCUS MUTANS:
 Causative agent of dental caries.
 Discovered by Clarke(1924);gram+ve cocci.
 Cultured in mitis salivarius agar containing
20%sucrose& 0.2%units/ml of bacitracin.
 Characteristically synthesises polysaccharides from
sucrose—more acidogenic.
 Cariogenic strains contain-lysogenic bacteriophage.
METABOLISM &CARIOGENECITY OF St.mutans:
 Most important substrate for s.mutans is
sucrose.
 Pathway by which s.mutans dissimilate sucrose:
By conversion of sucrose to adhesive
extracellular carbohydrate polymers by cell
bound and extracellular enzymes.
 S.mutans polymerizes glucose and fructose
moieties of sucrose to form glucans and
fructans.
 Lipoteichoic acid—extracellular polymer found in
culture of s.mutans.—adhesiveness of bacteria.
THE MINIMUM INFECTIVE DOSE IN MAN HAS
BEEN 104 to 105 S.mutans /ml OF SALIVA
 St.sanguis:
 α-hemolytic streptococcus species
originally isolated from patients with Sub
Acute Bacterial Endocarditis.
 Identified as small,firm colonies &
form extracellular polysaccharides in
sucrose broth.
 Consistently present in plaque in
carious and non carious sites.
 St.mitior:
 Commonly isolated bacteria in the oral cavity.
 Soft,round &black brown colonies on mitis
salivarius agar.

St.salivarius:
 Common in tongue throat and in saliva.
 Adheres well to epithelial surfaces.
 ACTINOMYCES:
 Gram +ve,filamentous organisms –include
A.naeslundi,
A.viscosus,A.israelii,A.odontolyticus.
 Isolated from root surfaces.
 A.viscosus form extracellular levans
&heteropolysaccharides consisting of
hexosamine and hexose.
 LACTOBACILLI:
 Gram+ve,non spore forming rods.form 1%
of oral flora.
 L.casei,L.acidophilus,L.fermentum,L.brevis.
 Isolation of these strains is done by the use of
ROGOSA agar medium.
 Multiply in low pH of plaque and carious
lesions.
SALIVA:
COMPOSITION:
pH and VISCOSITY:
The pH at which
any particular saliva ceases to be
saturated with calcium and phosphate
is referred to as “critical pH.”
Critical pH= 5.5
BUFFERING CAPACITY OF
SALIVA:

Chief buffer systems are

bicarbonate-carbonic acid
(HCO-/H2CO3,pk1=6.1)
and phosphate (HPO4-/H2PO4-,pk2=6.8).
 ANTIBACTERIAL PROPERTIES LIKE
ENZYMES:

1. Lysozyme(N-Acetylmuramide
glycanohydrolase)

2. Salivary peroxidase system

3. Immunoglobulins: IgA,IgG.
 Journal of Oral medicine and Oral
pathology:2006;vol 11;pg-449-455.
QUANTITY:
 Daily salivary secretion ranges from 500-
700ml
 Average volume in the mouth=1.1ml
 At rest=0.25 to 0.35ml/min.
 Sensory,electrical&mechanical
stimuli1.5ml/min.

Decreased salivary flow

-XEROSTOMIA
FACTORS
INFLUENCING
THE
EQUILIBRIUM
BETWEEN THE
THREE PRE
REQUISITES FOR
THE CARIES
PROCESS.
DESCRIBED BY –
KEYES AND
JORDAN.
CLINICAL CLASSIFICATION
OF DENTAL CARIES
 G.V BLACK’s classification of dental caries
 Classification of dental caries by Vimal sikri:
According to morphology of teeth.:
1.)pit and fissure caries
2.)Smooth surface caries
3.)Root caries
4.)Linear enamel caries
According to severity&progress of lesion.:
1.)Incipient caries.
2.)Rampant caries.
3.)Arrested caries.
4.)Recurrent caries.
5.)Radiation caries.
 According to age pattern:
1)Nursing bottle caries
2)Adolescent caries.
3)Geriatric caries.
 Classification of dental caries by sathish chandra:
According to surface topography and environmental
conditions,caries can be initiated in 4 distinct clinical
sites.:
1)Pit and fissure caries.
2)Smooth surface caries
3)Root surface caries
4)Cervical caries
According to rapidity of caries progression.:
1)Acute dental caries.
2)Rampant caries
3)Chronic dental caries
 Rampant dental caries: a)Nursing bottle rampant caries.
b)Adolescent rampant caries.
c)Xerostomia induced rampant
caries.
Whether caries attacks previously intact surface or
margin of a restoration:
1)Primary caries
2)Secondary caries
According to proximity of caries to the pulp.
 Classification of dental caries by Sturdevant:
Pit and fissure caries
Non cavitated—caries unlikely progression
Cavitated –caries likely progression.
 Proximal caries:
Non cavitated—caries unlikely no

progression.
Cavitated—caries likely to progress
 CLASSIFICATION OF DENTAL
CARIES
G.V.BLACK’S classification of dental caries based
on treatment and restoration design:
CLASS I CLASS II
CLASS III

CLASS IV CLASS V
CLASSVI
 Based on morphology or
anatomical site of the lesion:
1. pit and fissure caries
2. Smooth surface caries
3. Root caries
PIT&FISSURE CARIES SMOOTH
SURFACE CARIES
ROOT CARIES
 Rapidity of caries progression:
Acute dental caries
Rampant caries: Nursing bottle rampant caries
Adolescent rampant caries
Xerostomia induced rampant
caries
 Chronic dental caries:

Slowly progressing and

involves pulp at a much later
stage.

Allows sclerosis of dentinal

tubules and secondary dentin
formation.
 Whether caries attacks
previously intact surface or
margin of restorations:

primary caries

secondary caries.
 According to severity and progress of
lesion:
(STURDEVANT)

Incipient caries Cavitated

lesion
 Direction of lesion:(MARZOUK)

forward caries
backward caries
 HISTOPATHOLOGICAL FEATURES OF
ENAMEL CARIES.

ZONES OF ENAMEL CARIES:

1. TRANSLUCENT ZONE
2. DARK ZONE
3. BODY OF THE LESION
4. SURFACE ZONE
 DENTINAL CARIES:
Early dentinal changes
Advanced dentinal changes.
ZONES OF DENTINAL CARIES:
1. Zone of fatty degeneration of tomes fibres
2. Zone of dentinal sclerosis characterised by deposition of
calcium salts in dentinal tubules.
3. Zone of decalcification of dentin,narrow zone.
4. zone of bacterial invasion of decalcific but intact dentin.
5. Zone of decomposed dentin
AFFECTED DENTIN INFECTED DENTIN
 Softened  Softened
demineralised dentin contaminated with
that is not invaded by bacteria.
bacteria.  Outer layer stained
by 1%acid red 52 in
propylene glycol.
 Zones 2 and 3  Stains irreversibly
denatured collagen.
 Zones 4 and 5.
 ROOT CARIES:
METHODS OF CARIES
CONTROL
 Chemical measure of caries control:
 a) substances which alter the tooth
surface:
1) fluorides:
Water fluoridation
Topical fluorides
Fluoride dentrifices
Fluoride mouthwash/rinse
2)silver nitrate
3)zinc chloride and potassium ferro
cyanide.
 Substances which interfere with carbohydrate
degradation through enzyme alterations.:
vitamin k
sarcoside
Substances which interfere with bacterial growth and
metabolism.:
urea and ammonia compounds
chlorophyll
nitrofurans
penecillins.
Other antibiotics: erythromycin kanamycin
spiramycin tetracyclin
tyrothricin vancomycin
 Nutritional measures for caries control:
restriction of refined carbohydrate intake
phosphated diets.
 Mechanical measures of caries control done by dentist:
prophylaxis by dentist

pit and fissure sealants.

Mechanical methods of caries control by the
patient:
Tooth brushing

Mouth rinsing

Use of dental floss

Chewing gums
CARIES VACC INE

 Immunologically biological substance design to

protect an individual from disease. Derived

from Latin word meaning suspension of killed or

attenuated organisms administered for prevention of

disease.Vaccination is an artificial active mode of

immunization.
Appropriate immunisation agent:

Glucosyl transferase(GTF):
• Involved in synthesis of glucans
from sucrose.
•Inhibits s.mutans accumulation.

Wall associated proteins:

•Antigen A
•Antigen B
 Mechanism of Action of
Caries vaccine
Two Mechanisms of action are present :-
1 : Antibody IgA which are secreted by the salivary glands
and constitute the major part of oral antibody.
2. Mechanism Involves production of IgG Antibodies
which is a major serum antibody activated by specialized
cells in the intestine enters the mouth through gingival
crevicular fluid.
 EXPERIMENTAL DESIGNS AIMED
FOR SALIVARY IMMUNITY
1. Periglandular salivary
immunisation
2. Salivary gland immunization by
combined periglandular injection
and installation of streptococcus
mutans into the parotid duct.
3. Parenteral immunisation.
4. Oral submucous immunisation.
 CONCLUSION
 A CLEAR UNDERSTANDING OF THE
CONDITION IS ESSENTIAL IF THE
DENTIST IS TO PLAN AND EXECUTE
TREATMENT LOGICALLY EFFECTIVELY
AND IN THE PATIENTS BEST
INTEREST,INDEED UNLESS THE
DENTIST UNDERSTANDS THE
PROCESSES IT WILL NOT BE POSSIBLE
TO DECIDE WHETHER TREATMENT IS
NECESSARY AT ALL.
 REFERENCES
 Pickards manual of operative dentistry-8th edition
 Textbook of operative dentistry-sathish chandra.
 Shafers textbook of oral pathology-4th,5th editions.
 Operative dentistry-modern theory and practice-
Marzouk
 Textbook of operative dentistry-vimal sikri-2nd ed.
 Sturdevants art and science of operative dentistry-
5th edition
 Diagnosis and risk prediction of dental caries vol-2
 Clinical periodontology-caranza-8th edition
 Fundamentals of operative dentistry-summit-3rd ed
 Fluoride in dentistry-2nd ed.Ole Fegerskov
 Journal of community dentistry and oral
epidemiology-2001,29,278-288.
 Journal of oral medicine and oral pathology-
2006,11,449-455.
 Soben Peter-Text book or Preventive and
Community Dentistry.
THANK YOU