DENTAL CARIES

DR SUNNY PUROHIT
Dept. of Preventive & Pediatric Dentistry
SDCH
 Isan 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 often lead to cavitation.
 Dental Caries –Disease of modern Civilization

 Studies revealed that

Doliocephalic Skulls(Long Skull) from
Preneolithic Periods did not exhibit Caries
 Neolithic period – Initiation of Farming

 Brachycephalicskulls of Neolithic-Caries Present-

Just below Contact area
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 For caries to develop, three factors must occur
at the same time:
 A susceptible tooth
 Diet rich in fermentable carbohydrates
 Specific bacteria (regardless of other factors,
caries cannot occur without bacteria)

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 Pit and fissure caries occurs primarily on the
occlusal surfaces and buccal and lingual grooves
of posterior teeth, as well as in lingual pits of the
maxillary incisors.
 Smooth surface caries occurs on intact enamel
other than pits and fissures.
 Root surface caries occurs on any surface of
the root.
 Secondary, or recurrent, caries occurs on the
tooth surrounding a restoration.

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 It usually takes a period of time, from months to years,
for a carious lesion to develop.

 It is an ongoing process, characterized by alternating

periods of demineralization and remineralization.
 Demineralization is the dissolving of the calcium and phosphate
from the hydroxyapatite crystals.

 Remineralization is the calcium and phosphate being

redeposited in previously demineralized areas.

 It is possible to have the processes of demineralization and

remineralization occur without any loss of tooth structure.

Copyright © 2005 by Elsevier Inc. All rights reserved.

Copyright © 2005 by Elsevier Inc. All rights reserved.
Copyright © 2005 by Elsevier Inc. All rights reserved.
Copyright © 2005 by Elsevier Inc. All rights reserved.
Copyright © 2005 by Elsevier Inc. All rights reserved.
Copyright © 2005 by Elsevier Inc. All rights reserved.
 Many Theories
 3 theories which have stood the test of time
1.Acidogenic theory of Miller (Miller’s Chemico-
Parasitic Theory),
2.The Proteolytic theory and
3. The Proteolysis Chelation Theory
1.The Legend Of Worms-
 earliest reference to tooth Decay
 Ancient Sumerian Text Known as “Legend of
Worms”

 Homer-Pain in tooth due to worm

 Theancient Greek theory of the four body hu
mors (blood, yellow bile, black bile, and phle
gm) that determined health and disease.

 Caries is due to acid production and

disturbance in body humors.
 Also caries is similar to bone gangrene which
initiates within itself.
 Parmly in 1920

 Unidentified ‘Chymal Agent’ causes caries.

 Erdl -1843

 Filamentous
organisms present in surface
membrane of tooth

 Dresden-German Physician-Dental Caries-

”Denticolae”- Generic term for decay related
microorganism.
 Blend of above theories

 Willoughby D Miller (1882)

Theory: Caries caused by acids produced by

microorganisms of the mouth
Dental decay is a chemico-parasitic process
consisting of 2 stages:
1.Decalcification (preliminary step)
2.Dissolution (subsequent step)
Acids are produced by bacteria’s 
fermentation of sugar and starch
 Backboneof current knowledge and
understanding for etiology of dental caries

3 factors essential for caries production:

 Oral microorganism
 Carbohydrate substrate
 Acid
 Unable to explain:
 Site predilection
 Dental plaque
 Caries-free population

 Role of plaque:1897 by Mr Williams

 localizes acid produced by bacteria
 prevents anti- caries effect of saliva

20
 Gottlieb,1947
 Enamel lamellae
 Organic matrix would be attacked before
mineral phase of enamel
 The proteolytic enzymes liberated by
oral bacteria destroy the organic matrix
of enamel, loosening apatite crystals, so
that they are eventually lost and the
tissue collapses.
2 types of carious lesions:
1. Microorganism  enamel lamellae  attack
enamel and dentin (before clinical evidence of
caries)
2. No lamellae, bacteria in dental plaque  acids 
enamel decalcification.
The early lesion  chalky white
Schatz and Martin (1955)
Initial attack  breakdown of organic matter

Breakdown products chelate with minerals of enamel

dissolves it

Chelates (Metal-substance Complex with Covalent

bonds)can be formed at neutral or alkaline pH, the
theory suggests that demineralization of enamel could
arise without acid formation.
 Microorganisms

No caries
No caries
Host
(saliva
Substrate
and CARIES
teeth)
No caries
No caries

Time
 Micro flora: Acidogenic bacteria that colonize
the tooth surface.
 Host: Quantity and quality of saliva, the quality
of the tooth, etc.
 Diet: Intake of fermentable carbohydrates,
especially sucrose, but also starch.
 Time: Total exposure time to inorganic acids
produced by the bacteria of the dental plaque
 Position Of teeth
 Surface enamel more resistant than subsurface enamel
 Surface – More fluoride, zinc, iron and lead,
Less dissolution to acids
More inorganic material and less water
 Subsurface – More carbonate, magnesium, sodium
Decreased enamel density
and increase permeability

29
 Deep occlusal fissures
 Buccal or lingual pits

Mand 1 molar > max 1st molar> max & mand 2nd molars
Mand incisors & canines - least

 Surface susceptibilty
 molars → Occlusal
 lateral incisor → Lingual

30
 Physical protection provides a cleansing effect. Thick, or
viscous, saliva is less effective than a more watery saliva
in clearing carbohydrates.
 Chemical protection contains calcium, phosphate, and
fluoride. It keeps calcium there ready to be used during
remineralization. It includes buffers, bicarbonate,
phosphate, and small proteins that neutralize the acids
after we ingest fermentable carbohydrates.
 Antibacterial substances in saliva work against the
bacteria.
 If salivary function is reduced for any reason, such as from
illness or medications or due to radiation therapy, the
teeth are at increased risk for decay.

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 Composition of saliva

1. Fluoride in saliva
 Formation of fluoroapatite in surface enamel 
protection against caries.

 Inhibits Enolase Enzyme –Inhibiting Glucose transfers in

Micro organisams

 predetermined by the amount ingested.

 Composition of saliva

2.Organic components
a)Ammonia
 High ammonia concentration retards plaque
formation, neutralizes acid
 reduction of caries

 Urea converted to Ammonium carbonate which

increases the neutralizing power of saliva
 Composition of saliva

b)Histatins (Histidine rich proteins)

 Antibacterial action
 Released from Salivary glands present at the
back of tongue(Ebner’s Gland)
1. LACTOFERRIN

• Iron binding protein

• Prevents iron utilization by aerobic and facultative anaerobic bacteria

 prevents metabolism

2. Lysozyme

 Hydrolytic enzyme with direct antimicrobial effect

 Salivary gland fluid and crevicular fluid

 Acts in many ways

 Antibacterial properties of saliva
Lysozyme

1. Lysozyme - Positively charged enzyme

Binds to salivary ions like HCO3-, F-, I-, NO3-

Complex binds to the cell wall of bacteria

Hydrolysis of glycosidic bonds between polysaccharides

in the cell wall

Destabilization of cell wall

Autolysis
3. Salivary peroxidase system

Salivary Glands secrete salivary Periodase &

Thiocyanate(SCN-)

Reacts With H2O2 produced by certain Bacterias

Oxidation of Thiocynate(OSCN-)

Inhibits Metabolisam of Bacteria

 IgA is predominant immunoglobin in saliva.

• Inhibits adherence and prevents colonization on

mucosal surfaces and teeth.

 Primitive Man-Roughage/Raw Food
 Soil along with food

Flattened Occlusal and Proximal Surface –Less

caries
Modern Diet
Soft Sticky Carbohydrate-More carious
Less Roughage
 Total
exposure time to inorganic acids
produced by the bacteria of the dental
plaque
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