ROLE OF HOST IN

ETIOLOGY OF DENTAL
CARIES
 CONTENTS
1. Introduction
2. Tooth
-Crystal structure of hydroxyapatite
-Determinants of tooth susceptibility to caries
 Composition
 Morphology
 Surface
 Position

3. Saliva
- Composition of saliva
- Functions of saliva
- Saliva in relation to caries
 Oral clearance

 Buffer capacity

 Remineralization and demineralization

 Antimicrobial factors & salivary pellicle

4. References
INTRODUCTION
TOOTH
96
%
 Major mineral component:
Calcium phosphate crystals ~ Hydroxyapatite
Ca10(PO4)6(OH)2

A 3-dimensional representation of a conceptual unit cell of

hydroxyapatite. The a-and b-axes form a parallelogram with each side
9.42Å. The height represents the c-axis and is 6.88Å. Only hydroxyl
groups are shown
a. A diagrammatic representation of a HAP unit cell showing
the location of hydroxyl ions along the c-axis. Calcium ions
are located in two environments: 1) Calcium ions are also
located in the screw-axis position in the form of equilateral
triangles around the two hydroxyl groups. 2) Column-
calcium ions located inside the unit cell at the a-b plane and
one half the distance between two a-b planes.
b. Diagrammatic illustration of stacking of calcium ions in the
form of equilateral triangles around the hydroxyl groups
PO4
rod

Cross section
 Three primary constituents:
• OH-
• Ca2+
• PO43-

➢ Substitution of three primary constituents with

- fluoride
- carbonate
- other trace elements (impurities): Na, Cl, Mg, K, Zn, Si, Sr
 FLUORAPATITE
• Replacement of the dipolar OH- groups by fluoride ions,
which are larger, results in the formation of fluorapatite
• The fluoride ions substituting for the hydroxyl ions go to
the centers of the calcium triangles
• effects on the physical and chemical properties of the
crystal:
 Forms strong interaction
forces with Ca2+
 Stabilizes lattice structure
 Rate of dissolution is
lesser
 Improves crystallinity →
more stable
The net effect :
• increased stability
• increased rates of remineralization
• decreased rates of demineralization.
• All of these effects → cariostatic activity of fluorides
 CARBONATE HYDROXYAPATITE

Carbonate (CO3)2- substitute (PO4)3- or 2 (OH)-

Carbonate ions disturb the regular array of ions in the

crystal lattice
Less stable & more soluble in acid than pure HAP
• Dentin and enamel have similar mineral
compositions, the carbonate content of enamel
is approximately 3% while in dentine it is 5-
6%, making dentin mineral even more acid
 Dental hydroxyapatite (HAP) is often described as
"calcium deficient" and "carbonated" because some
calcium ions may be substituted by sodium, magnesium
and potassium, and some phosphates (PO ) by
carbonates (CO32- )

 Because of these substitutions the mineral in

enamel and dentin is much more acid soluble than
HAP which in turn is much more soluble than fluorapatite
(FAP)
 ACID SOLUBILITY:

Carbonated HAP > Pure HAP > Fluorapetite (FAP)

 PROPERTIES OF HAP
1) Hydration shell:
 hydroxyapatite, when exposed to an aqueous

solution, take on a definite film of bound

water called the hydration layer.
 The exact nature of the bonding of the water

is not clear, but is probably related to the

strong surface charge
2) Lack of Stoichiometry of Hydroxyapatite
Crystals:
 Hydroxyapatite crystals lack stoichiometry - that is

the concentration of the chemical constituents in the

crystals is different from that predicted by the formula
for hydroxyapatite [i.e. Ca10(PO4)6(OH)2]
 Eg.: The concentration of calcium in pure
hydroxyapatite is 39.9%, enamel contains only 36.5%

3) Isomorphous Substitution in Hydroxyapatite

Crystals:
 Cations and anions similar in size and charge to the

lattice ions may substitute for them on the surface

and the interior of the crystal.
 Example - Sr2+ and Ra2+ may substitute for Ca2+ in the

hydroxyapatite lattice.
 DISSOLUTION OF
HYDROXYAPATITE CRYSTALS
 Dissolution of tooth mineral → primary
mechanism in
dental caries
 Factors controlling dissolution of hydroxyapatite:

 Lattice impurities
 Crystal size
 Crystalline defect
 Rate of diffusion of dissolving ions
 Degree of saturation of saliva with minerals
 Degree of saturation (DS)

Ratio of the ionic activity product (IAP) of a substance in the solution to its
ionic product at saturation i.e solubility product (Ksp )

e.g., for hydroxyapatite Ca10(PO4)6OH)2 =

[Ca2+]10[PO43-]6[OH-]2
IAP (ionic activity products in solution)
DS =
Ksp (ionic activity products at saturation)

DS = 1 : i.e IAP = Ksp

Saturation condition
DS < 1 : i.e IAP< Ksp
Demineralization
Solution undersaturated with mineral
DS > 1 : i.e IAP > Ksp
Solution supersaturated with mineral Remineralization
 TRACE ELEMENTS IN ENAMEL

Incorporation of trace elements → alters physical

properties of HAP crystals especially solubility, hence
these are either more susceptible or less susceptible to
degradation
EFFECT TRACE ELEMENT
CARIOSTATIC F, P
MILDLY CARIOSTATIC Mo, V, Cu, Sr, B, Li, Au
EQUIVOCAL EFFECT Be, Co, Mn, Sn, Zr, Br, I
NO EFFECT Ba, Al, Ni, Fe, Pd, Ti
CARIES POTENTIATING Se, Mg, Cd, Pt, Si
MORPHOLOGIC CHARACTERISTICS: -

 Deep, narrow occlusal fissures or buccal

and lingual pits predispose to caries as they
tend to trap food and bacteria. Also enamel is
quite thin at the base of such deep pits and
fissures.

 The most susceptible teeth are mandibular 1st

molars followed by maxillary 1st ,
mandibular and maxillary 2nd molars.
TOOTH SURFACE:
 In mandibular first molars, the likelihood of

decay, in descending order, is occlusal, buccal,

mesial, distal and lingual.
 In maxillary first molars the order is occlusal,

mesial, lingual, buccal and distal.

 On maxillary lateral incisors, the lingual surface

is more susceptible to caries than the labial

surface due to the frequent presence of a pit at
this site.

POSITION:
 Malaligned, rotated or otherwise abnormally

situated teeth can be difficult to cleanse and are

likely to trap food debris and bacteria →
sufficient to dental caries.
 Tooth composition
▪ Structure & composition of a tooth determines
initiation and rate of progression of caries.
▪ Surface enamel more mineralized than subsurface
enamel and is more resistant to caries
 Surface – More fluoride, zinc, iron and lead,
- More inorganic material and less water
- Less dissolution to acids
 Subsurface – More carbonate, magnesium, sodium
- Decreased enamel density and
permeability
Therefore in initial carious lesions, the subsurface
enamel shows marked demineralization even though the
outer enamel is relatively intact.
 PRIMARY
VS
PERMANENT
TEETH
ENAMEL PRIMARY PERMANENT

THICKNESS 0.5 TO 1.5 MM 2 TO 2.5 MM

THICK AND
VARIABLE IN
DEPTH

FASTER AND HIGHER RATE OF CARIES IN

PRIMARY TEETH(Wang et al)

Wang L, Tang R, Bonstein T, Bush P, Nancollas G. Enamel Demineralization in Primary and

Permanent Teeth. Journal of Dental Research. 2006;85(4):359–63
ENAMEL PRIMARY PERMANENT
MINERALISATION LOWER ( LESS MORE
INORGANIC MINERALISED
CONTENT ) 37 % CALCIUM
MORE AND 18.1%
CARBONATES PHOSPHOROUS
AND CARBON PRESENT
DIOXIDE
(Correg et al)
Lower mineral content and higher amount of
carbonates lead to increase risk of dental caries in
primary teeth

Maria Angã©Lica Hueb De Menezes Oliveira, Torres CP, Gomes-Silva JM, Chinelatti
MA, Menezes FCHD, Palma-Dibb RG, et al. Microstructure and mineral composition of
dental enamel of permanent and deciduous teeth. Microscopy Research and Technique.
2009;
ENAMEL PRIMARY PERMANENT

FLOURIDE LOWER CONTENT HIGHER IN OUTER

ENAMEL

Murakami C, Bönecker M, Corrêa MSNP, Mendes FM, Rodrigues CRMD. Effect of

fluoride varnish and gel on dental erosion in primary and permanent teeth. Archives of Oral
Biology. 2009;54(11):997–1001.
 According to Arnim and Doyle, the mean
thickness of dentin in primary maxillary first
molar above mesiobuccal pulp horn is
1.54mm and can also be as less as 0.9mm.

 Similar dentin thickness in primary

mandibular first molar observed was 1.62mm
and also can be as less as 0.7mm

 Thus, rapid involvement of pulp is seen

associated with proximal carious lesions
in primary teeth.
SALIVA
FUNCTIONS
ROLE OF SALIVA AS A MODIFYING FACTOR IN
DENTAL CARIES

The principle properties of saliva that protect the teeth

against caries:
 Physical action - Dilution and clearance of

1)dietary sugars
2)bacteria
 Chemical action - Neutralization and buffering of

the acids in plaque.

- Supply of ions for
remineralization.
 Biological action - Antimicrobial factors.

- Salivary pellicle
PHYSICAL ACTION :
ORAL CLEARANCE
 ORAL CLEARNCE
Oral cavity
↓
substances with potentially harmful properties
↓
Direct effect on caries process, eg: fermentable
carbohydrate, mainly sucrose
↓
saliva dilutes and eliminates substances.

 This physiological process of diluting and

eliminating substances is referred as salivary
clearance/oral clearance.
 ORAL CLEARANCE
↓

Bacteria Sucrose
ORAL CLEARANCE OF BACTERIA
• When saliva is swallowed, any bacteria contained
therein are removed from the oral cavity and
pass into the stomach.

• The average unstimulated salivary flow rate is

about 0.3 mI/min and the amount of saliva
present in the mouth prior to swallowing is about
3 or 4 times of that volume.

• Thus, the half-life of any inert material

suspended in saliva in the oral cavity is only a
few minutes and is certainly very much less than
the mean generation time of oral
microorganisms
 ORAL CLEARANCE OF SUCROSE
 Sucrose dissolved in the small volume of
saliva may give rise to very high
concentrations that will vary locally and with
time after the exposure.

 Intake of sugar
taste or chewing
salivary glands → stimulated
increased flow rate
Swallow
eliminates some of the sugar
from the oral cavity
 Sucrose in the thin salivary film
↓rapidly diffuse
plaque layer (thicker).

 The amount of sugar passing the saliva–plaque

interface is dependent on the concentration
gradient of sucrose between saliva and plaque
fluid.

 Clinical significance - It is important for both

the therapist and the patient to know that sugar is
available for bacteria in the plaque long after the
sugar concentration in saliva has reached levels
below the taste threshold for sugar.
BIOLOGICAL
ACTIONS
 SALIVARY PELLICLE
 The saliva is separated from the surface of the
tooth by a thin, bacteria-free biofilm called the
acquired pellicle.
 It is an acellular layer of adsorbed salivary

proteins and other macromolecules.

 Thickness: 1–10 µm, becoming thicker with time.

 important role in protecting the tooth against

mechanical and chemical damage, but it also

serves as a diffusion barrier (e.g. to acids).
 lack of a pellicle will make tooth surfaces more

susceptible to acids and thus demineralization.

 Many of the proteins that contribute to the

formation of pellicle, e.g. most glycoproteins

 Macromolecules, such as α-amylase, lysozyme,
peroxidase, sIgA, carbonic anhydrases and
glycosyltransferases, participate selectively in
pellicle matrix formation, together with mucins and
breakdown products from macromolecules of
salivary, bacterial and even dietary background
 This thin layer forms the base for subsequent
adhesion of microorganisms
 Some proteins and peptides of the pellicle act as
receptors for oral bacteria such as Streptococcus
and Actinomyces species
 Clinical significance: The pellicle is not removed
mechanically by regular tooth brushing, but
detergents from dentifrice and polishing with rubber
cups and powders as well as acid etching and
bleaching remove the pellicle
ANTIMICROBIAL FACTORS
SALIVARY ENVIRONMENT

INNATE ANTIBODY MEDIATED

 Mucin  Secretory IgA

 Lactoferrin
 Salivary peroxidase
 Lysozyme
 Statherins & proline
rich proteins
SECRETORY IgA:

• Principle soluble immune component

• Varies with salivary flow rate . Max-
resting condition, decreases -stimulation
• Dimer 2H, 2L chains
FUNCTIONS :

• Virus neutralization, immune exclusion, “disposal of bacteria”

(blocking or competing) with binding sites

• Block bacterial receptors from adherence to tooth

• Enhanced by interaction – mucin

• Inhibits bacterial enzyme eg. Glucosyl tranferase

• Change in diffusion characteristic of plaque.

 LACTOFERRIN:
• Antimicrobial activity- inhibits iron dependent
metabolic process of microorganism.

 MUCIN:
• Protects hard and soft tissues by forming a
protective covering.
• Prevents bacterial cell aggregation and
adhesion to surfaces.

 LYSOZYME:
• Antimicrobial – causes lysis of microorganisms
 SALIVARY PEROXIDASE :
 Two principal sources – submandibular/parotid and GCF
 their influences microenvironments

Cofactors – hydrogen
Peroxidase Hypothiocyanate
peroxide & thiocyanate
enzymes
ions

Oxidizing
Toxic to
 Streptococci sulfhydryl
sensitive groups on bacteria
 Lactobacillii
enzymes
 SALIVARY PROTEINS –
(STATHERINS & PROLINE RICH PROTEINS )
 Calcium & phosphate salts of dental enamel are

soluble under typical condition of pH.

 Super saturation of calcium & phosphates maintain

enamel integrity.
 These prevent precipitation or crystallization of

supersaturated calcium & phosphate; therefore

maintaining salivary concentrations of minerals
 Aid in controlling crystalline growth of the enamel

by allowing the penetration of minerals into the

enamel for remineralization and by limiting mineral
egress.
CHEMICAL
ACTIONS
Concept of critical pH
 The pH at which saliva ceases to be saturated

with calcium and phosphate is referred to as

“critical pH”.

 Below this value the inorganic material of the

tooth may dissolve.

 Critical pH varies according to the calcium and

phosphate concentration but it is usually about
5.5.
 ROLE OF CALCIUM
Calcium in saliva

Protein bound Non protein

bound
Bound to statherins & Ionized Non-
ionized Binds to ion Binds to PO43-
Inhibits species
prolinespontaneous
rich proteins & HCO3-
precipitation CaPO4 with 2-ve charges
salts Eg.: Citrate
& Reduced conc. of
Keeps saliva Ca 2+

supersaturated Affects saturation of saliva

& HAP

Further accelerates
demineralization of teeth
 MODULATION OF
DEMINERALIZATION AND
REMINERALIZATION
Acids diffuse through plaque and the pellicle into the enamel
between enamel crystals.
↓ Critical pH
Crystalline dissolution
↓
Demineralization
↓
Dissolution of minerals Supersaturated saliva
↓ Salivary
proteins
Buffering action of saliva→influences pH Replaces lost minerals
of enamel
Inhibiting caries progression
REMINERALIZATION
 BUFFERING POWER OF
SALIVA
 Solutions containing both weak acids and
their salts are referred to as ‘buffer
solutions’.
 These solutions have the capacity of resisting

changes of pH when either acids or alkalies

are added to them.
 The buffer capacity of human saliva is

regulated by three buffer systems:

1) The carbonic acid / bicarbonate system.
2) Phosphate system.
3) The protein buffer system
BICARBONATE BUFFER
SYSTEM
 Most important buffer in saliva

 During a meal:
 Salivary flow rate increases
 Increases concentration of bicarbonate
 Increasing buffering capacity of saliva

 In stimulated saliva it is largely due to the

bicarbonate ion which provides 85% of the
total buffering capacity.
Bicarbonate determines saliva pH
PHOSPHATE BUFFER SYSTEM
 The phosphate buffer is active in unstimulated
saliva (Bardow et al., 2008).
 The mechanism for the phosphate buffer system is

due to the ability of the secondary phosphate ion,

H(PO4)2-, to bind a hydrogen ion and form a primary
phosphate ion H2(PO)4-.
 H2PO4 - ↔ HPO4 2-
+ H+
 Dihydrogen phosphate ion ↔Hydrogen Phosphate
ion
+ Hydrogen
ion
 It’s effectiveness is limited due to insufficient
 Nonetheless, in the resting state where there
is no food in the mouth, the concentration of
inorganic phosphate is rather high while the
concentration of carbonic acid/bicarbonate is
rather low.

 Hence the phosphate buffer is moderately

efficient in unstimulated saliva.
 PROTEIN BUFFER
SYSTEM
 A protein called pH rise factor, sialin, helps in
return of acidic pH to a neutral pH following an
acidic challenge.

 These do not have any significant buffering

action
 SALIVA AND THE RISK OF
DEVELOPING CARIES LESIONS

QUANTITY OF SALIVA COMPOSITION OF SALIVA

 QUANTITY OF SALIVA
 Mechanistic and cleaning properties of saliva in
the mouth are impaired
 Reduces flow rate
Slow oral sugar clearance rate
Prolonged periods of low pH in the plaque
Favors an acidic and more cariogenic microflora
Increased risk of caries
 Salivary deficiency
(xerostomia/ oligosialia/ asialia/ stomatitis
sicca)
 First reported by Hutchison in 1888.
 Definition: A permanent or temporary reduction in the
salivary flow.
 Causes of salivary deficiency:
1. Psychological or emotional disturbance
2. Immune disorders e.g. Sjogren’s syndrome,
Mickulickz’s disease.
3. Genetic conditions e.g. hypohydrotic ectodermal
dysplasia, 4. Total irradiation e.g. oncology patients.
5. Vitamin-B complex deficiency.
6. Use of drugs like tranquilizers, antihistamines,
antidepressants, antipsychotics
7. Congenital absence / malformation of salivary glands
 The management of patients with xerostomia
include the following:
1. Fluoride therapy

2. Dietary control

3. Oral hygiene maintenance

4. Avoidance of xerostomic drugs

5. Use of artificial saliva

 QUALITY OF SALIVA
 A major problem in studying saliva is that the
composition varies with flow rate, nature of
stimulation, duration, plasma composition,
time of the day and the serial dependency of
saliva samples i.e the effect of previous
stimulation on the composition of saliva
collected subsequently.

 Currently no consistent relationship has been

established between dental caries
prevalence and composition of saliva.
 CONCLUSION
 The tooth factor or a susceptible tooth is the most
important feature in caries etiology. The structure
and composition of teeth undoubtedly influences
the initiation and progression of a carious lesion.

 Saliva has numerous effects working towards

protection against caries, some by inhibition of
bacteria, some by dilution and elimination of
bacteria and their substrates, some by buffering
bacterial acids, and some by offering a reparative
environment after bacterial-induced
demineralization of teeth.
 REFERENCES

 Gordon Nikiforuk; Understanding Dental Caries; Karger

Publications;1985.
 Ole Fejerskov and Edwina Kidd; Dental Caries the
disease and its Clinical Management; Blackwell
Munksgaard Ltd; 2003.
 Shafer. A textbook of Oral Pathology. 4th Ed.
 Hara, A. T., & Zero, D. T. The Caries Environment:
Saliva, Pellicle, Diet, and Hard Tissue Ultrastructure.
Dental Clinics of North America. 2010; 54(3), 455–467.
 A review of saliva: Normal composition, flow, and
function. Sue P. Humphrey, RDH, and Russell T.
Williamson. J Prosthet Dent 2001;85:162-9.

 Biological factors in dental caries: role of saliva

and dental plaque in the dynamic process of
demineralization and remineralization (part 1).
John Hicks, Franklin Garcia-Godoy, Catherine
Flaitz. J Clin Pediatr Dent. 2003; 28(1): 47-52.

 Wang L, Tang R, Bonstein T, Bush P, Nancollas G.

Enamel Demineralization in Primary and
Permanent Teeth. Journal of Dental Research.
2006;85(4):359–63
 Maria Angã©Lica Hueb De Menezes Oliveira,
Torres CP, Gomes-Silva JM, Chinelatti MA,
Menezes FCHD, Palma-Dibb RG, et al.
Microstructure and mineral composition of dental
enamel of permanent and deciduous teeth.
Microscopy Research and Technique. 2009.

 Murakami C, Bönecker M, Corrêa MSNP, Mendes

FM, Rodrigues CRMD. Effect of fluoride varnish
and gel on dental erosion in primary and
permanent teeth. Archives of Oral Biology.
2009;54(11):997–1001.
THANK
YOU