DEPARTMENT OF CONSERVATIVE AND ENDODONTICS

COLLEGE OF DENTAL SCIENCES, DAVANGERE.

SEMINAR ON
DENTAL CARIES

Presented By
Dr.Meena Reddy
P.G. Student
2
ree Ganeshaya Namaha
MULTIFACTORIAL CAUSE OF DENTAL CARIES
Dental caries has been traditionally described as a multifactorial disease
in which there is an interlay of three principal factors namely ;
1) ost factors
a) !ooth factor
i) "orpholo#y and position in arch
ii) $hemical nature
b) Sali%a
i) $omposition& p and antibacterial acti%ity
ii) 'uantity and %iscosity of flow
c) (mmuni)ation
2) "icroflora
*) !he substrate + diet
a) Physical nature
b) $hemical nature
,ourth factor -
.) !ime
"ost important is the understandin# that the caries process does not
occur in absence of /Dental Pla0ue1 or dietary fermentable carbohydrate and
thus dental caries must be considered a /Dietobacterial disease1.
2 modern concept of caries includes the importance of social&
beha%ioural& psycholo#ical and biolo#ic factor which interact with the #enetic
bac3#round in a hi#hly comple4 and interacti%e manner.
*
Disease
Genetic 5n%ironmental
Biolo#ic ,actors
Social factors
Beha%ioural factors
Psycholo#ical factors
Dental $aries $onceptualised as an interaction between #enetic and
en%ironmental factors
6S! ,2$!67S -
a) !ooth "orpholo#y and 2rch ,orm -
!ooth morpholo#y has been lon# been reco#ni)ed as an important
determinant. !here are four factors which determine the tooth for caries
susceptibility.
1. (t is 3nown that P and , areas of posterior teeth are hi#hly susceptible to
caries& because food debris and microor#anism readily impart in the
fissures. (n%esti#ation ha%e shown the relationship between caries
susceptibility and depth of fissures.
2. $ertain surfaces of tooth are more prone to decay& when compared to
others. 5#. "andibular first molar li3elihood of decay in descendin#
order is occlusal& buccal& mesial& distal and lin#ual.
"a4illary first molar - 6cclusal& mesial& lin#ual + palatal& buccal and distal.
"4. lateral incisor - 8in#ual surface more susceptible.
!he difference in decay rates of %arious surfaces on some tooth are in
part due to morpholo#y. i.e. 5#. Buccal pit of mandibular molars& lin#ual
#roo%e of ma4illary molars& cin#ulam of ma4illary incisors.
.
!he distal surface of first permanent molars is freely accessible to sali%a
for about .9: years until 2
nd
molar erupt at 1;911 years. <hereas appro4imal
pla0ue may form on mesial surface from =9> years.
*. (ntraoral %ariation e4ists in susceptibility to caries between different tooth
types.
"ost susceptible one - "andibular first molar ? ma4illary first molar ?
mandibular and ma4illary& 2
nd
molar ? 2
nd
premolar& ma4illary incisors ? first
premolars. "andibular incisors and canines least susceptible.
.. (rre#ularities in arch form& crowdin# and o%erlappin# of teeth also fa%our the
de%elopment of carious lesions.
!66! $6"P6S(!(6N + $5"($28 N2!@75 -
Presence of inor#anic constituents& such as Dicalcium phosphatase
dehydrate and fluoroapatite etc ma3e the enamel resistant to some e4tent.
Surface enamel is harder than the underlyin# enamel. !hese differences
are li3ely to be related to the many difference between composition of the
surface and that of the rest of the enamel. !he surface enamel has more
minerals and more in or#anic matter but relati%ely less water. (n addition
certain elements& includin# fluoride& chloride& )inc& lead and iron accumulate in
the enamel surface while other constituents& such as carbonate and ma#nesium
are sparse in surface as compared with sub surface enamel.
$han#es of the enamel& such as decrease in density and permeability and
an increase in nitro#en and fluoride content with a#e. !hese alterations are part
of the /Post9operati%e maturation1 process whereby teeth become more
resistant to caries with time. !he concentration of fluoride of the surface layer
of enamel increases as the fluoride concentration of drin3in# water increases
and such enamel is less soluble in acids. ,urthermore hi#her the fluoride
concentration of water supply the lower the pre%alence of caries.
:
6S! ,2$!67S ? S28(A2 -
(n this conte4t sali%a refers to the mi4tures of secretions in oral ca%ity.
!his mi4ture consists of fluids deri%ed from maBor sali%ary #lands CParotid&
submandibular& sublin#ual)& from minor sali%ary #lands of oral mucosa and
traces from the #in#i%al e4udates. !his fluid is #i%en a term as oral fluid.
!he en%ironment of oral ca%ity particularly the sali%a in which teeth are
in constant contact and are bathed in it profoundly influences D.$. process.
!he comple4 nature of sali%a and the %ariation in its composition with %arious
factors li3e flow rate& nature of stimulation& duration of stimulation& plasma
composition and time of day which it is collected directly influences the dental
health.
"ost of the sali%a is produced durin# the meal items and as a response
to stimulation due to tastin# and chewin#. (n healthy indi%iduals teeth are
constantly bathed by upto ;.: ml of /restin# sali%a1 which helps to protect or
pharyn4. Sali%ation %irtually stops durin# sleep because of the sali%ary #lands
do not secrete spontaneously in humans.
Normal stimulated secretion rate in adults is 192 ml + minute. owe%er&
it may be less than ;.1 ml+minute in patients with sali%ary #land
malfunctionin#.
undred years a#o <.D."iller described the basic mechanism of caries
etiolo#y which is the foundation of our understandin# today. <hile "illerDs
e4periments showed that sali%a is an essential factor in the patho#enesis of
caries& little more than 2; years head reco#ni)ed the role of sali%a in protectin#
enamel and repairin# the effect of carious attac3. !he role of sali%a in caries
has since then been e4tensi%ely researched.
=
"aBor sources of sali%a are the maBor and minor sali%ary #lands. !he
mechanisms of secretion ha%e been e4tensi%ely studied and the importance of
neurotransmitter and hormonal influences on %arious maBor and minor sali%ary
#lands are well 3nown.
!he secretory products of these #lands can be di%ided into 2 maBor
cate#ories.
1. <ater and electrolytes.
2. "acro molecules particularly proteins and
#lycoproteins.
!he /acetyl choline1 released from the post#an#lionic parasympathetic
ner%e endin#s stimulates muscarinic choliner#ic receptors on secretory cells.
Nor epinephrine released from the adrener#ic ner%e endin#s of the
sympathetic ner%ous system stimulates adrener#ic receptors also locate don
secretory cells.
!he E9adrener#ic receptor locate din sali%ary #land cells& similar
to the F9adrener#ic receptor& and also responsi%e to epinephrine. 6ther neuro
transmitters& such as substance ?P& %aso acti%e intestinal peptide CA(P) and
2denosine !riphosphate C2!P)& also seem to play role sin stimulation of
secretion.
!he stimulation of one receptor often complements and amplifies the
response to another. "oreo%er& not all the sali%ary #lands respond in the same
manner to neurotransmitters. !he sublin#ual lin#ual& which contains mostly
mucus containin# acinar cells& is re#ulated primarily by the parasympathetic
ner%ous system and stimulation of muscarine receptors.
(ndi%idual neurotransmitters and hormones ha%e some what selecti%e
effects on
2
6 and electrolyte secretion on the one hand and secretion
>
macromolecules on the other& dependin# on the #land. !herefore if one alters
the e4ternal si#nals that influence the sali%ary #lands& one can effect both& the
amount and the composition of sali%a& which can inturn& effect the inte#rity of
the tooth structure.
S28(A2 ? B@,,57(NG ,8@(D -
(mportance of sali%a as buffer depends lar#ely on its ability to control
the reductions in p resultin# from bacterial action on metabolic substrates that
are found in dental pla0ue. Sali%a has a si#nificant bufferin# acti%ity and this
bufferin# acti%ity %aries from patient to patient CStephen 1G..).
!he wor3 of Stephan indicated a difference in restin# p %alues for
different patients and lower p %alues correlatin# with a hi#her le%el of caries
acti%ity. 7ecent studies& show that patients with low or no caries acti%ity had
restin# sali%ary p of around >.;. !hose with e4treme caries acti%ity had a
restin# p of around : ? ..: and p %alues between those 2 e4tremes were
reported for those with less se%ere caries acti%ity. !his %aries from person to
person and different a#e #roups.
2 maBor determinant of sali%ary p is its bufferin# capacity.
Bicarbonate is the maBor buffer in sali%a and its concentration in its sali%a
increases as sali%ary flow rate increases. !he #reater the acidity& the more
li3ely is the deminerali)ation of tooth surface. 2 reduction in sali%ary flow
leads to a correspondin# reduction in buffer capacity with important
implications on dental pla0ue p and caries susceptibility.
,@N$!(6N28 7685S 6, (ND(A(D@28 $6"P6N5N!S 6, S28(A2&
2N!(B2$!57(28 P76P57!(5S 2ND "(N5728(H2!(6N 5,,5$!S -
(n addition to the ability of sali%a to act as la%a#e %ehicle and to pro%ide
bufferin# of acid on the tooth surface& indi%idual components of sali%a ha%e
I
been shown to ha%e effects either on ? bacterial acti%ity& deminerali)ation and
reminerali)ation of tooth structure.
Some sali%ary substances ha%e direct ? Bactericidal or& bacterio static
effect.
<hile some other substances can cause a##re#ation of oral bacteria
resultin# in an increased clearance of oral bacteria.
82$!6,577(N -
(t is an iron bindin# protein with certain similarities to transferrin# the
iron bindin# protein found in blood.
(t is shown to ha%e antimicrobial acti%ity and it displays this acti%ity in the
oral ca%ity.
6r#anisms most susceptible are aerobic and facultati%e anaerobic bacteria.
(t appears to ha%e an antimicrobial acti%ity& that is independent of its ability
to bind to iron.
Growth of streptococcus mutans is sensiti%e to this and the inhibition
appears to be iron dependent.
8JS6HJ"5 -
(t is a hydrolytic en)yme that has direct antimicrobial effects.
(t clea%es the F 19. lin3a#e between N9acetyl #lucosamine and N9acetyl
muramic acid& which constitutes the repeatin# units of cell wall
peptido#lcyans of bacteria.
!he en)yme also appears to alter the intermediary #lucose metabolism in
sensiti%e bacteria and in some cases to cause a##re#ation perhaps
contributin# to clearance of bacteria from the oral ca%ity.
Sublin#ual and submandibular sali%a contain hi#her le%els of lyso)yme than
parotid sali%a.
8yso)yme alone does not lyse pre%ent #rowth of pure cultures of
predominant bacteria in 6.$. of man.
G
(n presence of Na lauryl sulfate& a deter#ent lyso)yme and alyse many
cario#enic and non cario#enic strepto cocci.
2lthou#h lyso)yme may not be effecti%e specifically a#ainst cario#enic
microor#anisms& it probably influences the ecolo#ical balance of the oral
mucosa by discriminatin# a#ainst transient or#anism introduced into the
mouth.
P576K(D2S5 -
!hey are produced by the acinar cells of some maBor #lands. Similar to
other pero4idases& the en)yme contains /henceD and uses /thiocyanate1 and
/hydro#en pero4ide1 produced by oral bacteria or present in #landular
secretions& to catalyse the formation of /hypothiocyanate1 and possibly the
/cyano sulfurous acid1.
ypothiocyanate o4idi)es sulfhydral #roups of oral bacteria resultin# in
inhibition of #lucose metabolism.

2
6
2
is more to4ic than hypothiocyanate to both oral bacteria and the
oral mucosa. Pero4idase thus protects the oral ca%ity from stron# o4idi)in#
effects of the pero4ide. Bacteria %ary in their sensiti%ity to hyopthiocyante
with S.mutans with bein# amon# the more sensiti%e.
8yso)yme and pero4idase ha%e been shown to inhibit adherence of
atleast one strain of S.mutans to sali%a coated hydro4yapatite. !he presence of
pero4idase& lactoferrin and lyso)yme in the dental pla0ue appears to be related
to a chan#e in composition of oral bacteria present in that pla0ue. !he relati%e
importance of this chan#e in pla0ue bacteria to caries incidence is not 3nown.
!he sali%ary #lands secrete sali%ary pero4idase and thiocyanate ion
which act on water #enerated by certain bacteria.
1;
!he o4idation reaction inacti%ates %arious en)ymes of the #lycolytic
pathway and thereby temporarily inhibit the #rowth& respiration and
metabolism of most species of oral bacteria.
E ? 2"J82S5 -
(s an en)yme that metaboli)es starch and other polysaccharides. (t is
produced by acinar cells of the maBor sali%ary #lands& particularly those of
serous type.
2mylase promotes the adherence of oral streptococci to hydro4yapatite.
(ts acti%ity to bind to the tooth surface as a component of pla0ue and to
metaboli)e lar#er polysaccharides into #lucose and mattose indicates that it
can pro%ide substantiate for cario#enic bacteria.
(n addition it is 3nown that S.mutans possess a #lucosyl transferase ion in
their outer surface that can use maltose and maltode4trains Cproduced by E9
amylase) to #enerate other polysaccharides 3nown as /#lucans1.
Glucan promotes adherence of streptococci and other bacteria to the tooth
surface& but #lucans %ary in their ability to promote adherence of oral
bacteria to the tooth surface& and therefore it is concei%able that a chan#e in
substrate for bacterial #lucosyl ion transferase would lead to chan#e in
adherence of the bacteria.
(t is at present impossible to determine the net effect of E9amylase on dental
caries. 2t least some potential effects of amylase on the tooth surface can
be %iewed as harmful. !he net effect of combinations of E9amylase with
other components of the pellicle is not well understood howe%er.
S!2!57(N -
(t is an acidic peptide that contains relati%ely hi#h le%els of praline& tyrosine
and phosphoserine.
(t inhibits spontaneous precipitation of $aP6
.
salts from supersaturated
sali%a and pre%ents crystal #rowth. By doin# so& it fa%ours reminerali)ation
11
of tooth surface. (t is able to function with other sali%ary proteins to protect
tooth surface from wear and from %arious physical forces.
(n addition to this& it can also bond to bacteria. (n doin# so it can enhance
the bindin# of cario#enic bacterial.
!his enhanced bindin# could indirectly promote caries acti%ity& but the net
effect with bacterial bindin# with staltherin is not 3nown.
(S!(NS -
!hey are #roup of histidine rich proteins that are another acinar cell
product that affects the inte#rity of the tooth surface.
(n addition to their demonstrated antifun#al effects which do not directly
relate to the caries process histatins ha%e antibacterial effects as well as the
ability to affect minerali)ation.
!he maBor forms in the oral ca%ity are istatin91& istatin9* and
istatin9:.
2n important role played by sitatin& is its ability to bind
/hydro4yapatite1 and pre%ent calcium phosphate precipitation from a super
saturated sali%a and to inhibit crystal #rowth Cthereby enhancin# the stability
of hydro4yapatite present in tooth surface).
P768(N597($ P76!5(NS -
!hey contribute si#nificantly to protection of the enamel surface by
bondin# with hi#h affinity to hydro4yapatite. !hey constitute a lar#e percent
of total protein in parotid and submandibular sali%a and are products of acinar
cells secretion.
!hey are of two types CSali%a)
2cidic proline rich
Basic proline rich
Both are secretory products of maBor sali%ary #lands.
!he acidic praline rich proteins cases in a similar way as istatin
i.e.bind ti#htly to hydro4yapatite and present precipitation of $aP6
.
from the
12
super saturated sali%a& thereby protectin# the enamel surface and pre%entin#
deminerali)ation.
!he acidic and basic types bind to oral bacteria includin# streptococci.
2s they bind to both bacteria and tooth surface this appear to ha%e an important
influence on the bacterial composition of the enamel pellicle.
Secretion is enhanced by stimulation of F9adrener#ic receptors in maBor
sali%ary #lands. Because the le%el of stimulation is a determinant of the
amount of these proteins& dru#s which act as the F9adrener#ic receptor could
affect the de#ree of oral adherence of certain bacteria to the tooth surface.
$JS!2!(NS -
Group of cysterine9enriched protease inhibitors. 2s protease inhibitors&
they pre%ent act action of potentially harmful proteases on soft tissues of oral
ca%ity.
!hey bind to hydro4yapatite and inhibits the precipitation of $aP6
.
and
protect the tooth by promotin# supersaturation of sali%a with calcium and
phosphate.
"ost of cystaines are secreted by submandibular secretion.
"@$(NS -
!hey are lar#e molecular wei#ht #lycoproteins composed mainly of
carbohydrate and produced from acinar cells from submandibular& sublin#ual
and some minor sali%ary #lands.
"aBor sali%ary mucins ? "G( and "GH.
"GL absorbs ti#htly to the tooth surface. (! has the primary role of
contributin# to the enamel pellicle& thereby protectin# the surface from
chemical and physical attac3 includin# acid challen#es.
Study of sali%a and its tooth protecti%e components re%eal force
functions.
1. Bufferin# ability
1*
2. $leansin# effect
*. 2ntibacterial action
.. "aintenance of sali%a supersaturated in $aP6
.

!he ability to a##re#ate bacteria appears to be shared by a number of
#lycoproteins present in human sali%a. !hese #lycoproteins can be in%ol%ed
both in adherence of bacteria to the tooth surface and in clearance from the oral
ca%ity.
,8@67(D5 -
,luoride is another important component of sali%a. !he ability of sali%a
to deli%er fluoride to the tooth surface& constantly mar3s sali%ary fluoride an
important player in caries protection lar#ely by promotion reminerali)ation and
reducin# deminerali)ation.
(""@N6G86B@8(NS -
!he maBor immuno#lobulin in sali%a and other e4ternal secretions is
secretory (#2 which differs from serum (#2. Secretory (#2 is the product of 2
distinct cell types. Secretory (#2 e4ists as a 11S dimmer constrictin# of 2 (G2
molecules Boined by a L9chain plus a secretory component CS$). S$ is a
receptor for polymeric immuno#lobulin 2 containin# L9chain; the (#2 binds to
S$ below the li#ht Bunction of #landular epithelial cells and is then transported
across the luminal surface.
Sali%ary (#2 are produced by plasma cells located in maBor and minor
sali%ary #lands. (t is then transported into sali%a lar#ely by the ductal cells of
the #land. (#2 respecti%e the principal immuno#lobulin found in sali%a. !i
e4ists in sali%a in appro4imate e0ual amounts of two isoforms& (#2& and (#2
2
.
!he secretory component is added to the molecule by secretory cells and act as
part of the membrane receptor for (#2. !he (#2 comple4 allows (#2 to be
1.
internali)ed and transported across the cell. !he (#2 receptor is cleaned off
durin# the secretion.
!he secretory component protects (#2 from proteolytic attac3.
Secretory (#2 has also been shown to inhibit the adherence to dental enamel
dependin# on the strain of the bacteria analy)ed. (ts presence in sali%ary
pellicle indicates that it is intimately related to the tooth surface. !he ability of
secretory (#2 to inhibit adherence appears to be relate to its ability to bind to
surface adhesi%es of bond as well as neutrali)e streptococci bacilli to bacterial
a##re#ation and remo%al from the oral ca%ity.
Secretory (#2 molecular are multi%alent antibodies and can pre%ent
ad%erse effect of bacterial to4ins and en)ymes.
!he results of se%eral studies attemptin# to correlate a protecti%e effect
of (#2 a#ainst dental caries ha%e been conflictin# and also in the role of (#2
and (#2
2
in dental caries. (t is not surprisin# that a characteristic correlation
between sali%ary (#2 le%els and de#ree of protection a#ainst dental caries has
not been readily shown in humans.
Sali%a is well adapted to protection a#ainst dental caries. Sal%ias
bufferin# capability& the ability of sali%a to wash the tooth surface to clean
bacteria& and to control deminerali)ation and minerali)ation& sali%ary
antibacterial acti%ities and perhaps other mechanisms all contribute to the
essential role in the health of teeth.
!5 "5$2N(S"92$(D P76D@$!(6N -
!he first step in the formation of the carious lesions is the increased
production of hydro#en ion in the bacterial pla0ue on the enamel surface.
!hese ions result from the process of #lycolysis& by which simple su#ars Cmono
1:
and disaccharides) enter the bacterial cells and are metaboli)ed by the #lycolic
pathways until or#anic acids are produced.
<hile some simple su#ars enter the mouth directly& much carbohydrates
are consumed in form of lon# chain polysaccharides& such as coo3ed and
uncoo3ed starches. ere we find the first and unhelpful action of sali%a caused
by the action of sali%ary en)yme amylase which be#ins the di#estion of lon#
chains to produce the simple units needed by the bacteria.
Starch lod#in# in sta#ulation sites may be subBected to en)ymatic
de#radation and coo3ed starch which is partly de#raded may become mildly
cario#enic as a result of prolon#ed amylase acti%ity.
2 more direct effect of sali%ary acid production is by bacterial inhibition
by a anti9bacterial effects of sali%ary en)ymes lyso)yme. !actopero4idase and
of lactoferrin and also other powerful inhibitor of pla0ue #lycolysis deri%ed
from both in#ested fluids and sali%a and that is the fluoride ion& which has an
inhibitory effect on pla0ue acid production.
2$(D $85272N$5 -
Stephan& in his studies had demonstrated that followin# su#ar inta3e&
acid production is rapid and within : minutes& the pla0ue will usually ha%e
fallen below #in#i%al o%er#rowth. !he speed at which the pla0ue p is
restored is dependent on many factors of which play and sali%ary bufferin#
capacity are amon# the important and most intensi%ely searched.
<hile the bufferin# capacity of whole sali%a rises on stimulation&
lar#ely because of increased bicarbonate ion production& it remains half of the
whole pla0ue Cwhich has cap of about 2; m e0ui%+lt).
Some I:M of pla0ue bufferin# capacity is due to hydro#en ions bindin#
by proteins of cell walls.
1=
2s the bicarbonate ion concentration in stimulated sali%a bathin# the
dental pla0ue is so hi#h& it is li3ely that the pla0ue ions are rapidly replenished
from sali%a durin# acid production.
!5 (6N($ S559S2< -
<hen the sali%a+ pla0ue bufferin# system can reduce the e4tent of the
fall in p when su#ars enter the mouth& prolon#ed and repeated #lycolysis can
e4haust the ability of system to contain hydro#en ion remo%al.
!he immediate effect of a fallin# pla0ue p is to
a) (ncrease the free ener#y of the ionic species at the enamel ? pla0ue
interphase.
b) 7ate of mi#ration of ions from both enamel and pla0ue.
2s the p falls below = the solubility limit of pla0ue fluid with respct to
hydro4yapatite increases.
<hen p e4ceeds the limit Ccritical p; the calcium and phosphate
mineral ion products of pla0ue fluid lea%e enamel under a concentration
#radient.
owe%er if the bufferin# action is effecti%e and the p rises& the
additional mineral ions in the pla0ue fluid will e4ceed its capacity to hold
themin solution when in contact with hydro4yapatite at the hi#her p. !his
state results in a %ice9%ersa mechanism causin# mineral ions to return to enamel
? reminerali)ation.
!hus the repeated fluctuations in pla0ue p produces a /see9saw1 of
ions across the interface between the enamel surface and the pla0ue fluid. (f
the see9saw actions produce a persistent deft for the enamel& then will occur.
!he role of sali%a in this mechanism is two fold.
(t can replenish the buffer systems of the pla0ue fluid and there is
e%idence of a relationship between sali%a and pla#ue fluid buffer components.
1>
(t can donate mineral ions to the pla0ue increasin# its de#ree of
saturation and reducin# deminerali)ation.
,inally& two other functions of sali%a should be mentioned. !he first is
the mechanism referred abo%e& by which hypominerali)ed newly erupted
enamel& is raised to the status of /mature enamel1 by deposition of mineral and
or#anic material from sali%a into its initially porous structure. <ithout this
transformation teeth in many mouths would ha%e little chance of escapin#
carious attac3 and its e4plains the susceptibility of the newly erupted tooth.
Second process is continuation of first and is the confirmation of an
absorbed layer of protein and #lycoprotein& the pellicle on the enamel surface.
S@""27J 6, !5 2N!($27(5S 2$!(6N 6, S28(A2 -
2ids in enamel maturation
!hey inhibit pla0ue #rowth and metabolism
"ay reduce #lycolysis in pla0ue
Spreads up su#ar clearance by maintainin# the pla0ue p.
Buffers p fall in pla0ue
2ids in reminerali)ation by pro%idin# mineral
(ncreases the rate of carbohydrate clearance
elps in increasin# the thic3ness of enamel pellicle
2ids reminerali)ation by pro%idin# fluoride
"2L67 2N!("($76B(28 P76!5(NS 6, @"2N S28(A2 - C!eno%uo
and 8a#erlof 1GG.)
1. Non (mmuno Globulin Proteins
9 8yso)yme
9 8actoferrin
9 Sali%ary pero4idase system
9 "yelopero4idase system
1I
2. 2##lutinins
9 Parotid sali%a #lycoproteins
9 "ucins
9 Secretory immuno#lobulin 2
9 F 92 micro#lobulin
9 ,ibronectin
*. istidine ? 7ich Proteins Cistatins)
.. Proline 7ich Proteins CStaltherin)
:. (mmuno#lobulins
9 Secretory (#2
9 (#G
9 (#"
(""@N5 ,2$!67S 2ND $27(5S -
!he soft and hard tissues of the oral ca%ity are protected by both1 non
specific1 and /specific1 immune factors& which limit microbial coloni)ation of
the oral surfaces and pre%ent the penetration of no4ious substances and
ensurin# dama#e to the underlyin# tissues.
Non specific immune factors in sali%a are ;
9 8yso)yme
9 8actopero4idase system
9 8actoferrin
9 2ntibacterial compounds and
9 i#h molecular wei#ht #lycoproteinDs
2ll these may act as bacterial a##lutinins& unli3e antibodies& these non specific
factors lac3 immunolo#ic memory and are not subBect to specific stimulation.
"aBor and "inor sali%ary #lands constitute one of the maBor sources for
specific host immune factors 5#. (#2 and (#"& (#G.
1G
(#2 mediates its protecti%e effect mainly throu#h primary bindin# of
anti#en. Bindin# can inacti%ate to4ins& inhibit en)yme based system and effect
many other mechanism in%ol%ed in microbial coloni)ation. !hus bindin# of
se%eral or#anisms result in their a##lutination and conse0uent clearin# from the
mouth.
2n additional source of immune factors is the G$,. !his contributes
more of (#G as well as some Cmonomeric) (#2.
!he cre%icular fluid also contains many of the complement components
and cell types that to#ether with (#G and (#" antibody can /indicati%eD or
/opsoni)eD bacteria.
!hese specific host immune factors in whole sali%a are assisted by the
pha#ocyto)in# non specific P"N8 cells& mi#ratin# from the #in#i%al cre%ice.
Numerous studies ha%e shown that an increased antibody le%el of either
(#2 or (#G to S.mutans can enhance its elimination and or interfere with its
cario#enic acti%ity.
"($76,8672 -
By now it is a#reed that caries cannot occur without microor#anisms. 2s
early as NochDs postulates& it was obser%ed that for caries to occur& bacteria
played a definite role. !he followin# factors further pro%e the role of bacteria in
caries
i) $aries will not occur in complete absence of microor#anisms.
ii) $aries can occur in animals e%en if 3ept on sin#le type of bacterial
#rowth.
iii) 2ll oral or#anisms are not cario#enic& but histolo#ically maBority can be
isolated from carious enamel and dentin.
!he part played by different micro or#anism at different sites is as
under.
a. 6$$8@S28 $27(5S -
2;
!here are differences in occlusal caries and root caries and also in
smooth surface and pit and fissure caries. 5%er since $lar3e disco%ered the
species B.mutans& it is considered to be the si#nificant microor#anism out of all
the oral flora. ,urther studies on S.mitis and S.sali%aris pro%ed that this
or#anism plays a %ital role in initiation of caries.
"ain etiolo#ical microor#anism in occlusal and pit and fissure caries is
S.mutans. S.mutans a) ,erments mannitol and sorbitol Csynthesi)ed insoluble
polysaccharide from sucrose) b) 2re lactic acid formers which easily colonic
on tooth surface& c) 2re more aciduric than other streptococci.
,ew of these properties ha%e also been shown by non cario#enic strains
such as enterococci& streptococci feacalis etc. !wo properties& which ma3e
them separate from other streptococci are ;
i) 2cid accumulation by S.mutans is substance #reater than that
of other oral streptococci.
ii) S.mutans contains lyso#enic bacteriopha#e which has not
been isolated from non cario#enic strains.
D55P D5N!(N28 $27(5S -
2s the en%ironment is different in deep dentinal lesions& it is certain that
the flora of deep caries would be different. !he predominantly present
microor#anisms are lactobacilli which account for 1+* of the oral flora. $ertain
#ram positi%e anaerobes and filaments are also present such as eubacerium&
actinomyces& bacillus& arachnia& bifidobacterium& eubacterium& propionic
bacterium. !he incidence of #ram positi%e facultati%e cocci is low.
$5"5N!28 + 766! $27(5S -
2s the name indicate& root caries starts at the cementum or $5L and
appears only when the cementum is e4posed. (! can occur at any tooth surface
but mandibular molars are more susceptible.
21
!he or#anism in%ol%ed in root caries are different from those in%ol%ed
in other smooth surface lesions. Predominantly actinomyces %iscous ha%e been
isolated other species of 2ctinomyces as 2.naeslundi and no caries etc ha%e
been isolated.
(n e4perimental animals %ariety of or#anism such as 2.%iscosus&
2.naeslundi& S.mutans and S.sali%arius ha%e been shown to produce root caries.
54act strains& which produce root caries is not clear but certainly the bacterial
flora is different in root caries as compared to others.
!5 S@BS!72!5 + D(5! -
Diet refers to the customary food& which we ta3e from time to time and
nutrition means the assimilated portion of diet& which affects the metabolic
process of body. Diet has shown to influence caries.
2 %ariety of factors ha%e been seen re#ardin# the role of diet in caries
production.
a) PJS($28 N2!@75 6, D(5! -
(t has been pro%ed that the physical nature of diet affects caries direct.
!he diet of primiti%e man consisted of raw food includin# sand and soil
coatin#& which led to attrition and cleansin# the debris& thereby reducin# caries.
"odern diet includes refined foods& soft drin3s and etables& which lead to
collection of debris predisposin# to more caries. ,urther it is obser%ed that the
mastication of food reduces the number of microor#anisms. "echanically
rubbin# and cleanin# definitely has role in caries reduction.
b) $5"($28 N2!@75 6, D(5! -
By chemical nature we are mainly concerned with the nutrients present
in our meals& fre0uency of inta3e and also their cario#enic potential. !he main
in#redient is carbohydrate& which is accepted as one of the most important
factor in dental caries process. 6nly refined carbohydrates are effecti%e. ,or
caries production followin# factors are responsible.
22
i) !ype of carbohydrate e#. "onosccharides& Disaccharides or
polysaccharides.
ii) ,re0uency of inta3e
iii) !ime of sta#nation
!he concentration of su#ar in a food can be a 3ey factor in the dental
caries process. Solution of su#ar contains ;.*M of su#ar in 1 liter of water.
,osdic3 stated that the concentration of ;.I " of su#ar must be present
to pass throu#h 1 mm of dental pla0ue and ferment to a harmful le%el Cp :.2)
within a : minutes. Small amount of concentrated caloric sweeteners are Bust
as cario#enic as lar#e amounts.
!ime for caries lesion to de%elop and fre0uency of between meal snac3.
(t ta3es 1I months = months from the incipient attac3in# forces of or#anic
acids on the tooth enamel surface until a carious lesion can clinically be
detected. (n case of 4erostemic patients caries can be detected clinically within
* months.
$aries pre%alence is directly related to the fre0uency of between meal
snac3in# O to 1+* of total carolic inta3e of adolescents comes from between
meal snac3s& but a maBor factor is their hi#h dental caries susceptibility.
$ario#enic Potential of ,oods -
,ood is classified as cario#enic if when it comes into contact with
pla0ue bacteria& the p falls below :.:& which is the tooth deminerali)ation p.
Some of these foods which are cario#enic are applies& caramel& bread&
chocolate& coo3ies etc. ,oods that non acido#enic li3e cheese #enerally
increases the p after comin# into contact with the tooth. !hese non cario#enic
not only increase the pla0ue p abo%e = but also contain relati%e hi#h protein
content& a moderate fat content to facilitate oral clearance& contain minimal
2*
concentration of fermentable carbohydrate& e4erta stron# bufferin# action& ha%e
hi#h mineral content and stimulate sali%ary flow.
Su#ar 2lcohols -
!hese ha%e little + no effect on pla0ue p. !hus it is a#reed that sorbitol
containin# chewin# #ums may not contribute si#nificantly for tooth decay.
Starch 7ich ,oods - !hey tend to retained on and around teeth for a prolon#ed
period of time and are ultimately de#raded to or#anic acids and depress the
pla0ue p for lon#er period of time contributin# to deminerali)ation phase of
dental caries process.
Su#ar 7ich ,oods - !here is a profound effect of readily fermentable carbon on
dental caries sucrose bein# the most cario#enic of the su#ars and #lucose&
fructose and lactose to a little lesser e4tent.
!he physical form of su#ar& that is in solution form it is much less
capable of causin# netal caries when compared to other forms. Stic3y su#ars
de%elop more caries than when compared to su#ars in non stic3y form and
solution form.
Aitamin content of diet ha%e reported to show si#nificant effect on
dental caries. Aitamin D has been shown with #reater relation to dental caries
because it helps in normal de%elopment of teeth& so def. causes malformations
and so increased caries incidence. Aitamin N has been tested as possible
anticaries a#ent by %irtue of its en)yme inhibitin# acti%ity in the carbohydrate
de#radation cycle. Aitamin B comple4 deficiency may e4ert a protecti%e
influence on the tooth since these essential #rowth factors of the acido#enic
flora and also ser%e as components of co9en)ymes in%ol%ed in #lycolysis.
$ertain minerals such as calcium and phosphorous and trace elements
such as selenium and %anadium ha%e some relation to dental caries. 7ole of
2.
calcium and phosphorous is contro%ersial. Def. of calcium durin# infancy and
(@. 8ife leads to poor calcification of teeth which may relate to occurrence of
caries. $aries incidence is si#nificantly hi#her in people residin# in
seleniferous areas and decrease in areas with increasin# %anadium
concentration.
,luoride in %arious forms also reduces the dental caries.
Basically followin# factors are responsible as for as diet and dental
caries is concerned.
i) Particle si)e and rou#hness of diet
ii) Pallatability of diet
iii) 5atin# and drin3in# pattern. 2fter diet and within diet
i%) 7etention and clearance of diet
%) 2#e at which diet is offered
7685 6, P82'@5 (N D5N!28 $27(5S -
(t is a #elatinous mass of bacteria adherin# to the tooth surface.
!he endo#enous microor#anism that are present in pla0ue are S.mutans&
S. sobrinus& lactobacillus species& 2ctinomyces species& nommutans
streptococci and yeast contribute the caries process.
Soft& translucent& and tenaciously adherent material accumulatin# on the
surface of teeth is commonly called pla0ue. Pla0ue is neither adherent food
debris& as is widely and erroneously thou#ht& nor does it result from the
hapha)ard collection of opportunistic microor#anisms. 2ctually accumulation
of pla0ue in teeth is a hi#hly or#ani)ed and ordered se0uence of e%ents. "any
of the or#anism found in the mouth are not found else where in nature.
Sur%i%al of microor#anisms in the oral en%ironment depend son their ability to
adherent to a surface.
2:
,ree floatin# or#anism are rapidly cleared from mouth by the sali%ary
flow and fre0uent swallowin#. 6nly a few speciali)ed or#anisms& primarily
streptococci& are able to adhere to oral surfaces such as mucosa and tooth
structure. !hese adherent bacteria ha%e special receptors for adhesion to the
tooth surface. 6nce they are attached& these pioneerin# or#anism& proliferate
and spread laterally to form a mat li3e co%erin# o%er the tooth surface. ,urther
#roup of bacteria produces a %ertical #rowth away from the tooth surface
Ce4ternal to). !he resultin# mi4ed streptococcal mat allows the adherence of
other or#anisms& such as filamentous and spiral bacteria& that otherwise are
unable to adhere directly to the tooth surface. !hus formation of a mature
pla0ue community in%ol%es a succession of chan#es and each chan#e depends
on the precedin# sta#e preparin# the local en%ironment for the ne4t sta#e.
Pla0ue $ommunities and abitats -
!here are si#nificant differences in the pla0ue communities found in
%arious habitats within the oral ca%ity. !he oral mucosa is populated by
or#anisms with receptor speciali)ed for attachment to the surface of epithelium.
!he dorsum of ton#ue has a pla0ue community dominated by S.sali%arius. !he
teeth ha%e a pla0ue community dominated by S.San#uis and S.mitis. !he
population si)e of "S on the tooth is hi#hly %ariable. Normally it is a %ery
small percenta#e of the total pla0ue population but it can be as lar#e as one half
the facultati%e streptococcal flora in other pla0ues.
<hite P and , on the crown may harbour a relati%ely simple population
of streptococci the root surface in the #in#i%al sulcus may harbor a %ery
comple4 community dominated by filamentous and spiral bacteria. ,acial and
lin#ual smooth surfaces and pro4imal surfaces also may harbour %astly
different pla0ue communities.
D5A586P"5N! 6, P82'@5 -
2=
!he de%elopment of pla0ue is an etiolo#ical phenomenon. !he pla0ue
community structure under#oes a succession of chan#es durin# periods of
unrestricted #rowth. !hese chan#es in the community structure conse0uently
chan#e the o%erall metabolism and other characteristic of the pla0ue.
$ommunity structural chan#es are predictable and are #o%erned by #eneral
principles of ecolo#y.
!he oral ca%ity is a well defined eco system bein# it has reco#ni)ed
#eo#raphic limits and #ather #eneral composition of biolo#ic community is
3nown. <ith the oral ecosystem are distinct habitats such as dorsum of ton#ue&
oral mucosa& #in#i%al sulcus and %arious tooth locations includin# P and , and
%arious smooth surface areas. !hese habitates ha%e uni0ue en%ironmental
conditions and harbour si#nificantly different communities of microor#anisms.
<ithin each habitual special combination of food and shelter are a%ailable to
support particular species of oral bacteria. !his special combination of food
and shelter is termed as an /ecolo#ical niche1.
!he #rowth of pla0ue is not P of a random accumulation of opportunistic
or#anism passin# throu#h the oral ca%ity. 7ather& an orderly se0uence of
replacement communities occupies the tooth surface& each community
modifyin# the local en%ironment of that site. !he a%ailable niches& the limitin#
factors and the en%ironment conditions chan#e as a result of the biolo#ic
acti%ity of each pla0ue community. !his process of mutual chan#e of the
community and its en%ironment is called /5colo#ic Succession1.
Pla0ue #rowth consist of surface attachment and their lateral spreadin#
as the attached or#anisms multiply. <hen the entire surface is co%ered #rowth
of colonies increases the thic3ness of the pla0ue. 2s the ori#inal coloni)in#
or#anisms proliferate& their pro#ency produces %ertical columns of cells called
/Palisades1. !he palisades can be in%aded by filamentous bacteria that
otherwise could not e4ist on the tooth surface.
2>
5arly Sta#es of Pla0ue Succession ;
<ithin 2 hours of professional remo%al of all or#anic material and
bacteria from a tooth surface& a new coat of structure less or#anic film& the
pellicle can completely co%er. !he pellicle is formed primarily from the
selecti%e precipitation of %arious components of sali%a. !he functions of
pellicle are ;
9 Protect the enamel
9 7educe friction between the teeth
9 Possibly pro%ide matri4 for reminerali)ation.
!he pellicle is formed from sali%ary proteins which include lyso)yme& albumin
and immuno#lobulin& (#2 and (#G. !he stron# affinity of sali%ary proteins for
e4posed hydro4yapatite is also of clinical important in operati%e dentistry&
because sali%ary contamination of a freshly etched enamel surface pre%ents
bondin# of composite restorations.
!he early sta#es of recoloni)ation of the cleaned tooth surface in%ol%e
adhesion between the pellicle and the pioneerin# or#anisms. S.san#uis alon#
with actinomyces %iscous& 2ctinomyces naeslundi and Peptostreptococcus are
the main pioneerin# species and are capable of attachin# to the pellicle within 1
hour after tooth cleansin#. !he adhesion process sis %ery selecti%e and re0uires
specific or#anism receptors capable of bindin# to certain areas on the
precipitated sali%ary proteins of the pellicle. 8i3e for e4ample the en)yme
#lucosyl transferase maybe of critical importance in the adherence of "S to the
pellicle when sucrose is present because it enhances the polymeri)ation of the
e4tracellular matri4 that ma3es "S forms such tenaciously adherent.
8ate Sta#es of Pla0ue Succession -
!he late sta#es of pla0ue succession are responsible for causin# either
caries + the periodontal disease. 5arly sta#es in pla0ue succession are #enerally
2I
lac3in# in patho#enic potential because they are primarily aerobic communities
and lac3 sufficient number or proper types of or#anisms to produce sufficient
0uantities of dama#in# metabolites.
owe%er as pla0ue matures& the production of cells and matri4 slow and
utili)ation of ener#y for the total community nut. 7esults in acid production
since mature pla0ue is primarily anaerobic& it reduces the a%ailable nutrients to
anaerobic metabolites that is fermentation products includin# wea3 or#anic
acids& amides and alcohol. "ature pla0ue communities rapidly metaboli)e
sucrose throu#h #lycolytic pathway to or#anic acids& primarily lactic acid. (N
cario#enic pla0ue& %irtually all the a%ailable successor is metaboli)ed to acid&
resultin# in se%ere and prolon#ed drop in p& thereby increasin# the potential
for enamel deminerali)ation. Deminerali)ation of enamel occurs at p of :.;
to :.:. 2 sin#le successor e4posure + rinse can produce p depression lastin#
upto 1 hour.
,2$!67S !2! S57A5 2S 5$686G($ D5!57"(N2N!S -
5colo#ic determinants are factors that e4ert ecolo#ic control o%er
habitats or nidus and ultimately determine the characteristics of dental pla0ue
community. Some of the determinants that control the o%erall composition of
the pla0ue community are shelter& p& o4y#en saturation and nutrient
a%ailability.
$urrent ypothesis to e4plain the role of pla0ue bacteria in the etiolo#y of
dental caries -
!here are two hypothesis concernin# the patho#enecity of pla0ue.
Non9Specific Pla0ue ypothesis -
!his promotes the uni%ersal presence of potential patho#ens in pla0ue
and therefore assumes that all accumulations of pla0ue are patho#enic.
Specific Pla0ue ypothesis -
2G
(t is based on the obser%ation that accumulation of pla0ue is not always
associated with the disease. (n this accumulation pla0ue can be considered
normal in the absence of the disease. Pla0ue is assumed to be patho#enic when
the disease is present.
!his hypothesis pro%ides a new scientific basis for the treatment of
caries that has radically altered caries treatment. Because only limited number
of microor#anisms are capable of caries production specific pla0ue hypothesis
treatment is aimed at elimination of specific patho#enic or#anisms but not total
pla0ue elimination.
5colo#ic Pla0ue ypothesis Carsh 1GG.)
Dynamic relationship e4ists whereby an en%ironmental chan#e in pla0ue
Ce#. 8ow p) dri%es a shift on the balance of the resident micro flora& thereby
shiftin# the balance towards enamel deminerali)ation. caries can be pre%ented
not only by inhibitin# the putati%e patho#ens Ce#. "S) but also by interferin#
with the en%ironmental chan#e dri%in# the ecolo#ic shift. 5#. By reducin# the
acid challen#e to pla0ue by the use of alternati%e sweeteners + fluoridated oral
health care products
"($76B(686GJ 6, D5N!28 $27(5S -
!he ori#in of oral microbiolo#y coincides with the disco%ery of bacteria
by 8ewenhoc3 in 1=I*. 8ewenhoc3 studied the morpholo#ical types of
bacteria from the oral ca%ity. "any theories were proposed for the cause of
dental caries.
5rdl in 1I.* put forth an another concept termed as the parasitic theory
of dental decay& which attributed dental caries to microor#anisms or denticolon.
(n 1I:;& Nlenc3e described a parasites labeled protococcus dentalis as
the cause of dental caries for it could dissol%e enamel and dentin.
*;
(N 1I=>& two German physicians& 8eler and 7ottenstein stated that
dental caries is started as purely chemical process but the li%in# or#anisms
caused its pro#ression into enamel and dentin.
8ater in 1II1& in%esti#ation of etiolo#y of dental caries were made in
NochDs laboratory in Berlin by B.D."iller. he presented that concept of the
role of acid sand bacteria in dental caries productions. !his theory was termed
as chemo parasitic theory.
$lar3e in 1G2.& described a new streptococcus species& S.mutans& which
was isolated from carious lesions in the teeth of British Patients& later
lactobacillus acidophilus was identified.
Between 1G2;Ds and 1G.; number of studies was carried out to study the
e4istence of microor#anisms responsible for dental caries by wor3ers li3e
2rnold and "ch$here and Bec3s& Lenser and "iller.
(N 1G=;& ,it)#erald and Neys isolate specific streptococci from rodent
carious lesions. $aries inducin# streptococci are now considered members of
S.mutans #roup.
!he most important factor in the patho#enesis of dental caries is the
capacity of a lar#e number of oral bacteria to produce acid from the dietary
carbohydrates. "iller in his study conclude that no sin#le #roup or specie
could be responsible for dental caries. (nstead& se%eral or all acido#enic
bacteria should be considered responsible.
2cido#enic bacteria usually found in lar#e numbers are streptococci&
lactobacilli& actinomyces and yeasts. !he ability of bacteria in pla0ue to
produce acids %aries when first e4posed to carbohydrates& all acido#enic
bacteria produce aids& but when p decreases& more and more of the bacteria
*1
loose their ability. <hen p reduces to the critical le%el only few bacterial
species produce acids. !hese aciduric bacteria are of #reat importance
Clactobacillus and S.mutans) in the patho#enesis of caries.
2part from S.mutans& S.san#uis& S.mitis 2ctinomyces %iscous and
2.naeslundi produces e4tracellular insoluble #lucans to %arious e4tent in the
presence of sucrose.
!he cario#enicity of different pla0ue bacteria is to an e4tent determined
by the type of the interbacterial matri4 they create. !hese insoluble e4tra
cellular #lucans increases in pla0ue as the sucrose consumption increases. !hus
the #lucans mechanically stren#then the pla0ue a#ainst the forces of
mastication and sali%a washin#& thus facilitatin# the a##re#ation of acido#enic
bacteria on the teeth.
,urther se%eral other #roups of or#anisms in dental pla0ue such as
S.mutans& S.mitis& 2. %iscous& 2.naesulundii and lactobacillus under#o
metabolism and produce intracellular polysaccharides which has the ability to
maintain acid production for prolon#ed periods in the absence of e4o#enous
su#ar sources& thereby contributin# si#nificantly to enamel dissolution.
S!75P!6$6$$@S "@!2NS -
6f all the bacteria& streptococci ha%e been studied most e4hausti%ely.
"ucous membrane in the mouth and other parts of the body are characteristic
habitats for streptococci. !he most prominent species of streptococci found in
oral ca%ity include S.mutans& S.mitis& S.mitior& S.Sali%arius and S.milleri.
2lthou#h S.san#uis& S.milleri and S.sal%arius ha%e occasionally been found to
induce fissure caries. S.mutans li3e bacteria comprise the most important #roup
of streptococci implicated in caries etiolo#y.
5colo#y -
*2
S.mutans does not coloni)e in the mouths of the infants prior to the
eruption of teeth. !he same way it disappears from the mouth after e4traction
of all the teeth. (nfants most li3ely become infected from their parents. Studies
which are utili)ed lacteriocin typin# and serotypin# the /fin#er print1
indi%idual strains ha%e shown that strains isolated from newly erupted teeth of
infants are one identical to those present in the sali%a of the mother.
S.mutans does not coloni)e teeth uniformly. !he or#anisms may be
more fre0uently isolated from fissures and interpro4imal surfaces. (t does not
spread readily from one tooth surface to the other. S.mutans may be spread to
other surfaces by the use of floss + dental e4posures.
S@$76S5 "5!2B68(S" 6, S!75P!6$6$$@S "@!2NS -
!he most important substrate for the in%ol%ement of S.mutans in the
caries process is the disaccharide sucrose. Sucrose not only ser%es as a primary
ener#y source but also permits the initiation of additional biochemical a#ents
which are responsible for the cario#enic potential of this microor#anisms.
!here are three pathways in%ol%ed by which S.mutans dissimilate
sucrose.
1. $on%ersion of sucrose to adhesi%e e4trcellular carbohydrate polymers
by all bound and e4tracellular en)ymes.
2. !he transport of sucrose into the cell interior accompanied + followed by
direct phosphorylation for ener#y utili)ation throu#h the #lycolytic
pathway leadin# to lactic acid production.
*. !he de#radation of sucrose to free #lucose and fructose by in%erta#e.
S!75P!6$6$$( 6!57 !2N S."@!2NS -
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!his E9hemolytic streptococcus species was ori#inally isolated from the
blood of patient with bacterial endocarditis. (n humans& this or#anism habitats
**
mainly in the oral ca%ity& especially in dental pla0ue. !he specie do not
coloni)e the oral ca%ity until the first teeth erupt at about = months of a#e.
Serolo#ical studies of S.san#uis indicate the presence at least *9. types.
<hile the serolo#y is comple4. !he or#anisms are easy to identify on sucrose
containin# media& because it produces small& firm colonies. S.san#uisis found
both in carious and non carious sites. (t ahs %ery low cario#enecity in
e4perimental animals with lesions limited to occlusal fissures.
S!75P!6$6$$@S "(!(67 -
6ften called S.mitis this or#anism does not hydrolyse ar#inins and
e3ulin as does S.san#uis. (t produces soft round and blac3 brown colonies on
mitis sali%arious medium& which contain sucrose. 2 characteristic feature of
this or#anism is the absence of si#nificant amounts of rhamnose in cell wall. (t
produces e4tracellular #lucan from sucrose& S.mitis is one of the most
commonly isolated bacteria in buccal mucosa. !his alon# with S.san#uis are
amon# the most predominant or#anism in dental pla0ue. (ts si#nificance in
human caries is un3nown and assumed to be %ery minor.
S!75P!6$6$$@S S28(A27(@S -
!his is found predominantly in ton#ue& soft tissue and in sali%a but not
in hi#h number in pla0ue. S.sali%arius adheres well to epithelial cells but not to
hard tissues& especially pellicle coated enamel. (ts low number in human
pla0ue su##ests that its into of #reat si#nificance in human caries initiation.
S!7P5!6$6$$@S "(8857( -
!his was ori#inally isolated from dental& brain and li%er abscesses. (t is
also found in #in#i%al cre%ice& cer%ical pla0ue but not in other intraoral sites.
2lthou#h some strains induce fissure caries in e4perimental animals& but its
importance in dental caries in humans is not 3now at present.
*.
S!75P!6$6$$@S S6B7(N@S -
!his alon# with S.mutans are now thou#ht to be the main etiolo#ical
a#ent in dental caries. But further studies are needed to pro%e this.
6!57 B2$!57(2 2SS6$(2!5D <(! $27(5S 82$!6B2$(88( -
(n 1G1:& Nli#ler reported the presence of hi#her numbers of lactobacilli
in carious lesions. 8actobacilli are stron# acid producers amon# the most
aciduric and acido#enic bacteria. !hese aciduric characteristic ha%e been
utili)ed for the de%elopment of selecti%e #rowth media for caries acti%ity base
don lactobacillus count. !hey are found in carious lesions and their numbers in
pla0ue and in sali%a correlate with caries e4perience. !he restrictions of
dietary carbohydrate and restorations of teeth reduce the number of lactobacilli
population. !hese are often seen in deep dental caries because of their acid
resistance. !hey may not be directly associated with caries initiation but rather
become secondary in%aders which contribute to the pro#ression of already
e4istin# lesion.
,(82"5N!6@S B2$!57(2 -
Se%eral types of filamentous or#anism ha%e shown to initiate root
surface caries. 2ctinomyces and 7ottia species ha%e been found in human
dental pla0ue and dental caries. 2 %iscous& an acido#enic bacterium that also
stores intracellular polysaccharides& is always amon# the predisposin# flora of
pla0ue o%erlyin# the root lesions.
G72" N5G2!(A5 $6$$( -
Aeilionella - 6f the #ram C9)%e cocci& this species is most commonly found in
pla0ue. !hese or#anism lac3 by en)ymes in%ol%ed in #lycolysis and the
he4ose morphosphate shunt and therefore do not utili)e su#ars as an ener#y
source. Aeilionella utili)es lactic acid by con%ertin# it to pripionic and other
wea3 acids.
*:
!hus is tells that there is decreased caries acti%ity when the pla0ue has
%eilionella in it. (n other words it is the composition of pla0ue micro flora
rather than Bust the 0uantity of pla0ue that determines the patho#enecity.
SP5$(,($ B2$!57(2 2SS6$(2!5D <(! 5N2"58 $27(5S -
"ost commonly found bacteria are lactobacilli which was reported
earlier by Goadby as bacillus microdentalis. (t was later identified as
lactobacillus species. 6ral lactobacillus comprise a spectrum of species amon#
which 8.casei and 8.,fermentium constitute the bul3 of strains.
S.mutans was first described by $lar3e in 1G2.& which is found
predominantly in the oral flora.
8actobacilli and S.mutans are found nearly in all carious lesions and
their proportion in pla0ue and sali%a is positi%ely related with caries fre0uency
acti%ity. S.mutans is more closely associated with initial caries lesions on
smooth buccal and lin#ual enamel surfaces than lactobacillus.
S.san#uis and S.mitis+ mitior are common in dental pla0ue and present
in numbers than found to be in%ersely relate dot caries acti%ity. (t is because
S.san#uis and S.mitis produce less acid than S.mutans.
S.sali%arius is also able to induce caries& but this constitutes only a
small fraction of mature micro biota of dental pla0ue.
2ctinomyces sp. 2re present in pla0ue o%er carious lesion and necrotic
carious dentin. 2lthou#h it was belie%ed that 2ctinomyces specie does not
initiate enamel caries& but a recent study report indicates a relationship of
actinomyces odontolycius to the initiation of caries in appro4imal areas of
deciduous molar teeth.
Jeasts are also isolated from sali%a& pla0ue and dental caries. !hese
or#anisms are aciduric but produce acid slowly. !he primary oral reser%oir of
yeast is the ton#ue and their numbers in dental pla0ue are low. !hey are
*=
therefore not li3ely to contribute to the initiation of dental caries. Btu they may
be isolated from caries lesions because of their aciduric property& which
enables yeasts to increase in numbers on the %arious oral surfaces in the acid
en%ironment e4itin# durin# hi#h caries acti%ity.
Se%eral studies ha%e shown than S.mutans and lactobacilli are related to
the de%elopment of dental caries on smooth enamel. (n fissures& S.mutans and
lactobacilli are not found in hi#her proportion than S.san#uis the opposite is
true in caries free fissures. !he initiation of caries tends to be preceded by
ele%ated number of both S.mutans and lactobacilli and to certain e4tent to
decreased number of S.san#uis.
(n conclusion& S.mutans and species within lactobacilli are stron#ly
associated with the initiation of caries in enamel. !hese or#anisms ha%e a
number of characteristic li3e ;
1. Both S.mutans and lactobacilli are acido#enic and ha%e a hi#h acid
production rate.
2. Specifically S.mutans& but also lactobacilli are able to produce insoluble
e4tracellular #lucans.
*. S.mutans and species within lactobaicllius ha%e the ability of intracellular
polysaccharides production.
.. Both the #roups are considered as aciduric or#anism.
!hese characteristic specially& the combination of aciduric and stron#ly
acido#enic capability should be re#arded as bestowin# %irulence to S.mutans
and lactobacilli.
$onse0uently& caries can be considered as a result of combined action of
all acid producin# bacteria in pla0ue contributin# to %arious de#rees.
"($76967G2N(S"S 2SS6$(2!5D <(! 766! S@7,2$5 $27(5S -
*>
2 %ariety of bacteria coloni)e supra#in#i%al root surfaces. !he #enera
often found are actinomyces& streptococcus includin# S.san#uis& S.mitis and
%eillonella. 7ecent studies show that two #ram C9)%e #enera cytopha#a and
capno cytopha#a strains of cytocapnopha#a are specifically able to coloni)e
root surfaces. !he #lidin# capacity of capno cytopha#a ma3es its able to
e4tensi%ely in %ade dentinal tubules.
2s in enamel caries& lactobacilli and S.mutans are associated with root
caries. 5%en caries other acido#enic bacteria li3e S.san#uis and actinomyces
specially found in lar#e numbers also contribute in the patho#enesis of root
caries. 2 %iscous is also one of the most dominant species in supra #in#i%al
pla0ue& which may contribute in production of root caries.
$ementum and dentin are rich in or#anic framewor3s. !he clinical and
histopatholo#ical features of root surface caries are not the same as enamel
caries. (n root caries& important microor#anisms may be not only the hi#hly
acido#enic and aciduric bacteria but also those possessin# proteolytic and
peptidolytic acti%ities.
"($7667G2N(S"S 2SS6$(2!5D <(! D5N!(N28 $27(5S -
<hen the caries lesion has penetrated into the dentin& the conditions for
microbial #rowth will chan#e. !he p of carious dentin can be low specially
when enamel lesion is small and a thic3 layer of carious dentin e4ists. ,urther&
the lar#e part of or#anic material in dentinal may fa%our #ram CQ)%e bacteria
and lactobacilli predominate the microbiota of carious dentin.
8ess is 3nown about the caries promotin# capacity of %arious or#anisms
in carious dentin. owe%er microbial products such as or#anic acids and
en)ymes are found ahead of the bacterial front. !hese substances may
ori#inate from the bacteria e4istin# both in necrotic and the deeper part of the
carious dentin.
*I
5arly studies concerned with the microfilaria of dental lesions showed
that the common bacteria found were positi%e allomorphic rods or #ram
positi%e filaments. "ore different studies to identify the flora of an ad%anced
lesion in dentin ha%e now been underta3en. !he dominant or#anism are ;
8actobacilli species - **M
2rachnia species - 12M
5ubacterium species - 11M
Propionibacteirum species - ;GM
Bifido bacterium species - ;>M
Peptostreptococcus species - ;=M
Streptococcus species - ;:M
2ctinomyces species - R 1M
!here is no 0uestion that dental caries is an infection. !he 0ualititati%e
nature of flora in pla0ue determines the metabolism and potassium for caries
production. !his %iew is termed specific pla0ue hypothesis. !he concept says
that certain pla0ues are more cario#enic than others because they contain
hi#her number of specification between species that cause cries specific
implicated most often in enamel caries are S.mutans and lactobacilli and in root
caries its actinomyces %iscous. 2ccordin# to this hypothesis most& but not
necessary all carious lesions are due to specific bacterial species. ,urther the
hypothesis implies that pla0ue in some sites is not disease producin#. !he
concept of this specific pla0ue hypothesis su##ests the de%elopment and
implementation of pre%ention procedures that treat dental caries as a specific
bacterial infection.
D5"(N5728(H2!(6N 2ND 75"(N5728(H2!(6N !66! S@7,2$5-
!he physiochemical inte#rity of dental enamel in the oral en%ironment is
entirely dependent on the composition and chemical beha%iour of the
surroundin# fluids i.e. sali%a and pla0ue fluids. !he main factors #o%ernin# the
*G
stability of enamel apatite are p and the free acti%e concentrations of calcium&
phosphate and fluoride in solution& all of which are deri%ed from the sali%a.
!he carious process is initiated by the bacterial fermentation of
carbohydrates& leadin# to the formation of %ariety of or#anic acids and
therefore fall in p. (nitially the
Q
will be ta3en up by the buffers in pla0ue
and sali%a& when the p continues to fall CQ increases) howe%er the fluid
medium will be depleted of 69 and P6
*
.
which react with
Q
to form
2
6
and P6
2
.
.
6n total depeletion of C69 and P6
*
.
) the p can fall below the critical
%alue of :.:& where the a0ueous phase becomes undersaturated with respect to
hydro4yapatite. !herefore& whene%er surface enamel is co%ered by a microbial
deposit& the on#oin# metabolic process within this barrier results influctuations
in p and occasionally steep falls in p& which may result in dissolution of the
minerali)ed surface. !he role of sali%a in this process is hi#hly dependent on
accessibility& which is closely related to the thic3ness of pla0ue.
So therefore& in principle dental enamel can be dissol%ed under two
different chemical conditions. 1) <hen the surroundin# a0ueous phase is
under saturated with respect to hydro4yapatite C2). 2) Supersaturated with
fluorapatite C,2).
<hen 2 is dissol%ed and ,2 is formed& the resultin# lesion is a carious
lesion. Dissol%in# 2 ori#inates from the sub surface enamel and ,2 is
formed in the surface enamel layers. !he hi#her the super saturation with
respect to ,2& the more fluoride is ta3en up in the enamel surface the better
minerali)ed the surface enamel layer becomes and less demateriali)ed is the
surface body of the lesion.
.;
6n other hand& if there is undersaturation with respect to both 2 and
,2& both apatites dissol%e concurrently and layer after layer is remo%ed and
this result sin an erosi%e lesion.
7685 6, $28$(@" -
(t is a bi%alent ion e4creted to#ether with )y#oma proteins& into the
lumen of the acini. !he calcium found in sali%a is dependent on the stimulation
rate of sali%a. Dependin# on p calcium is distributed in sali%a as ioni)ed and
bound forms.
!he free& ioni)ed calcium is especially important in the carious process
because it participates in establishin# the e0uilibrium between the calcium
phosphates of the dentinal hard tissues and its surroundin#. 2t p %alues
closed to normal the ioni)ed caries constitutes appro4imately :;M of the total
calcium concentration but it increases if sali%ary p is lowered. !hen bound+
unioni)ed calcium is distributed in such a way that it is more + less firmly
bound to inor#anic ions such as inor#anic phosphate& bicarbonate and fluoride.
!he tooth is usually separated from the sali%a by an intermediate layer
of inte#uments in the form of a pellicle or + pla0ue. !he total caries these
compartments is sli#htly hi#her& some times much hi#her than the sal%ia
because of hi#h concentration of bindin# sites for calcium and because of
precipitated calcium slats. !here is a stron# correlation between both total and
ioni)ed calcium in sali%a and dental pla0ue& showin# a flow of calcium o%er the
pla0ue sali%a interface followin# e4istin# diffusion #radients in ioni)ed
calcium. !his #radient will be lar#e after su#ar inta3e& liberatin# bound calcium
as the pla0ue p slowly increases the concentrations of ioni)ed calcium in
sali%a& pellicle and pla0ue will slowly reach an e0uilibrium.
7685 6, (N67G2N($ P6SP2!5 -
.1
!he concentration of these ions are dependent on the p of the sali%a.
!he lower the p the less concentration of the ions& indicatin# that the ion
production of .2. decreases considerably with decreasin# p. !he
phenomenon is the main cause of the deminerali)ation of the tooth s with
calcium& the content of inor#anic phosphate in sali%a is prere0uisite for the
stability of the tooth mineral in the oral en%ironment.
2bout 1;92:M of the inor#anic phosphates dependin# on p& is
completed to in or#anic ions such as calcium as is bound to proteins. 2 small
part& i.e. less than 1;M is in the /disease form1 which is a potent inhibitor of
the precipitation of calcium phosphate and influences the formation of calculus.
!his is the rationale for the inclusion of pyrophosphates in tooth paste intended
to inhibit calculus formation.
7685 6, ,8@67(D5 -
,luoride in the fluids surroundin# the enamel crystals has been shown to
ha%e potential to reduce the rate of deminerali)ation. <hen present in the
li0uid phase of deminerali)ation fluoride will be incorporated into the enamel
crystal and the enamel will become more resistant to deminerali)ation.
,luoride has also been shown to reduce the cid production in dental pla0ue.
!he hi#h initial fluoride concentration in the sali%ary film after fluoride
e4posure will establish a concentration #radient between the dental
inte#umentDs and the pla0ue. ,luoride will diffuse from sali%a into the pellicle
and the pla0ue& rapidly ele%atin# the concentration of fluorides in the pla0ue
fluid. "ineral $a,
2
may form in sali%a& pellicle and pla0ue fluid.
!he limitin# factor for the formation of $a,
2
is the calcium content of
the oral fluids. !herefore the use of fluoride chewin# #um after e%ery meal as
a combined sali%a stimulatin# and fluoride a#ent resultin# in increased calcium
release from the sali%a& foramen release and increased bufferin# effect& offers a
.2
rational and administered measure for caries control durin# are Bust after the
fall in p. $a,
2
releases fluoride slowly. ,luoride diffusin# into
microor#anism also pre%ent participation of en)yme enolase in the #lycolytic
pathway by bindin# ma#net sum essential for optimal function of the en)yme.
$8(N($28 P($!@75 6, !5 D5N!28 $27(5S P76$5SS -
2 pla0ue community of sufficient mass to become anaerobic at the tooth
surface has the potential to be cario#enic. 2 lar#e pop of "S %irtually& assures
this occurrence. 2 sucrose ? rich diet #i%es a selecti%e ad%anta#e to "S and
allows the or#anic to accumulate in lar#e numbers in the pla0ue community.
!he sucrose rich en%ironment also allows "S to produce lar#e 0uantities of
e4tracellular polysaccharides. !here form a #elatinous meta. !hat produces a
diffusion ? limitin# barrier in the pla0ue. !he combination of limited diffusion
and tremendous metabolism acti%ity ma3es the local en%ironment anaerobic
and e%ery acidic and thus an ideal en%ironment for dissolution of the subBacent
tooth surface. 6nce the tooth surface becomes ca%itated& a more retenti%e
surface area is a%ailable to the pla0ue community. !his allows filamentous
bacteria that ha%e poor adhesion abilities such as lactobacilli& to become
established in the lesion.
(n the absence of chan#e in the hostDs diet and oral hy#iene practices&
the ca%itations of the tooth surfaces produces a syner#istic acceleration of the
#rowth of the cario#enic pla0ue community and e4pansion of the ca%itations.
!his results in a rapid and pro#ressi%e destruction of tooth structure. 6ne
enamel caries penetrates to the D5L& rapid lateral e4pansion of the carious
lesion ta3es place because dentin is much less resistant to caries attac3. !his
shelted& hi#hly acidic and anaerobic en%ironment pro%ides an ideal niche for
lactobacilli& which was earlier throu#h to be primary etiolo#ic a#ent. But "S
are problem the most important or#anic in the initiation of enamel caries and
2.%iscous is the most li3ely or#anic to initiate root caries. 2fter caries initiation
lactobacilli than become residents of the carious lesion& once their niche is
.*
a%ailable. Because of their acido#enic potential and aciduric lifestyle&
lactobacilli are probably %ery important in the pro#ression of dentinal caries.
$8(N($28 S(!5S ,67 $27(5S (N(!(2!(6N -
!he characteristic of a carious lesion %ary with the nature of the surface
on which the lesion de%elops. !here are three distinctly different clinical sites
for caries initiation.
1) 7ecess of de%elopment pits and fissures of enamel.
2) Smooth enamel surfaces that shelter pla0ue
*) 7oot surface
Pits and ,issures -
!he pit and fissures of newly erupted teeth are coloni)ed by bacteria.
!hese early coloni)es from a /bacterial plu#1 that remains for a lon# time&
perhaps e%en the life of the tooth. !here are lar#e %ariation in the microfilaria
found in P and ,& su##estin# that each site can be considered a separate
ecolo#ic system. 8ar#e numbers of #ram Positi%e cocci especially S.san#uis
are found in the P and , of newly erupted teeth& whereas lar#e number of "S
are usually found inc %arious P and ,.
!he shape of Pit and ,issure contributes to their hi#h susceptibility of
caries. !here is considerable morpholo#ic %ariation in these structures. Some
pit and fissure ends blindly& other open near dentin and others penetrate to
entirely throu#h enamel.
Pit and fissure caries e4pands as it penetrate into the enamel. !his the
entry site may appear much smaller than the actual lesion& ma3in# clinical
dia#nosis difficult. $arious lesions of pit and fissure de%elops from attac3 on
their walls.
..
!he pro#ress of dissolution of the walls of a Pit and fissure lesion is
similar in principle to that of smooth surface lesion because there is wide area
of surface attac3in# e4tendin# inward& parallelin# the enamel rods. !he
occlusal enamel rods bend down and terminate on dentin immediately below
the de%elopment of enamel fault. !hus a lesion ori#inatin# in P and , effect a
#reater area of D5L than does a comparable smooth surface lesion. (n a $+s it
is a in%ested SAD with narrow entrance and wider at D5L.
S"66! 5N2"58 S@7,2$5S -
!he smooth enamel surfaces of a teeth present a less fa%ourable site for
pla0ue retention. Pla0ue usually de%elops on one those smooth surfaces that
are near the #in#i%a or under pro4imal contact. !he pro4imal surfaces are
particularly susceptible to caries because of e4tra shelter pro%ided to resident
pla0ue due to pro4imal contact area immediately occlusal to the pla0ue.
8esions startin# on smooth surface ha%e a broad area of ori#in and a conical or
pointed& e4tension towards the D5L. !he path of in#ress of lesion is rou#hly
parallel to lon# a4is of enamel rods in the re#ion. 2 $+s of enamel portion of
smooth surface lesion shows a A shape with a wide area of ori#in and the ape4
of A directed towards the D5L. 2fter caries penetrates the D5L softenin# of
dentin spreads rapidly laterally and pulpally.
766! S@7,2$5 -
!he root surface is rou#her than enamel and readily allows pla0ue
formation in the absence of #ood oral hy#iene. !he cementum co%erin# the
root surface is e4tremely thin and pro%ides little resistance to caries attac3.
7oot caries lesions ha%e less well defined mar#ins& tend to be @ shaped in $+s
and pro#ress rapidly because of lac3 of protection from an enamel co%erin#. (n
recent years pre%alence of root caries is increased because of the increasin#
number of older persons who retain more teeth& e4perience #in#i%al recession
and usually ha%e cario#enic pla0ue on e4posed root surfaces.
.:
$8(N($28 "2N(,5S!2!(6NS 6, D5N!28 $27(5S P76$5SS -
5278J $2NG5S -
!he earliest sta#e of caries is the first time deminerali)ation of enamel
after a pla0ue p depression below the critical p. !his cannot be detected
clinically but throu#h sophisticated e4perimental laboratory techni0ues.
<(!5 SP6! 85S(6N -
!he first %isual clinical presentation of dental caries is commonly
referred to as a /white spot lesion1. 2lthou#h it is considered to be an incipient
lesion& it is actually a relati%ely late state of caries process. !he lesion must
pro#ress to a depth of *;;9:;; m to be clinically detectable. !he clinical
appearance of the white spot is caused by loss of sub surface enamel& resultin#
in the loss of enamel translucency. !he surface enamel o%er the white lesion
can appear as bein# clinically intact and smooth& #enerally indicatin# that the
lesion is not acti%e. !hose white spots with rou#h surface because of increased
porosity indicate that the lesion is acti%e and may pro#ress. 2lthou#h
formation of white spots has been most e4tensi%ely studies with smooth surface
caries& it appears that P and , and root caries also start with sub surface
deminerali)ation.
2t the white spot sta#e the lesion may be arrested or re%ersed by
modifyin# any of the causati%e factors on increasin# pre%enti%e measures.
2lthou#h this sta#e is a re%ersible sta#e of clinical process& it can sometimes
leads to softenin# and loss of enamel surface due to hi#h cario#enic potential.
!he white spot sta#e can be considered as a #radually arrested lesion&
which may + may not pro#ress to a fran3 ca%itations. !herefore it is considered
as a pre ca%itated lesion su##estin# that it will e%entually lead to ca%itations but
not a ca%itated lesion.
(DD5N + 6$$@8! $27(5S -
.=
$oncerns ha%e been raised that there is an increased pre%alence of caries
pro#ressin# into dentin on tooth surface with clinically intact surfaces.
2pparently& the increased use of topical fluoride may he the effect of
preser%in# the inte#rity of enamel surface& which may mas3 the pro#ression of
dentinal caries lesions beneath the surface.
,72NN $2A(!2!(6NS -
2s the caries process pro#resses& the subsurface lesion e%entually leads
to the collapse of surface layer and formation of ca%itation re0uirin#
restoration. 2! this sta#e of caries process& tooth destruction pro#ress more
rapidly because the ca%itations fa%ours pla0ue accumulation and reduced
sali%ary access.
2775S!5D 85S(6NS -
$aries lesions can theoretically become arrested at any sta#e of caries
process& either because the causati%e factors ha%e chan#ed or protecti%e factor
are increased. 2 chan#e in the oral en%ironment can result in the arrest of
caries process.
2$@!5 D5N!28 $27(5S -
(t is that form of caries& which is a rapid clinical course and results in a
early pulp in%ol%ement by the carious process the process of rapid that there is
little time for the deposition of secondary dentin. !he dentin is usually stained a
li#ht yellow. $a%ity is deep& underminin# of enamel& pain is present& softenin#
of dentin.
$76N($ D5N!28 $27(5S -
(t is that form& which pro#resses slowly and tends to in%ol%e the pulp
much alter than acute caries. !he slow pro#ression of the lesion allows
sufficient time for both sclerosis of the dentinal tubules and deposition of
secondary dentin in response to the ad%erse irritation. !he carious dentin is
.>
often stained deep brown. !he ca%ity is #enerally shallow one with a minimum
softenin# of dentin. !here is little underminin# of enamel and pain is not a
common feature.
N@7S(NG B6!!85 $27(5S -
(t is a type of rampant caries effectin# the deciduous teeth. !here is
wide spread carious destruction of deciduous teeth& most commonly the four
ma4illary incisors followed by first molars and then cupids. !( is the absence
of caries in ma4illary incisors& which distin#uishes this disease from ordinary
rampant caries.
"ost of ions throu#h carious enamel can result in third dissolution of the
underlyin# dentin before actual ca%itations of the enamel surface. !he acid
attac3 at the e4ternal ends of the dentinal tubules initiates a pulpal response
Because the straie from hori)ontal liens of #reater permeability in the enamel&
they probably contribute to the lateral spread of smooth surface lesions. !he
striae appear to be accentuated in early lesions due to the decreased mineral
content.
(n the occlusal enamel& the striae of ret)ius and the enamel rod directions
are mutually perpendicular. 6n the a4ial surfaces of the crown& the striae
course dia#onally and terminate on the surface as sli#ht depression. $aries
preferentially attac3 the cases of the cords and the more permeable striae of
7et)iuss which promotes lateral spreadin# and underminin# of the adBacent
enamel.
$27(5S 6, 5N2"58 -
2s belie%ed by most in%esti#ations& the formation of this caries is
preceded by the formation of a microbial Cdental) pla0ue.
.I
!he process %aries sli#htly dependin# upon the occurrence of the lesion
on smooth surfaces and P and ,. So it is best to discuss separately.
S"66! S@7,2$5 $27(5S
P(! 2ND ,(SS@75 $27(5S
S"66! S@7,2$5 $27(5S -
!he surface of enamel& at has newly erupted teeth& is co%ered by a
membrane composed of the primary and secondary cuticle. !he si#nificance of
this membrane in forestallin# the de%elopment of a carious lesion is not 3nown.
$aries prone patients usually ha%e e4tensi%e deposits which must be
remo%ed prior to clinical e4amination. 6n clean dry teeth earliest e%idence of
caries on the smooth enamel surface of a crown is /white spot1. !hey are
chal3y white& opa0ue areas that are re%ealed only when the tooth surface is
desiccated and are termed as incipient caries. !hese areas of enamel loose their
translucency because of the e4tensi%e subsurface porosity and caused by
deminerali)ation. !hese incipient lesions will partially + totally disappear
%isually when the enamel is hydrated.
!he surface te4ture of this lesion is unaltered and is undetectable by
tactile e4amination with an e4plorer.
$linical $haracteristic of Normal and 2ltered 5namel.
ydrated Desiccated
Surface
te4ture
Surface
hardness
Normal
enamel
!ranslucent !ranslucent Smooth ard
(ncipient
caries
!ranslucent 6pa0ue Smooth Softened
2cti%e caries 6pa0ue 6pa0ue $a%itated Aery soft
2rrested caries
6pa0ue
dar3
6pa0ue dar3 7ou#hened ard
.G
!hese incipient lesion sometimes can be seen radio#raphs as a faint
radiolucency& limited to the superficial enamel. (t has been shown
e4perimentally and clinically that incipient caries of enamel can reminerali)e.
Non ca%itated enamel lesions retain most of the ori#inal crystalline
framewor3 of the enamel rods and the etched crystallites ser%es as mediatin#
a#ents for remineralisation. $alcium and phosphate ions from saline can
penetrate the enamel surface and precipitate on the hi#hly reacti%e crystalline
surfaces in the enamel lesion. !he supersaturation of sali%a with calcium and
phosphate ions ser%es as the dri%in# forces for the remineralisation process.
,urthermore& presence of trace amounts of fluoride ions durin# this
remineralisation process #reatly enhance the precipitation of calcium and
phosphate resultin# in remineralised enamel becomin# more resistant to
subse0uent caries attac3 due to incorporation of more acid resistant
fluorapatite.
2rrested + remineralised lesions can be seen clinically as intact& but
discoloured usually brown + blac3 spots. !he chan#e in court is presumably
due to trapped or#anic debris and metallic ions within the enamel. !hese
discoloured remineralised arrested caries areas are intact and are more resistant
to subse0uent caries attac3 than the adBacent unaffected enamel. !hey should
not be restored unless they are esthetically obBectionable.
H6N5S 6, (N$(P(5N! 85S(6N -
!he ability to artificially produce natural enamel lesions has resulted in
identification of a detailed description of the early sta#es of caries in enamel.
!he four re0uired obser%ed )ones ;
a) Hone 1 - !ranslucent )one
b) Hone 2 - Dar3 )one
c) Hone * - Body of lesion
d) Hone . - Surface )one
:;
!72NS8@$5N! H6N5 -
Deepest )one is this )one and represents the ad%ancin# front of enamel
lesion. !( is not always present. By means of polari)ed li#ht it has been shown
that this )one is sli#htly more process than sound enamel& ha%in# a prone
%olume of 1M compared to ;.1M in sound enamel& i.e. 1; times more than the
sound enamel. !he chemical analysis shows that there is fall in the ma#nesium
and carbonate le%els su##estin# that rich minerals are dissol%ed in these )one.
!he name refers to its structure less appearance when perfused with 0uinoline
solution and e4amined with polari)ed li#ht. ere the pores+%oids form alon#
the enamel prism boundaries presumably because of the ease of hydro#en ion
penetration durin# the carious process.
D27N H6N5 -
!his )one lies adBacent and superficial to the translucent )one and it is
3nown as dar3 )one because it does not transmit polari)ed li#ht. !he li#ht
bloc3a#e is caused by the presence of many tiny pores too small to absorb
0uinoline. !hese smaller air + %apour filled pores ma3e the re#ion opa0ue.
Pore %olume is 29.M.
Dar3 )one is not really a sta#e in the se0uence of the brea3down of
enamel& rather it is formed by deposition of ions into an area of pre%. only
containin# lar#e pores. 54perimental reminerali)ation has deminerali)ed
increases in the si)e of dar3 )one at the e4pansi%e of body of lesion. !here is
also a loss of crystalline structure in the dar3 )one& su##esti%e of the process of
deminerali)ation and reminerali)ation.
Si)e of dar3 )one is probably an indication of the amount of
remineralisation that has recently occurred. !his )one is narrow in rapidly
ad%ancin# lesion and wide in more slowly ad%ancin# lesions.
B6DJ 6, 85S(6N -
:1
!his )one lies between the relati%ely unaffected surface layer and the
dar3 )one. (t is the lar#est portion of incipient lesion and the area of #reatest
deminerali)ation. (n polari)ed li#ht the )one shows a pore %olume of :M in
spaces near the periphery to 2:M in the centre of the intact.
!he striae of 7etius C7est liens within enamel and containin# more
or#anism content) are well mar3ed in this indicatin# preferential mineral
dissolution alon# these areas of relati%e hi#her porosity.
Bacteria may lie present in this )one if the pore rid#e is lar#e enou#h to
permit their entity. Studies usin# !5" and S5" demonstrate the presence of
bacteria in%adin# between the enamel rods Cprisms) in the body )one.
S@7,2$5 H6N5 -
!his )one is relati%ely unaffected by the caries attac3. !his )one when
e4amined by the polari)in# microscope and micro radio#raphy& appears
relati%ely unaffected. !he #reater resistance of the surface layer may be due to
#reater de#ree of minerali)ation and + #reater concentration of fluoride in the
surface enamel. (t is about .; m thic3. owe%er remo%al of the hyper
minerali)ed surface by polish #in fails to pre%ent the reformation of a typical&
well minerali)ed surface o%er the carious lesion.
(t has a lower pore %olume than the body of the lesion C:M) and appears
radiopa0ue when compared to the unaffected adBacent enamel.
!hus the intact surface o%er the incipient caries is a phenomenon of
caries deminerali)ation process rather than any special characteristic of the
superficial enamel. Ne%ertheless the importance of the intact surface cannot be
o%eremphasi)ed& because it ser%es as a barrier to bacterial in%asion. 2rrestin#
the caries at this sta#e results in a hard surface that may at times be rou#h&
thou#h cleanable.
:2
P(! 2ND ,(SS@75 $27(5S -
!he caries process does not differ much in nature from smooth surface
caries e4cept as the %ariations in anatomic and histolo#ic structures dictate.
$aries in the fissure does not start at the base but it de%elops as a rin# around
the wall of a fissure. 2s the caries pro#resses& it e4tends towards dentin parallel
to enamel prisms and e%entually coalesces at the base of the fissure. !his
produces a cone shaped lesion with the base of cone toward dentin and not on
enamel surface as in smooth surface caries.
$27(5S (N D5N!(N -
(S!686GJ 6, D5N!(N -
(t is the hard portion of tooth co%ered by enamel on the crown and
cementum on the root. Dentin is a calcified product of the odontoblasts that line
the inner surface of the dentin. 5ach odontoblast has an e4tension C!omeDs
fiber) into a dentinal tubule. !he tubules tra%erse the entire thic3ness of dentin
from the pulp to the dentino enamel Bunction. ,illin# the space between the
tubules is the intertubular dentin& a ri#id bone li3e material composed of
hydro4yapatite crystals embedded in a networ3 of colla#en fibers. <alls of
tubules lined with smooth layer of mineral termed as peritubular dentin. 2 thin
membrane is always obser%ed linin# the tubule in normal dentin. !here is
contro%ersy re#ardin# the nature of linin# some say it is true plasma membrane
of odontoblast or the limitin# membrane similar to that found on the surface of
bone. (n either case the tubule allows fluid must and ion transport necessary
for the reminerali)ation of intertubular dentin& apposition of peritubular dentin
and+or perception of pain.
$8(N($28 2ND (S!686G($28 $272$!57(S!($ 6, D5N!(N28
$27(5S
Pro#ression of caries in dentin is different from pro#ression in the
o%erlyin# enamel because of structural differences of dentin. Dentin contains
much less mineral content and possess micro tubules that pro%ide a pathway for
:*
in#ress of acids and in#ress of mineral. !he D5L has least resistance to caries
attac3 and allows rapid lateral spreadin# once the caries has penetrated the
enamel. $aries ad%ance in dentin more than enamel because dentin pro%ide
much less resistance to acid attac3 because of less mineral content. $aries
produces a %ariety of responses in dentin& includin# pain& deminerali)ation and
the remineralisation.
6ften pain is not reported e%en when caries in%ades dentin e4cept when
deep lesions brin# bacterial infection close to the pulp. 5pisodes of short
duration pain may be felt occasionally durin# earlier sta#es of dentin caries.
!hese pains are due to stimulation of mechanoreceptors in pulp tissue by not of
fluid throu#h dentinal tubules that ha%e been opened to the oral en%ironment by
ca%itation.
!he pulp dentin comple4 reacts to caries attac3s by attemptin# to initiate
reminerali)ation and bloc3in# off the open tubules. !hese reactions result from
odontoblastic acti%ity and the physical process of deminerali)ation and
reminerali)ation. !hese le%els of dentinal reaction to dental caries can be
reco#ni)ed.
1. 7eaction to lon# term& low le%el acid deminerali)ation associated with a
slowly ad%ancin# lesion.
2. 7eaction to moderate intensity attac3.
*. 7eaction to ser%e rapidly ad%ancin# caries char. By %ery hi#h acid le%el.
!he dentin can react defensi%ely Cby repair) out low and moderate
intensity care attac3s as lon# as the pulp remains %ital and an ade0uate blood
circulation.
(N slow ad%ancin# caries - Aital pulp can repair deminerali)ed
dentin by reminerali)ation of the intertubular dentin and by apposition of
peritubular dentin. Dentin responds to the stimulus of it first caries
:.
deminerali)ation episode by deposition of crystalline material in the lumen of
the tubules and the intertubular dentin of affected dentin in front of the
ad%ancin# infected dentin of lesion. !his repair occurs only if the pulp is %ital.
Dentin that has more mineral content than normal one is called as
/Sclerotic dentin1. !his S.D. formation occurs ahead of the deminerali)ation
front of a slowly ad%ancin# lesion and may be seen under old restoration. S.D.
is shiny and dar3ly colored and function is to wall off a lesion by bloc3in#
Csealin#) the tubules.
!here is crystalline precipitates which from in the lumen of the dentinal
tubules in the ad%ancin# front of deminerali)ation )one Caffected dentin) once
these affected tubules becomes completely occluded by the mineral
precipitates& they appear clear when tooth is sectioned. !his portion of dentin is
called transparent dentin )one which is the result of both mineral loss in
intertubular dentin and precipitation of this mineral in the tubule lumen. !his is
softer than normal dentin.
!he second le%el of dentin response to moderate intensity irritants
results in bacterial in%asion of the dentin. !he infected dentin contains a wide
%ariety of patho#enic materials + irritants includin# hi#h acid le%els& hydrolytic
en)ymes& bacteria and bacterial cellular debris. !hese materials can cause
de#eneration and death of the odontoblasts and their tubular e4tensions below
the lesion& as well as mild inflammation of pulp. Groups of these empty tubules
are termed as dead tracts.
!he pulp may be irritated sufficiently from hi#h acid le%els + bacterial
en)yme formation to cause the formation of replacement odontoblasts which
produce reparati%e dentin + reactionary dentin on the effected portion of the
pulp chamber wall.
::
!hird le%el of dentinal response is to se%ere irritation. 2cute& rapidly
ad%ancin# caries with %ery hi#h le%els of acid production o%erpowers the
dentinal defenses and results in infection& abscess and death of the pulp. Small
locali)ed infection in pulp produce an inflammatory response in%ol%in#
capillary dilation& local edema and sta#nation of blood flow which results in
local ano4ia and necrosis.
"aintenance of pulp %itality is dependent on the ade0uacy of pulpal
blood supply. 7ecently erupted teeth with lar#e pulp chambers and short wide
canals with lar#e apical foramina ha%e much more fa%ourable pro#nosis than
fully formed teeth.
H6N5S 6, D5N!(N28 $27(5S -
$aries ad%ancement in dentin process throu#h three chan#es ;
i) <ea3 and or#anic acids demateriali)e the dentin.
ii) !he or#anic material of dentin particularly colla#en de#enerates
and dissol%es.
iii) !he loss of structural inte#rity is followed by in%asion of
bacteria.
2s the carious lesion pro#resses& %arious )ones of carious dentin may be seen.
!hese )ones are more clearly distin#uished in slowly ad%ancin# lesions. Btu in
rapidly pro#ressin# lesions the difference between the )ones become less
distinct. Be#innin# pulpally at the ad%ancin# ed#e of lesion adBacent to normal
dentin& these )ones are as followed.
i) Hone 1 - Normal dentin
ii) Hone 2 - Sub !ransparent Dentin
iii) Hone * - !ransparent dentin
i%) Hone . - !urbid dentin
%) Hone : - (nfected dentin
:=
Hone 1 - Normal Dentin
(t is the deepest area which has tubules with odontoblastic process that
are smooth& and no crystals are in the humans. !he intertubular dentin has
normal cross banded colla#en and normal dense apatite crystals. No bacteria in
the tubules. Stimulation of dentin produces a sharp pain.
Hone 2 - Subtranparent Dentin C2ffected)
(t has )one of deminerali)ation of the intertubular dentin and initial
formation of %ery fine crystals in the tubule lumen at the ad%ancin# front.
Dama#e to the odontoblastic process is e%ident& howe%er no bacteria are found
in this )one. Stimulation of dentin produces pain& and dentin is capable of
reminerali)ation.
Hone * - !ransparent Dentin -
(t is a layer of carious dentin that is softer than normal dentin and shows
further loss of mineral from the intertubular dentin and many lar#e crystals in
the lumen of dentinal tubules. Stimulation of this re#ion produces pain. No
bacteria are present. 2lthou#h or#anic acids attac3 both the mineral and
or#anic content of dentin& the colla#en cross lin3in# remains intact in this )one.
!he intact colla#en can ser%e as template for reminerali)ation of
intertubular dentin and thus re#ion remains capable of self repair pro%ided by
pulp remains %ital.
Hone . - !urbid Dentin
!his is a )one of bacterial in%asion and is mar3ed by widenin# and
distortion of the dentinal tubules& which are filled with bacteria. !here is %ery
little mineral present and the colla#en in this )one is irre%ersibly denatured.
!he dentin in this )one will not self repair. !his )one cannot be reminerali)ed
and must be remo%ed before restoration.
:>
Hone : - (nfected Dentin -
!he outermost )one& infected dentin& consist of decomposed dentin that
is termin# with bacteria. !here is no reco#ni)able structure to the dentin and
colla#en and mineral seem to be absent. Great numbers of bacteria are
dispersed in this #ranular material. 7emo%al of infected dentin is essential to
sound& successful restorati%e procedures as well as pre%ention of spreadin# the
infection.
:. T T T T
Nature has pro%ided us teeth to perform the functions of cuttin#&
#rindin# and admi4in# of food with sali%a. !he hard enamel co%er alon# with
the periodontal li#ament can withstand forces of for masticulation.
(t is %ery stran#e that the hardest tissue of the body ? the enamel& which
is indestructible otherwise& can disinte#rate in the oral en%ironment /$aries1
C8atin meanin# Sdry rotD) is the name #i%en to the process of slow
disinte#ration that may affect any of the biolo#ical hard tissue as a result of
bacterial action.
Dental caries is peculiarly a local disease& which in%ol%es destruction of
hard tissues of the tooth by metabolites produced by oral microor#anisms.
"any authors ha%e ri#htly referred it to as /$i%ili)ation
Dystrophy1. Dental caries is a multifactorial disease which is the most
pre%alent chronic disease affectin# human race. (t effectin# humans of all a#es
in all re#ions of the world.
(t is the disease that may be ne%er eradicated because of comple4
interplay of social& beha%ioural& cultural& dietary and biolo#ical ris3 factors that
are associated with its initiation and pro#ression. !he interaction amon# ris3
factors such as cario#enic bacteria& sali%a& fermentable carbohydrates and
:I
fluorides in the oral en%ironment& influence bacterial coloni)ation as well as
either deminerali)ation + reminerali)ation.
$27(686GJ -
Dental caries and periodontal disease are probably the most common
chronic disease in world. 2lthou#h caries has affected humans since
prehistoric times& the pre%alence of this disease has #reatly increase din modern
times on a world wide basis which is stron#ly associated with dietary chan#e.
owe%er e%idence indicates that this triad pea3ed and be#an to decline in many
countries li3e @.S.& 5urope& New Healand and 2sutralia. !he e4act cause not
3nown but attributed to the addition of trace outs of fluoride in drin3in# water.
!he decline in caries pre%alence is also related to socio economic status.
!hat is people of hi#her and middle classes the decline is prominent but in
lower socio economic classes and rural residents there is hi#her pre%alence of
caries. (t is obser%ed by N2N5S CNational ealth and Nutritional
54amination Sur%ey) that I;M of caries occurred of children which are of
lower socioeconomic status.
!he limited se#ment of population e4periences most of disease and this
effect is called as polari)ation. Pre%alence of caries decrease is in de%eloped
countries and increasin# in less de%eloped countries because of the cost of
caries to society is enormous.
$onsiderin# the ma#nitude and almost all uni%ersal impact of caries&
eradication of caries depends on a%ailability of four thin#s.
1) Potent eradicator weapon CAaccine)
2) Stron# and efficient public health ser%ice support
*) Popular support for the pro#nosis
.) 2n efficient sur%eillance system to monitor caries acti%ity on
a population le%el.
:G
$aries eradication is not achie%ed because these four basic re0uirements ha%e
not been met.
D5,(N(!(6N 6, $27(5S -
Dental caries in simple terms can be defined /as the irre%ersible& slow
pro#ressin# decay of hard tissues of the tooth1.
(t can be defined as the microbial disease of calcified tissues of teeth&
characteri)ed by deminerali)ation of the inor#anic portion and destruction of
or#anic substances of the tooth ? Shafer.
2s a locali)ed post erupti%e& patholo#ical process of e4ternal ori#in
in%ol%in# softenin# of the hard tooth tissue and proceedin# to the formation of
ca%ity ? <6.
Dental caries is an infectious microbial disease of the tooth that results
in locali)ed dissolution and destruction of the calcified tissues ? Sturde%ant.
1. (ncipient + (nitial + Primary carious lesion - !hat describes the first attac3
on a tooth surface.
2. 7ecurrent + secondary lesion - 6ne occurred that is obser%ed under +
around the mar#ins or surroundin# walls of an e4istin# restoration.
*. 2cute + rampant caries - 7apidly in%adin# process that usually in%ol%es
se%ere teeth. 8esions are soft and li#ht colored and are fre0uently
accompanied by se%ere pulp reactions.
.. Pit and fissure caries - !hose ori#inatin# in the pits and teeth and a
buccal& lin#ual and occlusal surfaces of posterior teeth.
:. Smooth surface carious lesion - !hose carious lesions ori#inatin# in and
around all surfaces and pits.
=. ,orward bac3ward - !he first component of enamel to be in%ol%ed in the
carious process is the interprismatic substances. !he disinte#ratin#
substances will proceed %ia this substance causin# the enamel prisms to
be undermined. !he resultant caries in%ol%ement in enamel will ha%e a
cone shape.
=;
(n con%e4 surfaces CP and ,) base of cone will be away from D5L& while in
conca%e surfaces. !he base of cone will be away for the D5L.
!he first component to be in%ol%ed in dentin is the protoplasmic
e4tension within the tubules. !hese e4tensions ha%e their ma4imum spacin# at
the D5L but as they approach the pulp chamber and root canals the tubules
become more densely arran#ed with fe%er interconnection. 6ne can therefore
in a#ainst caries cones in dentin will ha%e a cone shape base of cone toward
D5L.
Decay starts in enamel and then in%ol%es dentin. So whene%er the caries
cone in enamel is lar#er or atleast the same si)e as that in dentin& it is called
forward caries.
owe%er& if the carious process in dentin pro#resses much faster in
dentin than it doe sin enamel from its dentinal side. 2t this sta#e& therefore it
becomes bac3 ward decay.
$hronic $arious 8esions - Aariable depth& lon#er standin# and tend to be fewer
in number. Dentin in this condition is hard in consistency and dar3 in colour.
Smile carious lesions - $aries associated with a#in# process ;
9 54clusi%ely on root surface of teeth.
9 ,ollow #in#i%al recession.
7esidual caries - $aries that is not remo%ed durin# a restorati%e procedure
either by accident& ne#lect or intention.
Simple carious lesion - (n%ol%es only one surface of the tooth.
$ompound carious lesion - 6nly 2 surfaces of teeth.
$omple4 carious lesion - * or more surfaces of teeth.
=1
$82SS(,($2!(6N 6, D5N!28 $27(5S -
6n the basis of clinical features& dental caries may be classified to *
basic factors.
1. "orpholo#y - 2ccordin# to the anatomical site of lesions.
2. Dynamics - 2ccordin# to se%erity an rate of pro#ression of lesions.
*. $hronolo#y - 2ccordin# to a#e patterns at which lesions predominate.
2. $lassification Based on "orpholo#y -
$lassified !ype (
!ype ((
(. Pit and fissure caries - Pit and fissures caries are limited to the occlusal
surfaces of molars and bicuspids the buccal pits of molars& and lin#ual surfaces
of ma4illary anterior teeth.
((. Smooth surface caries
a) (nterpro4imal lesions - "esial + distal contact points.
b) $er%ical lesions - 6n buccal + lin#ual surfaces near the dentin enamel
Bunction.
B. Blac3Ds $lassification C!herapeutic $lassification)
Based on morpholo#ical classification of dental caries.
$lass ( - Structural defects of teeth such as pits& fissures and sometimes
defecti%e #roo%es. !hey usually ha%e * locations ;
a) 6cclusal surfaces of molars and premolars.
b) 6cclusal 2+*
rd
of buccal and lin#ual surfaces of molars
c) 8in#ual surfaces of anterior teeth.
$lass (( - ,ound on pro4imal surfaces of bicuspids and molars.
$lass ((( - ,ound on pro4imal surfaces of anterior teeth that donot in%ol%e or
necessitate remo%al of the incisal an#le.
=2
$lass (A - ,ound on the pro4imal surfaces of anterior teeth and in%ol%e +
re0uire the remo%al and restoration of incisal an#leCs).
$lass A - ,ound at the #in#i%al third of the facial and lin#ual surfaces of
anterior + posterior teeth.
$lass A( - <ere not ori#inally included in Blac3Ds classification. !hey are also
found on molar and premolar cusp tips& a4ial an#les of teeth& or any hi#hly
cleansable areas.
$) $lassification related to de#ree and rate of pro#ression of caries
1. (nfancy CSooth + Nursin# Bottle) caries
(tDs a form of rampant caries effectin# the deciduous dentition. !his is
due to prolon#ed use of ;
9 Nursin# bottle C"il + "il3 formula& fruit Buice)
9 Breast feedin#
9 Su#ar + oney sweetened pacifiers.
2. 2dolescent caries
*. Geriatric + Senile caries
2ccordin# to Sturde%ant ? Base don location& e4tent and rate.
8ocation of $aries -
1. Primary caries - 6ri#inal carious lesion of the tooth.
a) $aries in enamel P and ,
b) Smooth surface
c) 7oot surface
i) Bac3ward caries - Spread of caries alon# the D5L e4ceed the caries
in the conti#uous enamel& caries e4tends into this enamel from D5L.
ii) ,orward caries - $aries where the caries cone in enamel is lar#er or
at least same si)e as that of dentin.
iii) 7esidual caries - $aries that remains in a completed ca%ity
preparation either accidentally or by the operator.
=*
2. Secondary caries
54tent of $aries -
1. (ncipient caries C7e%ersible)
2. $a%itated caries CNon re%ersible)
7ate of caries -
1. 2cute Crampant) caries
2. $hronic Cslow + arrested) caries
N5< $2A(!J $82SS(,($2!(6N -
Gi%en by Graham L. "ount <. 7osy ume C2ustralian Dental Lournal
1GGI)
!his classification is desi#ned to simplify the identification of lesion and
to define their comple4ity to pro%ide benefits for the profession and their
patients. (t has been proposed accordin# to S(!5 and S(H5 of the lesion.
!he three sites of carious lesion -
(t can occur in three sites on the crown + root of a tooth& that is in those
areas subBect to the accumulation of pla0ue. !hese are ;
Site 1 - P and , and enamel defects on occlusal surfaces of posterior teeth and
on other smooth surfaces& such as cin#ulum pits on anteriors Cincludes all
lesions of blac3 class ( but also other smooth surfaces).
Site 2 - 2ppro4imal surfaces immediately below the areas in contrast with
adBacent teeth Call lesions associated with contact areas) includes all anterior
and posterior teeth. (ncludes all lesions of Blac3Ds class ((& ((( and (A lesions.
Site * - Describes cer%ical 1+* of crown followin# #in#i%al recession either in
enamel or dentin or e4posed root around full circumference of tooth. (ncludes
Blac3Ds class A and also e4tends to root surface for recession.
!he abo%e three sites are then #rades as . si)es accordin# to e4tent of
pro#ress and #i%es the #uidance for mana#ement of any sta#e.
=.
Si)e 1 C"inimal) - "inimal in%ol%ement of dentin Bust beyond treatment by
minerali)ation alone.
Si)e 2 C"oderate) - "oderate in%ol%ement of dentin still sufficient amount of
enamel present supported by dentin and not li3ely to fail under occlusal load.
!hat is remainin# tooth structure is sufficiently stron# to support the
restoration.
Si)e * C5nlar#ed) - 5nlar#ed and more e4tensi%e lesion. 7emainin# tooth
structure is wea3ened to the e4tent that cusps or incisal ed#es are split or are
li3ely to fail if felt e4posed to occlusal load + incisal load. !he ca%ity desi#n
will ha%e to be modified and enlar#ed to the e4tent that the restoration will ta3e
the main occlusal load and protect the remainin# tooth structure.
Si)e . C54tensi%e) - !here is e4tensi%e loss of tooth structure& such as loss of a
cusp.
Si)e
"inimal
1
"oderate
2
5nlar#ed
*
54tensi%e
.
Site
Pit + ,issure 1 1.1 1.2 1.* 1..
$ontract 2rea 2 2.1 2.2 2.* 2..
$er%ical * *.1 *.2 *.* *..
!567(5S 6N 5!(686GJ 6, $27(5S -
Dental caries is a multifactorial disease. !he process by which a tooth
can be destroyed easily in oral ca%ity& which is indestructible otherwise& is %ery
difficult to understand. !ill today no sin#le theory can e4plain the
phenomenon of caries.
(n %iew of uni0ue characteristics of the tooth %is9U9%is caries& the caries
does not fall into any of the common patholo#ical lesions of oral ca%ity.
Dental caries is not inflammatory in ori#in& nor a de#enerati%e in nature and
neither it is neoplasm. (t is a local disease which in%ol%es destruction of hard
tissues of tooth by metabolites produced by microor#anisms.
=:
Numerous reference to dental caries& includin# early theories to e4plain
mechanism of caries ha%e been found. Before we underta3e correct concept of
caries etiolo#y lets diseases in brief the early theories.
!567(5S ? 5278J $6N$5P!
9 $@775N! $6N$5P!
5278J $6N$5P!
a) <orm theory
b) umoral theory
c) Aital theory
d) $hemical + parasitic theory
e) Septic theory
$@775N! $6N$5P!S -
a) 2cido#enic theory C$hemico9Parasite !heory) ? "iller& 1IG;.
b) Proteolytic theory ? Gottlieb C1G..)& ,risbic C1G..)& Pincus C1G.=).
c) Proteolytic cheltion theory ? Schat)& "artin 1G:..
d) Sucrose ? $helation theory ? 5##ars ? 8una C1G=>)
e) 8e%ineDs theory ? 8e%ine 1G>>
f) Phosphate ? Se0uestration theory
#) 2utoimmune theory
h) Genetic theory
5278J !567(5S -
a) <orm !heory C:;; B$)
!he earliest reference of tooth decay and tooth arched& probably
appeared around 1. cent B.$. when oracle lo%e inscriptions were e4ca%ated
from the ruins of the Jin# Dynasty& showed the character meanin# ScariesD.
2ccordin# to the concept of that time& the cause of caries was thou#ht to be
/in%asion of worms into teeth. !herefore the character of caries was shown as
a worm o%er tooth surface. !he association of systemic disease and teeth was
==
probably obtained from writin#s of a physician around ==I B.$. !he physician
ahs mentioned that the inflammation in his le#s and arms was due to tooth and
that it must be e4tracted.
!he le#end of worm was disco%ered on ones of the many day tablets
e4ca%ated near the Niffer& @r and other countries with the 5uphrates %alley of
lower "esopotamian. !he early history of (ndia& 5#ypt and <ritin#s of omer
also ma3es reference to the worm as the cause of tooth ache.
b) umoral !heory -
2ccordin# to Galem the ancient Gree3 physician considered that a
persons physical and mental constitution was determined by the relati%e
proportions of the four humours of the body namely ;
Blood - San#uine
Phle#m - Phel#niate
Blac3 bile - "elanocholic
Jellow bile - $holeric
2ll diseases includin# caries could be e4plained by an imbalance of these
humours. 2ccordin# to Galen dental caries was produced by internal action of
acids and corrodin# humours.
$ertain authors such as ippocrates fa%oured this concept and also
added that the accumulated debris around the teeth help to corrodin# action.
e further stressed that sta#es of Buices o%er the tooth surface caused tooth
ache.
c) Aital !heory -
!he %ital theory& re#arded dental caries as ori#inatin# within the tooth
itself& analo#ous to bone #an#rene. !his theory& proposed at the end of 1I
th
century& remained dominant until the middle of 1G
th
century. 2 clinically well
=>
3nown type of caries is clear& e4tensi%e penetration into dentin& e%en into the
pulp& but with a barely detectable catch in the fissure.
d) $hemical + 2cid !heory -
(n 1>
th
and 1I
th
centuries& there emer#ed a concept that teeth were
destroyed by acids formed in the oral ca%ity. !he e4act nature and e4act
mechanism of acid formation was not 3nown.
7obertson C1G*:) proposed that dental decay was caused by acid formed
by fermentation of food particles around the teeth.
Different postulates were #i%en - one su##estion was that putrefaction of
protein #a%e rise to ammonia& which was subse0uently o4idi)ed to nitric acid
and another was that food was decomposed to sulphuric acid. !ill then acti%ity
of bacteria was not reco#ni)ed
c) Parasitic + Septic !heory -
(n 1I.*& 5rdl described filamentous parasites in the /surface membrane1
Cpla0ue) of the tooth. Shortly thereafter& ,icinus C1I.>)& a Dresden physician&
obser%ed filamentous microor#anisms& which he called denticoloar in material
ta3en from the carious ca%ities. !hey said that these bacteria caused
decomposition of enamel cutile.
$@775N! !567(5S -
!he etiolo#y of dental caries is #enerally a#reed to be a comple4
problem& complicated by many indirect factors& which obscure the direct
cause + causes. !here is no uni%ersally accepted opinion n the etiolo#y of
dental caries.
2$(D6G5N($ !567J + "(8857DS $5"($69P272S(!($ !567J -
!his theory is a blend of the abo%e two theories Cchemical and parasitic)
because it states that caries is caused by acids produced by microor#anisms of
=I
mouth. 2nd the writin#s of "illers <.D. helped to establish this concept firm
basis. <or3 of <illou#hley D."iller C1I:*91G;>) had a most profound effect
on the understandin# of caries etiolo#y and subse0uent caries research. "iler
concluded that /no sin#le species of microor#anisms caused caries but rather
that the process was mediated by an oral or#anism capable of producin# acid
and di#estin# protein.
"iller hypothesi)ed that /dental caries + decay is a chemico9parasitic
process consistin# of two sta#es ;
1) Decalcification of enamel which results in the total destruction
and decalcification of dentin as a preliminary sta#e.
2) Dissolution of the softened residue.
!he acid which effects this primary decalcification is deri%ed from the
fermentation of su#ars lod#ed in the retainin# centre of the teeth.
,urther wei#ht was added to this theory by <illiams C1IG>) who
obser%ed dental pla0ue on the enamel surface. Pla0ue was considered to be a
means of locali)in# or#anic acids formed by microor#anisms in contact with
the tooth surface. !he pla0ue partially pre%ented dilution and neutrali)ation of
or#anic acids by the sali%a.
!he theory has been accepted by the maBority of in%esti#ators in a form
essentially unchan#ed since inception. !he bul3 of scientific e%idence does
implicate carbohydrates& oral microor#anism and acids and for this reason
decreases further consideration.
P76!568J!($ !567J CG6!!8(5B 2ND D(2"6ND 2ND
2PP85B2@"& 1GG.) -
!he classical chemicoparasitic theory is not uni%ersally accepted.
(nstead& it ahs been proposed that the or#anic + protein elements are the initial
pathway of in%asion by microor#anisms. !he human tooth contains only about
=G
1.: ? 2M of or#anic material of which ;.*: ? ;..M is protein. 2ccordin# to
this theory the or#anic component is most %ulnerable and is attac3ed by
hydrolytic en)ymes of microor#anisms. !his precedes the loss of the inor#anic
phase.
Gottleib C1G..) said that the /initial action was due to proteolytic
en)ymes attac3in# the lamellae& rod sheaths& tufts& and walls of the dentinal
tubules. !he yellow pi#mentation which was seen was attributed to pi#ments
produced by the proteolytic or#anisms.
,rusbie C1G..) described cares as& caries is initiated by at sli#htly
al3aline p produced by the proteolytic acti%ity in%ol%in# depolymerisation
and li0uefaction of the or#anic matri4 of enamel.
6nce the or#anic part sets free after the dissolution of inor#anic part&
these salts are dissol%ed subse0uently by acido#enic bacteria.
Pincus C1G.G) contended that proteolytic or#anisms attac3ed the protein
elements& such as dental cuticle and then destroyed the prism sheaths. !he
loosened prisms then fell out mechanically. e also su##ested NasmythisD
membrane and the enamel proteins are mucoproteins which acted upon by
sulphatase en)ymes of #ram ne#ati%e bacilli yieldin# sulfuric acid. !he
released sulfuric acid could combine with the calcium of mineral phase.
!hou#h enamel contains 1; to 1.:M of or#anic matri4 out of which
;.=M is protein& initiation of caries with brea3down of this small amount of
protein is hi#hly 0uestionable. !ill date si#nificant loss of enamel tissue then
proteolytic acti%ity has not been pro%ed e4perimentally. "oreo%er en)yme
system capable of attac3in# 3eratin has also been not demonstrated. !herefore
this theory by and lar#e lac3s e4perimental support.
>;
,risbier C1G..) described caries as a proteolytic process in%ol%in#
depolymerisation and li0uefaction of the or#anic matri4 enamel. !he less
soluble inor#anic salts could then be freed from their or#anic bond fa%ourin#
thrice solution by acido#enic base that secondarily penetrate alon# widenin#
paths of in#ress.
P76!568JS(S ? $582!(6N !567J -
$helation is a process in%ol%in# the comple4in# of a /metallic ion1 to a
/$omple4 substance1 throu#h a coordinate co%alent bond which results in a
hi#hly stable& poorly dissociated or wea3ly ioni)ed compound C$helar law).
!his theory proposed by Schat) et al C1G::) implies a simultaneous
microbial de#radation of the or#anic components Chence proteolysis; and the
dissolution of minerals of the tooth by the process of chelation.
Numerous naturally occurrin# chelatin# a#ents e4ists& the most common
of these bein# the citrates. 2mino acids are also 3nown to act as chelators& as
well as hydro4yl and 3etoesters of eyerhaf emben system pathway&
phosphorylated and nonphosphorylated compounds in the he4ose
monophosphate shunt& polymorphates includin# these in%ol%ed in
phosphpsylate& certain antibiotics lipids carbohydrates& en)ymes& %itamins&
o4alates etc.
$helation ha been proposed as an e4planation for tooth decay whereby
the inor#anic components of enamel can be remo%ed at neutral + al3aline p.
!he proteolysis ? chelation theory considers dental caries to be a bacterial
destruction of teeth where the initial attac3 is essentially on or#anic
components of enamel. !he bea3 down of this or#anic matter ha%e chelatin#
properties and thereby dissol%e the minerals in the enamel. !hus both the
or#anic and inor#anic constituents of enamel are simultaneously demolished.
>1
2ccordin# to this theory& decalcification is mediated by a %ariety of
comple4in# a#ents such as acid anions& amines& peptides& polyphosphates and
carbohydrate deri%ati%es. !hese substances are microbial brea3down products
of either the or#anic components of enamel + dentin + of food that is in#ested
and diffuses throu#h the pla0ue. 6ral 3eratinocyte bacteria are thou#ht to be
in%ol%ed in the process. Difference in 3eratin content of the enamel in children
with hi#h caries and low caries e4perience are considered important. (t should
be noted that only a small fraction of enamel mass any resemblance to the
3eratin of hair.
Se%eral reconciliations must be made if proteolysis ? chelation theory is
to be accepted. !hese include ;
1) !he obser%ation of increased caries incidence with increased su#ar
consumption. !his is because increased su#ar + carbohydrate consumption
leads to ;
a) Stimulatin# + increasin# proteolysis.
b) Producin# conditions under which 3eratinous proteins are less stable.
c) $ompel4in# calcium
2) !he obser%ation of increased lactobacillus counts with hi#h caries acti%ity.
!his is because of the result of carious process rather than the cause thus Schat)
su##ested that ;
a) Proteolysis may pro%ide ammonia which presents a p drop that would tend
to inhibit #rowth of lactobacilli.
b) !he release of calcium from hydro4yapatite by chelation mi#ht encoura#e
the #rowth of lactobacilli& since calcium has been reported to produces this
effect.
c) $alcium e4erts a %itamin spacin# action on some lactobacilli.
*) !he obser%ation of decreased caries incidence followin# topical + systemic
administration of fluoride.
>2
a) !his may occur throu#h formation of fluroapatite which stren#thens the
lin3a#es between the or#anic and inor#anic phases of the enamel thereby
pre%entin# a reducin# comple4in#.
(A. 85A(N5DS !567J -
8e%ine established the chemical relationship of enamel pla0ue and the
factors which determined the mo%ement of minerals from Sali%a + pla0ue to
enamel and %ice %ersa which he termed as /(onic See9Saw mechanism1.
(n this mechanism be emphasi)e that deminerali)ation are
reminerali)ation of enamel is a continuous process. (, in a #i%en inter%al of
time& more ions ha%e the enamel than enter it& then there is a net
demineralisation which amounts to start of the carious process. (t has been
pro%ed that passa#e of ions is not a one way process and that ions are
constantly bein# e4chan#ed between enamel and pla0ue. 2t times& the chemical
condition at enamel pla0ue interface may fa%our outward most of ions and at
other times the situation may be re%ersed. !his delicate balance of ion is
dependent on many factors. !he three most important factors which are
respecti%ely are ;
a) p of pla0ue
b) $alcium and phosphate ion concentration at the interface
c) ,luoride ion concentration
(f p falls below : Ccritical p; e#. Durin# carbohydrate in ta3e&
mineral ions are liberated from the hydro4yapatite crystals of enamel surface
and diffuse into pla0ue within 2; minutes sali%ary buffer neutrali)e the acid.
2t this sta#e& the pla0ue is super saturated with ions some of the ions are lost
and others are deposited onto the enamel. <ith such repeated episodes& o%erall
deminerali)ation occurs which leads to caries.
,or this phenomenon to occur the& actual mineral ion concentration of
sali%a is important. (, free calcium and phosphate ions are hi#her in sali%a
>*
because of dietary and other sources& there would be a #reater tendency of ions
to mo%e from pla0ue to enamel. 7e%erse is true if ion concentration is sali%a is
low.
2nother factor which plays an important role in see9saw mechanism is
fluoride. ,luoride fa%ours mo%ement of ions from pla0ue to enamel. !he initial
deposit appears to be in the form of calcium fluoride. ,luoride concentration as
low as : ppm can but the see9saw mechanism.
6!57 !567(5S -
2ccordin# to him oral fluids protect the enamel by pro%idin# a
protecti%e co%erin# on the enamel surface attrition ma3es fissures wider and
remo%es the superficial layer of enamel alon# with initial carious lesion& if
present. !he new layer of enamel becomes protecti%e a#ain with the help of
oral fluids. (n areas where the oral fluids cannot reach e#. $ontact area cannot
be made protecti%e a#ainst the carious attac3.
$aries starts in contact areas where the protecti%e action of oral fluids is
not there i.e. the perimeter of the contact alia. Smaller the area& more is the
perimeter +unit area; as the area becomes lar#e& the perimeter + unit area falls.
Similarly smaller the contact area the perimeter + unit area as the contact
becomes more Cmay be physiolo#ic + attrition) the perimeter + unit area falls.
!he effect of acid attac3 depends on perimeter+unit area.
Greater the perimeter stron#er the attac3. 2s the len#th of perimeter +
unit area falls with increase in si)e of contact area& the carious lesion pro#ress
faster in a smaller contact area.
2ccordin# to Dr.Bandlish the meticulous contact throu#h brushin# and
cleanin# reduces the caries not by remo%in# pla0ue but remo%in# enamel.
>.
P76!568J!($ !567J
$582!(6N -
$helate results from combinin# an inor#anic metal ion with at least 2
electron rich functional #roups in a sin#le or#anic molecule.
$helatin# a#ent is a molecule capable of sei)in# and holdin# a metal ion
in a claw li3e #rip and formin# a heterocyclic rin#. !he atoms holdin# the
metal ion are called li#ands and are usually 6
2
& N
2
sulphur.
(n biolo#y there are well 3nown chelates includin# haemo#lobin
Ccontainin# iron) chlorophyll& Aitamin B912& en)ymes cytochrome o4idase
C(ron and $opper) and carbo4y peptidase ? 2 CHinc).
54ample of chelate structures are lactate or citrate and calcium. $alcium
is held co%alently by two o4y#enDs of the carbo4yl #roups and in a coordinate
co%alent bond in%ol%in# mushard electrons of the alcohol #roups.
$itrate can effecti%ely form chelates of calcium and may be important
for the physiolo#ical mobili)ation of calcium from s3eleton and transport of
comple4es calcium to serum. 8actate is of ne#li#ible importance as an or#anic
chelator of calcium.
$helation has been proposed as an e4planation for tooth decay whereby
the inor#anic components of enamel can be remo%ed at neutral or al3aline p.
!his prot9chel theory considers. Dental caries to be a bacterial
destruction of teeth where the initial attac3 is essentially on or#anic
components of enamel.
!he brea3 down products of this or#anic material ha%e chelatin# props
and thereby dissol%e the mineral in the enamel. !hus both or#anic and
inor#anic constitutes of enamel are simultaneously demolished.
2ccumulation to this theory& decalcification of enamel is mediated by a
%ariety of comple4in# a#ents& such as acid anions& amines& amino acids&
>:
peptides& polyphosphates and carbohydrate deri%ati%es. !hese substances are
microbial brea3 down products of either or#anic components of enamel + dentin
of food that is in#ested and diffuses throu#h the pla0ue.
6!57 !567(5S -
Phosphate ? Se0uestration !heory -
Postulated that steady state e0uilibrium e4ists between inor#anic
phosphate of sali%a and mineral phase of enamel.
2ccordin# to this theory& as bacteria ta3e up phosphate& inor#anic
phosphate must be remo%ed from enamel to maintain the e0uilibrium.
Bacterial ? Phosphatase theory -
,ound that bacterial al3aline phosphatase was found to release
phosphate from enamel in %itro. (t was speculated that this en)yme could
participate in caries destruction by actin# on phosphoproteins of enamel.
Difficulty with this theory is that this en)yme is an intracellular en)yme
so lysis of cells has to occur to free the en)yme.
!567(5S -
$5"69P272S(!($ !567J ? "(8857DS -
Blend of abo%e 2 theories because ;
=. States that caries is caused by acids produced by microor#anisms of mouth.
>. (t is customary to credit this theory to <.D."iller who helped to establish
this concept on firm basis. But howe%er contributions were #i%en by many.
a) Pasteur - Disco%ered that microor#anism transform su#ar to lactic acid
in the process of formation.
b) 2nother ,rench man 5mil "a#itot& deminerali)ed that fermentation of
su#ars caused dissolution of tooth mineral in %itro.
>=
c) (n Berlin& 8efer and 7ottenstien C1I=>) #a%e additional e4perimental
e%idence implicatin# that acids and bacteria are the causati%e a#ents of
caries.
!hey described a specific micro or#anism& hepato thri4 bacillus& in the tubules
of carious dentin and thou#ht that it was respecti%ely for enlar#in# the tubules
and facilitates rapid penetration of acids.
!hen wor3 of an 2merican& <.D. "iller C1I:*91G;>) at @ni%ersity of
Berlin had a most profound effect on the under standin# of caries etiolo#y and
subse0uent caries research.
"iller demonstrated the followin# factors ;
1. 2cid was present with in the deeper carious lesions& as shown by reaction
on litmus paper.
2. Different 3inds of food Cbread& su#ar etc) mi4ed with sali%a and incubated
at *>
o
$ could decalcify the entire crown of a tooth.
*. Se%eral type of oral bacteria Cat least *; types) could produce enou#h acid
to cause dental caries.
.. Different microor#anism in%ade carious dentin. !hen $ concluded;
a) No sin#le species of microor#anism caused caries.
b) 7ather the process was mediated by an oral microor#anism capable
of producin# acid and di#estin# protein.
D5N!28 D5$2J -
(t is a chemo9parasitic process consistin# of 2 sta#es ;
1. Decalcification + softenin# of tissues Cfor enamel Decalcification
si#nifies its total destruction).
2. Dissolution of softened residue
,urther it was added to this by <illiams C1IG>) who obser%ed dental pla0ue on
enamel surface pla0ue was considered to be a means of locali)in# or#anic acids
formed by micro or#anisms.
>>
(n sali%a& chief buffer systems are $6
*
and P6
.
. Bicarbonate is by far the
most important sali%ary buffer due to se%eral reasons.
1. (t can buffer rapidly by losin# $6
2
Ccompared with blood).
2. (ts pN CPoint at which p chan#es the least Cacid9base) is close to that
encountered in pla0ue& therefore it is more effecti%e in that ran#e.
*. 2s flow rate increases& the $6
*
Cbicarbonate) concentration increases&
whereas P6
.
falls sli#htly with increased flow rate.
.. 2fter remo%in# of $6
*
by a current of $6
2
free air at p:& the
bufferin# capacity of sali%a is reduced mar3edly.
Dialysis of sali%a which remo%es both $6
*
and P6
.
but not protein ? leads
to total loss of sali%ary buffer capacity. !his indicates that sali%ary proteins
can be disre#arded as buffers.
@rea is continuously secreted in sali%a& pla0ue microor#anism can
con%ert urea to other intro#enous products and ammonia. !he N
*
thus
formed can also ser%e as buffer.
>I