HISTOPATHOLOGY OF DENTAL CARIES

Dental caries is a microbial disease of the calcified tissues of the teeth, characterized by desensitization of the inorganic portion and destruction of the organic substance of the tooth. The caries involvement of the tooth structure is an interesting process as it progresses as a series of exacerbations and remissions. This process can be best studied by: 1. Transmission and Scanning Electron !. "istochemical studies. #. $se of %adioactive isotopes. Dental caries can be best studied are: a. &aries of enamel. b. &aries of dentin. c. &aries of cementum ' %oot caries. (A) CARIES OF ENAMEL : Depending on the site of icroscopy.

(&&$%%E)&E is of t*o types: 1+ ,f the caries occurs in the developmental pit and fissures ' occlusal surface it is termed as -,T . /,SS$%E &0%,ES.

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&aries occurring on any other surface is termed S ((T" S$%/0&E &0%,ES.

I] PIT AND FISSURES are of ! types: 1. Shallo* pit and fissures. !. Deep pit and fissures. During the union of enamel lobes in the calcification process organic elements of enamel forming organs get entrapped resulting in a natural pit' thin fin *hich separates the lobes. 1 The caries process begins once the bacterial pla2ue gets deposited on these sites of the tooth surface. The entrapped organic material gets attac3ed by the enzymatic and bacterial action *hich causes a material passage*ay into the enamel. 4ater, this natural fissure becomes a miniature culture tube for progress of bacteria *hich causes dissolution of the remaining enamel and later creeps in to the dentin. The basic difference bet*een shallo* pit and fissures and deep pit and fissures. 1 0 relatively thic3 layer of enamel is present at the base of the pit. !

"ence )( DE)T,)04 ,)5(45E E)T.

DEEP PIT & FISSURES 1 The enamel thic3ness at the base of the pit is thin cause of increased depth. 1 There ,S DE)T,)04 ,)5(45E E)T. 0lmost all the teeth are effected by pit and fissure caries except for 4(6E% ,)&,S(%S and &$S-,DS. The carious lesion starts on the lateral *alls of the fissures that eventually fuse at the base of the fissure. ,n -,T 0)D /,SS$%E the enamel rods are said to flare laterally at the bottom of the pit and caries is said to follo* the path of enamel rods hence a characteristic angular ' inverted 758 shaped lesion is formed *hose. 90SE 111111111 is to*ards DE)T,) and 0-E: 111111111 is to*ards ($TE% S$%/0&E. (nce the caries reaches Dentino1Enamel ;unction it spreads laterally and to*ards pulp. 0 greater number of Dentinal tubules are involved in pit and fissure compared to smooth surface caries. #

Thus, clinically: 1. 0 7catch8 may be felt *ith an explorer. !. Softening at the base of pit and fissure. #. (pacity surrounding the pit and fissure indicating undermining ' demineralization of Enamel. <. %adiographic evidence of dental caries under the occlusal enamel further indicates the need for: Treatment: 1 1 1 %estoration of pit and fissures. Topical fluoride application. Enameloplasty.

II] SMOOTH SURFACE CARIES : The carious process begins only follo*ing the deposition of a layer of dental pla2ue. 1=microflora > food debris+ !< to <? hours later. THE INCIPIENT LESION CLINICALLY : The first sign of Dental &aries is an area of Decalcification ' less translucency of the affected area *hich appears ' resembles a &"04@A 6",TE S$%/0&E.

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This *hite spot is seen *hen the enamel is thoroughly dried.

)o &05,T0T,() is evident =but the surface may be rougher than normal enamel as assessed by a dental probe+.

The *hite spot is normally seen in the: a. Bingival area of the buccal and labial surfaces of the clinical cro*n. b. -roximal subcontact sites.

"(6E5E% care must be exercised to distinguish a carious *hite spot from a non1carious *hite spot =Enamel hypoplasia+ CARIES WHITE SPOT 1 ,t *ill partially ' totally disappear visually if moistened.

ENAMEL HYPOPLASIA 1 ,t is unaltered by *etting ' drying.

HISTOLOGICALLY : This chal3y *hite area is mainly due to: a. 4oss of interprismatic ' inter rod substance of enamel resulting in increased prominence of the enamel rods.

b.

Due to the roughening of the ends of enamel rods hence the enamel rods are more susceptible to acid attac3.

,t has been sho*n experimentally and clinically that ,ncipient caries of enamel can %E ,)E%04,DE. )on cavitated enamel lesions retain most of the original crystalline frame *or3 that severes as a nucleating agent for remineralization &a and -( < ions from saliva precipitate crystalline surfaces in enamel lesion :1 0t this stage if there is availability of / ions. %emineralization lesion *ill be concentrated *ith /4$(%0-0T,TE. The presence of /luorapatite provides additional resistance to further caries attac3. 1 0 remineralized lesion appears as a bro*n ' discoloured spot =trapped organic debris and metallic ions are presumably the cause of the discolouration+. 0t this stage, the incipient lesion may be arrested ' even revered by remineralization. Except ' if esthetically obEectionable caries restoration of an incipient lesion is an elective procedure. &E%T0,) ST$D,ES carried out by 6,S4(S%, sho*ed that the interprismatic organic substance of enamel *as made up of a certain

$&(-(4AS0&&"0%,DE *hich is said to undergo degradation early in the caries process. 0s the caries progresses other histopathological changes occurring are: =,,,+ 0ppearance of transverse dar3 lines ' bands at right angles to the enamel rods. These lines are due to changes occurring in the enamel prisms. =,5+ The incremental lines of retgins undergo accentuation. This dar3ening appearance of the ,4% in the carious lesion is an optimal phenomenon *hich occurs due to the loss of minerals due to the carious process =as a result of *hich G the organic structures appear more prominent+. 1 The path of ingress of an advancing carious lesions is roughly parallel to the long axis of the enamel rods. 1 The advanced smooth surface caries obtains a typical 758 shaped' cone shaped lesion *hose base is to*ards the enamel and apex to*ards the dentin. 1 Eventually there is a loss of continuity of the enamel surface.

HISTOPATHOLOGY : This is due to the disintegration of the enamel prisms follo*ing decalcification of the inter prismatic substance follo*ed by accentuation of debris and microorganisms. 9efore the complete disintegration of enamel several zones can be appreciated starting from the advancing end of the lesion. 4ight microscopic studies of the enamel lesion has revealed < zones G *hich represent various degree of hard tissue transformation. a+ 0 translucent zone G *hich is the advancing front of the lesion. b+ 0 dar3 zone G separating the translucent zone from the body of the lesion. c+ The body of carious lesion G %adioluscent region. d+ 0 relatively intact enamel surface layer. These zones should not be interpreted as distinct entities but represent a continuum of changes in caries process. ONE ! : TRANSLUCENT of the enamel lesion. , 1 1 ,t is not al*ays present. CIJ of longitudinal sections sho* this zone. ONE : is present at the advancing end

This zone has been sho*n to be slightly more porous than sound enamel =at Eunction sites such as the prism boundaries+ having a pore volume of 1J than I.1J of normal enamel.

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This zone is best visualized by polarized light. There is no evidence *hether the organic matter is removed ' altered in this zone.

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There is less demineralization. The loss of carbonate and magnesium along *ith &a >> and -( < results in pore formation.

ONE " : DAR# ONE 1 1 4ies adEacent to translucent zone. ,t is termed as positive zone because it is usually presence. 1 1 Done is present due to mineralization of enamel. The pores are not small than in translucent zone -ore volume G !J to <J. ONE $ : %ODY OF THE LESION 1 ,t is deep to the relatively unaffected enamel surface layer. K

This zone lies inbet*een the dar3 zone and the surface layer.

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,t is the area of greatest demineralization. $nder light G the ground sections revealed:

1. Enhanced striae of retgins. !. &ross striations in the enamel prisms. 1 ,t has a pore volume of CJ at the periphery and !CJ at the center of the lesion. 1 ,t is considered as the *idest zone.

ONE & : SURFACE ONE: 1 0n important feature of an progressing initial carious lesion is the presence of an apparently intact enamel surface overlying an area of sub1surface demineralization. 1 1 This is the most superficial zone. ,t is the most unaffected zone G due to the great resistance of the surface zone to decalcification. 1. 9ecause of the greater degree of mineralization of the surface =hypermineralized surface+.

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!. ,ncreased concentration of fluoride in the surface enamel G here the pore volume is less than CIJ. Thus *hen only enamel is affected the patient experiences: 1. Sensitivity. !. (n mastication because of the increased forces, the unsupported brittle enamel *ill brea3 do*n G cavity formation. &linically: 1 1 Softened enamel may be flabed a*ay by the explorer. -roximal lesions detectable on bite1*ing radiographs should be carefully examined clinically. =,ncipient enamel lesions visible ' Eust detectable on bite1 *ing are unli3ely to have cavitated surfaces+. Treatment : -reventive measures ie.: 1. /luoride application. !. -atient education. ay help in preventing the progress of lesion cause the outer layer of enamel is the most caries resistant and is capable of *ithstanding damage. (%) CARIES OF DENTIN

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Spread of caries is more in dentin compared to enamel because of:

1. Decreased calcification =mineralization+. !. Existence of path*ays =dentinal tubules+. 1 (nce the enamel caries reaches the dentino1enamel Eunction it spreads laterally along the DE; *ith the rapid involvement of a great number of dentinal tubules. Each dentinal tubules acts as a tract along *hich

microorganisms travel to the pulp. 1 Thus, there *ill be pulp response1*hich forms the sclerotic and secondary dentin. 1 &0%,ES (/ DE)T,): ,) &",4D%E) ,S /0STE% because: 1. Dentinal tubules are shorter and *ider. !. 4ess amount of mineralization. #. Thic3ness of enamel and dentin is less and pulp chamber is *ider and large. 1 ,n cases of caries spreading in an enamel lesion clinically only a small lesion may be present but the underlying dentin a large cavity may be formed.

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0s the carious lesions progress is various zones of caries in dentin can be appreciated *hich assumes a triangular shape.

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6ith 90SE G to*ards dentino1enamel Eunction. 0nd 0-E: G to*ards the pulp.

The zones are: 1. Done of fatty degeneration. !. Done of dentinal tubules. #. Done of decalcification. <. Done of bacterial invasion. C. Done of decomposed dentin. 1 causes: 1+ /irstly the fatty degeneration of the tomes dentinal fibres resulting in deposition of fat globules in the further end of dentinal tubules. 1 ,t has been suggested that this fatty degeneration contributes to the: 1. ,mpermeability of the dentinal tubule. The initial penetration of caries in the dentinal tubules

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!. 0lso sclerosis of dentinal tubule. !+ Secondly as the caries penetrates there is a reaction of the vital dentinal tubules and vital pulp *hich lay do*n a &04&,/,& 90%%,E% thus protecting the dentinal tubules from further invasion of microorganisms. 1 This calcific barrier is termed as dentinal sclerosis ' transparent dentin =as this zone appears transparent in polarized light and dar3 in reflected light+. SLOW PROGRESSI'E LESION (CHRONIC) LESION 0 T",&@ transparent dentinal zone is present. Sclerosis resulting from aging is 1 -hysiological dentinal sclerosis. sclerosis RAPIDLY AD'ANCING (ACUTE) LESION P()*+,-,.+/a- S0D0 at #C years. The rate at I.C mm thic3 0 thin zone of transparent dentin seen Rea/t+1e D0S0 &an be seen radiographically in the form of a more radio1opa2ue =light+ area in the S shape of the 1< %esulting from mild irritation1 %eactive dentinal

*hich

caries

,) the

(4DE% caries

tubules progressive depends on 0ge. ,) A($)BE% ,)D,5,D$04S

,)D,5,D$04S

spread is sclerotic dentin.

SD Shiny the spread of caries is fast. and hard to explorer. /resh D 0llo*s penetration of a sharp explorer lp. Even before the carious process becomes E5,DE)T clinically a

fe* bacteria are seen to be present in the dentinal tubules. These are termed as -,()EE% 90&TE%,0. These bacteria are said to be present in the dentinal tubules prior to the occurrence of

DE&04&,/,&0T,(). #+ &lose examination of the dentin behind the zone of dentinal sclerosis reveals a zone of decalcification of dentin. This decalcified zone occurs prior to bacterial invasion. The initial decalcification involves the *alls of the dentinal tubules allo*ing them to distend slightly. <+ The dentinal tubule pac3ed masses of

microorganisms =closer examination reveals adEacent tubules *ith different strains of microorganisms i.e. tubule *ith social organism adEacent *ith bacilli type. ,n the early stages of dental caries acidogenic organisms are responsible for decalcification of dentinal tubules as these 1C

organisms depend on the carbohydrate substrate present at the surface. 0s the carious lesion progresses deeper the carbohydrate source moves further a*ay, the organisms found in the dentinal tubule are proteolytic in nature i.e. they depend on the proteins of dentinal tubules. "ence the organisms responsible for the initiation of the caries =0&,D(BE),&+ are replaced by other organisms =-%(TE(4AT,&+ as the lesion progresses. AD'ANCED DENTINAL CHANGES: C+ /urther decalcification of the individual dentinal tubule in their confluencing and increasing in diameter. The dentinal tubules undergo further pac3ing *ith

microorganisms. Tiny li2uifaction foci form due to brea3do*n of dentinal tubule. These foci are ovoid area of destruction parallel to the course of the dentinal tubules. 1 0s areas of li2uifaction foci undergo, expansion the adEacent dentinal tubule undergo. Distortion and their course is bent around li2uifaction foci.

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,n areas of globular dentin the decalcification process is said to be faster.

,n last stages destruction of dentin occurs through a processes of decalcification and proteolytic brea3do*n. These are numerous focal areas of destruction present and dentin, becomes 4E0T"E%A in consistency.

The caries extends at angular angles, along brachs of DT thus resulting in clefts.

These clefts account for the manner in *hich carious dentin can be excavated =as thin layers using hand instruments+.

0bove this is the necrotic layer *hich histologically is structureless and granular in appearance and contains masses of bacteria.

SECONDARY DENTINAL IN'OL'EMENT 1 The carious process is the same as in primary dentin but here the process is much slo*er as: 1. The dentinal tubules are fe*er in number. !. ore irregular in course.

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"ence,

delaying

the

penetration

of

invading

microorganisms but sooner ' later the involvement of the pulp results. 1 Sometimes the caries process may spread laterally bet*een primary and secondary dentin producing

separation of the t*o layers. ROOT CARIES : This is mainly said to occur in older individuals ' or as those age suffering from debilitating disease undergoes recession exposing the cementum covering the root. "ence there is increase in the prevalence of root caries. 1 %oot caries is found at the cemento1enamel Eunction or more apically, on the cementum. 1 %oot surface caries progresses round rather than into the tooth. =proteolyses of Sharpey8s fibres being

fragmentation ' cavitation+. 1 The spread of filamentous organisms along the Sharpeys fibres ' inbet*een bundles of Sharpey8s fibres are responsible for caries spread.

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ACTI'E LESION 1 bro*n. 1

INACTI'E LESION Dar3er smooth surfaces. "arder consistency =on probing+ *ith in

Aello*ish ' light 1 Soft and leathery 1 consistency.

0fter decalcification of cementum destruction of the remaining cementum occurs. 0s the process continues microorganisms invade into the underlying dentinal tubule *ith subse2uent matrix destruction and pulpal

involvement. Treatment: -ain : due to stimulation of odontoblastic process *hen acid in caries reaches DE;. CONCLUSION S, -4,/,ED EL$0T,()S depicting the caries progress is as follo*s: &ariogenic bacterial pla2ue (rganic acids =in pla2ue+ Demineralized tooth =Dentin+ > Suitable local substrate Tooth mineral 9acterial proteolytic enzymes (rganic acids

>

4oss of enamel

>

&avitation

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