CLINICAL FEATURES & HISTOPATHOLOGY OF DENTAL CARIESPRESENTATION BY:SAGAR HIWALE

MDS 1ST YEARDEPARTMENT OF CONSERVATIVE AND ENDODONTICS

JAIPUR DENTAL COLLEGE AND HOSPITAL

CONTENTS CLASSIFICATION OF DENTAL CARIES1.BASED ON ANATOMICAL SITE2.BASED ON PROGRESSION3.BASED ON VIRGINITY OF LESION4.BASED ON EXTEND OF CARIES5.BASED ON TISSUE INVOLVEMENT6.BASED ON PATHWAY OF CARIES SPREAD 7. BASED ON NUMBER OF TOOTH SURFACE INVOLVED8. BASED ON CHRONOLOGY9 .BASED ON WHETHER CARIES IS COMPLETLY REMOVED OR NOT DURING

TREATMENT.10.BASED ON TOOTH SURFACE TO BE RESTORED11.BLACK’S CLASSIFICATION12.WHO SYSTEM.13.GJ MOUNT CLASSIFICATION HISTOPATHOLOGY OF CARIES – ENAMEL HISTOPATHOLOGY OF CARIES – DENTIN

CLASSIFICATION OF DENTAL CARIES

1.BASED ON ANATOMICAL SITE

OCCLUSAL(PIT AND FISSURE)

ROOT CARIES

SMOOTH SURFACE CARIES(PROXIMAL AND CERVICAL CARIES)

LINEAR ENAMEL CARIES

PIT AND FISSURE CARIES PIT AND FISSURE CARIES of the primary type

develops in the occlusal surface of molar and premolar,in the buccal and lingual surface of the molar and in the palatal surface of the maxillary incisors.

Shape, morphological variation and depth of pit and fissures contributes to their high susceptibility to caries.

Enamel in the extreme depth is very thin or occasionally absent and thus allows the exposure of dentin.

Pit and fissures affected by early caries may appear brown or black and will feel slightly soft and ‘catch’ a fine explorer point.

Entry site may appear much smaller than actual lesion, making clinical diagnosis difficult.

Carious lesion of pits and fissures develop from attack on their walls.

In cross section, the gross appearance of pit and fissure lesion is inverted V with a narrow entrance and a progressively wider area of involvement closer to the DEJ.

MORPHOLOGY OF FISSURES

NANGO (1960):Based on the alphabetical description of shape– 4 types

V&U type: self cleansing and somewhat caries resistant

U type: narrow slit like opening with a larger base as it extend towards DEJ .Caries susceptible; also have a number of different branches

K type: also very susceptible to caries

Smooth surface caries Less favorable site for plaque attachment, usually

attaches on the smooth surface that are near the gingiva or are under proximal contact..

In very young patients the gingival papilla completely fills the interproximal space under a proximal contact and is termed as col. Also crevicular spaces in them are less favorable habitats for s.mutans.

Consequently proximal caries is less lightly to develop where this favorable soft tissue architecture exists.

The proximal surfaces are particularly susceptible to caries due to extra shelter provided to resident plaque owing to the proximal contact area immediately occlusal to plaque.

Lesion have a broad area of origin and a conical, or pointed extension towards DEJ.

V shape with apex directed towards DEJ.

After caries penetrate the DEJ softening of dentin spread rapidly and pulpally

Linear enamel caries Linear enamel caries ( odontoclasia ) is seen to occur in

the region of the neonatal line of the maxillary anterior teeth.

The line, which represent a metabolic defect such as hypocalcemia or trauma of birth, may predispose to caries, leading to gross destruction of the labial surface of the teeth.

Morphological aspects of this type of caries are atypical and results in gross destruction of the labial surfaces incisor teeth

ROOT SURFACE CARIES The proximal root surface, particularly near the cervical line, often is

unaffected by the action of hygiene procedures, such as flossing, because it may have concave anatomic surface contours (fluting) and occasional roughness at the termination of the enamel.

These conditions, when coupled with exposure to the oral environment (as a result of gingival recession), favor the formation of mature, caries-producing plaque and proximal root-surface caries.

Root-surface caries is more common in older patients.

Caries originating on the root is alarming because 1. it has a comparatively rapid progression 2. it is often asymptomatic 3. it is closer to the pulp 4, it is more difficult to restore

The root surface is refer the enamel and readily allows plaque formation in the absence of good oral hygiene.

The cementum covering the root surface is extremely thin and provides little resistance to caries attack.

Root caries lesions have less well-defined margins, tend to be U-shaped in cross sections, and progress more rapidly because of the lack of protection from and enamel covering.

2.BASED ON PROGRESSION

ACUTE CARIES

CHRONIC CARIES

ARRESTED CARIES

ACUTE CARIES

Acute caries is a rapid process involving a large number of teeth.

These lesions are lighter colored than the other types, being light brown or grey, and their caseous consistency makes the excavation difficult.

Pulp exposures and sensitive teeth are often observed in patients with acute caries.

It has been suggested that saliva does not easily penetrate the small opening to the carious lesion, so there are little opportunity for buffering or neutralizaton

CHRONIC CARIES These lesions are usually of long-standing involvement,

affect a fewer number of teeth, and are smaller than acute caries.

Pain is not a common feature because of protection afforded to the pulp by secondary dentin

The decalcified dentin is dark brown and leathery. Pulp prognosis is hopeful in that the deepest of lesions

usually requires only prophylactic capping and protective bases.

The lesions range in depth and include those that have just penetrated the enamel.

ARRESTED CARIES:-

Caries which becomes stationary or static and does not show any tendency for further progression

Both deciduous and permanent affected With the shift in the oral conditions, even

advanced lesions may become arrested . Arrested caries involving dentin shows a

marked brown pigmentation and induration of the lesion [the so called ‘eburnation of dentin’]

Sclerosis of dentinal tubules and secondary dentin formation commonly occur

Exclusively seen in caries of occlusal surface with large open cavity in which there is lack of food retention

Also on the proximal surfaces of tooth in cases in which the adjacent approximating tooth has been extracted

3.BASED ON VIRGINITY Of LESION

INITIAL/PRIMARY RECURRENT/SECONDARY

PRIMARY CARIES(INITIAL)

A primary caries is one in which the lesion constitutes the initial attack on the tooth surface.

The designation of primary is based on the initial location of the lesion on the surface rather than the extent of damage.

SECONDARY CARIES (RECURRENT)

This type of caries is observed around the edges and under restorations.

The common locations of secondary caries are the rough or overhanging margin and fracture place in all locations of the mouth.

It may be result of poor adaptation of a restoration, which allows for a marginal leakage, or it may be due to inadequate extension of the restoration.

In addition caries may remain if there has not been complete excavation of the original lesion, which later may appear as a residual or recurrent caries.

4. BASED ON EXTENT OF CARIES

INCIPIENT CARIES

OCCULT CARIES

CAVITATION

INCIPIENT CARIES The early caries lesion, best seen on the smooth

surface of teeth, is visible as a ‘white spot’. Histologically the lesion has an apparently intact

surface layer overlying subsurface demineralization.

Significantly may such lesion can undergo remineralization and thus the lesion is not an indication for restorative treatment

These white spot lesion may be confused initially with white developmental defects of enamel formation, which can be differentiated by their position away from the gingival margin], their shape [unrelated to plaque accumulation] and their symmetry [they usually affect the contralateral tooth].

Also on wetting the caries lesion disappear while the developmental defect persist

It is believed that bite wing and OPG radiographs along with noninvasive adjuncts like fiber optic transillumination (FOTI),laser luminescence, electrical resistance method (ERM) are used for diagnosis these occlusal lesions.

These lesion are not associated with microorganisms different to those found in other carious lesion.

These carious lesion seem to increase with

increasing age. Occult carious lesion are usually seen with low caries

rate which is suggestive of increase fluid exposure.

It is believed that increased fluid exposure encourages remineralization and slow down progress of the caries in the pit and fissure enamel while the cavitations continues in dentine, and the lesions become masked by a relatively intact enamel surface.

These hidden lesions are called as fluoride bombs or fluoride syndrome.

Recently it is seen that occult caries may have its origin as pre-eruptive defects which are detectable only with the use of radiographs.

Once it reaches the dentinoenamel junction, the caries process has the potential to spread to the pulp along the dentinal tubules and also spread in lateral direction.

Thus some amount of sensitivity may be associated with this type of lesion.

This may be generally accompanied by cavitation

5.Based on tissue involvement1. Initial caries2. Superficial caries 3. Moderate caries 4. Deep caries 5. Deep complicated caries

Dental caries can be divided into 4 or 5 stages

Initial caries: Demineralization without structural defect. This stage can be reversed by fluoridation and enhanced mouth hygiene

Superficial caries (Caries superficialis):Enamel caries, wedge-shaped structural defect. Caries has affected the enamel layer, but has not yet penetrated the dentin.

3. Moderate caries (Caries media): Dentin caries. Extensive structural defect. Caries has penetrated up to the dentin and spreads two-dimensionally beneath the enamel defect where the dentin offers little resistance.

4. Deep caries (Caries profunda): Deep structural defect. Caries has penetrated up to the dentin layers of the tooth close to the pulp.

5. Deep complicated caries (Caries profunda complicata) :Caries has led to the opening of the pulp cavity (pulpa aperta or open pulp).

6.BASED ON PATHWAY OF CARIES SPREAD

1.FORWARD CARIES 2.BACKWARD CARIES

“Forward-backward” classification is considered as graphical representation of the pathway of dental caries. ENAMEL

First component of enamel to be involved in carious process is the interprismatic substance. The disintegrating chemicals will proceed via the substance, causing the enamel prism to be undermined.

The resultant caries involvement in enamel will have cone shape.In concave surface (pit and fissures) base towards DEJ.In convex surfaces (smooth surface) base away from DEJ.

DENTIN First component to be involved in dentin is

protoplasmic extension within the dentinal tubules.

These protoplasmic extension have their maximum space at the DEJ, but as they approach the pulp chamber and root canal walls, the tubules become more densely arrange with fewer interconnections.

So caries cone in dentin will have their base towards DEJ.

Decay starts in enamel then it involves the dentin. Wherever the caries cone in enamel is larger or at least the size as that of dentin, it is called forward decay (pit decay)

However the carious process in dentin progresses much faster than in enamel, so the cone in dentin tends to spread laterally creating undermined enamel. In addition decay can attack enamel from its dentinal side. At this stage it becomes backward decay.

7.BASED ON NUMBER OF TOOTH SURFACE INVOLVED

Simple

Compound

Complex

A caries involving only one tooth surface

A caries involving two surfaces of tooth

A caries that involves more than two surfaces of a tooth

8. BASED ON CHRONOLOGY

EARLY CHILDHOOD CARIES

ADOLESCENT CARIES

ADULT CARIES

It has been stated that over a lifetime, caries incidence i.e. the number of new lesions occurring in a year, shows three peaks-at the ages 4-8,11-19 and 55-65 years

EARLY CHILDHOOD CARIES Early childhood caries

would include, two variants: Nursing caries and rampant caries.

The difference primarily exist in involvement of the teeth[ mandibular incisors ] in the carious process in rampant caries as opposed to nursing caries.

CLASSIFICATION OF EARLY CHILDHOOD CARIESTypeI(MILD )

Involves molars and incisorsSeen in 2-5 yearsCausecariogenic semisolid food +lack of oral hygeine

TypeII (MODERATE)

Unaffected mandibular incisorsSoon after first tooth eruptsCauseinappropriate feeding +lack of oral hygeine

TypeIII(SEVERE)

All teeth including mandibular incisorsCausemultitude of factors

NURSING CARIESSeen in infant and toddlerAffects primary dentitionMandibular incisors are not involvedETIOLOGYImproper bottle feeding Pacifier dipped in honey/other sweetner

RAMPANT CARIESSeen in all ages,including adoloscennceAffects primary and permanent dentitionMandibular incisors are also affectedETIOLOGYMULTIFACTORIAL Frequent snacks Sticky refined CHO Decreased salivary flow Genetic background

TEENAGE CARIES (ADOLESCENT CARIES) This type of caries is a variant of rampant caries

where the teeth generally considered immune to decay are involved.

The caries is also described to be of a rapidly burrowing type, with a small enamel opening.

The presence of a large pulp chamber adds to the woes, causing early pulp involvement

ADULT CARIES With the recession of the

gingiva and sometimes decreased salivary function due to atrophy, at the age of 55-60 years, the third peak of caries is observed.

Root caries and cervical caries are more commonly found in this group.

Sometime they are also associated with a partial denture clasp.

9.BASED ON WHETHER CARIES IS COMPLETLY REMOVED OR NOT DURING TREATMENTRESIDUAL CARIES Residual caries is that which is not removed during

a restorative procedure, either by accident, neglect or intention.

Sometimes a small amount of acutely carious dentin close to the pulp is covered with a specific capping material to stimulate dentin deposition, isolating caries from pulp.

The carious dentin can be removed at a later time.

10.BASED ON SURFACES TO BE RESTORED

Most widespread clinical utilization O for occlusal surfaces M for mesial surfaces

D for distal surfacesF for facial surfacesB for buccal surfacesL for lingual surface

Various combinations are also possible, such as MOD –for mesio-occluso-distal surfaces.

11.BLACK’S CLASSIFICATIONClass 1 lesions: Lesions that begin in the

structural defects of teeth such as pits, fissures and defective grooves.

Locations include Occlusal surface of

molars and premolars. occlusal two thirds of

buccal and lingual surfaces of molars and premolars.

Lingual surfaces of anterior tooth.

Class 2 lesions:They are found on the proximal surfaces of the bicuspids and molars.

Class 3 lesions:Lesions found on the proximal surfaces of anterior teeth that do not involve or necessitate the removal of the incisal angle.

Class 5 lesions: Lesions that are found at the

gingival third of the facial and lingual surfaces of anterior and posterior teeth.

Class 4 lesions:Lesions found on the proximal surfaces of anterior teeth that involve the incisal angle.

Class 6 (Simon’s modification):

Lesions involving cuspal tips and incisal edges of teeth.

12.World health organization (WHO) systemIn this classification the shape and depth of the

caries lesion scored on a four point scaleD1. clinically detectable enamel lesions with intact

(non cavitated) surfacesD2. Clinically detectable cavities limited to enamelD3. Clinically detectable cavities in dentinD4. Lesions extending into the pulp

CLASSIFICATION BY GJ MOUNT AND HUME (1998) This new system defines the extent and

complexity of a cavity and at the same time encourages a conservative approach to the presevation of natural tooth structure.

This system is designed to utilized the healing capacity of enamel and dentin.

The three sites of carious lesion

Site1- pit and fissure and enamel defects on occlusal surface of posterior teeth or other smooth surfaces.

Site2- proximal enamel immediately below area in contact with adjacent teeth

Site3 – the cervical one third of crown or following gingival recession,the exposed root.

Four sizes of carious lesion Size1- minimal involvement of dentin

treatment by remineralization alone. Size2- moderate involvement of dentin

following cavity preparation,remaning enamel is sound,well supported by dentin and not likely to fail under normal occlusal load.

The remaining tooth structure is sufficient strong to support the restoration.

Size3- the cavity is enlarged beyond moderate.The remaining tooth structure is weakened to the extend that cusp or incisal edges are split or are likely to fail or left exposed to occlusal or incisal load the cavity need to be futher enlarged so that the restoration can be designed to provide support and protection to the remaining tooth structure.

Size4- extensive caries with bulk loss of tooth structure has already occurred.

RADIATION CARIES

Radiography is frequently associated with xerostomia due to decreased salivary secretion,an increase in viscosity and low PH.

lead to a rampant form of caries Three types of defects due to radiation1. Lesion usually encircling the neck of teeth

amputation of crowns may occur 2. Begins as brown to black discolouration of

tooth .occlusal surface and incisal edges wear away3. Spot depression which spreads from any surface

HISTOPATHOLOGY OF CARIES

HISTOPATHOLOGY OF CARIES - ENAMEL

Caries process in enamel progresses through following stagesA. Early submicroscopic lesionB. Phase of nonbacterial enamel crystal destructionC. Cavity formationD. Bacterial invasion of enamel

* C & D Occur almost simultaneously

EARLY LESION – SMOOTH SURFACE Earliest visible changes are

seen as a chalky white spot on the tooth just adjacent to contact point.

Electron microscopic study reveals the early changes as loss of inter rod enamel, accentuation of striae of Retzius and perikymata.

As caries progresses, the lesion of smooth surface caries has a distinctive conical shape with its base towards enamel surface and apex towards DEJ.

This conical lesion when observed in a light microscope reveals four different zones as seen from deepest advancing zone first1. Translucent zone 2. Dark zone3. Body of lesion 4. Surface zone

1.TRANSLUCENT ZONE: - Unrecognizable clinically &

radiologically. Occurs due to formation of

submicroscopic pores at enamel rod boundaries.

This zone is slightly more porous than sound enamel having a pore volume of 1% compared to 0.1% of sound enamel.

2. DARK ZONE: - Lies superficial to translucent

zone. Called positive zone as it is

always present. Pore volume is 2 – 4%.

Increased porosity in this zone is due to greater degree of demineralization in this zone.

3. BODY OF LESION: - Forms bulk of the lesion and lies

between relatively unaffected surface zone and dark zone.

Area of greatest demineralization, having a pore volume of 5% near the periphery to about 25% in the center of body of lesion.

4. SURFACE ZONE: - Interestingly, this zone not only

remains intact during the early stages of attack by caries, but also REMAINS MORE HEAVILY MINERALIZED.

Pore volume of only 1%. Ions for remineralization come either

from those within plaque or from reprecipitation of calcium and phosphate ions diffusing outwards as deeper layers are demineralized.

Eventually, this zone is demineralized by the time caries penetrates dentin.

HISTOPATHOLOGY OF CARIES – DENTIN (EARLY CHANGES)

The initial (non infected) lesion in dentin forms beneath enamel before any cavity has formed.

Even though acids formed from fermentation of carbohydrate substrate diffuse into dentin, they leave the organic matrix intact.

Once bacteria penetrate enamel, they spread laterally along DEJ and attack dentin over a wide area.

The infected lesion of dentin is helped in its course by the presence of tubules within dentin which provide an easy pathway to the bacteria.

Bacteria now liberate proteolytic enzymes and bring about destruction of organic matrix of dentin which is already softened by demineralization.

The first change to occur in the caries process within dentin is fatty degeneration of the tome’s fibers, with deposition of lipid globules within these fibers.

This is then followed by dentinal sclerosis, which is minimal in rapidly advancing acute caries and maximum in slow, chronic caries.

This is considered as a protective measure by dentinal tubules to seal off the invading bacteria.

In spite of all these attempts to prevent spread of caries process, dentin is continually destroyed.

Thus behind the zone of dentinal sclerosis a narrow zone of decalcification is seen, just ahead of bacterial invasion of dentinal tubules.

At this stage, only a few tubules are invaded even before clinical evidence of caries.

These bacteria are called “Pioneer bacteria”.

HISTOPATHOLOGY OF CARIES – DENTIN (ADVANCED CHANGES)

Continued decalcification of dentinal tubules leads to their confluence, although the structure of organic matrix may still be maintained for some time.

Confluence of tubules occurs due to packing of the tubules with the invading bacteria.

The coalescence and breakdown of adjacent dentinal tubules leads to formation of “Miller’s liquefaction foci”.

It is an ovoid area of destruction of tubules parallel to the course of tubules and is packed with necrotic debris derived from destruction of tubules.

Continued dentinal destruction by decalcification followed by proteolysis occurs at many focal areas which ultimately coalesce to form a necrotic leathery mass of dentin.

In this mass, clefts occur at right angles to tubules and parallel to the course of lateral branches of tubules or along the collagen fibers of organic matrix.

Due to these clefts, carious dentin can be peeled away in thin layers by hand instruments.

Observing from the pulpal side at the advancing edge of carious lesion following different zones can be seen –

ZONE 1 – Zone of fatty degeneration of Tomes’ fibers

ZONE 2 – Zone of dentinal sclerosisZONE 3 – Zone of decalcification ZONE 4 – Zone of bacterial invasionZONE 5 – Zone of decomposed dentin

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ZONES OF DENTINAL CARIES

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