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Dental Caries

PRESENTATION BY:RAJESH JAIN MDS 1ST YEAR DEPARTMENT OF CONSERVATIVE AND ENDODONTICS ITS DENTAL COLLEGE HOSPITAL AND RESEARCH CENTER GREATER NOIDA

PRESENTED ON :-30th JULY 2012

MODERATOR Dr.Rohit Kochhar

Contents
Introduction Review of literature History Definitions Theories of dental caries Etiology Classification Histopathology

Diagnosis
Caries protection Conclusion

References

Introduction
Dental caries is the most common chronic disease (5 billion people worldwide) It is costly in terms of time and work hours lost, money spent. In addition the expense incurred in education of health professional required to cope with this disease in terms of prevention, treatment and oral rehabilitation.

Review of literature
Psoter WJ, Reid BC, Katz RV. 2005 stated that Enamel hypoplasia, salivary glandular hypofunction and saliva compositional changes may be mechanisms through which malnutrition is associated with caries, while altered eruption timing may create a challenge in the analysis of age-specific caries rates. Hillman JD, Dzuback AL, Andrews SW(1976) concluded that streptococcus mutans was the main organism responsible for dental caries. Dreizen S, Brown LR(1987)stated that there is a strong corelation between Xerostomia and dental caries. Burke F.J.T (1998) states that presented trend in treating caries directed more towards prevention & minimal intervention rather than the traditional drill and fill dentistry.

HISTORY
Aristotle, Hippocrates and Shakespeare have all written on dental caries in their writings.

Some theories put forward are the Worm theory, Vital theory etc.
L. S. Parmly (1819)-first contributed to current understanding of caries mechanism Emil Magitot experimented using Pasteur findings. He produced artificial carious lesions in extracted teeth. W.D.Miller (1890) Chemo parasitic theory. Gottlieb (1941) Proteolysis theory. Schatz & Martin(1955) Proteolysis chelation theory.

Definitions
Dental caries is a microbial disease of the calcified tissues, characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth. (Shafer) Dental caries is an infectious microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues. (Sturdevant) Dental caries is defined as a progressive, irreversible multifactorial in nature affecting the calcified tissues of teeth, characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth. (Soben peter)

Theories of dental caries 1. Worms Theory 2. Humor Theory 3. Vital Theory 4. Chemical theory 5. Parasitic at septic theory 6. Chemical Parasitic theory 7. Proteolytic theory 8. Proteolysis Chelation theory 9. Acidogenic theory 10.Levines theory 11. Bandlish theory

a] Millers Chemo-parasitic / Acidogenic theory b] The proteolytic theory c] The sucrose-chelation theory

a)Acidogenic theory(w.d miller -1882)


Caries is a chemo parasitic process Caused by acids produced by microorganisms of the mouth Decalcification of the enamel which results in total destruction and decalcification of the dentin (preliminary stage)

Dissolution of the softened residue (final stage)

In a series of experiments following facts were demonstrated Acid was present in deep carious lesions Several types of bacteria could produce acid Lactic acid was an identifiable product Different kinds of food could decalcify the entire crown Different kinds of microorganisms had potential to invade carious dentin
Draw backs

Phenomenon of arrested caries,caries on unerupted teeth is not explained Smooth surface caries was not accounted Particular type of organisms causing caries was not explained

b)Proteolytic theory (gotilleb,fresbie,pincus)


The organic or protein elements are the initial pathway of invasion by microorganisms

The organic component is most vulnerable and is attacked by hydrolytic enzymes of microorganisms ,this precedes the loss of inorganic phase

Critics
organic matrix (small %) sufficient ??

lacks experimental support

c)chelation theory (schatz)


chelation; is a process involving the complexing of a metallic ion to a complex substance through a coordinate covalent bond which results in a highly stable, poorly disassociated or weakly ionized compound. bacterial attack on the enamel initiated by microorganisms, consists in a breakdown of protein and other organic components in the enamel, chiefly keratin . This results in the formation of substances which may form soluble chelates with the mineralized components of the tooth and there by decalcifying the enamel even at a neutral or alkaline ph.

Draw backs
Organic matrix (small %) dissolution can produce sufficient amount of chelates .
Break down of organic matter by proteolysis in initiating caries lacks experimental support

ETIOLOGY OF DENTAL CARIES

I. PRIMARY FACTORS:
1.TOOTH a. Susceptible tooth surface b. biochemical characteristic of tooth 2.DENTAL PLAQUE 3.DIET 4.TIME

Mechanism of carious lesion

Microorganisms found in various types of carious lesions


Pit and fissures S.mutans, S.sanguis,lactobacillus sp.actinomyces S.mutans, S.salivarius Actinomyces viscosus, A.naeslundii, s.mutans, s.sanguis,s.salivarius Lactobacillus sp, Actinomyces viscosus, A.naeslundii

Smooth surface caries Root caries

Deep dentinal caries

II.MODIFYING FACTORS:
1. SALIVA 2. SYSTEMIC HEALTH 3. SEX 4. RACE 5. GEOGRAPHIC ENVIRONMENT 6. OCCUPATION

CLASSIFICATION
I. STURDEVANT

Based on - Location
- Extent - Rate of progression

According to location:
a. Primary caries b. Caries of pit and fissure origin c. Caries of enamel smooth surface origin d. Backward caries e. Forward caries f. Residual caries g. Root surface caries

h. Secondary (recurrent) caries

According to extent:
a. Incipient (reversible) caries
b. Cavitated (irreversible) caries

According to rate of progression:


a. Acute (rampant) caries

b. Chronic (slow or arrested) caries

Blacks classification of tooth preparation


Class-I: - caries on the occlusal surfaces of molars and premolars - occlusal 2/3 of the buccal and lingual surfaces of molars - lingual surfaces of the anterior teeth. Class II- restorations on proximal surfaces of posterior teeth. Class III- restorations on anterior teeth that do not involve the incisal angles.

Class IV- Restorations on anterior teeth that involve the incisal angles. Class V- Restorations on all gingival third of facial or lingual surfaces of all teeth (except pit and fissure lesions) Class VI- restorations on incisal edge of anterior teeth or the occlusal cusp heights of posterior teeth.

proposed by Simon 1. Simple caries: one surface is involved Compound caries: two surfaces are involved Complex caries: three or more surfaces are involved

2.

3.

WHO classification
The shape and the depth of the carious lesion can be scored on a 4 point scale D1 -Clinically detectable enamel lesions with intact (non cavitated) surfaces D2 -Clinically detectable cavities limited to enamel

D 3 -Clinically detectable lesions in dentin (with and without cavitation of dentin)


D 4 Lesions into the pulp.

Limited to the occlusal surfaces of molars and premolars - buccal pits of molars - lingual surfaces of maxillary anterior teeth Poor self-cleansing features Usually occurs before smooth surface caries Clinically - black or brown in color - slightly soft consistency - catch the tip of a fine explorer Adjacent enamel appears bluish white Internal Caries

PIT AND FISSURE CARIES

Smooth Surface Caries


Develops on - proximal surfaces of the teeth - gingival third of the buccal and lingual surfaces (cervical caries) Preceded by the formation of dental plaque. Usually initiate just below the contact point. Clinically- initially as faint white opacity or yellow brown pigmented area. Adjacent enamel appears bluish white.

Cervical Caries
Appears as crescent shaped lesion.

May extend proximally.


Almost always an open cavity. Lack of oral hygiene on the part of patient.

Backward Caries
Lateral spread of the lesion along the DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the junction.

Forward Caries

Caries cone in enamel is larger or at least the same size as that in dentin

Residual Caries
Caries that remains in a completed cavity preparation Not acceptable if - present at DEJ - prepared enamel wall

Root Surface Caries


In old age patients

Initiates at the surface of a mineralized dentin and Cementum which have greater organic content
Usually have rapid clinical course

Recurrent (secondary) caries:


Occurs at the junction of the restoration and the cavosurface of the enamel May extend beneath the restoration

Indicates unusual susceptibility to caries attack, poor cavity preparation, defective restoration. Also indicates presence of microleakage.

Incipient (reversible) caries:


First evidence of caries activity in enamel Clinically as white opaque region Subsurface demineralization has occurred but no cavitation May take up extrinsic stains May undergo remineralization- called as caries reversibility or consolidation of early enamel carious lesion

Cavitated (irreversible) caries:


Lesion that has advanced into dentin with broken surface Remineralization is not possible

Treatment include cavity preparation and restoring with suitable material.

Linear enamel caries (odontoclasia):


Atypical form of dental caries in primary dentition Lesion predominates on the labial surface of the maxillary anterior teeth in the region of neonatal zone Lesion is crescent shape Increase caries susceptibility of posterior teeth.

Odontoclasia:

- variant of linear enamel caries


- results in gross destruction of the labial surfaces of incisor teeth

- cause may be an inherent


structural defect

Acute dental caries:


Rapid clinical course resulting in early pulp involvement Frequently in children and young adults Entry of lesion remains small while rapid spread along the DEJ Clinically appears light yellow in colour Pain is often present

Chronic dental caries


Common in adults

Large entrance of the lesion


Dentin is stained deep brown Moderate lateral spread of caries at DEJ

Pain is not a common clinical finding.


Slowly progressive lesion that involves pulp much later

Rampant caries:
Sudden and rapid onset and almost uncontrollable destruction of teeth Involves teeth that are ordinarily caries free (mandibular incisors) Ten or more new increments of carious lesion in one year

Nursing Bottle (Infancy or Soother) Caries


Rapidly progressing caries affecting primary dentition usually during first 2 years of life 4 maxillary anterior are affected first If unchecked, maxillary and mandibular molars may also get involved Lower anterior are spared (characteristic feature)

Adolescent caries:
Acute caries attack at 11-18 years of age

Lesion in teeth and surfaces that are relatively immune to caries


Small opening in enamel with extensive undermining

Rapid clinical course


Little or no secondary dentin formation

Arrested caries:
Caries which becomes static or stationary and does not show any tendency for progression Almost exclusively occurs on occlusal surfaces Both dentitions are affected Lesion appears as large open cavity with lack of food retention Superficially softened and decalcified dentin gets burnished and has brown stained polished appearance Eburnation of dentin

Xerostomia induced caries (radiation caries)


Complication of radiation therapy of oral cancer lesion Radiation induced xerostomia produces caries conducive environment Carious lesion develops as early as 3 months after onset of xerostomia May be caused by other factors like salivary gland tumors, autoimmune diseases, prolong illness

Senile Caries
Caries activity that spurts up during the old age.

They are located exclusively on the root surfaces of the teeth.


Also seen in association with partial denture clasps.

Causes: gingival recession, decreased salivary secretion, poor oral hygiene.

Histological Features of early enamel caries


Loss of inter-rod substance

prominent enamel-rods
Appearance of transverse striations of enamel rods due to segmental demineralization Accentuation of incremental striae of

Retzius

Histological Features of Advanced enamel caries


Classified on the basis of pore volume and mounting media used
Zone 1 Translucent zone

Zone 2 Dark zone


Zone 3 Body of lesion Zone 4 Surface zone

These zones are from the dentin towards the outer enamel surface

NORMAL ENAMEL DEJ SURFACE LAYER

BODY OF THE LESION


DARK ZONE TRANSLUSCENTZONE

TRANSLUCENT ZONE: Unrecognizable clinically & radiologically.

Occurs due to formation of submicroscopic pores at enamel rod boundaries and striae of Retzius. This zone is slightly more porous than sound enamel having a pore volume of 1% compared to 0.1% of sound enamel.

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.

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.

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.

Dentinal Caries
Once lesion spreads to DEJ, there is lateral spread of caries Surface enamel gets unsupported enamel rods enamel # greater cavitation Zones of dentinal caries. Zones start from pulpal side towards dentinal side

1.
2. 3.

Zone of Fatty Degeneration of Tomes process


Zone of Sclerosis Zone of Decalcification without Bacterial Invasion

4. 5.

Zone of Decalcification with Bacterial Invasion Zone of Decomposed Dentin / Infected dentin

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
5 4 3 2 1

ZONE 2 Zone of dentinal sclerosis

ZONE 3 Zone of decalcification


ZONE 4 Zone of bacterial invasion ZONE 5 Zone of decomposed dentin

Fatty Degeneration of Tomes Process


Innermost layer of dentinal caries towards pulp

Due to deposition of fatty tissue in odontoblastic processes


Seen usually in rapidly progressing caries No crystals or bacteria in lumen of tubules Intertubular dentin normal

Zone of Sclerosis/Sub-Transparent Dentin


As the microorganisms cause destruction to dentin, initially there is an attempt to stop the advancement of caries by depositing the minerals. There is a deposition of mineral in intertubular dentin. Zone is called transparent zone Odontoblasts are also start depositing dentin. At the periphery of sclerotic dentin, dead tracts are present.

Zone of Decalcification without Bacterial Invasion / Transparent Dentin


Decalcification is by bacterial acid diffusion
Very narrow zone, softer than normal dentin Further loss of minerals from inter tubular dentin Large crystals within lumen of dentinal tubules

Zone of Decalcification with Bacterial Invasion / Turbid Dentin


Initially only few tubules are involved & micro-orgs also less
These are acidogenic, pioneer bacteria (initiators), present long before lesion is clinically detected

Bacteria multiply within tubules & are seen in advancing


front of lesion

Zone of Decomposed Dentin / Infected Dentin


Outermost zone, large scale destruction of dentin High concentration of bacteria Removal of zone

DIAGNOSIS OF DENTAL CARIES


METICULOUS CLINICAL EXAMINATION TACTILE EXAMINATION RADIOGRAPHIC EXAMINATION TOOTH SEPARATION FIBEROPTIC TRANSILLUMINATION XERORADIOGRAPHY DIGITAL RADIOGRAPHIC METHODS COMPUTER AIDED RADIOGRAPHIC METHODS DIGITAL FIBEROPTIC TRANSILLUMINATION

METICULOUS CLINICAL EXAMINATION:

Careful examination under clean and dry condition with good illumination can reveal various signs of caries like:- brown discoloration of pits and fissures - opacity beneath pits and fissures or marginal ridges - frank cavitation of the tooth surface

TACTILE EXAMINATION:
Use

of dental explorer may help in detection of dental caries. Tactile findings suggestive of caries are: - softness at the base of a pit and fissures and discontinuity of enamel surface - catch at the explorer tip - cavitation at base of pit and fissure Cautions:excessive pressure with explorer can cause cavitation where was not present earlier infective m.org may be transferred to uninfected area

RADIOGRAPHIC EXAMINATION:
-Conventional , intraoral periapical and bitewing radiograph are employed to diagnose dental caries - bitewing is of more diagnostic value Uses of bitewing: detecting proximal caries Examining many teeth in one radiograph Checking cervical margin of restoration Monitoring the progress of arrest caries

Scoring the progress of caries on bitewing:


0= sound enamel 1= radiolucency only in enamel 2= radiolucency in enamel extending up to DEJ 3= radiolucency in enamel and outer half of dentine 4= radiolucency in enamel reaching inner half of dentine

TOOTH SEPARATION:
To detect initial proximal caries, separation of the contacting teeth can be achieved using wedges or mechanical separator Once the proximal surface is accessible, visual examination and gentle probing may help in diagnosis of the carious lesion

FIBEROPTIC TRANSILLUMINATION:
Carious lesion have lowered index of light transmission, when teeth are examined with the fiberoptic light source, caries appears as a dark shadow After drying the tooth, a fiberoptic probe can be placed in the buccal or lingual embrassures directly beneath the contact area between two adjacent teeth. If caries is present , dark shadow is seen beneath the marginal ridge Non invasive No radiation hazard No permanent record Difficulty in placing probe

XERORADIOGRAPHY:
Image is recorded on an aluminium plate coated with a layer of selenium particles These selenium particles are charged uniformly and stored in a unit called condition When x-ray is passed onto the film , it causes selective discharge of the particles which forms a latent image. This is converted into positive image by a process known as development in the process per unit Less radiation exposure No wet processing Electric charge over the film may cause discomfort

DIGITAL RADIOGRAPHIC METHODS:


offers more superior means of detecting caries
Can be obtained by 2 methods i)video recording and digitization of a conventional radiograph ii)direct digital radiography The direct digital radiography system was RVG It uses a charged couple device which works like a miniature video camera This records images produced by conventional x-ray and stores it in the computer memory for image processing and viewing Reduced radiation dose ,no need of dark room, no processing error, instant image visualization and can be magnified

COMPUTER AIDED RADIOGRAPHIC METHOD:


This method uses the measurement potential of computers in assessing and recording the size of carious lesions. Provides graphic visualization of the size and progression of the carious lesion especially a proximal caries. Computer software have been developed for automated interpretation of digital radiographs in order to standardize image assessment Helps in monitoring the carious process Time consuming and expensive

DIGITAL FIBEROPTIC TRANSILLUMINATION:


New technique which combines fiberoptictransillumination and digital CCD camera. Images captured by the camera are sent to a computer for analysis, which produces digital images that can be viewed This method overcomes the shortcomings of FOTI Non invasive Can detect incipient and recurrent caries very early Does not measure the depth of the lesion

PREVENTION OF DENTAL CARIES


An

ounce of prevention is worth a pound of dental cure.


-Old Dental Public Health Proverb

AIMS OF PREVENTION AIMS OF PREVENTION (Sturdevant):


1.Limiting pathogen growth & metabolism

2.Increasing resistance of tooth surface to demineralization


3.Caries control methods which include operative procedures

CLASSIFICATION OF METHODS FOR PREVENTION


According to SHAFER:

CHEMICAL MEASURES
Substances which alter tooth surface/structure
Fluorine Bis-biguanides Silver nitrate Zinc chloride & potassium ferrocyanide

Interfere with carbohydrate degradation through enzymatic alterations


Vitamin K Sarcoside

Interfere with bacterial growth & metabolism


Urea & ammonium compounds Chlorophylls Nitrofurans Penicillin's Other antibiotics Caries vaccine Ozone technology

NUTRITIONAL MEASURES
Diet counseling restriction of refined carbohydrates Phosphated diets Calcium phosphate rich diet. Sugar substitutes Non-caloric sweeteners-aspartame, saccharine Caloric sweeteners-sorbitol, Xylitol, Mannitol

MECHANICAL MEASURES
Dental prophylaxis

Tooth brushing
Mouth rinsing Dental floss

Oral irrigators
Chewing gum Pit & fissure sealants Preventive resin restorations

conclusion
Dental caries is an oral infection. Dental caries has a multi-factorial causation involving the interaction of host factors (tooth surface, saliva, acquired pellicle), diet, and dental plaque (biofilm). Besides these other modifying factors like socioeconomic status and behavioral patterns also greatly influence the caries process in a complex manner. A good understanding of the caries process can help in formulation of better diagnosis, prevention and treatment of dental caries .

References
1) 2) 3)
Sturdevant's Art and Science of Operative Dentistry5th edition pg74-110 Cariology Ernest Newbrun- 3rd edition Diagnosis & Risk prediction of dental caries-Per Axelsson.

4)
5)

Textbook of operative dentistry-Ramya Raghu 2nd edition pg 50-70


Essentials of Preventive and Community dentistrySoben Peter -2nd edition pg117-130