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DENTAL CARIES

Contents
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    

Introduction Etiology of dental caries Histopathology of dental caries Diagnosis of dental caries References

Introduction
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Dental caries continues to be a major problem in dentistry and should receive significant attention in everyday practice, not only from the standpoint of restorative procedures but also in terms of preventive measures designed to reduce the problem. Caries is on the decline in the industrial countries but it is on the increase in the developing countries due to increased sugar consumption.

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Dental caries is an irreversible microbial disease of the calcified tissues of the teeth, characterized by demineralisation of the inorganic portion and destruction of organic substance of the tooth , which often leads to cavitation. It is essential to understand that cavitation in teeth are signs of bacterial infection. It has effected humans since prehistoric times, but the prevalence of this disease has increased greatly in modern times due to dietary changes.

Dental caries 5 .

Calcium and Phosphates can again enter the tooth. The process is strongly facilitated by fluorides 6 A CAVITY occurs if the Demineralization "wins" over the Remineralization over time . they form acids which start to dissolve the enamel . Plaque is often found close to the gum. in fissures and at other "hidden" sites. saliva can wash away sugars and buffer the acids. which consists mainly of bacteria. in between teeth.an early caries lesion occurs due to loss of Calcium and Phosphates Remineralization: When sugar consumption has ceased. Demineralization: When sugar and other fermentable carbohydrates reaches the bacteria.Tooth is covered by plaque.

4. 3. A tooth surface without caries. 2. . 6. The demineralization proceeds and undermines the tooth. The first signs of demineralization. 5. A filling has been made but the demineralization has not been stopped.Progression of dental caries 7 1. The tooth has fractured. The enamel surface has broken down.

. It can also be defined as localized chemical dissolution of the tooth surface caused by metabolic events taking place in the biofilm (dental plaque) covering the affected area. to WHO it is defined as a localized post eruptive pathological process of external origin involving softening of the hard tooth tissue and proceedings to the formation of a cavity.8   Acc.

.9   It may develop at any tooth site where biofilm develops and remains for a period of time. Biofilm is characterized by continued microbial activity resulting in continued metabolic events in the form of minute pH fluctuation. Biofilm is a prerequisite for caries lesion to occur.

EPIDEMIOLOGY 10  Dental caries may be considered a disease of modern civilization . Anthropologic studies of VON LENHOSSEK revealed that the Dolicocephalic skulls of men from pre Neolithic periods (12000 BC) did not exhibit dental caries but skulls from Bracycephalic man of the Neolithic periods (12000 to 3000 BC) contained carious teeth. since prehistoric man rarely suffered from this form of tooth destruction . The cervical areas of teeth in older persons were frequently affected . .

CARIES SUSCEPTIBILITY OF INDIVIDUAL TEETH 11           BREKHUS (1931 ) studied a group of students at the university of Minnesota and reported the following caries susceptibility incidence of the teeth Upper and lower first molar : 95 % Upper and lower second molars : 75 % Upper second bicuspids : 45% Upper first bicuspid :35% Lower second bicuspids : 35% Upper central and lateral incisor : 30 % Upper cuspids and lower first bicuspids : 10% Lower central and lateral incisors : 3 % Lower cuspids : 3% .

ETIOLOGY OF DENTAL CARIES .

Development of dental caries depends on : Microflora: acidogenic bacteria that colonize the tooth surface. 4. 2.but also starch. Host :quantity and quality of saliva . Diet : intake of fermentable carbohydrates. 3. especially sucrose . . quality of the tooth.Etiology 13  1. Time : total exposure time to acids produced by the bacteria of the dental plaque.

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Caries Tetralogy[Newbrun 1982] 15 Includes a fourth factor. time to the still existing concept of Keyes. . depicting the significance of changes taking place over a period.

Classification of dental caries 16 ACCORDING TO MORPHOLOGY -Pit and fissure caries -Smooth surface caries  ACCORDING TO CHRONICITY -Acute dental caries -Chronic dental caries  ACCORDING TO PROGRESSION -Primary caries -Secondary (Recurrent )caries -Arrested caries  .

17 ACCORDING TO SEVERITY AND PROGRESSION -rampant caries -nursing caries -radiation caries  ACCORDING TO PART OF TOOTH STRUCTURE INVOLVED -Enamel caries -Dentinal caries -Cemental caries  .

 Retention of food debris and microorganisms.  Early caries appear brown or black.  Lateral spread of caries through a narrow opening at the DEJ. . soft ‘catch’ of a fine explorer point.18 PIT AND FISSURE CARIES  Pit and fissure with high steep walls and narrow bases are prone to develop caries.

19 SMOOTH SURFACE CARIES  Early appears as a faint white opacity of the enamel without loss of the continuity of the surface.  Proximal caries begins just below contact point.  Preceded by the formation of a microbial or dental plaque. .it assumes bluish white appearance.  As caries penetrates enamel.  The typical cervical carious lesion is crescent shaped cavity with chalky area.

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ACUTE DENTAL CARIES  Rapid clinical course resulting in early pulp involvement with pain.  Progress rapidly so less time for secondary dentin depositionis present  E.g.Nursing bottle caries commonly affects 4 deciduous maxillary incisors. It is a type of RAMPANT caries which primarily affects all deciduous incisors.

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CHRONIC DENTAL CARIES  Progresses slowly and tends to involve pulp much later.  Sufficient time for sclerosis of dentinal tubules and secondary dentin deposition.  Carious dentin stains deep brown.  PAIN is not a common feature.

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RECURRENT CARIES  Caries occuring in immediate vicinity of a restoration.  Usually due to inadequate extension of the original restoration favoring retention of debris.  Poor adaptation of filling material to the cavity which produces a leaky margin.

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ARRESTED CARIES  Static or stationary caries which do not show any tendency for further progression.  Occurs exclusively in caries of occlusal surfaces characterised by a large open cavity which lack food retention.  EBURNATION OF DENTIN : gradual burnishing of superficial softened and decalcified dentin until it takes on a hard brown stained, polished appearance.

24 RAMPANT CARIES  It occurs as a sudden . involving surfaces of teeth that are ordinarily caries free(proximal and cervical surfaces of anterior teeth including the mandibular incisors get affected)  A caries increment of 10 or more new lesions over a period of about a year is characteristic of rampant caries attack . rapid and almost uncontrollable destruction of teeth .

25 NURSING CARIES  It is a specific form of rampant decay of primary teeth of infants and toddlers.  Affects maxillary primary incisors due to prolonged nursing habit esp. when the child is sleeping  Also named as baby bottle tooth decay or early childhood caries .

26 RADIATION CARIES  Common complication of radiotherapy of oral cancer lesions and radiation induced xerostomia .

Plaque is assumed pathogenic only when signs of disease are present. Latter one promotes that accumulation of plaque could be regarded as normal in the absence of disease.Hypothesis concerning the etiology of caries 27     Two hypothesis: Older one : promotes the universal presence of potential pathogens in plaque and assumes that all accumulation of plaque are pathogenic. .

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The difference between two hypothesis was identified and discussed by Loesche: First one : non specific plaque hypothesis Second one: specific plaque hypothesis Problem with non-specific hypothesis was that it requires a therapeutic goal that completely eliminates plaque in all patients that requires a continuous therapy directed to total plaque elimination.

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Acc . to specific theory ,plaque can be identified as pathologic only when they are associated with clinical disease. So treatment can be aimed at elimination of the specific pathogenic organisms.

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Caries- latin word –rot or decay. Its etiology is agreed to be a complex problem complicated by many indirect factors that obscure the direct causes. Many theories have evolved through years of investigation and observation attempting to explain its etiology.

The early theories
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1.

2.

The legend of worms : the earliest reference is from the ancient sumerians known as legend of worms. This dates back around 5000 BC . The idea behind this was that caries was caused by worms and worms are the cause of toothache. Endogenous theory: it was advocated by Greek physicians, who proposed that dental caries is produced by internal action of acids and corroding humors.They also proposed the Vital theory of tooth decay,which postulated that tooth decay originated from within the tooth itself.

Ficnus in 1847 attributed dental caries to denticolae(decay related to microorganisms). He proposed that unidentified chemical agent was responsible for caries. .32 3. 4. Parasitic theory:Erdl in 1843 was first to relate microorganisms to caries as a positive agent. Chemical theory:Parmly in 1820 observed that dental decay affected externally and not internally. But this was soon disseminated as it was proposed that dental caries commenced as a purely chemical process and bacteria were essential for caries as an exogenous source of the acids.

which results in its total destruction and the de-calcification of dentin as a preliminary stage. the de-calcification of enamel . “Dental decay is a chemico-parasitic process consisting of two stages .followed by dissolution of the softened residue” . He stated that caries is caused by acids produced by microorganisms of the mouth.Miller‟s chemico-parasitic theory OR Acidogenic theory 33    Proposed by Willoughby D Miller in1882.

A no.34    The acid that affects the de-calcification is derived from the fermentation of starches and sugars lodged in the retaining centres of the teeth. . some were acidogenic and others were proteolytic. of these bacteria were capable of producing lactic acid. He isolated numerous microorganisms.

3. 2. He proposed that caries was not caused by any single organism but a variety of microorganisms.35   1. Essential factors in caries process: Microorganisms Carbohydrate substrate Acid production .

36   This theory is the backbone of current knowledge and understanding of the etiology of dental caries. . Drawbacks : theory was unable to explain the predilection of specific sites on a tooth to caries and the initiation of smooth surfaces was not accounted by this theory.

. This theory proposed that the organic material(enamel lamellae and rod sheaths) or protein elements are the initial pathway of invasion by microorganisms. They also admit that acid formation accompanied the proteolysis. Proposed by Gottlieb and Gottlieb(1944).The proteolytic theory 37     The previous theory was not wholly accepted. Then this theory came into existence.

.38    Pincus(1949) proposed that enamel proteins are mucoproteins. This acid dissolves the enamel. In support of this theory Gram negative bacilli capable of producing sulfatase were also isolated. yielding sulphuric acid upon hydrolysis. combining with the calcium to form calcium sulphate.

No such enzyme has also been demonstrated in the oral cavity.39    Drawbacks : no sulfatase has been demonstrated at the site of carious lesion. The proteolysis of organic matrix of dentin may indeed occur after demineralization and there is no satisfactory evidence to support the claim that the initial attack on enamel is proteolytic. .

The proteolysis-chelation theory 40    Proposed by Schatz et al (1955). Chelation is a process involving the complexing of a metallic ion to a complex substance through a coordinate covalent bond(highly stable . . Proposed a simultaneous microbial degradation of the organic components (proteolysis) and the dissolution of minerals of the tooth by the process known as chelation. poorly dissociated).

41   This theory considered caries to be a bacterial destruction of teeth where the initial attack is essentially on the organic components of the enamel. . Thus this theory suggested that demineralization of enamel could arise without acid formation. this breakdown product has chelating property hence dissolves the minerals in enamel (at a neutral or alkaline ph).

42   Drawback : it was concluded that saliva and plaque do not contain substances in sufficient amount to chelate calcium in detectable amounts from enamel. . Also chelation is unlikely to be involved in the initiation of the lesion. it may play a minor role in the established lesion.

Sucrose chelation theory 43    Proposed by Egglers-Lura (1967). This theory stated that calcium saccharates and calcium complexing intermediaries require inorganic phosphate which is subsequentaly removed from the enamel by phosphorylating enzymes. He proposed that sucrose itself and not the acid derived from it cause dissolution of enamel by forming an ionized calcium saccharates. .

it is highly improbable that depletion of phosphate in plaque by oral microbial metabolism results in phosphate withdrawl from enamel.44  Drawback : since saliva is an abundant source of inorganic phosphates for bacterial utilization. .

Accumulation of plaque on teeth is highly organized and ordered sequence of events . translucent and tenaciously adherent material accumulating on the surface of teeth and not readily removed by rinsing with water .Role of plaque in dental caries 45    Dental plaque is soft. It is composed of bacteria and their byproducts.

A few specialized organisms (streptococci ) are able to adhere to oral surfaces like mucosa and tooth surface. These bacteria produce a sticky matrix that allows them to coadhere to each other .46    It is estimated that 1mm³ of plaque weighing about 1mg contains more than 200 million bacteria. .

. These bacteria proliferate and spread laterally to form a mat-like covering over the tooth surfaces.growth of colonies increases the thickness of plaque . (mainly streptococcal strains). When the entire surface is covered .Plaque growth 47    The initial bacteria are called pioneer bacteria or colonizers. Further growth of bacteria produces a vertical growth away from the tooth surface forming vertical columns called palisades .

Proliferation of new invading bacteria produce entangled masses of filaments forming “corncob” like structure. .which are unable to adhere directly to the tooth surface.48  These bacteria allow the adherence of other organisms like filamentous bacteria.

the pellicle.49 Early stages of plaque succession    After professional removal of all organic material and bacteria from the tooth surface . covers the tooth surface. a cell free . Some of the proteins of pellicle are biologically active and have a significant impact on microorganisms attemptimg to colonize the tooth surface. . Within 2 hrs. a new coating of organic material begins to accumulate immediately. structureless organic film.

viscosus and peptostreptococcus are the main pioneering species capable of attaching to the pellicle within 1 hr after tooth cleaning. . S. sangius . A.50   The early stages of recolonization of the cleaned tooth surface involves adhesion between the pellicle and the pioneering bacteria.

The enzyme glucosyltransferase may be crucial in the adherence of organisms to the pellicle when sucrose is present as it enhances the polymerization of the extracellular matrix that helps in the formation of tenaciously adherent colonies.51   The adhesion process is selective and requires specific organism receptor capable of binding to certain areas on the precipitated salivary proteins of the pellicle. .

Late stages 52     Late stages are mainly responsible for causing caries. In early stages there are primarily aerobic communities lacking pathogenic potential. increasing the potential for enamel demineraliztaion. As the plaque matures. This increased production of acid leads to prolonged drop in pH . .more and more acid is produced from metabolism mainly lactic acid.

plaque builds rapidly to sufficient depth to produce anaerobic environment. If left undisturbed .Tooth habitat for pathogenic plaque 53     The tooth surface is stable and covered with the pellicle and thus the ideal site for the attachment of many oral streptococci. Some favorable tooth habitats for plaque are: Pit and fissures .

54    Smooth enamel surface immediately gingival to the contact area and in the gingival 1/3 of facial and lingual surface. Subgingival areas. . Root surface near the cervical line.

The appearance of microorganisms in pits and fissures is followed by caries 6-24 months later. The relative proportion of organisms most probably determine the cariogenic potential of the pits and fissures.Pits and fissures 55     Highest prevalence of all dental caries. Provide excellent shelter for organisms. .

.56  Sealing the pits and fissures just after tooth eruption may be the most important event in their resistance to caries.

So proximal caries are less likely to develop where the favorable soft tissue architecture exists.gingival papilla fills completely the interproximal spaces under the proximal contact. In very young patient.Smooth enamel surfaces 57    The proximal enamel surfaces gingival to the contact area are the 2nd most susceptible area to caries. .

These surface areas are habitats for the caries. . The gingival aspect of the facial and lingual smooth enamel surface is not rubbed by the bolus of food and not properly cleaned by the brush.producing mature plaque. apical migration of papilla creates more habitats for surface colonizing bacteria.58    Conversely.

the facial and lingual root surface when exposed to the oral environment harbors caries producing plaque. caries producing plaque and thus root caries lesion.Root surface 59    The proximal root surface . because of its concave anatomic surface. This favors the formation of mature. Also. often is unaffected by the action of oral hygiene procedures. .

60 .

Role of microorganisms 61     To initiate carious lesion in enamel . It was proposed that one or more organisms are implicated in the initiation of caries . the organisms must also be able to colonize the tooth surface.Strepococcus mutans. The second bacteria closely related to caries is Lactobacillus. The most important bacteria responsible for carious lesion are.

62        While others distinctly different organisms may influence the progression of disease. mitior S. mutans S.milleri . salivarius S.oralis S. Cariogenic bacteria: S .

casei A. viscosus A.63       S. neaslundii . sangius Peptostreptococcus intermedius Lactobacillus acidophillus L .

Smooth surface   S. salivarius (by chance) .Localization of bacteria related to caries 64 Type of caries 1. organisms  Pit and fissure    2. mutans (very significant) S. mutans (very significant) Lactobacillus (very significant) S . Sangius (uncertain) Actinomyces (by chance) S.

viscosus (very significant) A. Root surface     4. naeslundii (very significant) . (very significant) A. naeslundii (very significant) S.65 3. Deep dentinal caries  A. mutans (significant) Lactobacilli sp.

Role of acids 66    Carbohydrate degradation occurs through enzymatic breakdown and the acid formed are chiefly lactic acid although others such butyric acid are also formed. The mere presence of acid in the oral cavity is of far less significance than the localization of acids upon the tooth surface. Generally . monosaccharides and disaccarides result in the greatest fall in plaque pH. .

lactobacilli)  Heterofermenters  .67 Anaerobic catabolism of carbohydrates called fermentation predominates in plaque. Bacteria :  Homofermenters (streptococci. After breakdown one molecule of glucose breaks down into two molecules of lactic acid.

Butyric acid. . Ethanol etc are called hetero-fermentative.68    Organisms which produce 90 % or more lactic acid as the end product are called homofermentative. Organisms which produce a mixture of metabolites including other organic acids such as propionic . The proportion of lactic acid and other organic acid formed by plaque may be markedly affected by growth conditions and the type of bacteria present.

and a suitable substrate that must be present for a sufficent time. a cariogenic flora. . caries require a susceptible host.69 Caries is a multifactorial disease in which there is interplay of four primary factors :  Host  Microbial flora  Substrate  Time Thus.

Components   Tooth  Composition Morphologic characteristics Position Composition pH Quantity Viscosity Antibacterial factors B.70 Factors A. Saliva      .

Diet  Physical factors (quality of diet) Local factors (carbohydrate content. Systemic conditions .71  C.Fluoride content) D. Vitamin content.

because of its high content of mineral salts and their crystalline arrangement. Composition of enamel : enamel is the hardest calcified tissue in the body. . organic=4%.Tooth factors 72    Composition of teeth : the composition of teeth undoubtedly influence the initiation and the rate of progression of a carious lesion . Enamel: inorganic=96%.

5mm on the cusps of the molars.73    Enamel attains a maximum thickness of 2. Acc. Surface enamel is more highly mineralized . thinning down to almost a knife edge at the neck of the tooth. to Brudevold et al surface enamel is more resistant to caries than subsurface enamel. .

lead. Contains less water and has more organic material than subsurface enamel.74     Tends to accumulate greater quantities of fluoride. Also initial carious lesions indicate that marked decalcification is observed in subsurface enamel while the outer surface is relatively intact. The surface dissolves at a slower rate in acids. These factors apparently contribute to caries resistance and are partly responsible for slower degradation of surface enamel than the underlying enamel in initial carious lesion . iron etc than subsurface enamel. zinc .

resulting in rapid penetration and spread of caries to the pulp. .75    Composition of dentin: dentin forms the bulk and general form of the tooth. Dentin : inorganic=65% organic=35% The dentinal tubules form a passage for invading bacteria .

Cementum : inorganic=45-50% organic=50-55% Cementum has the highest fluoride content of all the mineralised tissues. covering the anatomic roots of human teeth. .76    Composition of cementum: cementum is the mineralized dental tissue.

Physical characteristics 77   Tooth size:it has been assumed that low caries may have smaller teeth and the larger teeth were found more caries susceptible and are found in the oral cavity for a shorter time period . the effect of tooth size would be negligible in comparison with the combined effects of other factors. .

3. Caries susceptibility in the permanent dentition may be ranked in the following order : Fissures of molars Mesial and distal surface of first molars. Mesial surface of 2nd molars and Distal surface of 2nd premolars. 2. The morphologic characteristics of tooth have been suggested as influencing the initiation of dental caries. .Morphologic characteristics 78   1.

1st premolar 6.79 4. incisors. . Mesial and distal surfaces of the maxillary first premolars. Proximal surface of max. 5. Distal surfaces of the canines and mesial surface of md.

occlusal fissures or buccal or lingual pits. Such fissures tend to trap food. so caries may develop rapidly in these areas.80   Fissures : the only morphologic feature which conceivably might predispose to the development of caries is the presence of deep. . bacteria and debris. narrow.

. the inclined planes become flattened .81  But as the attrition advances. and the predisposition towards the caries diminishes. providing less opportunity for entrapment of food in the fissures.

1st molar: occlusal > buccal > mesial > distal >lingual. 1st molar: occlusal >mesial>lingual> buccal>distal. whereas other surfaces rarely show decay. md. Max.82     Surfaces: certain surfaces of teeth are more prone to decay . Max. LI: lingual surfaces are more susceptible. .

but caries initiation is affected only to a very little extent. . The rate of caries progression may be influenced .83  All available evidences indicate that alteration of the tooth structure by disturbances in formation or in the calcification is of only secondary importance in dental caries.

So root caries tend to develop along the CEJ.Morphology of CEJ 84  An exposed CEJ is a potential area of plaque retention . .

the surface of intact cementum and the CEJ are very rough . And the rough surface is highly retentive to plaque . root surfaces like the CEJ are not exposed to the oral cavity. Morphologically. . healthy adult.Exposure of root surfaces 85    In the young . compared to the enamel surface. Prevalence of exposed root surfaces is agerelated or from gingival recession associated with periodontal disease.

The position seems to be a minor factor in the etiology of caries. out of position . rotated or otherwise not normally situated may be difficult to cleanse and tend to favor the accumulation of food and debris. .Position of tooth 86    Teeth which are malaligned. This in susceptible persons would be sufficient to cause caries in a tooth .

but around 1900 there were several case reports on the deleterious effects of absence of saliva. Who made the 1st observation of the influence of saliva on caries is hidden in the mists of time. exerts control over its oral flora.Saliva and dental caries 87  Introduction :saliva is the primary means by which the pt.  .

Saliva provides the ions needed to remineralize the teeth. Saliva has manifold functions in protecting the integrity of the oral cavity from food residue . Saliva has antibacterial. antifungal and antiviral capacities. . debris and bacteria : Saliva has some buffering effect against strong acids and bases.Functions of saliva 88  1. 3. 2.

3. 4. The principal properties of saliva that protects the teeth against caries are: Dilution and clearance of dietary sugars. . Neutralization and buffering of the acids in plaque. 2. Supply of ions for remineralization.89  1. Both endogenous and exogenous antiplaque and antimicrobial factors.

This is a physiological process referred to as salivary clearance or oral clearance.90   An important function of saliva is dilute and eliminate substances. which eliminate some of the sugar from the oral cavity which inturn helps in caries prevention . resulting in swallow. After an intake of sugar. the salivary glands will be stimulated by the taste or chewing to increase the flow rates.

. 1946.  This value was determined by SchmidtNeilsen.  Critical pH= 5.5  The main determinants of critical pH are the total calcium and phosphate conc.91 pH of saliva:  The pH at which saliva ceases to be saturated with calcium and phosphate is referred to as critical pH . in saliva.

demineralization occurs as phosphate ion of apatite crystals get converted to hydrogen phophates by increased hydrogen ion. solubility of tooth depends on the pH of surrounding medium.92    At this pH no demineralization or remineralization will take place. Thus. Below this pH. .

. whereafter it slowly returns to normal.93   In the pH range of 2-6 the solubility increases by a factor of 10 for each pH drop of one unit. Stephan curve: he stated that inspite of saliva buffer capacity the plaque pH will drop immediately after the sugar intake to values below critical pH.

94 .

6.2 Following exposure to sugars the pH drops very rapidly(in few minutes) to lowest level(5.pH of plaque is reasonably constant.9-7.2critical pH) and at this pH. Repeated fall of pH over a period of time leads o more and more mineral loss from the tooth surface.resulting in initiation of dental caries Later slowly it returns to original value over a period of 30-60 minutes.the tooth mineral dissolves.5 to 5.the tooth surface is at risk During this critical period.95     Under resting conditions.approximately .

which increases caries risk.96 Quantity of saliva:  In patients with reduced quantity of saliva(salivary gland aplasia or xerostomia) . . the cleaning properties of saliva in the mouth are impaired.  the unstimulated flow rates has been found to be diagnostically more important than the stimulated one.  Which leads to low oral sugar clearance.

.2 ml/min have an elevated demineralization rate and a high risk of developing caries. This low flow rates also favors acidic environment.97   Individuals with unstimulated flow rates <0. with an increase in cariogenic microflora.

In such cases the rate of progression of caries is also faster as compared to cases with normal flow rates.98   Thus. . but may also change the ecology of mouth. a low saliva flow rate not only will prolong clearance time and periods with low plaque pH.

sublingualand accessory glands.  The significance of this factor is not clear.  The viscosity of saliva is due largely to the mucin content derived from submaxillary.99 Viscosity :  Occasional workers have reported that a high caries incidence is associated with thick mucinous saliva. .

such as taste. intensity .Role of diet 100    The role of diet and nutrition factor deserves special consideration because of the often observed differences in caries incidence of various population who subsist on dissimiliar diets. Following consumption . a certain amount of saliva is stimulated by particular characteristic of food. depending on the quality of salivary gland function . A diet rich in fermentable carbohydrate is indisputably a very powerful risk factor for caries.

Disaccharides  Sucrose  Maltose  Lactose .Monosaccharides  Glucose  Fructose 2.Fermentable carbohydrates 101 1.

Polysaccharides  Glucan  Fructan  Mutan  Starch .102 3.

The dietary sugar all diffuse rapidly into the plaque and are fermented to lactic acid or can be stored as intracellular polysaccharides by the bacteria. . Sucrose is refined from sugar cane or beet and is the most common dietary sugar .103    Sucrose is regarded as the most important in dental caries.

Thus .104    This mechanism prolongs the fall in pH and promotes a suitable environment for acidogenic bacteria. sucrose favors colonization by oral microorganisms and increase the stickiness of plaque. allowing it to adhere in larger quantities to the teeth. . Sucrose is unique as it is the substrate for production of extracellular polysaccharide (fructans and glucan) and insoluble matrix polysaccharide (mutans).

sucrose is considered to be somewhat more cariogenic than other sugars. fructose. maltose give identical fall in pH but for lactose fall in pH is smaller.105     Because of this effect on the quality of plaque . All are rapidly fermented on plaque-covered tooth surfaces. Also other dietary disaccharides and monosaccharides are regarded as risk factors. Glucose. .

cyclamate. xylitol. mannitol Non-caloric : saccharin. Caloric: sorbitol. .106      In frequently consumed snack food such as sweets and drinks less fermentable and noncariogenic sweeteners are increasingly being used as substitute for potentially cariogenic sugars. These are : caloric or non-caloric sweeteners. aspartame They cannot be fermented by acidogenic bacteria.

.  Mechanical cleansing by detergent foods may have some role in caries control.  Physical properties of food may improve the cleansing action and reduce retention of food with in the oral cavity and increase saliva flow Physical nature of Diet:  Roughage food cleans the teeth from adherent debris during mastication. solubility and oral hygiene.  Soft refined food tends to adhere to the teeth and are not removed because of general lack of roughage.107 Physical properties of food and cariogenicity:  The Physical properties of food may be significant by affecting food retention. food clearance.

No effect on humans.  Vitamin K: It may act as a anticaries agent by virtue of its enzyme inhibiting activity in carbohydrate degradation cycle. .108 Carbohydrate content of diet  Most important factor in dental caries Vitamin content of Diet  Vitamin A: Definite effect on developing teeth in animals.  Vitamin D: Children suffering from Vit. D deficiency may exhibit slightly higher degree of caries experience. B6 acts as an anticaries agent by selectively altering the oral flora by promoting the growth of non cariogenic organisms which suppress the non cariogenic forms.  Vitamin B complex: Vit.

Fluorine content of diet: Dietary fluoride is relatively unimportant compared to fluoride in drinking water because of its metabolic unavailability. .109   Calcium and phosphorus dietary intake : Disturbance in calcium and phosphorus metabolism during the period of tooth formation may result in severe enamel hypoplasia and defects of the dentin.

. and no provision for between meal snacks.  The institutional diet provided was nutritious .  The dental caries rate experienced was relatively low. with little sugar.Dietary studies 110 Vipeholm study: (Gustafsson et al -1954):  This study was conducted in a mental institution for 5 yrs in Vipeholm hospital.

4.111  1. 7. 6. 3. 2.for 3 yrs) 24.toffee group(120 gm sugar-18 months) . 5. 7 groups: Control group Sucrose group(300gm sucrose) Bread group (345gm bread-50gm of sugar) Chocolate group(65gm – daily-for last 2yrs) Caramel group((22caramel-70gm sugar) 8-toffee group (60gm sugar.

If sugar is consumed in between meals. Increased caries riskIncrease in sugar content. 2. Clearance time of the sugar correlates closely with caries activity. 6. Upon withdrawl of the sugar rich foods.Conclusions 112  1. It varies widely in between individuals. . 3. if sugar consumed in a form that will be retained on tooth. 5. 4. the increased caries activity rapidly disappears.

113  This study showed that the physical form of carbohydrates is much more imporatnt in cariogenicity than the total amount of sugar ingested. .

1958):  The dental status of children between 3-14 yrs of age at Hopewood house was studied for 10yrs.  All lived on a strictly institutional diet.114 Hopewood house study (Sullivan. .  The absence of meat and a rigid restriction of refined carbohydrate were the two principal features.

. calculus uncommon but gingivitis in 75% of children. Conclusion: the children‟s oral hygiene was poor.6 53% of the children were caries free. DMFT /child after 10 yrs -1.115     The meals were supplemented by vitamin concentrates and an occasional serving of nuts and a sweetening agent such as honey.

116  This showed that dental caries can be reduced by diet control even in the presence of unfavourable oral hygiene. .

117 Turku sugar study (Scheinin. Xylitol group-52 people .  3 groups: 1. Sucrose group-35 people 2. Makinen -1975):  This study was done to test the effects of chronic consumption of sucrose. Fructose group-38 people 3. fructose and xylitol on dental caries.

Fructose was cariogenic as sucrose for the first 12 months but became less so at the end of 24 months.118    A dramatic reduction in the incidence of dental caries was found after 2 yrs of xylitol consumption. It was also found that frequent between meal chewing of a xylitol gum produced an anticariogenic effect. .

 Newburn 1969. malaise.  Persons affected with this rare metabolic disorder have learned to avoid any food that contains fructose or sucrose. tremor . vomiting. and even coma due to fructosemia. Because the ingestion of these foods causes symptoms of nausea. found that caries prevalence was extremely low in persons with HFI. . excessive sweating .119 Hereditary fructose intolerance (Froesch 1959):  It is caused by the remarkably reduced levels of hepatic. fructose -1-phosphate aldolase into two or three carbon fragments to be further metabolized.

acc to GV Black when the family remains in one locality . . the susceptibility to caries will be very similar in the great majority of cases. the children living under the conditions similar to those of parents in their childhood .Systemic factors 120   Heredity :it has been linked with the dental caries incidence in scientific literature for many years. In 1899.

which predisposes to caries immunity or susceptibility. it may be mediated through inheritance of tooth form structure. .121  But there is still no such evidence that heredity has a definite relation to dental caries incidence.the possibility exists that if there is such relation.

So caries incidence is actually a local problem. In nearly all cases it is revealed that the woman has neglected her oral care.122    Pregnancy and lactation: it is a common clinical observation that a woman during the later stages of pregnancy or shortly after birth of the child will manifest a significant increase in caries activity. .

Also psychiatric drugs impair salivary gland functioning. cough mixtures and antibiotics may affect caries risk Psychiatric patients: carbohydrates favor uptake of tryptophan to the brain and serotonin production is enhanced.123    Intake of medicine containing sucrose – fiber supplements for constipation. . Thus its intake may induce relaxation.

Socio-economic status: higher caries prevalence in children with low socioeconomic background. bakery workers.124    Occupation: in which frequent food sampling is required. may be associated with increased caries risk. their lesser involvement in oral hygiene and lesser involvement in topical and supplementary F regimes. This is due to lesser parental knowledge . .Eg.Confectionary industry.

HISTOPATHOLOGY OF DENTAL CARIES .

It forms a cone shaped lesion with the Apex towards the DEJ and the base towards the surface of tooth. which resembles a smooth. beneath the dental plaque. chalky white area. with increased prominence and roughening of the ends of the enamel rods.Caries of enamel 126   Smooth surface caries: The earliest manifestation of incipient enamel caries is the appearance of an area of decalcification. There is loss of continuity of the enamel surface and the surface feels rough to the point of an explorer. There is loss of interprismatic substance. .

so that early involvement frequently occurs.127 Pit and fissure caries:  Pit and fissures are often of such depth that food stagnation with bacterial decomposition in the base to be expected. Because of its shape it tends to produce more undermining of enamel. .  When caries occurs it follows the direction of enamel rods and forms a cone shaped lesion with its apex at the outer surface and its base towards the DEJ. The enamel in the bottom of the Pit or fissure may be very thin.

128 Enamel Caries :  Zone 1-translucent Zone  Zone 2.Surface Zone .Dark Zone  Zone 3.Body Of The Lesion  Zone 4.

Zone 4: Surface Zone: Appears relatively unaffected.129 Four zones are clearly distinguishable. It is formed as a result of demineralization. Zone 2: Dark Zone: It is referred to as the positive zone. because it is always present. . It is not always present. Zone 1: The translucent Zone: Advancing front of the enamel lesion. Zone 3: Body of the Lesion: It is the area of greatest demineralization.

that tends to seal them off against further penetration by microorganisms. The initial penetration of the dentin by caries may result in dentinal sclerosis resulting in calcification of dentinal tubules. .Caries of dentin 130  It begins with the natural spread of the process along the DEJ and the rapid involvement of great numbers of dentinal tubules. It most commonly occurs in older adults.

forming necrotic mass of dentin of a leathery consistency. As the carious lesion progresses.  .131  The destruction of dentin through a process of decalcification followed by proteolysis. various zones of carious dentin may be distinguished which tends to assume a triangular shape with the apex towards the pulp and the base towards the enamel.

132 Dentin caries:  Zone 1: Zone of fatty degeneration of Tomes fibres  Zone 2: Zone of Dentinal sclerosis  Zone 3: Zone of decalcification of dentin  Zone 4: Zone of bacterial invasion  Zone 5: Zone of decomposed dentin .

Zone 3: Zone of decalcification of dentin – a narrow zone.133 Following zones are seen: Zone 1: Zone of fatty degeneration of Tomes fibres. . Zone 5: Zone of decomposed dentin. preceding bacterial invasion. Zone 4: Zone of bacterial invasion of decalcified but intact dentin. Zone 2: Zone of Dentinal sclerosischaracterized by deposition of calcium salts in dentinal tubules.

Microorganisms invade the cementum either along sharpey’s fibers or between bundles of fibers. As carious process continues there is invasion of microorganisms in to dentinal tubules. Lesion spreads laterally between the various layers.134 Caries of cementum (Root caries)     Dental plaque and microbial invasion are an essential part of the cause and progression of this lesion. Microorganisms involved in root caries are filamentous rather than coccal. .

DIAGNOSIS OF DENTAL CARIES .

This is what caries diagnosis is about: detection of signs and symptoms of caries .136  Clinical inspection of the teeth at the chairside does not allow the dentist to observe the caries process itself. What dentists can do is to examine the consequences of microbial metabolic activity when looking for signs of lesions that have formed as a result of it.

in dental practice. . diagnosis is closely linked with the management options.2003) The logic is that the course of the diseases may be changed for the better if they are detected and treated before they reach a stage at which they elicit symptoms or require more invasive intervention. Therefore.137   Diagnosis is defined as the “art or act of identifying a disease from its signs and symptoms”(Merriam-Webster.

and those who are at high risk for developing carious lesions. . those that require nonsurgical treatment .138  The primary objective of caries diagnosis is to identify those lesions that require surgical (restorative) treatment .

Why do we diagnose caries? 139 Diagnosis is important in:  Detecting and excluding disease  Assesing prognosis  Contributing to the decision making process with regard to further diagnostic and therapeutic management  Informing the patient  Monitoring the clinical course of the disease .

140 Diagnostic tests need to be valid and reliable.  Validity means that test should measure what it is intended to measure e.g. dentist would recognize the same white spot lesion with matt surface as an active lesion.g. a white spot lesion with a matt surface indicates an active lesion which has not yet cavitated  Reliability or reproducibility means that the test can be repeated with the same result e. There should be intra.as well as interexaminer reproducibility .

but may be caused by different mechanisms.either during enamel formation or posteruptively.Differential diagnosis 141   When performing a caries diagnosis it should be appreciated that not all opaque lesions on the tooth surface represent dental caries. All opacities reflect a decreased mineral content in the enamel. .

appears as fine white horizontal striae reflecting the perichymatal pattern of enamel.banana or kidney shaped.142   Dental fluorosis has a symmetric distribution on homologous teeth & in mild cases. reflecting the retention of plaque along the curvature of the gingival margin . Such lesion is arch.they are suggestive of inactive non-cavitated carious lesions(smooth on probing). When such white lines merge in the gingival part of the tooth.

143 .

Prerequisites for detection and diagnosis 144    The diagnosis of caries require good lighting and dry.clean teeth When teeth have been cleaned.each quadrant of mouth is isolated with cotton wool rolls to prevent saliva wetting the teeth once they have been cleaned Thorough drying should be carried out by gentle blast of air from three-in-one syringe as white spot lesions are more obvious when the teeth are dry and saliva can obscure small cavities .

Methods of caries detection 145 Conventional techniques:  Visual observation  Tactile inspection  Radiography: • Intra-oral periapical radiographs • Bitewing radiographs .

146 Recent advances:  Dental digital radiography  Caries-detector dyes  Fiber-optic transillumination  Quantitative lightinduced fluorescence      Laser fluorescence Ultrasound Xeroradiography Electroconductivity measurements Microbiologic methods .

frank cavitation of tooth surface. discoloration & frank cavitations. .opacity beneath pit & fissure or marginal ridge.Visual observation 147 It encompasses the use of criteria such as detection of white spot.brownish discoloration of pit and fissures .  Careful examination of teeth under clean & dry condition using good illumination reveal:.  .

A consistent examination pattern ensures that no teeth or surfaces are missed .148  For practical purposes.then jump to the lower left molars and finish up with the lower right molars.begin with the upper right molars and move tooth by tooth and surface by surface to upper left molars.

With the use of slides pictures of posterior teeth tell us more about discoloration.149  Various aids Magnification loupes  Slides have been used to gather information about caries. decalcification & translucencies  Use of separators in detection of proximal caries .

Magnification loupe 150 .

5 Flip Up Loupes • 3.151 Loupes are comfortable to wear  Inexpensive  Freely available in various magnifications  E.g: • 2.5 Custom TTL Loupes • NEW Custom TTL Loupes on Safety Frame  .5x Galilean Flip-Up Optics • 2.0x and 3.

Tactile inspection 152 The teeth are examined by the aid of dental mouth mirror and a sharp probe  The mouth mirror is used to displace the cheeks and lips and to facilitate vision in difficult to reach areas on the teeth  .

153   Reflected light from the mouth mirror can be applied to search for dark shadows.which may be suggestive of dentinal lesions Transmitted light from the operating lamp is particularly helpful for examining the approximal surfaces of anterior teeth .

inter proximal explorer is used to detect proximal caries.curved explorer is used for examination of pit and fissures . .154  An explorer is useful in caries diagnosis as a tool to remove plaque and debris and check the surface characteristics of suspected carious lesions. . .

155  The surface texture of lesion is sensed through minute vibrations of the instrument by the supporting fingers when moving the tip of the probe at an angle of 20-40 degrees across the surface .

thereby running the risk of causing irreversible damage to the surface layer of an incipient lesion.which may potentially accelerate localized lesion progression .156  One should definitely abstain from poking vigorously into the tissue.

this this concern has not been confirmed as transferred microorganisms would not survive unless their new econiche favored their existence .e. mutans streptococci) to other teeth in the same mouth. However.157  Some researchers are concerned that probing of suspected carious lesions may serve to spread infective plaque(i.thereby facilitating carious lesion development.

158  • • • •  Tactile finding suggestive of caries are:„binding‟ or „catch‟ of explorer tip Frank cavitation at the base of pit or fissure Softness at base of pit or fissure Opacity surrounding the pit or fissure Feeling of „catch‟ may be due to non carious reasons also. this may depend on: • shape of fissure • sharpness of explorer • force of application • path of explorer placement .

Radiographs 159  Conventional . intra-oral periapical & bite wing radiographs are used to diagnose dental caries. .

. . wear.extent of caries as seen in the radiographs is usually lesser than actual defect.radiolucency may be due to caries. Disadvantages:.only a 2-D image of 3-D object. prone to observer bias.keeps a permanent record for maintaining progress or arrest of carious lesions.disclose site inaccessible to other diagnostic methods. fracture. .doesn‟t reveal the earliest stages of caries development. .160 Advantages:. or due to cervical burn out.non-invasive method .radiographic diagnosis is subjective . .. .

 Role in detecting proximal caries:• Early proximal enamel lesions are seen as small radiolucent notch below contact area. • caries involving the buccal and lingual grooves on molars mimic occlusal lesions due to superimposition.161 BITEWING RADIOGRAPH: Role For detecting occlusal caries:• Initial enamel caries are difficult to detect on bitewing radiographs due to 3 D shape of occlusal surface. • Advanced proximal caries are seen as dark .

162 .

Diagrammatic representations of caries on bitewing radiograph 163 .

.  Monitoring the progress or arrest of caries.  Noting the size of pulp chamber.  Checking cervical margins of restoration.  Examining many teeth in one radiograph.164 Uses:  Detecting incipient proximal caries.

g a fine probe with an exit diameter of 0. It is used as an adjunct to visual and radiographic method .Fiberoptic transillumination 165      Diagnostic method by which visible light is transmitted through the tooth from an intense light source.5 mm Principle of it is that there is a different index of light transmission for decayed & sound tooth Tooth which is decayed has a lower index of light transmission than the sound tooth structure It is effective specially when used in anterior region.e.3-0.

166     If the transmitted light reveals a shadow when the tooth is observed from the occulusal surface this may be associated with the presence of a carious lesion The narrow beam of light is of crucial importance when the technique is used in premolar and molar region For optimal performance the probe should be brought in from the buccal or lingual aspect at an angle of about 45 degrees to the approximal surfaces pointing apically.while looking for dark shadows in the enamel or dentin Shadows are best noticed when the office light is switched off .

167 .

168 Advantage:  Does not produce overlapping images as in case of posterior crowding  Can be easily used in pregnant women when radiation has to be avoided Disadvantage :  FOTI fails to detect incipient proximal caries .

169 .

 Advantages:.non invasive  .instantaneous image projections .170 Digital fiberoptic Trans illumination Image captured by the camera are sent to a computer for analysis . which produce digital images that can be viewed.image quality is easy to control .can detect incipient & recurrent caries very early .

171 .

stain and dental caries.172  - Disadvantages :doesn‟t measure the depth of lesion Difficult to distinguish between deep fissure . .

Therefore. tooth separation has been introduced Orthodontic elastic separators are applied for 2-3 days around the contact areas of surfaces to be diagnosed.after which assess to inspection and probing is improved .Tooth separation 173   Neither radiographs nor FOTI can help to identify the presence of a cavity on contacting approximal surfaces.

174 .

 It requires an extra visit Therefore.at present this technique is not recommended for routine use in general practice  .175 This technique may create some discomfort.especially in patients with established dentitions.

The amount of discharge is related to radiation striking photoreceptor. .Xeroradiography 176   Advance technique alternative method to conventional radiography In xero radiography image is recorded on photo conductive selenium coated plate rather than X ray film. This photoreceptor is placed intra orally & exposed to X ray beam causing selective discharge. Selenium coated plate is charged & placed in to light tight cassette.

177 During developing the selenium plate is exposed to cloud of charged powder particle called TONER . USES:  help to diagnose initial caries  . next the plate is dried to remove the liquid vehicle of toner particles. Processed image is transferred to opaque elastic base with the help of clear adhesive tape.

DISADVANTAGES:-Expensive -Development process should be completed within 15 minutes -Electric charge over the film may cause discomfort to the patient.178 ADVANTAGES:-“Edge enhancement” can demarcate area of varying dentition specially at margins. . -no wet processing. -Less radiation exposure. -Both -ve & +ve prints are possible.

retrieval & transmission to remote sites in digital format. . storage. manipulation. Has allowed image acquistation. Introduced in 1987  The application of computer technology to radiography.Digital radiographic method 179    This method offer a more superior means of detecting caries than conventional radiographs.

The signal from CCD is sent to computer where it is digitized in 256 gray levels & is viewed on screen with enhanced density & contrast.180    • • Digital imaging sensor is used (CCD) instead of radiographic film. It is of two types: Direct digital radiography In-Direct digital radiography .

181 Direct digital radiography:  Image is acquired by detector that is sensitive to electro magnetic energy & data is converted into digitized form  It is of two types: 1: photo stimulable phosphor {PSP} 2: charged couple device sensor {CCD} Other type: -complementary metal oxide semiconductor {CMOS} .

182 PSP:  The interactions between X-ray photons & crystals of PSP excite the electrons of phosphor. . Further on irradiation with ruby laser.trapped electrons are released causing emission of shorter wave length of light in blue region of spectrum. The intensity of emitted blue light is proportional to amount of X ray absorbed by phosphor which can be detected by photo multiplier tube. The output of tube is digitized to form image.

USES of digital radiography: 1: Early detection of caries. it helps to measure root canal length. After exposure. . an electric charge is created. When CCD interacts with X ray. 2: In endodontics. electric charge is sequentially transferred to computer which is acquired as an image later. 3: It also helps to assess bone loss. working length & distance between apex and obturating material.183 CCD:  Consists of a chip of pure silicon.

184 .

185   The software has been designed to assist in locating and classifying proximal surface caries in digital intraoral radiographs The analysis is completed in seconds and an enlarged image of the radiograph being evaluated is displayed. along with the possible decay area .

186  This helps to identify and calculate the probability of enamel and dentin caries based on a unique histological database. .  We simply select the area of interest and the software automatically outlines any consistent alignment of radiolucent features directing our attention to the area of interest for closer examination.

Contrast and density of image can be enhanced.Instant image visualization .Reduce radiation dose.No processing error . .No need for dark room .187 ADVANTAGES:.Image can be magnified .Expensive . DISADVANTAGES:.

vanguard electronic caries detector. . On the other hand . carious enamel has a measurable conductivity which increase with degree of demineralization. .188 Electric conductance measurement sound enamel is an insulator due to its high inorganic content .  Two devices were developed in 1980‟s .caries meter  • Both instrument measures the electrical conductance between the tip of a probe placed in a fissure and connector attached to an area of high conductance.

resistance of above 6. . Resistance below 2.00.000 indicates caries.189    Low conductance of tooth is primarily caused by enamel Increased conductance & decreased resistance are indicative of the presence of hypo &/or demineralization When a potential of less 1volt applied.50.000 ohms indicates caries free tooth.

190 Factors affecing electronic resistance measurement:  Porosity  Surface area  Thickness of tissues  Hydration of enamel  Temperature .

191 .

192 .

enamel cracks can cause misleading reading. radiographs or FOTI . -time consuming procedure -Requires the use of sharp metal explorer which can cause traumatic defect in pits and fissures. Disadvantages -Hypomineralized area . .193 Advantages -More accurate in diagnosis of early occlusal caries than visual method . -Can monitor the progress of caries.

is earliest change in carious lesion  For detection of enamel caries • Calcien • Zyglozl-22  For detection of dentin caries • Fuschin • Acid red system • 9-aminoacridine .Caries detecting dyes 194 Principle Increased porosity.through the development of capillary like micro voids.

195 Limitations:  Does not stain bacteria but organic collagen matrix of less mineralized dentine  No differentiation between infected and affected dentine possible  High risk of over treatment  Also stains healthy dentine with naturally high collagen content: circumpulpal dentine .

196 .

when Benedict observed that normal teeth fluoresce under UV illumination. Aids in the detection of occlusal caries The machine emits light at a wavelength of 655nm and this is transported through a fibre bundle to the tip of a handpiece.Laser Fluorescence 197    Use of fluorescence for detection dates back 1929. The tip is placed against the tooth surface & rotated .

198 .

199     The laser light will penetrate the tooth.giving high reading when active caries is not present . Different fibers in the tip receive the reflected light and fluorescence from the lesion.thought to be produced from bacterial porphyrins The received light is measured & its intensity is an indication of size and depth of carious lesion The machine does not detect the mineral loss Reproducibility has shown to be good but can be confused by staining and calculus.

. It has been recently found that when illuminated with argon laser. In carious teeth emission spectra shifts to more than 540nm i. fiery. red range of EM spectrum.410 & 530nm on carious & non carious teeth.e.200    Monochromatic light is used at 350. and orange-red in color.carious tissue appears as dark.

201 .

202

Diagnodent:  Based on principle of fluorescence.  It uses a diode laser light source & a fiber optic cable that transmits light to a hand held probe.  Emitted fluorescence is collected at probe tip, processed & presented on display as an integer between -9 to99.  -9 indicates healthy teeth & increased fluorescence indicates caries particularly value above 20.

203

204

The Diagnodent operates at a wavelength of 655 nm. At this specific wavelength, clean healthy tooth structure exhibits little or no fluorescence, resulting in very low scale readings on the display. However, carious tooth structure will exhibit fluorescence, proportionate to the degree of caries, resulting in elevated scale readings on the display of the Diagnodent. An audio signal allows the operator to hear changes in the scale values. This enables the focus to be on the patient, not solely on the device.

205

Limitations:  Cannot determine the depth of lesion.  Reading may alter due presence of food debris, plaque.  Not able to detect recurrent caries. Alloy restoration exhibits little or no fluorescence, while the composites, ceramics & cements emit their own fluorescence.  Reading changes at different angulations of probe tip.  Caries indicator dyes cannot be used simultaneously with diagnodent.

Quantitative light fluorescence 206    This methodology began with observation in1978 by a scientist in Sweden that the use of a laser light of selected wavelength markedly enhances the visibility of early non carious lesions QLF uses light with wavelengths around 405 nm to excite yellow fluorescence at wavelengths above 520 nm. . Its diagnostic capacity is based on the mechanism that the intensity of natural fluorescence of a tooth is decreased by scattering due to a caries lesion.

207 Two-photon image of a carious tooth Carious area shown in green .

208

The initial work was based around the use of multiphoton microscopy to build up a three dimensional image of the tooth. This revolutionary technique enables the dentist to see right into the tooth but is complex to use and not suitable for general dental practitioners.

Ultrasonography
209

Involves use of sound waves for detection With the use of this instrument, sonic velocity & specific accoustic impedance can be determined for dentin & enamel as well as for soft tissue & bone. In ultrasound frequency vibration is greater than 20 Khz. which is more than audible range{1500-20,000hz/sec}. In sonography, sound waves are used in frequency of 1-20Mhz.

210

Scanners used for sonography generate electric impulse that are connected into ultra – high frequency sound waves by transducer{ device which convert electric energy into sound energy} Transducer is a thin piezo electric crystals made up of great number of dipoles arranged in geometric pattern. Electric impulse generated by scanner causes dipole in crystals to re-align themselves with electric field & thus sudden change causes a series of vibrations that produce the sound waves that are transmitted into the tissues being

211

When ultra sonography beam passes through or interacts with tissues of different sound, energy causes obstruction, reflection , refraction diffusion. Sonic waves that reflected back towards transducer cause change in the thickness of piezoelectric crystal, which produces an electric signal which is amplified and displayed on monitor.

Microbiologic method 212  Fluorogenic enzyme assay: it is a new method to count cells “in situ”. Increasing cell number has close correlation with alkaline phosphatase activity and this relationship did not change with time in culture. based on a fluorogenic enzyme assay that measures the activity of alkaline phosphatase. The method is rapid and efficient. making it a useful method for studying streptococcus and lactobacillus activity in active root lesions. This method is able to estimate relative cell numbers over a range from about 104 to 105×105 for many cell types. .

.213   Lactobacillus colony count test : This test estimates the number acidogenic Lactobacillus bacteria in the patient’s saliva by counting the number of colonies appearing on the tomato peptone agar plates (pH 5. selective streptococcal medium.mutans colony forming units per volume of saliva from the root lesion.0). It is cultured on the Mitis Salivarius Agar (MSA). Streptococcus mutans count test: This test measures the number of S.

They must be convenient to use.214    All the above mentioned methods may be used as an adjunct to visual inspection.not too expensive and must be reproducible Only laser fluorescence(diagnodent) and digital radiography are currently used in practice and seem to be suitable techniques for detection of caries . However to be used in practice the methods must be better than clinical-visual and radiographic examination.

3rd Ed. Nikiforuk Gordon. Kidd Edwina. Roberson TM.Textbook of oral pathology.Dental caries:the disease and its clinical management.4th Ed. Preventive and Community Dentistry.Sturdevant‟s Art & Science of Operative Dentistry. Understanding dental caries part1 Newbrun.Cariology Hiremath SS. Kidd Edwina.References 215         Fejerskov Ole.2nd Ed.5th Ed. Levy. Hine. Textbook of preventive and community dentistry . Soben Peter. Essentials of dental caries Shafer.

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