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DENTAL CARIES Prepared by Dr Sundeep Bhagwath





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Dental caries is defined as an “irreversible disease of calcified tissues of teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth, which often leads to cavitation”. - Shafer, Hine and Levy



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CARIES IN PREHISTORIC MAN: - Caries is considered a disease mainly of modern civilization, as prehistoric humans rarely suffered from it. In those instances where it was noted, it was usually found to occur in older persons teeth with attrition and food impaction. Caries in such persons was seen to occur below the contact areas and also on the CEJ.

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CARIES IN MODERN MAN: - Occurs universally. No human being is immune. Commonest infection to occur in oral cavity. Directly linked to dietary habits of modern man – processed, soft food. Primitive man’s diet was coarse, raw and mostly uncooked.

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FACTORS AFFECTING CARIES PREVALENCE: - RACE: People living in same geographical area but belonging to different race have differing caries incidence. Generally, Chinese, Blacks, Indians have lesser caries incidence than the Caucasian whites.

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2. AGE: Dental caries more prevalent in children up to 12 years. Incidence decreases somewhat in younger and middle age group. Incidence increases again by the older age.

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3. GENDER: Incidence of caries is significantly higher in females than males. This may be due to the fact that teeth in females erupt earlier compared to males.

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4. FAMILIAL: There appears to be heredity involved. Children of parents with low caries experience also show lesser caries incidence and vice versa.



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No universally accepted opinion of etiology. Many theories have been proposed but only 3 have stood the test of time 1. Miller’s Chemico – parasitic theory 2. Proteolytic theory 3. Proteolysis - chelation theory


I. CHEMICO PARASITIC THEORY W.D.Miller stated in 1887 that “Dental decay is a chemico - parasitic process consisting of two stages, the decalcification of enamel, which results in its total destruction and the decalcification of dentin as a preliminary stage followed by dissolution of the softened residue”.

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The acid which caused the decay was derived from fermentation of starches and sugars lodged in the retaining centers on teeth. In his experiment he incubated a mixture of bread, meat and sugar with saliva at body temperature It produced enough lactic acid within 48 hours to decalcify sound dentin

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In his hypothesis, Miller assigned essential roles to 3 factors – 1. Carbohydrate substrate 2. Acid which caused dissolution of tooth minerals 3. Oral micro organisms which produce acid and also cause proteolysis.

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OBJECTIONS TO THE HYPOTHESIS: - Unable to explain predilection of specific sites on tooth to caries. Initiation of smooth surface caries not explained. Unable to explain why some populations are caries free and some are caries prone. However, this theory is accepted by majority in unchanged form. Also, bulk of evidence DOES implicate carbohydrates, acids and Microorganisms.

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ROLE OF CARBOHYDRATES: - Numerous studies confirm the fact that presence of readily fermentable carbohydrates are responsible for increased caries incidence. Cariogenic carbohydrates are dietary in origin since human saliva contains negligible amounts of carbohydrates. Also, whatever is present, is bound to salivary proteins and thus not available for microbial degradation.

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Cariogenicity of carbohydrates depend upon – frequency of its ingestion, physical form, chemical composition, route of administration and presence of other food components. Thus, carbs in detergent foods are less cariogenic than those in sticky, retentive foods. Polysaccharides are less easily fermented than monosaccharides by the plaque organisms. Meals high in fats, proteins or salt reduce the retentiveness of carbs.

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2. ROLE OF MICROORGANISMS: - Two gram positive coccal forms of bacteria have been implicated in dental caries from over a century – L.acidophilus and S.mutans. However, it is now recognized that one or more different types of bacteria are involved in “initiation” of caries and a completely different species of bacteria may be involved in “progression” of caries. Also, a different diet – bacterial interaction is involved in producing root and coronal caries.

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The various cariogenic species of bacteria include – S.mutans, S.salivarius, S.sanguis, S.mitior, S.millieri, L.acidophilus, Peptostreptococcus intermedius, A.naeslundi, A.viscosus etc. Different bacteria show selectivity for the tooth surfaces they localize and attack, e.g. S.mutans, Lactobacilli species attack the pit and fissures, while A.naeslundi and A.viscosus prefer root surfaces. The Lactobacilli species and A.naeslundi also show preference to deep dentinal lesions.

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3. ROLE OF ACIDS: - It is understood that acids are produced by enzymatic breakdown of sugars by cariogenic bacteria. Acids produced are – Lactic acid mainly and butyric acid to some extent. However only production of acid is of no consequence. It must be localized and retained on the tooth surface for it to cause the caries. Its accepted that dental plaque does this.

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4. ROLE OF DENTAL PLAQUE: - Plaque defined as a soft, unmineralized, bacterial deposit or biofilm which forms on teeth and dental prostheses that are not adequately cleaned. Resists cleansing by physiological oral forces like salivary washing and tongue movements but is removable by tooth brushing.

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Considered as a contributing factor for at least initiation of caries. However mere presence of dental plaque doesn’t necessarily mean caries will occur.

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COMPOSITION OF DENTAL PLAQUE => Water – 80% Solids – 20% Dry weight of plaque composed of Bacterial & Salivary proteins – 50% Carbohydrates & Lipids - 25% Inorganic ions, mainly Ca++ & Po4--- - 10% CLASSIFICATION OF DENTAL PLAQUE => Plaque classified as – SUPRAGINGIVAL & SUBGINGIVAL. Supragingival plaque – essential role in causing caries, while subgingival plaque – role in periodontal diseases.

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MECHANISM OF FORMATION => Plaque formation proceeds through following stages Deposition of a cell free layer, ACQUIRED PELLICLE which is derived from salivary glycoproteins. This layer acts as nutrient for plaque bacteria. Prepared by Dr Sundeep S Bhagwath

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2. Colonization of pellicle by Gram positive bacteria like S.sanguis and S.mutans within 24 hours. 3. Maturation of plaque by further colonization with filamentous and other bacteria. Also there is build up of plaque substance by polysaccharides produced by plaque bacteria.


II. PROTEOLYTIC THEORY In contrast to acidogenic theory, this theory postulated by Gottleib, Diamond and Applebaum states that caries is essentially a proteolytic process. According to them, the organic or protein elements like enamel lamellae, rod sheath etc are the initial pathway of invasion by microorganisms.

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OBJECTIONS TO THE THEORY: - Out of 0.56% of organic matrix, 0.18% is Keratin. However, no enzyme systems capable of attacking keratins have been isolated so far. Studies in germ free rats have shown that caries can occur in the absence of proteolytic organisms. However, even though proteolysis may not play any role in initiation of caries, their role in progression of more advanced carious lesions cannot be ruled out.


III. PROTEOLYSIS – CHELATION THEORY Schatz et al in 1955 proposed that caries occurred as a result of simultaneous degradation of organic substances (Proteolysis) and dissolution of tooth minerals by a process called Chelation.

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Chelation is a process of complexing of a metallic ion to a complex substance through a co-ordinate covalent bond resulting in a highly stable, poorly dissociated ionized compound. Examples are – Chlorophyll molecule in green plants where 4 pyrrole nuclei are linked to magnesium and Hemoglobin where 4 pyrrole nuclei are linked to iron.

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According to this theory, the initial attack on the tooth is on the organic components of enamel. Breakdown products of the proteolysis have chelating properties which form chelates with mineralized components of enamel and thereby decalcify the enamel even in neutral or even alkaline pH.


OBJECTIONS TO THIS THEORY: - Direct evidence for proteolysis – chelation as a mechanism for causing caries is lacking. Recent studies have shown that saliva as well as plaque do not contain substances in sufficient concentrations to chelate calcium from enamel. However, although chelation may not be actually responsible for initiating caries, it may still have some role to play in advanced carious lesion where the pH levels return to neutral.


MULTIFACTORIAL CONCEPT OF CARIES ETIOLOGY Dental caries – a multifactorial disease – interplay of 3 primary factors plus time also. Mere presence of bacteria and a suitable substrate on a tooth surface at a given time is not enough to cause caries. So, variations in caries incidence occur because of number of indirect or CONTRIBUTING FACTORS.


CONTRIBUTING FACTORS A. TOOTH 1. Composition 2. Morphologic characteristics 3. Position B. SALIVA 1. Composition 2. pH 3. Quantity 4. Viscosity 5. Antibacterial factors C. DIET 1. Physical factors 2. Local factors D. SYSTEMIC CONDITIONS


CONTRIBUTING FACTORS - TOOTH 1. COMPOSITION OF TOOTH: - Structure & composition of a tooth determines initiation and rate of progression of caries. Surface enamel more mineralized than subsurface enamel and is more resistant to caries. It also accumulates more fluoride, zinc, lead ions than subsurface enamel. Therefore in initial carious lesions, the subsurface enamel shows marked demineralization even though the outer enamel is relatively intact.

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2. MORPHOLOGIC CHARACTERISTICS: - Deep, narrow occlusal fissures or buccal and lingual pits predispose to caries as they tend to trap food and bacteria. Also enamel is quite thin at the base of such deep pits and fissures. Certain surfaces of teeth are more prone to decay like e.g. in mandibular 1st molars the likelihood of caries in descending order is occlusal, buccal, mesial, lingual and distal. The most susceptible teeth are mandibular 1st molars followed by maxillary 1st , mandibular and maxillary 2nd molars.

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3. POSITION: - Malaligned, rotated or otherwise abnormally situated teeth can be difficult to cleanse and are likely to trap food debris and bacteria. This, in susceptible persons is sufficient to cause dental caries.


CONTRIBUTING FACTORS - SALIVA 1. COMPOSITION: - Many inorganic and organic components of saliva have been investigated for anti cariogenic effects. However, results have been conflicting. In normal circumstances, saliva is supersaturated with calcium and phosphate ions w.r.t enamel hydroxyapatite. This not only prevents enamel from dissolving but even tends to precipitate apatite in the surface enamel of carious lesions.

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2. pH OF SALIVA: - The “critical” pH at which the inorganic material of tooth begins to dissolve is about 5.5, since above this pH, saliva is supersaturated with Ca and Po4 ions. Although much has been discussed about buffering capacity of saliva, its relation with caries incidence is not so simple! Acid production during caries occurs at a localized site on tooth, which in initial stages at least, is covered by dental plaque. This plaque prevents a free exchange of ions.

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3. QUANTITY OF SALIVA: - Caries incidence is significantly higher in people with less or no saliva flow, as is seen in cases of salivary gland aplasia and xerostomia. Continuous flow of saliva is required for mechanical removal of bacteria and food debris from the tooth surfaces.

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4. VISCOSITY OF SALIVA: - Sound scientific evidence is lacking to support the view that viscous saliva is associated with high caries incidence as some studies have reported. The reverse has also been shown to be true in some other studies.

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5. ANTIBACTERIAL PROPERTIES: - Saliva contains many antibacterial factors like lysozyme, lactoferrin, sialoperoxidase, bistatin, thiocyanate ion, IgA etc. However their efficacy has been doubtful as saliva always appears to contain bacteria capable of causing caries if carbohydrates are present.


CONTRIBUTING FACTORS - DIET 1.PHYSICAL FORM: - Very important factor responsible for difference between caries incidence of primitive and modern man. Already explained that diet of primitive man contained plenty of roughage which mechanically cleansed the teeth of any adhering to the teeth.

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Also, the coarse nature of the diet induced early attrition of occlusal and proximal surfaces leading to reduction in food entrapment. Diet of modern man in contrast is soft and lacking in roughage. As a result, food sticks tenaciously to teeth and is not cleansed mechanically.

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2. CARBOHYDRATE CONTENT OF DIET: - Accepted all over as one of the most important factors in caries process. Observed that different ethnic populations have differing caries incidences – postulated that it could be due to difference in diet, especially carbohydrate content.

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Diet of caries free ethnic races contain low amounts of carbohydrates, that too found in fruits and vegetables, while diet of caries prone westerners contains more carbohydrates due to intake of processed food. Exceptions – certain populations in India have a high carbohydrate content yet are relatively caries free.

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3. LIPID CONTENT OF DIET: - Understood that medium chain fatty acids and their salts have antibacterial effects at low pH. Mechanism of action not understood. Its potential as anticariogenic food needs more investigation.

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4. VITAMIN CONTENT OF DIET: - Of all vitamins, only Vit D and Vit K appear to have some role in the caries process. Vit D may have an indirect effect on caries process. Its deficiency can cause enamel hypoplasia which can make the tooth more susceptible to caries. Vit K has enzyme inhibiting action in carbohydrate degradation cycle. Can be utilized as an anticariogenic agent.

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5. CALCIUM & PHOSHORUS CONTENT:- Available evidence indicates that there is no relation between dietary calcium and phosphorus and dental caries. 6. FLUORINE CONTENT: - While topical and water fluoridation has been known to be effective in caries control, dietary fluorine may have no role as it is unavailable metabolically.


CONTRIBUTING FACTORS – SYSTEMIC FACTORS 1. HEREDITY: - Racial tendency for high or low caries may be explained by heredity. However, local factors like change in dietary habits can change this tendency. Possible that caries tendency may be inherited through tooth form & structure. Prepared by Dr Sundeep S Bhagwath

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2. PREGNANCY & LACTATION: - Commonly observed that during pregnancy, women tend to neglect their oral health owing to all her attention being diverted to that of care for the newborn. Thus increased caries incidence during pregnancy & lactation is more a problem of neglect !



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I. BASED ON MORHOPLOGICAL SITE: - 1. Pit and fissure caries 2. Smooth surface caries II. BASED ON RATE OF PROGRESSION:- 1. Acute dental caries 2. Chronic dental caries III. BASED ON WHETHER LESION IS NEW OR UNDER PREVIOUS RESTORATION: - 1. Primary (virgin) caries 2. Secondary (recurrent) caries


PIT & FISSURE CARIES Usually develops on occlusal surface of molars and premolars, buccal and lingual surfaces of molars and on lingual surface of maxillary incisors. Prepared by Dr Sundeep S Bhagwath

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Deep pits and fissures are naturally more prone to caries due to their poor self cleansing properties and tendency to entrap food debris and bacteria.

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Also, enamel at the base of such pits and fissures is thin or even absent, thereby exposing dentin. Early lesions in such locations appear brown / black and “catch” a fine explorer point. Upon reaching the DEJ, there is lateral spread of caries and penetration of dentinal tubules.

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All this occurs without apparent fracturing away of overlying enamel. Thus there may be a large carious lesion inside with only a pinpoint opening seen on the tooth surface.

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Not all pit and fissure caries progress in this way. In many cases, carious lesion begins as an open cavity and becomes larger progressively. In such cases, the progress of caries is much slower and pulpal involvement is also much delayed.


SMOOTH SURFACE CARIES Develops on proximal surfaces of all teeth or on gingival 1/3rd of buccal and lingual surfaces. Here, the caries is preceded by formation of dental plaque, quite unlike the pit and fissure caries. Presence of plaque ensures retention of carbohydrate and bacteria on tooth surfaces, leading to subsequent acid production and demineralization of enamel.

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Smooth surface caries usually begins just below the contact point and appears in initial stages as a faint white opacity of enamel without loss of continuity of enamel surface. The early chalky white spot becomes roughened owing to superficial decalcification of enamel.

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As caries reaches the DEJ, there is rapid lateral spread. Quite often, caries extends buccally and lingually but not till the actual buccal and lingual surfaces, as these areas are more accessible to the toothbrush.


CERVICAL CARIES Cervical caries occurs on buccal, lingual or labial surfaces. Extends occlusally from gingival crest region to the convexity of smooth surface that marks the self cleansing portion of tooth. Laterally, it extends towards the proximal surfaces. Thus this lesion is a crescent shaped cavity beginning in its initial stages as a chalky white lesion.


CERVICAL CARIES It almost always occurs as an open cavity unlike the smooth surface or pit and fissure caries. Occurs on all the teeth without predilection as it is directly related to lack of oral hygiene. No excuse for it to occur on anybody’s teeth since it can always be prevented by maintaining good oral hygiene.


ROOT CARIES Defined as “Soft progressive lesion that is found anywhere on the root surface that has lost connective tissue attachment and is exposed to oral environment”. Predominantly seen in teeth of older individuals showing gingival recession and exposed root surfaces. Lesion begins on cementum / dentin, occurring most frequently on buccal and lingual root surfaces.


ROOT CARIES For root caries to begin, formation of dental plaque and bacterial invasion are essential. However, the microflora may be different for root caries compared to coronal caries. Most commonly the invading bacteria are filamentous rather than cocci. Bacteria appear to invade either along Sharpey’s fibers or between the fiber bundles just like invasion of dentinal tubules. Once, dentin is involved, progression is similar to coronal caries but for a slower rate of progression. Why?


ACUTE DENTAL CARIES It is that form of caries that follows a rapid clinical course and results in early pulpal involvement by carious process. Predominantly affects children and young adults probably because their dentinal tubules are larger and show no sclerosis. The point of entry of caries is small even though there is rapid spread of caries at DEJ, producing large internal cavitation.

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The small point of opening doesn’t allow the buffering ions of saliva to neutralize acids formed within the cavity. The affected dentin is usually stained light yellow compared to deep brown / black of chronic caries. Pain is more likely to be seen in acute dental caries than chronic caries, but this is not a hard and fast rule.


RAMPANT DENTAL CARIES Characterized by sudden, rapid destruction of teeth affecting even relatively caries free surfaces like proximal and cervical surfaces of mandibular teeth. 10 or more carious lesions over a one year period is characteristic of rampant caries.

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Prominently observed in deciduous dentition of young children and permanent dentition of teenagers. Dietary factors like high carbohydrate intake etc as well as physiological factors affecting saliva are major contributors to etiology of rampant caries.


NURSING BOTTLE CARIES Also called baby bottle syndrome and bottle mouth syndrome. It is a type of rampant caries and occurs due to – Nursing bottle containing milk, milk formula or sweetened water. Breast feeding Sugar or honey sweetened pacifiers

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Usually, the above aids are used at sleeping time after one year of age. Clinically seen as widespread caries of the 4 maxillary incisors followed by 1st molars and then canines. Absence of caries in mandibular teeth distinguishes it from ordinary rampant caries. If milk or other carbohydrates are rapidly cleared from mouth, they aren’t cariogenic, but if they pool in the mouth, then they can cause rampant caries. Mandibular teeth usually escape the process as the pooled milk or sweet products are washed away by saliva


CHRONIC DENTAL CARIES That type of caries which progresses slowly and involves the pulp much later than acute caries. Most commonly seen in adults. Opening to the lesion is invariably large r than that of acute caries. As a result, there is lesser food impaction and greater access to saliva. Also, the slow progress of caries allows enough time for dentinal sclerosis and deposition of tertiary dentin in response to irritation.

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The carious dentin is stained deep brown As compared to acute caries there is considerable SURFACE destruction with a shallower cavity and little undermining of enamel, while there is only moderate spread of caries along the DEJ. Pain is NOT a prominent feature here due to the protection provided to the pulp by tertiary dentin formation.


RECURRENT CARIES Occurs around or beneath an existing restoration. Usually due to inadequate extension of restoration resulting in food impaction

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Can also occur if a restorative material is not properly adapted to margins of cavity leading to leaky cavity margins. This “renewed” carious process follows a similar pattern as that of primary caries.


ARRESTED CARIES It is that caries which becomes static or stationary and does not progress any further. Can occur in both deciduous and permanent dentition. Occurs almost exclusively on occlusal surface caries.

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Characterized by large, open cavity in which there is no food retention and the softened decalcified dentin is gradually burnished until it assumes a brown polished appearance. Called “Eburnation of dentin”. Sometimes arrest can also occur in initial proximal caries, when the adjacent tooth is extracted for some reason. This is due to the automatic creation of a self cleansing area


RADIATION CARIES Rampant caries occurring in patients receiving radiotherapy in head & neck region is called as RADIATION CARIES. Xerostomia is a major complication of radiotherapy of head & neck region. This, coupled with increase in viscosity and low pH of saliva results in decreased anticariogenic actions of saliva.




HISTOPATHOLOGY OF CARIES - ENAMEL Caries process in enamel progresses through following stages A. Early submicroscopic lesion B. Phase of nonbacterial enamel crystal destruction C. Cavity formation D. 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.

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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 first 1. Translucent zone 2. Dark zone 3. Body of lesion 4. Surface zone

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1.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.

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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.

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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.

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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.


EARLY LESION – PIT & FISSURE Caries process not much different from smooth surface. Caries most often starts on both side of fissure and visual changes like yellow or brown discoloration are seen. Also, enamel being usually thin at the base of pits and fissures, dentin involvement occurs much earlier.

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In contrast to smooth surface caries’ lesion, the caries here follows direction of enamel rods, forming a cone shaped lesion with its base towards DEJ and apex directed occlusally. As a result therefore, greater number of dentinal tubules are affected when lesion reaches DEJ.


CAVITY FORMATION & BACTERIAL INVASION The enamel crystallites are progressively dissolved until the disintegration becomes visible macroscopically. Now the pathways are large enough for the bacteria to physically enter the enamel, destroy organic matrix by proteolysis and then proceed to DEJ and dentinal tubules.


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.

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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.

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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.

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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 (ADNANCED 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.

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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.

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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.


ZONES OF DENTINAL CARIES 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 sclerosis ZONE 3 – Zone of decalcification ZONE 4 – Zone of bacterial invasion ZONE 5 – Zone of decomposed dentin

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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 sclerosis ZONE 3 – Zone of decalcification ZONE 4 – Zone of bacterial invasion ZONE 5 – Zone of decomposed dentin 1 2 3 4 5


BIBLIOGRAPHY Dental Caries: The disease and its clinical management. 1st ed. Blackwell Munksgaard, Iowa. Soames JV, Southam JC. Oral pathology/. 3rd ed. Oxford 2002. Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 6th ed. Elsevier, NOIDA, India 2009. Acknowledgements: All pictures used in the presentations are courtesy of above mentioned authors.

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