DENTAL CARIES

Dental Caries : Dental caries is an irreversible

microbial disease of the calcified tissues of the teeth , characterized by demineralization of the inorganic portion and destruction of the organic substances of the tooth , which often leads to cavitation

EPIDEMIOLOGY OF DENTAL CARIES

The most common epidemiological measures of dental caries is the DMF index (decayed missing or filled teeth); this measure of the number of teeth are diseased , missing or filled at the time of examination. DMF may be reported as the number of teeth (DMFT) OR SURFACE AFFECTED (DMFS).

Important measures to prevent Caries

Extensive water fluoridation Use of antibiotics Increased oral hygiene awareness Increased parental care Improvement in the preventive dentistry More availability of skillful dental professionals

PATHOPHYSIOLOGY OF DENTAL CARIES

Major theories of dental caries

1- Acidogenic theory 2- Proteolytic theory 3- Proteoltic chelation theory 4- Sucrose chelation theory 5-Autoimmune theory

ACIDOGENIC THEORY
THIS THEORY IS ALSO KNOWN AS MILLER'S CHEMOPARASITIC THEORY. Its proposes that acid formed due to fermentation of delay carbohydrate by oral bacteria leading to progressive decalcification of the tooth Acidogenic Theory states two stages : a) Initial stage : production of organic acid occurs as a result of fermentation of carbohydrate by the plaque bacteria. b) Later stage : The acid cause decalcification of enamel followed by dentin and cause total destruction and dissolution of soften part of the tooth . Final result is cavity formation. A/c to miller there are four important factors which can influence the process of tooth destruction in dental caries : Dietary Carbohydrate Microorganism Acids Dental Plaque

DIETARY CARBOHYDRATE

Fermentated dietary carbohydrate play an important role in the causation of caries eg. Glucose , fructose & sucrose. Among them sucrose is more potent These sugars are easily& rapidly fermented by cariogenic bacteria in oral cavity to produce acid at or near the tooth surface & cause dissolution of hydroxyappetite crystals of enamel followed by dentin. Risk of caries incidence increases greatly of the dietary sugar is sticky in nature which remain adheres to the tooth surface for long time after taking the meal. Following the ingestion of these sugar the pH of the plaque falls to 4.5 to 5 within 1 to 3 min and neutralization occurs after 10 to 30 min. Due to low molecular weight the plaque diffused sucrose , glucose & fructose..

MICRO-ORGANISM

A large number of micro-organism play individual role in dental care production and among them the most important one is streptococcus mutants. a) Its readly ferments the dietary carbohydrate to produce acid which caries tooth destruction b) It synthesizes dextron from sucrose which helps inadhering the plaque bacteria as well as the acid on the tooth surface. c) S.mutants hasthe ability to adhere and to grow on hard and smooth surface of the tooth. The actinomycosis grp are important organism to cause root caries The Lactobacillus acidophillus is important organism for the progress of dental caries.

ROLE OF ACIDS

During the process of caries formation a large variety of acids are produced in the oral cavity due to the bacterial fermentation of dietary carbohydrate. These acids are lactic acid , aspartic acid , acetic acid , glutomic acid & butyric acid. They can cause demineralization of enamel and dentin and cause the tooth decay.

ROLE OF BACTERIAL PLAQUE

Plaque is a thin , transparent film produced on tooth surface. The dental plaque helps in initiation of dental caries by: It harbours the cariogenic bacyeria on the tooth surface. It holds the acid on the tooth surface for long time. It protects the acid from getting neutrilization by buffering action of saliva.

PROTEOLYTIC THEORY

A/c to this theory , the proteolytic enzyme liberated by cariogenic bacteria causes destruction of organic matrix of enamel as a result of which the inorganic crystals of the enamel becomes detached form one another and finally the whole structures collapse leding to cavity formation. This theory cannot explain the role of sucrose , pH & fluoride in dental caries.

PROTEOLYTIC CHELATION THEORY

A/c to this theory during caries first of all proteolytic break down of the organic portion of the enamel matrix takes place. Following this chelating agent is formed by the combination of the proteolytic breakdown products acquired pellicle and fat debris etc. The chelating agent (-ve charged) released the calcium ions (+ve charged) from enamel and dentin this process is called a chelation.

SUCROSE CHELATION THEORY

This theory propose is that if there is very high concentration of sucrose in the mouth there can be formation of complex substance like calcium saccharide and calcium complexing inter mediaries. These complexes cause release of calcium and phosphorus from the enamel and there by resulting in tooth decay

AUTO IMMUNE THEORY

This theory suggests that few odonoblast cells at some specific sites within the pulp of few specific teeth are damaged by autoimmune mechanism.

HISTOPATHOLOGICAL FEATURES OF ENAMEL CARIES

I- EARLY ENAMEL CARIES

There will be loss of inter prismatic or inter rod substances with increase in prominence of these enamel rods. Dark line often appears at right angles of the enamel rods , suggesting segments. Accentuation of the incremental straie of ratzius often occurs.

II - ADVANCED ENAMEL CARIES

It presents several zones in the tissues , out of which four zones are clearly visible starting from the inner advancing front of the lesion the zones are :

ZONE I : TRANSLUSCENT ZONE-- It is the deepest zone lies at the advancing front of the enamel lesion. This zone is more porous then the normal enamel The pore are larger than the normal enamel Pore volume being 1% The zone appears structure less the zone contains more fluoride than fluoride than normal enamel.

ZONE II : DARK ZONE---

Located just superficial to the translucent zone & its dark appearance is due to the excessive demineralization of enamel. This zone is narrower in rapidly advancing caries and it is wider in slowly advancing lesion. This zone contains 2 to 4% pore volume. The pore are larger than the normal but smaller than theory of translucent zone. This zone reveals same degree of reminerlisation of caries lesions.

ZONE III : BODY OF LESION---

The zone is situated between the dark zone and surface layer of enamel It represents the area of greatest demineralization Pore volume 5 to 25% This zone contains appetite crystals larger than those of normal enamel The larger crystals results from the reprecipation of minerals dissolved from the deeper zone.

ZONE IV : SURFACE ZONE---

The surface zone when examined by the polarizing light appears relatively unaffected . it may be due to surface reminerlization by the salivary minerals.

HISTOPATHOLOGICAL FEATURES OF DENTINAL CARIES

The dentinal caries histologically presents 5 zones in the tissue which are :

ZONE I : NORMAL DENTIN-- This zone represents the inner most layer of the carious dentin , here the dentinal tubules appears normal. There is evidence of fatty degeneration of the tomes process. No crystals in the lumen of the tubule No bacteria in the tubules Inter tubular dentin has normal cross banded collagen and normal dense appetite crystals.

ZONE II : SUB-TRANSPARENT DENTIN---

This is the zone of dentinal sclerosis and is characterized by the deposition of very fine crystals structures within the dentinal tubules . Superficial layer shows area of demineralization and damage of the odontoblastic processes No bacteria in the tubules The dentin is capsule of remineralization

ZONE III : TRANSPARENT DENTIN---

This zone appears transparent and this is because of decalcification of dentin It is softer than normal dentin No bacteria in tubules Cross banded inter tubular collagen is still intact This zone is capable of self repair and remineralization

ZONE IV : TURBID DENTIN--This zone is marked by widening and distortion of dentinal tubules which are packed with micro-organism There is very little amount of minerals in dentin , denaturation of collagen fibers also take place The zone cannot undergo self repair or remineralization This zone must be removed before restoration. ZONE V : INFECTED DENTIN--This is the outermost zone of the carious dentin It is characterized by complete destruction of dentinal tubules In this zone the area of decomposition of dentin are called liquefaction focii of miller which occur perpendicular to dentinal tubules are called transverse clefts In the process the entire dentinal structures become destroyed and cavitation begins from DEJ.

CLASSIFICATION OF CARIES
A BASED ON LOCATION OF THE LESION
Smooth Surface Caries Proxim al Occlusa l/ Lingual Surface

Pits & Fissure s Caries

Root Caries

Occlusa l

Buccal/Li ngual Pit

B--- BASED ON TISSUE INVOLVED

i) Enamel Caries

ii) Dentinal Caries

iii) Cementum Caries

B--- BASED ON VIRGINITY OF LESION

i) Primary Caries

ii) Secondary Caries

B--- BASED ON PROGRESSIVE OF LESION

Progressive Caries

Arrested Caries
Rapidly Progressive Slowly Progressive

PITS & FISSURE CARIES

This type of lesion occurs in the developmental pits & fissures of the tooth. The teeth & their specific areas or surfaces affected by the pit & fissure caries include occlusal surfaces of molars and premolars , buccal and lingual surfaces of molars & lingual surfaces of maxillary incisors. The lesions usually brown or black with little softening & opaqueness of the surface . When the lesion is examined by a fine explorer tip a catch point is often felt where the explorer tip catches the area. The lesions are smaller in the beginning but becomes wider as they spread towards the dentin due to the typical orientation of enamel rod.

SMOOTH SURFACE CARIES

This type of carious lesion occur in relation to smooth surface of teeth eg. proximal surface or gingival areas of the buccal and lingual aspect of tooth. The lesion begins as a well demarcated chalky white opacity of enamel with no loss of continuity of surface. The white spot lesion becomes pegmented yellow or brown & it often extend buccally & lingually.

RAMPANT CARIES

A condition which is characterized by sudden , raped and almost uncontrollable destruction of teeth Affecting surfaces of teeth that are relatively caries free These include the proximal and cervical surfaces of the mandibular incisors which are relatively caries free A caries increment of 10 or more new carious lesions over a period of abt a yr is characteristic of rampant caries. They are most often observed in primary dentition of young children and the permanent dentition of teenagers Dietary factors affecting oral substitute and oral flora and physiological factors affecting saliva are often significant in the development of rampant caries

NURSHING BOTTLE CARIES

IT is also called as NEW/BABY BOTTLE SYNDROME & BOTTLE MOUTH SYNDROME This type of rampant caries affect deciduous dentition. ETIOLOGY It occurs due to prolong use of A nursing bottle containing milk or milk like fruit juice or sweetened water Breast feeding Sugar or honey sweetened pacifiers The disease presents clinically as widespread carious destruction of deciduous tooth if the habit prolonged The carious process in affected teeth may be so severe that only root stumps remain The mandibular incisor usually escape because they are covered and protected by tongue

ADOLESCENT CARIES

There are 2 chronological periods when acute , rapidly progressing caries is commonly observed Acute exacerbations in caries rate are usually seen at 4 to 8 yrs of age and at 11 to 18 yrs of age The acute caries attack in the later period is usually characterized as adolescent caries These are usually seen in teeth and surface that are relatively immune to caries with a relatively small opening in enamel with extensive undermining of enamel because of rapid progression of lesion there is little time for the formation of reparative dentin It is important to detect cases of rampant caries in the adolescent at an early stage so that preventive procedures may be rigorously applied

RECURRENT CARIES

Recurrent caries is the type which occurs in the immediate vicinity of a restoration . It is usually due to inadequate extension of the original restoration which favors retention of debris or to poor adaptation of the filling material to the cavity which produces a leaky margin . It has been thought that recurrent caries occurs beneath restorations if all the carious dentin is not removal before inserting the filling

ARRESTED CARIES

Arrested caries has been described as caries which become static and does not show any tendency for further progression The deciduous and permanent dentitions are both affected by this condition It occurs almost exclusively in caries of occlusal surface and is characterize by a rlarge open cavity in which there is lack of food retention and in which the superficially softened and decalcified dentin is gradually burnished untill it takes on a brown stained polished appearance and is hard. This has been brown stained polished appearance and is hard. This has been referred to as eburnation of dentin

 sclerosis of dentinal tubules and secondary dentin formation commonly occur in case of arrested caries Another form of arrested caries is that sometimes seen on the proximal surface of teeth in case in which the adjacent approximately tooth has been extracted reveling a brown stained area at or just below the contact point of the retained tooth. This represents very caries which in many cases is arrested following the extraction because of the fermentation of a self cleansing area Manifested certain typical acquired characteristics The presence of brown pigmentation The change from a soft to a hard texture the change from a chalky whiteness to light brown No increase in the size of the lesion No further progress of lesion as long as the pigmentation remained

CONTRIBUTING OR SECONDRY FACTORS IN DENTAL CARIES

DIETARY FACTORS Carbohydrate with types: like monosaccharide's , disaccharide or polysaccharide & the amount consumed and whether between meals MICRO-ORGANISMS Acidogenic streptococcus mutants & Actinomycosis SYSTEMIC FACTORS Hereditary Pregnancy & lactation HOST FACTORS Poor oral hygiene & improper brushing technique may lead to dental caries IMMUNOLOGICAL FACTORS The functional role of circulating antibodies as protective agent against tooth decay has been demonstrated in non human primate

RADIOLOGICAL FEATURE OF DENTAL CARIES

Radiographs are often helpful in the detection of dental caries and usually the detection of dental caries & usually the IOPA , panoramic & bitewing radiographs. The bitewing radiographs are especially indicated for the detection of proximal caries The pit and fissure caries radiographically appears as a triangle shaped radiolucent area , with its base located towards the DEJ The sooth caries also produces a triangle shaped radiolucent area, but its base is located towards the surface of the tooth..

CARIES ACTIVITY TEST

CARIES ACTIVITY TEST (CAT) Measures the dergree to which the local environmental challenge favours the probability of carious lesion. Cat sterilises the need for personalised preventive measures provides an index of the success of thearupetic procedures and monitors the effectiveness of education programme. A. LACTOBACILLI COLONY TEST: It measures the no of aciduric bacteria in pt.

Saliva by counting the no of colonies which appear on tematopeptone agar plates a selective medium with ph 5.0 after inoculation of the pt saliva & incubation. INTERPRETATION
NO OF LACTOBACILLI/ML SALIVA CARIES ACIVITY 0-1000 1000-5000 5000-10,000 >10,000 LITTLE/NONE SLIGHT MODERATE MARKED

B. CALORIMETRIC SYNDER TEST : It measures the acid produced by flora by seeing changes in ph indicator which is compared to an uninoculated controlled tube after 24 48 72 hrs of incubation. A sample of stimulated saliva is inoculated in glucose and agar containing medium of ph 4.7 to 5 , the medium has a color indicator which changes from blue to green at ph 4.7 to 5 to yellow at 4.

INTERPRETATION TIME IN HRS COLOR CARIES ACTIVITY COLOR CARIES ACTIVITY 24 YELLOW MARKED GREEN CONTINUE TEST 48 YELLOW DEFINITE GREEN CONTINUE TEST 72 YELLOW LIMITED GREEN INACTIVE

C. STREPTOCOCCUS MUTANTS LEVEL TEST: The no of streptococcus mutants formed per unit volume of saliva is the basic of the test a sample is obtained using tongue blades or wooden spatula on mitis salivarius agar (MSA) a selective streptococcal medium with increase in conc of sucrose (21%) & 0.2% bacitracin per ml at 37c for 48 hrs. The frequency of isolation of S.mutants is high prior to initiation of lesion. D. BUFFER CAPACITY TEST : The test evaluate quantity of acid required to lower the ph of saliva through an arbitrary ph interval or in other words the amount of acid or base necessary to bring color indicators to this end point. Importantly buffer capacity could be quantities either using a ph meter or color indicator. This test relates the suffering capacity of saliva and caries activity.

PREVENTING & CONTROLLING METHOD OF CARIES

CHEMICAL MEASURES SUBSTANECS WHICH ALTER THE TOOTH SURFACE A. FLUORIDE It has cariostatic activity Fluoride makes the teeth more resistant to acid attack to oral cavity It decreases microbial acid production & enhances the remineralization of underlying enamel It is given in the form of i. Communal water fluoridation ii. Fluoride containing dentifrices iii. Fluoride mouth rinses iv. Dietary fluoride supplement

B. C. D. A. A. B. C. D. A. B.

BIS-BIGUANIDES Cholrhexidene SILVER NITRATE ZINC CHLORIDE SUBSTANCES WHICH INTERFERE WITH CARBOHYDRATE DEGRADATION THROUGH ENZYMATIC ALTERATION Vitamin k : prevents acid formation in minimum of glucose into saliva SUBSTANCES WHICH INTERFERE WITH BACTERIA GROWTH & METABOLISM Urea & ammonium compound Chlorophyll Nitro furans Penicillin NUTRITIVE MEASURES High in fat , low in carbohydrate free from sugar Phophate diet causes in indication of caries

MECHANICAL MEASURES A. Tooth brushing B. Mouth rinsing C. Dental floss D. Detergent foods E. Pits & fissures sealent