Lecture II : DENTAL CARIES Dental Caries is a progressive bacterial damage to the teeth exposed to the saliva is the destruction

on and disintegration of the hard tissues of the tooth breakdown of enamel, dentin or cementum thus open the path of bacteria to reach the pulp toothache a bacterial disease of the calcified tissues of the teeth characterized by demineralization of the inorganic and destruction of the organic substance of the tooth a complex and dynamic physicochemical process: movements of ions between the tooth and external environment, as well as biological processes associated with the interaction of bacteria with the external environment exists around the world, recognized throughout history In industrialized countries, sharp increase in the first half of 20th century; but since early 70s there has been a steady decrease in disease activity among children continuing among adult life => more people are retaining more teeth for much longer In some developing countries: prevalence increasing associated with urbanization and availability of refined CHOs Etiology of Dental Caries: Various theories for the etiology of dental caries have been proposed, but there is now overwhelming support for the acidogenic theory (postulated by W. D. Miller in 1889). Acidogenic Theory: proposes that acid formed from the fermentation of dietary CHOs by oral bacteria leads to a progressive decalcification of the tooth substance with a subsequent disintegration of the organic matrix confirmed in 1954 by Orlando and assoc (USA)= showed that caries did not develop in germ-free animals Other theories: subsequently discarded because of lack of experimental evidence Fig, A diagrammatic representation of the parameters involved in the etiology of dental caries

A clean enamel surface is covered within seconds by an adsorbed layer of glycoprotein from the saliva the pellicle on to which coccal bacteria adhere over the following 2 hrs. After 24 hrs, 95% of the total cultivable flora of plaque consist of streptococci. at this time bacteria have multiplied, formed colonies, become enmeshed in plaque matrix = consist of many subst of host, bacterial, dietary origin When there is excess sugar, the principal component of matrix are: extracellular glucans synthesized by plaque bacteria Otherwise, matrix consist mainly of salivary glycoproteins partially degraded by bacteria Strep remains the predominant group of bacteria in plaque for about 7 days, after which anaerobic filamentous bacteria becomes evident. By 14 days, they are the predominant group. The organisms are arranged in parallel units or in palisades, consisting of coccal, bacillary, filamentous, or spirochetal forms Organisms packed closely adjacent to enamel, becoming dispersed towards salivary surface, many of the organisms are dead Plaque is important in the etiology of dental caries because acid is generated within its substance to the extent that enamel may be dissolved dietary sugars diffuse rapidly in plaquebacterial metabolism acids: lactic acid (mainly) + acetic and propionic acids pH falls within 10 mins as much as 2 units at 30-60 mins later, pH slowly returns to original figure, due to buffering mech, ionic exchanges at the saliva-plaque-enamel interface during acid phase, mineral ions may be lost from the system by diffusion out of the plaque into saliva, repeated episodes may lead to overall demineralization and initiation of enamel caries frequency and duration of acid phase affect development of caries enamel caries cavity formation: plaque becomes removed from saliva, buffering mech bec inefficient, plaque bec more acidic for longer periods plaque orgs can store extracellular glucans form sugars which can be metabolized into acid when other COHs are not present inc bulk of plaque= interfering with buffering systems

Role of bacteria and plaque: Experiments with germ free animals have shown that bacteria are essential for the development of dental caries. Bacteria are present in dental plaque, which is found in most tooth surfaces. Plaque= consists predominantly of bacteria suspended in an amorphous matrix derived from salivary mucoids and extracellular bacterial polysaccharides (glucans). Leukocytes, and desquamated epithelial cells may become entrapped.

In Dental Plaque cariogenic bacteria ferment COH to acid cariogenic bacteria can store carbohydrate intra and extracellularly extracellular polysaccharides increase plaque bulk bulky plaques can interfere with outward diffusion of acid and inward diffusion of salivary buffers ions see-saw across the plaque-enamel interface depending on pH

fluoride ions encourage precipitation of minerals in to enamel and inhibit baterial metabolism

Notes:

Microbiology of Dental Caries species strongly implicated: --mutans streptococci, e.g. S. mutans; S. sobrinus --lactobacilli, e.g. L. casei; L. acidophilus species possibly associated: -- other streptococci, e.g. S. mitis -- actinomyces, e.g. A. viscosus ---all induce experimental caries in animals Factors supporting the role of S.mutans in the etiology of dental caries Rapid generation of acid from sucrose Synthesis of extracellular polysaccharides -adhesion to tooth - increase in plaque bulk Synthesis of intracellular polysaccharides Present in high numbers 9in plaque associated with developing lesions High numbers at a particular tooth site predispose to subsequent caries Highly cariogenic in animal models of experimental caries Immunization against S. mutans reduces caries incidence in animal models significance of role of S. mutans not fully resolved but overall conclusion is it is very important in the development of caries Caries of enamel may develop in some individuals in the absence of S. mutans; in some indiv high levels of S. mutans in tooth surface did not subsequently develop caries

Sucrose significantly more cariogenic than other sugars; significantly more available in human diet Glucose, fructose, maltose, galactose, lactose are also highly cariogenic in experimental animals Dietary sugars intrinsic (mainly fruits and veges) extrinsic ( added sugars, milk, fruit juices) Dietary recommendation: reduction of extrinsic sugars except milk Other carbohydrates such as sorbitol and xylitol, are very low cariogenic agents, partly because of their slow rate of fermentation.

Diet and dental caries caries prevalence increases when populations become exposed to sucrose-rich diets extrinsic sugars are more damaging than intrinsic sugars sucrose is the most cariogenic sugar frequency of sugar intake is of more importance than amount consumed Etiological Variables Factors influencing site attack and rates of progression in dental caries are largely unknown but may include: Factors intrinsic to the tooth: 1. Enamel composition inverse relationship between enamel solubility and enamel fluoride concentration 2. Enamel structure developmental enamel hypoplasia and hypomineralization amy affecte rate of progression of caries but not initiation 3. Tooth Morphology deep, narrow pits and fissures favor plaque retention and food 4. Tooth position malaligned teeth predispose to retention of plaque and food Factors extrinsic to the tooth 1. Saliva saliva component and quality affect caries pattern flow rate, viscosity, buffericng capacity, availability of calcium and phosphates for mineralization, and the presence of antimicrobial agents (Igs, thiocyanate ions, lactoferrin, lysozyme) 2. Diet presence of phosphates in the diet may reduce incidence of caries increasing the proportion of fat in the diet reduces cariogenic effect of sugarsphysical effect traces of molybdenum and vanadium in the diet may reduce caries 3. Immunity

Role of Carbohydrates Evidences: 1. The increasing prevalence of dental caries in developing countries and previously isolated ethnic groups associated with westernization, urbanization and increasing availability of sucrose in their diet. Ex: Inuit, native North and South Americans, African tribes, rural population in Asia 2. The decrease in the prevalence of dental caries in World War II because of sugar restriction, followed by rise to previous levels when sucrose became available in post war era. 3. The Hopewood House study: a childrens home in Australia where sucrose and white bread were virtually exluded from the diet. The children had low caries rate dwhich increased dramatically when they moved out of the home.

PATHOLOGY OF DENTAL CARIES Classification by site of attack 1. Pit or fissure caries occurs on the normal surfaces of molars and premolars, buccal and lingiual of molars, lingual surfaces of maxillary incisors detected by sticks or a catch on explorer evidence suggests that early fissure is becoming more difficult to diagnose by probing 2. Smooth surface caries occurs on proximal surfaces begins just below the contact point as a welldemarcated chalky-white opacity of the enamel; at this point it cannot be detected by probing or radiographs as caries progresses, surrounding enamel bec bluish-white, surface bec roughened before frank cavitation occurs Diagnosis of Caries early occlusal caries may be difficult to detect radiolucencies in approximal areas that do not reach the amelodentinal junction do not usually indicate enamel cavitation 3. Cemental or Root caries when root surfaces is exposed to the oral environments as a result of periodontal disease shallow, saucer-shaped and illdefined boundaries Recurrent caries around the margins or base of a previously existing restoration

chem. Analysis: fall in Mg and carbonate material sissolution of materials occurs mainly from the junctional areas between prismatic and interprismatic enamel sometimes missing or present along only part of the lesion

2.

Dark Zone 2-4 % by volume of pores some remineralization occurs due to reprecipitation of minerals thought that this zone is narrow in rapidly advancing caries, and widr is slower caries Body of the lesion pore volume of between 5 and 25% contains larger appatite crystals remineralization increased prominence of striae of Retzius Surface Zone about 40 um thick, shows surprisingly little change in early lesions area of active remineralization

3.

4.

4.

Enamel caries a dynamic physicochemical process involving dissolution and reprecipitation of minerals zonation of the early (white spot) lesion reflect different degrees of remineralization surface zone is an area of active remineralization the morphology of the lesion differs in pit and fissures compared dwith approximal surfaces Dentin Caries Processes in dentine caries defence reaction of pulpodentinal complex sclerosis reactionary dentin formation sealing of dead racts carious destruction demineralization proteolysis

Classification by rate of attack 1. Rampant or acute caries rapidly progressing inv many or all erupted teeth rapid coronal destruction leads to early involvement of the pulp 2. Slowly progressive or chronic caries inv the pulp much later than acute caries slow progression allows for defence reactions of the pulp (sclerosis and reactionary dentin) Arrested caries enamel, dentine or root caries that has become static or shows no tendency for further progression

3.

Zones: 1. Zone of sclerosis 2. Zone of demineralization 3. Zone of bacterial invasion 4. Zone of destruction 5. Reactionary or tertiary dentin

Enamel Caries Zones: 1.

Translucent Zone 1st recognizable histologic change 1 % by volume of pores dentin; 0.1% by vlome of pores of enamel