Definition of dental caries

DENTAL CARIES & ETIOLOGY Definition of Dental Caries • According to Shafer, Hine and Levy Dental caries is a microbial disease of the calcified tissues of the teeth, characterized by demineralization of inorganic portion and destruction of the organic substances of tooth.

• According to Cawson Dental caries can be defined as progressive, irreversible bacterial damage to teeth exposed to the oral environment.

• G.V. Black defined caries of the teeth as a chemical dissolution of the calcium salts, first of the enamel then of the dentin by lactic acid.

• According to Kidd and Simth caries is a disease of the calcified tissues of the teeth caused by the action of micro-organisms on fermentable carbohydrates.

• Thomas F. Lundeen and Theodore M. Roberson defined dental caries as an infections microbiological disease that results in localized dissolution and destruction of the calcified tissues of the teeth and progresses as a series of exacerbations and remissions.

• Ernest Newburn defined dental caries or tooth decay, as a pathological process of localized destruction of tooth tissues by microorganisms.

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Introduction Dental caries has been recognized throughout history and exists around the world, although the prevalence and severity varies in different populations caries is one of the most common of all diseases and partly because of its relatively rapid progess is the main cause of loss of teeth in younger people. The ultimate effect of caries is to breakdown enamel and dentine and to open a path for bacteria to reach the underlying tissues. This causes infection and inflammation of the pulp and later of the periapical tissues. Infection can spread from the periapical region to the jaw and beyond.

The etiology of dental caries is generally agreed to be a complex problem complicated by many factors which observe the direct cause or causes. There is no universally accepted opinion of the etiology of dental caries.

To better understand the current concept of the etiology of caries, earlier theories will be discussed briefly.

Early Theories Of Caries Etiology A. Worms Theory: According to an ancient Sumerian text, tooth ache was caused by a worm that drank the blood of the teeth and fed on the roots of the jaws. This legend of 2

the worm was discovered on one of many clay tablets excavated near Niffer and other cities within the Eupharates valley of the lower mesopotamin area and estimated to date from about 5000 BC. The idea that caries is caused by a worm was almost universal at the time, as evidenced by the writings of Homer and Popular Lore of China, India, Finland and Scotland. As a cure he advocated fumigation with seeds of leeks, onion and hyposcyamus. Fumigation was used by Chinese and Egyptians in earlier times, and fumigation devices continued to be used in England as late as the 19th century.

At least at the subconscious level this theory survives to our day when we refer to a tooth ache as a growing pain.

B. Humors Theory: The ancient greeks considered that a person’s physical and mental constitution was determined by the relative proportions of the lower elemental fluids of the body, blood, phlegm, black bile and yellow bile which correspond to the 4 humors – Sanguine, Phlegmatic, melancholic and choleric. All diseases including caries, could be explained by an imbalance of these humors.

Hippocrates while accepting the prevailing greek philosophy, drew attention to

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the Stagnation of food and suggested that both local and systemic factors were related to the cause of caries.

C. Vital Theory: The vital theory regarded dental caries as originating within the tooth it self, analogous to bone gangrene. This theory proposed at the end of the 18 th century, remained dominent until the middle of the 19th century. A clinically well known type of caries is characterized by extensive penetration into the dentin and even into the pulp, but with a barely detectable catch in the fissure. It is not so surprising therefore, that the vital theory attracted may supporters.

D. Chemical Theory: Parmly (1891) rebelled against the vital theory and proposed that an unidentified “chymical agent� was responsible for caries. He stated that caries began on the enamel surface in locations where food putrified and acquired sufficient dissolving power to produce the disease chemically. Support for the chemical theory cam from Robert Son (1835) and Regnart (1938), who actually carried out experiments with different dilutions of inorganic acids (such as sulfuric and nitric) and found that they corroded enamel and dentin.

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E. Parasitic or Septic Theory: In 1843, Erdl described filamentous parasites in the “surface membrane” (plaque?) of teeth observed filamentous microorganisms, which he called denticolac, in material taken from carious cavities. He implied that these bacteria caused decomposition of the enamel and then the dentin. Neither Erdl nor Ficinus explained how these organisms destroyed tooth structure.

F. Auto Immunity: In 1978 the famous John Hunter proposed that the initial event in dental caries took place with in the tooth, caries being secondary to inflammation of the pulp. Jackson and Burch, in recent years have revived this “intrinsic” concept of caries aetiology. They suggest that clones or regions of odontoblasts in specific sites within the pulp of specific teeth are damaged by an autoimmune process so that the defense capacity of the overlying dentine and enamel is compromised and conclude that caries should be regarded as a degenerative disease.

These authors argue that if, for example, caries develops on the mesial surface of a maxillary central incisor it is reasonable to assume the disease will eventually involve the adjacent of the adjoining tooth, because of a common plaque environment. However, they have shown that from the age of 22-60 years, 5

the ratio of the number of attacks on single central incisors to those on both incisors remain approximately constant at 1: 0.7. They conclude that the initiating events correspond to a form of somatic gene mutation in central growth control stem cells; descent mutant cells synthesize auto antibodies which damage specific groups of odontoblasts and thus determine the sites of caries susceptibility.

G. Chemo-Parasitic Theory (Acidogenic Theory): The chemo-parasitic theory is a blend of the chemical theory and parasitic theory because it states that caries is caused by acids produced by microorganisms of the mouth. It has been customary to credit this theory to W.D. Miller (1890), whose writings and experiments helped to establish this concept on a firm basis.

However, Miller owes much to the observations of this predecessors and contemporaries. Pasteur has discovered that microorganisms transform sugars to lactic acid in the process of fermentation. Another Frenchman, Emil Magitot (1867), demonstrated that fermentation of sugars caused dissolution of tooth mineral in vitro. Artificial lesions similar to caries were produced when sound adult teeth, covered by wax except for a small opening, were exposed to dilute acids or fermenting mixtures for an extended period of time.

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In a series of experiments Miller demonstrated the following facts: 1. Acid was present with in the deeper carious lesion, as shown by reaction on litmus paper.

2. Different kinds of foods (bread, sugar not meat) mixed with saliva and incubated at 37째C could decalcify entire crown of a tooth.

3. Several types of mouth bacteria (at least 30 species were isolated) could produce enough acid to cause dental caries.

4. Lactic acid was an identifiable product in carbohydrate saliva incubation mixtures.

5. Different kinds of micro-organisms invade carious dentin.

Miller concluded that no single species of microorganism caused caries, but rather that the process was meditated by an oral microorganism capable of producing acid and digesting protein.

Further weight was added to the chemo-parasitic theory by Williams (1897), who observed dental plaque on the enamel surface. Plaque was considered to be a means of localizing organic acids formed by microorganisms in contact with the tooth surface.

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Role of Carbohydrates Numerous studies have demonstrated a direct relationship between fermentable carbohydrate in the diet and dental caries. The evidence includes.

1. When teeth were incubated in mixtures of saliva and bread or sugar, decalcification occurred or fat was used in place of the carbohydrates.

2. The decrease in the prevalence of caries during world war II because of sugar restriction followed by a rise to previous levels when sucrose became available in the post war period.

3. The Hopewood House study a childrens home in Australia where sucrose and white bread were virtually excluded from the diet. The children had low caries rates which increased dramatically when they moved out of the home.

Different carbohydrates have different cariogenic properties sucrose is significantly more cariogenic than other sugars. Partly because it is readily fermented by plaque bacteria and partly because of its conversion by bacterial glycosal transferase into extra cellular glucans. Sucrose is also readily converted into intracellular polymers. Glucose, fructose, maltose, galactose, and lactose are also highly cariogenic carbohydrates in experimental caries in animals, but the principal carbohydrates available in human diets are sucrose and starches.

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Starch solutions applied to bacterial plaque produce no significant depression in pH due to the very slow diffusion of the polysaccharide into the plaque which must be hydrolysed by extracellular anylase before it can be assimilated and metabolized by plaque bacteria. Other carbohydrates such as sorbitol and xylitol, are very low cariogenic agents, partly because of their slow rate of fermentation.

Proposed relationship between caries score and dietary sucrose intake in humans.

In young children with newly erupted teeth and frequent sucrose ingestion, the S-shaped curve shifts to the left (solid linc). In older persons with mature enamel and limited sucrose ingestion, the curve shifts to the right and does not reach as high a caries score (broken line).

Groups of people with high sugar consumption: 1. Sugar Cane Chewers: There appear to have been six surveys of people who habitually chew sugar-cane. An habitual chewer might chew 4 to 5 kg of cane per day, which could contain about 500 grams of sugar. The results are equivocal 37% of the 98 adults examined by Harris and Cleaton – Jones were caries free and their mean

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caries experience was 3.2 DMFT. The 147 adults in the study of Drizen and Spies had a mean DMFT of 15.1 which was similar to that reported by Kumzel (16.5 DMFT) for adult white workers in Cuba.

2. Workers in the confectionary industry: There have been 2 studies comparing the caries experience of confectionary industry employees with similar groups of other workers. The caries experience of 722 Israeli confectionary workers was 71% higher than the caries experience of 812 workers from textile factories.

3. Femyl ketoneuria: This is a rare inherited metabolic defect in which there is a deficiency of the liver enzyme, phenyl alomine hydroxylase.

4. Children taking syrup medicines long term: Paediatric medicines are conveniently given in syrup form: Usually sucrose based. Roberts and Roberts compared the caries experience of 44 children, aged 9 months to 6 years, who had been receiving syrup medicines for atleast 6 months, with the caries experience of 47 similarly aged children who attended the same out patient clinic but either did not take medicines or tablets.

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The children taking the syrup medicines had much higher caries experience than the control children.

Human Interventional Studies The number of planned, interventional studies on human subjects in the field of diet and dental caries is few. This is because of the difficulties of placing groups of people on rigid dietary regimes for long periods of time.

1. The Vipeholm studies: The vipeholm study is probably the largest single study in the field of dental caries ever undertaken.

The main purpose of the study was to investigate how caries is influenced. i.

By the ingestion meals of refined sugar with only a slight tendency to be retained in the mouth (non sticky form).

ii.

By ingestion at meals of sugar with a strong tendency to be retained in the mouth (sticky form eg., sugar rich bread) and

iii.

By the ingestion between meals of sugar with a strong tendency to be retained in the mouth (sticky form, eg., toffees etc.).

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There was one control group and six main test groups, although the ‘bread’ and ’24-toffee’ groups were both divided into separate male and female groups.

The groups lived in separate wards eliminating the possibility of exchange of diet between groups of the 633 patients examined in 1946, 436 completed the main study in 1951. In general, their caries experience was low 15.6 DMFT at the age of 32 years, compared with 18.4 DMFT found in 20 year old Swedish army conscripts.

The main conclusions of the Vipehom study are: 1. Consumption of sugar, even at high levels is associated with only a small increase in caries increment if the sugar is taken upto 4 times a day at meals and none between meals.

2. Consumption of sugar both between meals and at meals is associated with a marked increase in caries increment.

2. The Turku shugar studies: In order to test whether the cariogenecity of sugars was also different in human subjects, a clinical study was conducted in Turku, Finland, between October, 1972 and October, 1974. The object was to study the effect on dental

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caries increment of nearly total substitution of sucrose in a normal diet with either fructose or xylitol. The 125 subjects were allocated to 3 groups – Sucrose (S), Fructose (F) and xylitol (X).

In summary, the Turku sugar study required a considerable amount of careful planning and organization. Almost total substitution of sucrose by xylitol resulted in a substantial reduction in caries incidence.

The Role of Microorganisms: Although there are differences of opinion as to how and which microorganisms, produce carious lesions. It is uniformly agreed that caries cannot occur without microorganisms, the over whelming evidence implicating microorganisms in the etiology of caries is summarized below: 1. Germ free animals do not develop caries.

2. Antibiotics fed to animals are effective in reducing the incidence and severity of caries.

3. Totally unerupted and un exposed teeth do not develop caries, yet when exposed to the oral environment and microflora can become carious.

Rarely, impacted 3rd molars with soft tissue covering are found to be carious, in which case a sinus tract to the oral cavity can be found.

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4. Oral bacteria can demineralize enamel and dentin invitro and produce caries like lesions.

5. Microorganisms have been histologically demonstrated invading carious enamel and dentin. They can be isolated cultivated from carious lesions.

Localization of oral flora related to caries: Careful evaluation of reports on caries indicates that different organisms display some selectively as to which tooth surface they attack and suggests that there are atleast 4 types of processes involved.

1. Pit and fissure caries: This is the most common carious lesion found in modern humans. Many organisms can colonize in fissures, which provide mechanical retention for the bacteria. Gnotobiotic rats monoinfected with either S. Mutans, A. nauslundii, or Actinomycetes Israeli develop fissure lesions. S. Sanguis is the predominant viable organism. S. mutans and lactobacilli are low in newly formed plaque in fissures but increase overtime. A wide variety of microbes may be able to initiate pit and fissure caries.

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2. Smooth surface caries: A limited number of organisms have proved able to colonize smooth surface in large enough numbers to cause decay. S. mutans is very significant in this respect. Streptococci are predominant organisms in both old and young plaques. Subsequently there is a shift in the relative proportions, and in older plaques filamentous organisms (veillonella and actinomyeces species) form fairly large groups. Lacto bacilli comprise less than 1% of the plaque flora.

3. Root Caries: Root caries is a soft, progressive lesion of the root surface involving plaque and microbial invasion. It has been known by a variety of terms, including cemental caries, cervical caries, radicular caries, and even “senile� caries. Some of the organisms involved in root caries are different from those in other smooth surface lesions because the initial lesion is in cementum and dentine, not enamel.

In rodents, gram +ve filamentous rods, including actinomyces species, have been associated with this type of lesion. Strains of Nocardia and S. Sanguis, besides causing enamel may at times also cause root caries. In humans the mutans groups of streptococci has been associated with surface with root caries when compared to intact root surfaces.

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4. Deep Dentinal Caries: Because the environment in deep dentinal lesions is different from that at another locations, it is not unexpected that the flora here is also different. The predominant organism is lactobacillus which accounts for approximately 1/3 rd of all bacteria. Frequently isolated gram +ve anaerobic rods and filaments are arachnia, Bifidobacterium, Eubacterium, and propionibacterium. Actinomyces, of deep dentinal lesions. The incidence of gm +ve facultative cocci is low.

Oral Streptococci: Irrespective of the age of plaque and the previous diet, the predominant organisms are gm +ve cocci of the genus streptococcus, which form young plaque.

These streptococci have been divided into various groups, based on their colonialmorphologyical characteristics.

Streptococcus sangius: This is one of the predominant groups of streptococci colonizing on the teeth. Formerly it was called streptococcus S.B.E. because of its involvement in sub acute bacteria endocarditis.

Caries from this strain occurs primarily in sulci and is significantly less extensive than that from S. mutans, which causes smooth surface caries as well, 16

S. Sanguis grows as small zoological colonies with a firm consistency and forms extracellular polysccharides in sucrose broth. On blood agar, S. sanguis causes α (green) hemolysis.

S. mutans: In 1924 Clarke isolated a streptococcus that predominated in many human carious lesions and that he named streptococcus mutans because of its varying morphology. For the next 40 years, S. mutans was virtually ignored, until the 1960s when it was “re discovered” and its prevalence in plaque confirmed.

Characteristics of this group of streptococci have been described as non motile, catalase negative and gram +ve cocci in short or medium chains. On mitis salvarius agar they grow as high convex to pulvinate (cushion shaped) colonies.

These colonies are opaque; the surface resembles frosted glass. Hemolysis of blood agar is variable and may be α (green) or (no change) and occasionally β (clear).

S. mutans exhibits several important properties: 1. It synthesizes insoluble polysaccharides from sucrose.

2. It is a homo fermentative lactic acid former.

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3. It colonizes on tooth surface.

4. It is more acideuric than other streptococci.

Biomechanical composition of S. mutans cell walls: S. mutans possesses: 1. An outer capsule of glucan or levan when grown in the presence of sucrose and 2. A cell wall polysaccharide. This is composed either of rhamnose, glucose, and galactose, or galactose and rhamnose, or glucose and rhamnose (which is the most common type found).

In addition to these components, the cell wall possesses as peptidoglycan and glycerol teichoic acid.

Ecology of S. mutans: Accumulated evidence of the ecology of S. mutans indicates that this organism can survive in the mouth only when solid surfaces such as teeth or dentures are present.

Although the favorite habital of S. mutans is the tooth surface, it does not uniformly colonize all tooth surfaces but instead localizes on certain surfaces.

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The exact mechanism by which S. mutans can adhere to and accumulate on the surface of teeth is unknown. It has been thought that S. mutans is a pathogen because of its ability to produce extracellular glucans from sucrose. Many bacteria, however, can synthesize polysaccharides such as glucans or dextrans and yet are unable to produce carious lesions.

Human salivary concentrations of S. mutans range from undetectable to 106 to 107 colony forming units (CFU/ml), with a mean concentration of about 105 CFU. Salivary combination of cusps and glasses or eating utensils such as spoons may account for the transmission of S. mutans from parent to child. There is good evidence implicating the childs mother as the principal vector, especially mothers with high concentrations of S. mutans in there plaque and saliva (more than 10 5 CPU/ml).

All

types

of

S.

mutans

are

highly

susceptible

to

penicillin,

chloramphenical.

S. Salivarius: These colonies grow as large, heaped, mucoid, or gummy colonies on mitis salivarius agar. In sucrose broth they form a water soluble polymer of fructose

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known as levan, as well as in soluble glucans. They can be recovered from the mouths of infants shortly after birth.

S. mitior: S. mitior is a heterogenous species. On mitis salivarius agar it forms soft, circular black brown colonies.

Oral Lactobacilli: Lactobacilli, or organisms resembling lactobacilli, have been reported in the oral cavity ever since miller enunciated the chemo-parasitic theory.

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Homo fermentative

Hetero fermentative

L casei

L fermentum

L acidophilus

Lactobacillus brevis

Lactobacillus plantarum

Lactobacillus buchneri

Lactobacillus salivarius

Lactobacillus cellbiosus

In isolates of lactobacilli from human carious dentin, the homo fermentative out number the hetero fermentative variety.

It was found that lactobacilli constitute only a minor fraction (1/10,000) of the plaque flora.

Lactobacilli have a relatively low affinity for tooth surface.

Oral Actinomyces: Actinomyces is a gram positive non motile, non spore forming organism occurring as rods and filaments that vary considerably in length.

Facultative anaerobic

Anaerobic

A. Naeslundii

A. Israeli

A viscsus

Actinomyces meyeri A odontolyticus

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All species of actinomyces ferment glucose, producing mostly lactic acid, lesser amounts of acetic and succemic acid, and traces of formic acid. Most interest has centered on A viscous and A naeslundii because of their ability to induce root caries.

Role of Dental Plaque The dental plaque is a structure of vital significance as a contributing factor to atleast the initiation of carious lesion. It has been recognized for many years and was demonstrated in histologic preparations by Williams in 1897.

Miller though that the plaque protected the enamel against attack by the carious process. In contrast G.V. Black regarded the plaque as important in the caries process and, in 1989 described it thus; “the gelatinous plaque of the caries fungus is a thin, transparent film that usually escapes observation, and which is revealed only by careful search�.

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Definition: Plaque is a tenaciously adherent deposit on the tooth surface.

Plaque can be supra or sub gingival and differs in composition and in its effects in these different sites. Plaque is involved in the genesis of both dental caries and periodontal disease.

Chemical composition of plaque: Plaque contain about

80% water and 20% solids.

Of the dry weight

40-50% proteins (major component) 13-18% carbohydrates 10-14% lipids.

Proteins of plaque: The proteins found in plaque originate from bacteria, saliva, or gingival fluid. Several salivary proteins, such as amylase, lysozyme, IgA, IgG and albumin have been identified in plaque. IgG, IgA and IgM are mainly derived from gingival fluid.

Carbohydrates of plaque: Glucose is the main carbohydrate found in hydrolyzed extracts of plaque.

Appreciable amounts of arabinose, ribose, galactose and fucose can be detected.

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Much of the carbohydrate exists in the form of extracellular polymers, either as glucans (homopolymers of glucose), fructans (homopolymers of fructose), or heteropolysaccharides, all of which are synthesized by different plaque microorganisms.

The glucans occur either as dextrans, predominantly 2 (1.6) linked, or as “mutans” which are mostly 2 (1.3) linked. In addition, an amylase type glucan, mostly 2 linkage is made by Neisseria species. The fructans made by streptococcus salivarius and A viscous are of the levan type.

In organic components of plaque: The inorganic content of plaque depends on is location and age. Plaque contains calcium, phosphate and fluoride in higher concentrations than those of saliva. The fluoride concentration in plaque (14 to 20 ppm) is higher than in saliva (0.01 to 0.05 ppm).

Microbial composition of plaque: Plaque consists of a mélange of organisms that varies depending not only on the site and the customary diet but also on how much time the plaque has had to “mature”.

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Supra gingival microbiota: Supragingival plaque contains mostly gm +ve facultative anaerobes. S sanguis is the most commonly found streptococcus and constitutes about 10% of the cells. A. viscous, A. nalslundii and A. Israeli are found in almost all plaque samples. Other gm +ve organisms that are regularly detected include S mitis, S mutans, Rothia dentocariosa, peptostreptococcus species, and staphylococcus epidermitis.

Gm +ve species found include veillonella alcabescens, veillonella parvula, fusobacteria, and bacteroids oralis.

Subgingival microbiota: Mature plaque from a healthy gingival sulcus comprises about 50% to 85% gm +ve cocci and rods 15% to 30% gm –ve cocci and small rods *5 each of fusobacteria and filaments and about 2% spirochetes. Actinomyces and streptococcus species are the major components of cultivable flora. Spirochetes of the genera Treponenna and Borrelia are indigenous to the gingival sulcus area.

Formation and Development of Dental Plaques: The first stages appears to be the deposition of a structureless cell free pellicle. This starts almost immediately; it does not appear to be due to bacterial 25

action. This cell free pellicle has also been shown to form in germ free animals and seems to be derived by deposition of salivary mucinous substances such as: Glycoproteins: It is possible that further deposition of this pellicle is facilitated by bacterial action precipitating these proteins.

Within 24 hours this cell layer becomes colonized by microorganisms, mainly streptococci and particularly sanguis and mutans strains. After 48 hours these streptococci comprise some 70% of the cultivable flora. As the plaque matures filamentous organisms proliferate and form the second largest groups after the streptococci. In addition a wide variety of other bacteria join the plaque population and include, lactobacilli, actinomyces, diptheroids and various Gm+ve anaerobes.

Effect of thickness of plaque: Even in the presence of suitable organisms and substrate, plaque needs to form in a certain critical thickness for caries to develop. Thick plaque can accumulate at the necks of teeth in the angle between the gingival margin and the tooth. Caries can then develop to produce cervical caries.

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A critical thickness of plaque is therefore necessary to maintain the concentration of acid at the tooth surface, to resist salivary bulfering and to form reserve carbohydrate stores if caries is to develop.

Acid production in plaque: Sugars can diffuse rapidly into plaque and acid production quickly follows.

It was once thought that the dental plaque, which is permeable to carbohydrates with the possible exception of starch, acted to hold the carbohydrate at a restricted site for a relatively long time. Stephan (1940) showed that this concept was in correct and that carbohydrates permeating the plaque were degraded rapidly. He used an antimony microelectrode capable of measuring the pH in a dental plaque in situ. The pH of plaques in different persons varied, but averaged about 7.1 in caries free persons to 5.5 in persons with extreme activity, investigation of actual provisional cavities opened ‘mechanically’ showed that the lowest pH varied from 4.6 to 4.1 Stephen also studied the pH in dental plaque after rinsing of the mouth with a 10% glucose or sucrose solution.

Within 2-5 minutes after the rinse, the pH in the plaque had fallen to between pH 4.5 and 5.0 and gradually returned to the initial pH level within 1-2 hours. Further studies indicated difference in reductions in pH in caries-free and caries active

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subjects. The plaque pH in the caries free group did not fall below 5.0 units after the glucose rinse, while the pH in the caries active group fell below 5 units after the glucose rinse in over half the cases.

The maxillary anterior teeth exhibited a greater pH drop in the plaque than the mandibular anterior teeth, indicating that the saliva influences plaque and production.

H. Proteolytic Theory: The classical chemo-parasitic theory was not been universally accepted.

Instead, it has been proposed that the organic or protein elements are the initial pathway of invation by microorganisms. The human tooth contains only about 1.5% to 2%. Organic material of which 0.3% to 0.4% is protein. According to the proteolytic theory, the organic component is most vulnerable and is attached by hydrolytic enzymes of microorganisms. This precedes the loss of inorganic phase.

Gottleib (1944) maintained that the initial action was due to proteolytic enzymes attacking the lamellar rod sheaths, tufts, and walls of dentinal tubules.

He suggested that a coccus, probably staphylococcus aureus, was involved because of the yellow pigmentation that he considered pathognomonic of dental caries. According to Gottleib, acid alone produces chalky enamel but not true 28

caries. Gottleib ideas were based on the observations of histological specimens and on the similarly between carious enamel and enamel whose organic components were stained with silver nitrate. There has been no bacteriological confirmation of his proposed link between staphylococcus pyogenes and caries.

Fresbie (1944) also described caries as a proteolytic process involving the polymerization and liquefaction of the organic matrix of enamel. The less soluble inorganic salts could then be freed from their “organic bond”, favoring their solution by acidogenic bacteria that secondarily penetrate along widening paths of impress.

Pincus (1949) contented that proteolytic organisms first attacked the protein elements, such as the dental cuticle, and then destroyed the prism sheaths.

The loosened prisms would then fall out mechanically. He also suggested that sulfatases of g-ve bacilli hydrolyzed “mucoitin sulfate” of enamel or “chondroitin sulfate” of dentin and produced sulfuric acid. The released sulfuric acid could combine with the calcium of the mineral phase. It should be noted that the composition of organic components of enamel does not resemble that of connective tissue and an abundance of sulfated polysaccharides has not been demonstrated.

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Pincus theory remains, therefore, without experimental support.

I. Proteolytic – Chelation Theory: This theory was advanced by Schatz and his co-workers to explain the cause of dental caries.

Chelation: Chelation is a process involving the complexing of a metallic ion to a complex substance through a coordinate covalent bond which results in a highly stable, poorly disassociated or weakly ionized compound.

Chelation is independent of pH of the medium, so that removal of such metallic ions as calcium from even a biologic calcium phosphorus system may occur at a neutral or even alkaline pH. This theory states that the bacterial attack on the enamel, initiated by keratinolytic “microorganisms, consists in a break down of the protein and other organic components of enamel, chiefly keratin. This results in the formation of substances which may form soluble chelates with the mineralized component of the tooth and there by decalcify the enamel at a neutral or even alkaline pH.

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Enamel also contains other organic components besides keratin, such as mucopolysaccharides, lipid and citrate, which may be susceptible to bacterial attack and act as chelations.

The proteolysis chelation theory resolves the arguments as to whether the initial attack of dental caries is on the organic or inorganic portion of enamel by staining that both may be attacked simultaneously. But several reconciliations must be made if the proteolysis chelation theory is to be accepted. These include 1.

The observation of increased caries incidence with increased sugar consumption.

2.

The obsrvation of increased lactobacillus counts with high caries activity and

3.

The observation of decreased caries incidence following topical or systematic administration of fluoride.

Increased caries incidence concomitant with increased carbohydrate

consumption might occur through the action act of the carbohydrate in: 1.

Stimulating or increasing proteolysis.

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2.

3.

Producing conditions under which kerationous proteins are less stable, and Complexing calcium.

Increased caries incidence accompanying increased lactobacillus counts

might be explained by the microorganisms being the results of the caries process, rather than its cause. Thus Schatz has suggested that: 1. Proteolysis may provide ammonia which prevents a pH drop that would tend to inhibit growth of the lactobacilli.

2. The release of calcium from hydroxyapatite by chelation might encourage the growth of lactobacilli, since calcium has been reported to produce this effect; and 3. Calcium exerts a vitamin – sparing action on some lactobacilli.

The weaknesses and strengths of this theory are as follows: 

Proteolysis is not an important step in the carious process.



Carious lesions and plaque are acid in the presence of suitable substrate.

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

Chelation, on the otherhand, is a wide spread biological process, and aminoacids, citrate, and lactate, which are capable of chelate formation are present in saliva and plaque. It is not clear whether these chelators are present in sufficient quantities.



What portion of calcium is removed as an ionic salt versus a calcium chelator complex is also not clear.

J. Sucrose Chelation Theory: Eggars – Lura has proposed in a series of papers (1948 – 1968) that the very high sucrose concentrations often encountered in the mouths of caries active individuals form calcium saccharate; that is a direct interaction between sucrose and calcium takes place. This, however, is unlikely to be a significant process because of the rapidly with which sucrose is metabolized to acid and polysaccharide, and because calcium saccharates can only form at high pH, above the range usually found in the mouth.

K. Phosphate Theory: Several theories have been proposed dealing with the role of phosphate in the caries formation. Using radioactive phosphorus, Luoma showed that inorganic phosphate was taken up by plaque bacteria during metabolism of carbohydrates, 33

the phosphate being required for phosphorylation of sugars and for polyphosphates that store energy. It has been postulated that a steady state equilibrium exists between the inorganic phosphate of saliva and the mineral phase of enamel.

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L. Phosphate Sequestration Theory: According to sequestration theory, as bacteria take up phosphate, inorganic phosphate must be removed from the enamel. However, invivo there is a continual flow of saliva containing soluble inorganic phosphates that are more available to bacteria than the insoluble mineral phase of enamel provided the saliva can diffuse through the plaque to the bacteria.

M. Nutritional Deficiency Theory: This theory consider as a nutritional deficiency caused either by in sufficient phosphate intake or by an improper dietary calcium to phosphate ratio.

Neither of these latter explanations has adequate statistical or experimental support.

N. Alkaline Phosphatase Theory: Bacterial alkaline phosphate was found to release phosphate from enamel in vitro. It was speculated that this enzyme could participate in caries destruction by acting on phosphoproteins of enamel. A commercial enzyme preparation obtained by sulfate precipitation was utilized, but it was subsequently observed that ammonium sulfate itself can release phosphate from teeth. Another difficulty

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with this theory is that the alkaline phosphatase of the bacteria is an intracellular enzyme. Therefore, lysis of cells would have to occur to free the enzyme.

Contributing Factors In Dental Caries The indirect factors that might influence the etiology, of caries are as follows: A.

Tooth

1.

Composition.

2.

Morphologic characteristics.

3.

Position.

B.

Saliva

1.

Composition. a.

Inorganic.

b.

Organic.

2.

pH.

3.

Quantity.

4.

Viscosity.

5.

Antibacterial factors.

C.

Diet

1. Physical factors. a.

Quality of diet.

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2. Local factors. a. Carbohydrate content. b. Vitamin content. c. Fluorine content.

A. 1.

Tooth factor Composition: Brudevold and his associates in 1965 indicated that surface enamel is more

resistant to caries than subsurface enamel. Surface enamel is more highly mineralized and tends to accumulate greater quantities of fluoride, zinc, lead, chloride and iron than the underlying enamel. The surface is lower in carbon dioxide, dissolves at a slower rate in acids, contains less water and has more organic material than subsurface enamel. These factors apparently contribute to caries resistance and are partly responsible for the slower disintegration of surface enamel than of the underlying enamel in initial carious lesions.

2. Morphologic characteristics The only morphologic feature that conceivably might predispose to the development of caries is the presence of deep, narrow occlusal fissures or buccal or lingual pits. Such fissures tend to trap food, bacteria and debris and since

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defects are especially common in the base of fissures, caries may develop rapidly in these areas.

For example, in mandibular first molars the likelihood of decay in descending order is occlusal, buccal, mesial, distal and lingual, where as in maxillary first molars the order is occlusal, mesial, palatal, buccal and distal. On maxillary lateral incisors, the palatal surface is more susceptible to caries than the buccal surface.

The most susceptible permanent teeth to caries are the mandibular first molars, closely followed by the maxillary first molars and the mandibular and maxillary second molars. The second premolars, maxillary incisors and canines and the least likely to develop lesions.

3. Position The position of teeth seems to be a minor factor in the etiology of dental caries.

Teeth which are malaligned, out of position, rotated or other wise normally situated may be difficult to cleanse and tend to favor the accumulation of food and debris.

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B. Saliva : 1. Composition: A. Inorganic: The concentrations of inorganic calcium and phosphorus show considerable variation depending upon the rate of flow. Becks and Wain Wright did extensive studies on salivary calcium and phosphorus and noted to the rate of flow. Karshan reported that the calcium and phosphorus content of saliva is low in caries active persons. There are numerous other inorganic components of saliva such as sodium, magnesium, potassium, carbonate, chloride and fluoride.

B. Organic: Organic constituent like salivary cholesterol was determined by Krashow and Oblatt and reported as varying from 2.3 to 50.0 mg/100ml. Its significance is unknown. Mucin content of saliva has also been determined, but its significance and the factors modifying its concentrations are like wise obscure.

The ammonia and urea content of saliva has been studied by many workers. Turkheim in 1925 noted that the saliva of caries immune persons exhibited a greater ammonia content than saliva from persons with caries. Grove and Grove found that the only apparent difference between the saliva of caries susceptible and caries immune persons was in ammonia content. They reported

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that the ammonia nitrogen of saliva from caries susceptible ranged from none to 8.0 mg/100ml. While ammonia nitrogen in saliva from the caries immunes ranged from 4.0 to 10.0 mg/100ml. They suggested that a high ammonia concentrations retarded plaque formation and neutralized acid, at least to some extent.

A number of different enzymes have been isolated from saliva. The most prominent and important oral enzyme is amylase, or ptyalin, a substance responsible for the degradation of starches.

2. pH of saliva: The pH at which any particular saliva ceases to be saturated with calcium and phosphate is referred to as the “critical pH�, below this value, the inorganic material of the tooth may dissolve.

Most of the studies dealing with the pH of the saliva and its relation to dental caries have shown no positive correlation. Reported correlations are of no biological significance.

3. Quantity: The quantity of saliva secreted in a given period of time may, theoretically atleast influence caries incidence. This is especially evident in cases of salivary

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gland aplasia and xerostomia in which salivary flow may be entirely lacking, with rampant dental caries the typical result.

Xerostomia may be the consequence of a variety of different human pathological conditions, as listed below.

1. Sarcoidosis may involve reduced salivary gland functions.

2. Sjogren’s syndrome.

3. Theurapeutic radiation of the head and neck leads to xerostomia if glands are with in the primary beam.

4. Surgical removal of salivary glands for neoplasms may cause localized xerostomia.

5. Chronic administration of anticholinergic or para sympatholytic drugs can produce clinical manifestation of xerostomia.

6. Diabetes mellitus.

7. Parkinsons disease.

8. Congenital absence or mal formation of salivary glands.

9. Acute virus infection involving salivary glands results in temporary xerostomia.

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4. Viscosity of saliva: Occasional workers have reported, however, that a high caries incidence is associated with a thick mucinous saliva. The viscosity of saliva is due largely to the mucin content, derived from the submaxillary, sublingual and accessory glands.

5. Antibacterial properties of saliva: Clough in 1934 tested 41 different salivas for their effect on the growth of L. acidophilus inhibition of growth was demonstrated by all salivas except one. ďƒ˜

Van Kesteren and associates found that the saliva probably contains atleast 2 antibacterial substances, one of which resembles lysozyme the other being distinctly different.

ďƒ˜

Using L. acidophilus as the test organism, Hill in 1939 found that saliva from caries free persons had a greater inhibiting effect than saliva from caries active persons.

ďƒ˜

The significance of antibacterial factors in saliva has been questioned by many workers, including Bibby (1956), who pointed out that

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regardless of the quantity of saliva, saliva always appears to contain bacteria capable of producing caries if carbohydrates are present.

The Buffer capacity of the saliva: A buffer is a solution that tends to maintain a constant pH. The Buffer capacity of the saliva is another factor that has received considerable attention because of its potential effects on acids in the oral cavity. ďƒ˜

Karshan and his associates (1931) pointed out that titrable alkalinity is a better indication of buffer capacity than is the pH, but they found that saliva from caries immune and caries susceptible persons exhibited essentially the same tetratable alkalinity.

ďƒ˜

Sellman in 1949 studied the buffer capacity of saliva and its reaction to dental caries and found that the total amount of acid needed to reduce the salivary pH of a given pH level was always greater for saliva from caries resistant persons.

ďƒ˜

The relation between buffer capacity of saliva and dental caries activity is not as simple as might be supposed. The acid production significant in the caries process, occurs at a localized site on the tooth. This

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rate, particularly in the early stages of caries, is protected by the dental plaque, which appears to act as an osmotic membrane preventing a completely free exchange of ions. ‘Thus eventhough buffer ions are present in the saliva, these may not be totally available at those specific sites where they are needed on the tooth surface.

The entire problem of the buffer capacity of saliva and its relation to dental caries require further investigation.

C. Diet: Diet refers to the customary allowance of food and drink taken by an person from day to day. Thus, the diet may exert an effect on caries locally in the mouth by reacting with the enamel surface and by serving as a substrate for cariogenic microorganisms.

1. Physical factors: a. Quality of diet: The physical nature of the diet has been suggested as one factor responsible for the difference in caries experience between primitive and modern man.

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The diet of the primitive man consisted generally of raw unrefined foods containing a great deal of roughage, which cleanses the teeth of adherent debris during the usual masticatory excursions. In addition, the presence of soil and sand in incompletely cleaned vegetables in the primitive diet induced severe attrition of both occlusal and proximal surfaces of the teeth, the following causes a reduction in the probability of decay.

In the modern diet, soft refined foods tend to cling tenaciously to the teeth and are not removed because of the general lack of roughage. Augmenting this collection of debris on the teeth is the reduction of mastication due to the softness of the diet.

2. Local factors: a. Carbohydrate content – Discussed already.

B. Vitamin content The vitamin content of the diet has been reported by many workers to have a significant effect on dental caries incidence. ďƒ In case of Vitamin D deficiency malformation, particularly enamel hypoplasia has been described.

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 The relation of rickets to dental caries is not well defined, however the only possible way in which infantile rickets could influence dental caries incidence is through an alteration in the tooth structure which makes the teeth more susceptible to caries.  Vitamin K ahs been tested as a possible anticaries agent by virtue of its enzymes inhibiting activity in the carbohydrate degradation cycle.  Vitamin B6 (Pyridoxine) has been proposed as an anticaries agent on the hypothetical ground that it selectively alters the oral flora by promoting the growth of non cariogenic forms.  Vitamin C deficiency is well recognized as producing severe changes in the periodontal tissues and pulps of the teeth.

Systemic factors: There are certain factors disassociated from the local environment or at least not intimately associated with it, which have been related to dental caries incidence and which may be conveniently discussed under this general heading.

Hereditary has been linked with the dental caries incidence in the scientific literature for many years. In 1899 G.V. Black wrote “when the family remains in

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one locality, the children under the conditions similar to those of the parents in their childhood, the susceptibility to caries will be very similar in the great majority of cases. This will hold good even to the particular teeth and the localities first attacked, the order of occurrence of cavities, and the particular age at which they occur.

The racial tendency for high caries or low caries incidence in some incidence at least, appears to follow hereditary patterns. The fact that local factors may easily alter this caries tendency would indicate that hereditary does not exert a strong influence in determining individual caries susceptibility.

One of the most significant studies is that reported by Klein in 1946 on the results of examination of 5400 persons in 1150 families of Japanese avastry. In this study the DMF was established for each individual, and 30 percent of the fathers with the lowest DMF rate were designed arbitrarily as “low DMF”. The 30% with the highest DMF were designed as middle DMF. The same groupings were used for the mothers and for the sons and daughters of these parents. It was found that a “high DMF” father and “high DMF” mother produced off spring, both sons and daughters, with a high DMF rate. On the other hand, if the father and mother were both low DMF the children also were in a low DMF group.

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Pregnancy and lactation: The available evidence indicates that pregnancy does not cause increased caries.

Caries Activity Tests Caries activity tests have been used in dental research for many years, and some tests have been adapted for routine use in the dental office. There is no ideal test in existence at the present time, although caries cavity tests are a valuable adjunct for patient motivation in a plaque control program.

A. Lactobacillus Colony Count: Action: This test, first introduced by Hadley in 1953, estimates the number of acidogenic and aciduric bacteria in the patients saliva by counting the number of colonies appearing on tomato peptone agar plates after inoculation with a sample of saliva.

Equipment: The necessary equipment includes saliva collecting bottles, paraffin, 9 ml tubes of saline, 2 agar plates 2 bent glass rods, facilities for incubating, and a Quebec. By having the subject chew paraffin before break fast and then collecting the saliva in a bottle. The specimen is shaken to mix it. A 1 : 10 dilution is

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prepared by pipetting 1 ml of the saliva sample into a 9 ml tube of sterile saline solution. This is shaken and 1:100 dilution is made by pipetting 1 ml of the 1:10 dilution another 9 ml tube of sterile salt solution. The 1:100 dilution is mixed thoroughly, and 0.4 ml of each dilution is spread on the surface of an agar plate with a bent glass rod. The plates are labeled and incubated at 37째C for 3 to 4 days.

A count of the number of colonies is then made by using the Quebec counter.

B. Snyder Test: Action: The Snyder test measures the rapidity of acid formation when a sample of stimulated saliva is inoculated into glucose agar adjusted to pH 4.7 to 5 and with bromocresol green as colour indicator. Indirectly the test is also a measure of acidogenic and aciduric bacteria.

Equipment: The equipment includes saliva collecting bottles, paraffin, a tube of Synder glucose agar containing bromocresol green and adjusted to pH 4.7 to 5, pipettes, and incubating facilities.

Procedure: Saliva is collected before breakfast by having the subject chew paraffin. A tube of Synder glucose agar is melted and then cooled to 50째C. The saliva specimen is shaken vigorously for 3 min. The 0.2 ml of saliva is pipetted into the tube of agar and immediately mixed rotating the tube. The agar is allowed 49

to solidity in the tube and is incubated at 37°. The colour change of the indicator is observed after 24, 48 and 72 hours of incubation by comparison with an incubated tube against a white background.

This test meets some of the “ideal test” characteristics. Synder and others have found a high correlation between the synder did acid production test and lactobacillus plate count. Also, Synder and others have found a high correlation between clinical caries activity and +ve. Synder test results on a group basis. The best agreement was between a –ve Synder test and the absence of caries activity.

C. Reductase Test: Action: The test measures the rate at which an indicator molecule, diazoresorcinol, changes from blue tored to colorless or leukoform on reduction by the mixed salivary flora. Rapp claims the test “measures the activity of a single enzyme, reductase. This enzyme is involved in some very definite and limiting reactions in the formation of products dangerous to the tooth surface.

Equipment: The reductase test comes in a kit that includes calibrated saliva collection tubes with the reagent on the inside of the tubes cap, plus flavored paraffin.

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Procedure: Saliva is collected by chewing a special flavored paraffin and expectorating directly into the collection tube. When the saliva reaches the calibration mark (5ml) the reagent cap is replaced. The sample is mixed with a fixed amount of diazoresorcinol, the reagent upon which the reductase enzyme is to react. To change in color after 30 seconds and after 15 minutes is taken as a measures of caries activity.

D.

Buffer Capacity Test:

Action: Buffer capacity can be quantitated using either a pH meter or color indicators. The test measures the number of millimeters of acid required to lower the pH of saliva through an arbitrary pH interval, such as from pH 7.0 to 6.0 or the amount of acid or base necessary to bring color indicators to their end point.

Equipment: Needle equipment includes a pH meter and titration equipment, 0.05n lactic acid, 0.05 N base, paraffin and sterile glass jars containing a small amount of oil.

Procedure: 10 millimeters of stimulated saliva are collected under oil at least 1 hour after eating; 5ml of this are measured into a breaker. After correcting the pH meter to room temperature, the pH of the saliva is adjusted to by addition of lactic acid or base. The level of lactic acid in the graduated cylinder is re-recorded.

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Lactic acid is then added to the sample until a pH of 6.0 is reached. The number of millimeters of lactic acid needed to reduce pH from 7.0 to 6.0 is a measure of buffer capacity.

E.

Fosdick calcium dissolution test:

Action: The test measures the milligrams of powdered enamel dissolved in 4 hours by acid formed when the patients saliva is mixed with glucose and powdered enamel.

Equipment: Powdered human enamel, saliva collection bottles, sterile test tubes, test tube agitation equipment and equipment for determining the calcium content of the saliva. Saliva is stimulated by moving the subject chewgum or paraffin, in which case a 5% solution of glucose needed.

Procedure: 25 millimeters of gum stimulated saliva are collected. Part of this is analyzed for calcium content. The test is placed in an 8 inch sterile test tube with about 0.1 gms of powdered human enamel. The tube is sealed and shaken for 4 hours at body temperature after which it is again analyzed for calcium content.

The chewing of gum to stimulate the saliva produces sugar, if the paraffin is used, a concentration of about 5% glucose is added. The amount of enamel dissolution increases as the caries activity increases.

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Procedure: Saliva is collected before breakfast by having the subject chew paraffin. A tube snyder glucose agar is melted and then cooled to 50째C. The saliva specimen is shaken vigorously into the tube of agar and immediately mixed by rotating the tube. The agar is allowed to solidify in the tube and is incubated at 37째C. The color change of the indicator is observed after 24, 48 and 72 hours of incubation by comparison with an uninoculated tube against a white background.

F.

Dewar test:

Action: This test is similar to the fos dick calcium dissolution test except that the final pH after 4 hours is measured instead of the amount of calcium dissolved.

Summary & Conclusion The etiology of dental caries is generally agreed to be a complex problem complicated by many factors which obscure the indirect cause or causes. There is no universally accepted opinion of the etiology of dental caries.

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