Etiology

Dental caries is considered as the most prevalent disease in humans, second only to the common cold. Dental decay is complex and multifactorial. Various theories have been proposed to explain the etiology of dental caries.

The acidogenic theory, proteolytic theory and proteolysischelation theory have been the most discussed.

Role of carbohydrates

According to Miller’s observations, teeth decalcify when incubated in saliva and bread/sugar mixture and show no change when incubated with fat. His simple experiment demonstrated the cariogenic effects of carbohydrates.

However, the cariogenic potential of dietary carbohydrates varies on their physical form, chemical composition and frequency of intake. It is a well known fact that carbohydrates which have a slow clearance rate from the oral cavity are more cariogenic than those which have a higher clearance rate. The risk of caries incidence increases greatly if the dietary sugar is sticky in nature, and when there is increased frequency of ingestion of the sugars.

Polysaccharides are less easily fermented by plaque bacteria than monosaccharides and disaccharides. Glucose, sucrose and fructose which are highly fermentable have a greater role to play in the causation of dental caries. These sugars are readily broken down by the bacteria to produce acids that in turn cause the dissolution of the hydroxyapatite crystals of the enamel and dentin.

Sucrose is readily fermented by the cariogenic bacteria (mainly Streptococcus mutans) to produce acids, which can demineralize the tooth. S. mutans use sucrose to synthesize an extracellular insoluble polysaccharide with the help of the enzyme ‘dextran’, which helps in adhering the plaque firmly on to the tooth surface.

The pH of plaque falls to 4.5–5 in about 1–3 minutes of sugar intake. It is estimated that pH returns to neutral levels in approximately 30 minutes.

The physical nature of the diet intake also has a bearing on the incidence of carious lesions. Coarse fibrous foods aid in greater clearance rate from the oral cavity thereby minimizing the carious incidence. However, sticky refined food and sweetened soft drinks predispose to debris accumulation and the increased likelihood of carious lesions.

Role of microorganisms

Lactobacillus acidophilus along with a combination of other bacteria such as S. mutans and Actinomyces species are closely associated with the causation of dental caries. It is believed that a few types of bacteria may be intimately involved in the initiation of the carious process whereas some may be involved in the progression of the carious process.

Role of acids

Miller in his observations reported that many of the microorganisms in the oral cavity were capable of producing acids and these acids were usually present in deeper carious lesions. In many of the lesions studied, lactic acid was identified in carbohydrate saliva combined mixtures. A specific microorganism, Leptothrix buccalis, was isolated from the dentinal tubules, suggesting that the microorganisms and the acids may have a synergistic action to dissolve the organic portion of the tooth.

Role of dental plaque

Plaque as described by GV Black is a ‘gelatinous plaque of the caries fungus in a thin, transparent film that usually escapes observation, and which is revealed only by careful search’. It generally consists of salivary components such as mucin and desquamated epithelial cells and of microorganisms. However, long-standing plaque may accumulate to a perceptible degree in 24–48 hours. It is estimated that cariogenic plaque contains 2 × 10⁸ bacteria/mg weight.

The pH of plaque also varies in caries free and individuals with high caries activity. The pH is about 7.1 in caries free individuals and approximately 5.5 in individuals with high caries activity.

a. Tooth factor

b. Saliva

Morphology and position in arch

Compared to the smooth surfaces of teeth, deep pits and fissures are more prone to carious attack because of food lodgment and bacterial stagnation. Owing to their, complex occlusal morphology consisting of numerous pits and fissures, the permanent mandibular first molars followed by the maxillary first molars and mandibular and maxillary second molars are more prone to carious attack.

Apart from the morphology of the tooth, the position of the tooth in the arch has a heavy bearing on the incidence of carious lesions.

Irregularities in the arch form, crowding and overlapping of the teeth also favor the development of caries as these regions provide an excellent environment for plaque accumulation.

Partially impacted third molars are more prone to caries and so are the buccally or lingually placed teeth.

Chemical nature

The chemical components of enamel such as dicalcium phosphate dihydrate and fluorapatite make the enamel resistant to carious attack to a certain extent.

The presence of mineral ions such as Ca, F, Zn and Fe in higher concentrations, decreases the enamel solubility.

Higher the solubility of the enamel surface greater is the possibility of caries development. Hence, they can be seen in case of enamel hypoplasia.

The mineral content of enamel tends to increase with advancing age. Such teeth have an increased resistance to carious attack.

Composition

Hay et al (1982) and Lagerlof (1983) in their reports reiterated the fact that human salivary secretions are supersaturated on calcium and phosphate.

The concentrations of inorganic calcium and phosphorus show considerable variation within resting and stimulated saliva. Caries prone individuals have low calcium and phosphorus levels. Salivary proteins such as statherin, acidic proline-rich proteins (PRPs), cystatins, and histatins help in the maintenance of the homeostasis of the supersaturated state of saliva. According to Hay and Moreno (1989), statherin is present in stimulated saliva in concentrations sufficient to inhibit the precipitation of calcium and phosphate salts. Studies by Gibbons and Hay (1988) have shown that statherin may contribute to the early colonization of the tooth surfaces by certain bacteria, such as Actinomyces viscosus.

The acidic PRPs account for 25–30% of all proteins in saliva, and they have high affinity for hydroxyapatite in vitro (Hay and Moreno, 1989). The acidic PRPs bind free calcium, adsorb to hydroxyapatite surfaces, inhibit enamel crystal growth, and regulate hydroxyapatite crystal structure (Hay and Moreno, 1989).

The amount and quality of acidic PRPs and agglutinins are found to be different in caries-free and caries-active individuals as shown by the studies of Rosan et al (1982) and Stenudd (1999).

The role of cystatins in the caries process is still unclear. However, they may play a minor role in the regulation of calcium homeostasis in saliva. Phosphorylated and non-phosphorylated cystatins bind to hydroxyapatite.

Salivary flow rate, pH and buffer capacity

Saliva has the most important function of caries prevention by way of its flushing and neutralizing effects, commonly referred to as ‘salivary clearance’ or ‘oral clearance capacity’. As a thumb rule, the higher the flow rate, the faster the clearance and the higher the buffer capacity. Reduced salivary flow rate and the concomitant reduction of oral defense systems may cause severe caries and mucosal inflammation. Though, patients with impaired saliva flow rate often show high caries incidence (Papas et al, 1993; Spak et al, 1994) or caries susceptibility, it is still a mystery as to how much saliva is adequate enough.

The pH of saliva at which it ceases to be saturated with calcium and phosphorus is referred to as the ‘critical pH’. Normally, the critical pH is 5.5. Below this value, the inorganic content tends to demineralize. The normal pH of resting saliva is 6–7.

Quantity and viscosity of flow

The consistency or viscosity of the saliva and the amount of saliva produced has a significant influence on the incidence of dental caries.

The average person produces at least 500 ml of saliva over a period of 24 hours. The unstimulated flow rate is 0.3 ml/min, whereas the flow rate during sleep is 0.1 ml/min and during eating or chewing, it increases to 4.0 to 5.0 ml/min. Any reduction in this quantity of saliva as seen in diseases such as Sjögren’s syndrome, diabetes, etc. predisposes to dental caries.

Increased viscosity of saliva may hinder its natural cleansing action thereby promoting the deposition of plaque on the tooth surface. Likewise when the salivary viscosity is low, the amount of minerals and bicarbonates are inadequate thereby limiting its anticaries activity.

Physical nature of diet

It is believed that coarse and fibrous food helps in cleansing the debris from the tooth surface thereby minimizing the incidence of carious lesions. However, refined and sticky starchy food aid in the formation of dental caries.

Chemical nature of diet

It is a well-known fact that food with high refined carbohydrate content has the greatest potential to give rise to carious lesions.

The type of carbohydrate (monosaccharide, disaccharide or polysaccharide), frequency of intake and the time for which the ingested food remains stagnant in the oral cavity or on the tooth surface determine the incidence and severity of the carious lesions.

Animal studies have shown that sugar in the solid and sticky form is more harmful to the tooth than the same amount of sugar in a liquid form.

It is believed that vitamin B deficient individuals have lower incidence of dental caries. Vitamin B is essential for the growth of oral acidogenic flora and also serves as a component of coenzymes involved in glycolysis.

Vitamin D plays an important role in the normal development of teeth. Various studies have shown that the teeth are hypoplastic and usually have higher incidence of dental caries in vitamin D deficiency.

Teeth may be poorly calcified in individuals exposed to low doses of calcium during intrauterine life and infancy. Such poorly calcified teeth may be susceptible to carious attack. Higher levels of selenium is known to predispose to the carious lesions affecting permanent teeth.

Fluoride content in the diet has no significant role because of its metabolic unavailability. Therefore, the fluoride content in cooking salt and its effect on reducing the incidence of carious lesions is still questionable. However, fluoridated water minimizes the caries incidence.

Phosphates, molybdenum and vanadium in the diet helps in minimizing the incidence of carious lesions.

Role of heredity

Literature review reveals various studies to assess the genetic modifications in dental enamel, genetic modification of immune response, genetic regulation of salivary function and inherited alterations in sugar metabolism.

Bachrach and Young (1927) compared the caries incidence of monozygotic twins with same-sex dizygotic (93 pairs) and different-sex dizygotic (78 pairs) twins. Their results showed that the monozygotic twins had a more similar caries incidence than dizygotic twins and that different-sex dizygotic twins had the greatest variance. The authors concluded that heredity plays a subsidiary part in the incidence of caries. It is believed that heredity affects the dental decay only in as much as it controls the shape of a tooth and its pits and fissures and its position in the dental arch.

Senpuku et al (1998) and Acton et al (1999) have correlated specific HLA-DR types with binding S. mutans antigens and S. mutans colonization.

Acton concluded that ‘genes within MHC modulate the level of oral cariogenic organisms’.

Mariani et al (1994) in their study of celiac disease, enamel defects and HLA typing observed that HLA-DR3 was associated with increased enamel defects and HLA-DR5, 7 were associated with a reduced frequency of enamel defects. Studies have shown that the genes in the HLA complex are associated with altered enamel development and increased susceptibility to dental caries.

Role of immunity

Salivary IgA and immunoglobulins secreted in the gingival crevicular fluid such as IgG, IgM and IgA along with neutrophil leukocytes and macrophages play an important role in the prevention of dental caries. It is believed that the immune response exerted by the gingival crevicular immune system is more potent compared to the salivary immune mechanism.

Salivary IgA prevents S. mutans from adhering to the tooth surface. The IgG antibodies acting as opsonins, facilitate phagocytosis and the death of S. mutans by the action of macrophages and neutrophil leukocytes.

a. Pit and fissure caries

b. Smooth surface caries

c. Root surface caries

a. According to morphology of teeth

b. According to severity and progress

c. According to age pattern

d. According to rapidity of progress.

i. Pit and fissure caries (also called type-1 caries): Caries occurring on anatomical pits and fissures of all the teeth. The specific areas or surfaces involved include occlusal surfaces of molars (Figure 2) and premolars, buccal and lingual surfaces of molars (Figure 3) and lingual surfaces of maxillary incisors.

    The lesions are smaller in the beginning but become wider as they spread toward the dentin due to orientation of enamel rods.

    In these places there can be entrapment of food leading to fermentation of carbohydrates with lack of neutralization of acid produced by salivary buffers which leads to destruction of enamel and dentin. The enamel bordering the pit and fissure may appear opaque and bluish-white as it becomes undermined.

    Clinically these lesions appear brown or black, with little softening and opaqueness of the surface. When the lesion is examined by a fine explorer tip, a ‘catch point’ is often felt, where the explorer teeth catches the area.

    When the lesion reaches the dentinoenamel junction (DEJ), they spread laterally to cause undermining of the enamel.

ii. Smooth surface caries (also known as type-2 caries): These carious lesions occur on the smooth surfaces of the teeth (e.g. proximal surfaces or gingival areas of the buccal and lingual aspect of tooth).

    Proximal caries usually begins just below the contact point, and appears in the early stage as a well demarcated faint white opacity of the enamel without apparent loss of continuity of enamel.

    The white spot lesion becomes pigmented yellow or brown and it often extends buccally and lingually.

    The surrounding enamel becomes bluish white as the lesion continues to progress (Figure 4). The surface of the affected enamel becomes rough and later on, there is formation of a cavity (Figure 5).

iii. Root caries: Caries occurring at the cementoenamel junction or cementum. This occurs predominantly in the older age when there is gingival recession.

iv. Linear enamel caries: Caries occurring on the labial surfaces of anterior teeth. This is also known as ‘odontoclasia’. The caries occurs at neonatal zone because of trauma at birth or metabolic disturbances.

i. Incipient caries: Initial carious lesion limited to the teeth is called incipient caries and is characterized by a virtually intact surface but a porous subsurface (subsurface demineralization).

ii. Rampant caries: This is an acute fulminating type of carious process, which is characterized by simultaneous involvement of multiple number of teeth (may be all teeth) in multiple surfaces (Figure 6A, B).

iii. Arrested caries

iv. Recurrent caries: It occurs at the interface of tooth and restorative material because of many factors such as defective cavity preparation, microleakage and combination of these (Figure 7).

v. Radiation caries: One of the complications of radiotherapy of oral cancer lesions is xerostomia, which leads to an early development of widespread caries.

1. It has been variously attributed to prolonged use of

2. Invariably there is a prolonged habitual use of one of the above after 1 year of age, usually as an aid for sleeping at night or naptime.

3. Clinically presents as widespread destruction of deciduous teeth, most commonly the four maxillary incisors, followed by the first molars and then the cuspids if the habit is prolonged.

4. The lower teeth are not usually affected as they remain under the cover of the tongue, so the absence of caries in the mandibular incisors distinguishes this disease from ordinary rampant caries.

5. Both the nursing bottle and rampant cause early pulp involvement.

i. Acute dental caries

ii. Chronic dental caries