Dental Caries, Pulp and Periapical Lesions
The World Health Organization (WHO) defines caries as a localized post-eruptive, pathological process of external origin involving softening of the hard tooth tissue and proceeding to the formation of a cavity.
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.
Willoughby Miller in 1882 suggested that dental decay is a chemoparasitic process. He believed that caries was caused by a variety of microorganism and the acids in the oral cavity were synthesized by the action of microorganisms.
He recognized four important factors in his study of the carious process which are: role of microorganisms, role of carbohydrate substrate over the tooth surface, role of acids and the role of dental plaque.
According to Miller, the carious process occurs in two distinct steps: in the initial stages there is decalcification of enamel and destruction of dentin, and in the second stage there is dissolution of the softened residue of the enamel and dentin.
The acidic attack which causes destruction and dissolution of the residue is carried by the proteolytic action of the bacteria. This two-step process is supported by the presence of carbohydrates, microorganisms and dental plaque.
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 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.
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.
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.
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 initial work on the proteolytic theory was done by Heider and Bodecker in 1878 and Abbott in 1879. Studies showed that the organic portion of the tooth plays an important role in the development of dental caries.
He believed that the yellow pigmentation that is characteristic of caries was due to pigment produced by the proteolytic organisms. He also proposed that the Staphylococcus plays a vital role in initiating proteolytic activity.
Pincus in 1949 proposed that the proteolytic breakdown of the dental cuticle is the first step in the carious process. He proposed that the Nasmyth’s membrane and the enamel proteins are mucoproteins, which are acted upon by the sulfatase enzyme of the bacilli yielding sulfuric acid. The sulfuric acid thus produced combines with the calcium of the hydroxyapatite crystal and destroys the inorganic component of the enamel.
Chelation is a process in which there is complexing of the metal ions to form complex substance through coordinated covalent bond which results in poorly dissociated and/or weakly ionized compound. Chelation is independent of the pH of the medium.
The proteolysis-chelation theory considers dental caries to be a bacterial destruction of organic components of enamel and the breakdown products of these organic components to have chelating properties and thereby dissolve the minerals in the enamel even at the neutral/alkaline pH. Mucopolysaccharides, lipids and citrates may also act as secondary chelators.
This theory proposes that if there is a very high concentration of sucrose in the mouth of a caries-active individual, there can be formation of complex substances like calcium saccharate and calcium complexing intermediaries by the action of phosphorelating enzymes. These complexes cause release of the calcium and phosphorus ions from the enamel and thereby resulting in tooth decay.
According to this theory few odontoblasts, within the pulp of few certain teeth are damaged by the autoimmune mechanisms, leading to a compromised defense mechanism and the loss of integrity of enamel or dentin. These targeted sites are potential sites for the development of carious lesions.
This theory is based on the fact that plaque bacteria produces enzymes. Enzymes involved may include phosphatase (dissolves apatite), chondroitin sulfatase (dissolves dentinal chondroitin sulfate), hyaluronidase (dissolves dentinal hyaluronic acid) and proteases (dissolve dentinal collagen). All these enzymes are produced by plaque bacteria.
This theory is a combination of the acidogenic and the enzyme theories. It is believed that the acids produced have a major role in enamel dissolution and the enzymes probably play a greater role in dentinal dissolution.
This theory was proposed by Levine in 1977. According to this theory, there is a chemical relationship between enamel plaque and the factors which determine the movement of minerals from saliva/plaque to enamel and vice versa, which was termed as the ionic see-saw mechanism.
Levine proposed that the demineralization and remineralization of enamel is a continuous process. If in a given interval of time, more ions leave the enamel than enter it, then there is a net demineralization, which heralds the beginning of the carious process. It was proved that the ions are constantly exchanged between enamel and plaque. This theory emphasizes the importance of pH of plaque, calcium and phosphate ion concentration at the interphase and fluoride ion concentration.
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.
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 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.
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.
The buffer capacity of both unstimulated and stimulated saliva involves three major buffer systems: the bicarbonate (HCO−3), the phosphate, and the protein buffer systems. These systems have different pH ranges of maximal buffer capacity. The bicarbonate and phosphate systems have pH values of 6.1–6.3 and 6.8–7.0, respectively.
Since most of the salivary buffering capacity operative during food intake and mastication is due to the bicarbonate system, sufficient saliva flow provides the oral cavity with the neutralizing components.
The phosphate and protein buffer systems make a minor contribution to the total salivary buffer capacity, relative to the bicarbonate system. The phosphate system is, in principle, analogs to the bicarbonate system but without the important phase-buffering capacity, and it is relatively independent of the salivary secretion rate.
The buffer effect of saliva is influenced by the hormonal and metabolic changes, as well as by altered general health. It is generally accepted that the buffer effect is greater in men than in women (Heintze et al, 1983). In women, the buffer effect decreases gradually, independent of flow rate, toward late pregnancy and promptly recovers after delivery. Introduction of either hormone replacement therapy in menopausal women (Laine and Leimola-Virtanen, 1996) or low-dose oral contraceptives (Laine et al, 1991) can slightly increase the buffer capacity.
Carbonic anhydrases (CAs) participate in the maintenance of pH homeostasis in various tissues and biological fluids of the human body by catalyzing the reversible hydration of carbon dioxide. Recent research suggests that salivary CA VI plays a role in protecting the teeth from caries (Kivela et al, 1999a, b). CA VI has been reported to bind to the enamel pellicle and retain its enzymatic activity on the tooth surface.
It is also believed that the urea and saline in saliva become hydrolyzed to produce ammonia and the later can cause rise in the salivary pH. This rise in pH can counter the attacks on the tooth surface during the progression of caries.
The primary oral innate defense factors are peroxidase systems, lysozyme, lactoferrin, and histatins. In vitro studies have shown that these proteins are known to limit bacterial or fungal growth, interfere with bacterial glucose uptake or glucose metabolism and promote aggregation and, thus eliminate bacteria. Hanstrom et al (1983) and Tenovuo and Larjava (1984) reported that the salivary peroxidase and myeloperoxidase systems eliminate H2O2, which is highly toxic for mammalian cells.
The immunoglobulins, IgG, IgM, IgA, and secretory IgA (sIgA), form the basis of the specific salivary defense against oral microbial flora, including Streptococcus mutans. The most abundantly available immunoglobulin in saliva is dimeric slgA, which is produced by plasma cells located in the salivary glands. Two IgA subclasses are present in saliva; IgAl forms the major component of immunoglobulins, although the relative amount of IgA2 is higher in saliva than in other secretions (Tappuni and Challacombe, 1994).
The IgG concentration decreases to non-detectable levels after some months but appears again after tooth eruption (Brandtzaeg, 1989). Low concentrations of IgG can be detected in stimulated parotid saliva (Brandtzaeg, 1989), but most of the IgG detected in whole saliva enters the mouth from the gingival crevicular fluid, thus originating from sera.
In most children above 3 years of age, salivary IgAs against S. mutans can be detected, and their amount increases with the length of exposure (Smith and Taubman, 1992). Salivary Igs can bind to the salivary pellicle, and they are found also in dental plaque (Newman et al, 1979; Fine et al, 1984). In the oral cavity, immunoglobulins act by neutralizing various microbial virulence factors, limiting microbial adherence, and agglutinating the bacteria, as well as by preventing the penetration of foreign antigens into the mucosa. IgGs are also capable of opsonizing bacteria for phagocytes, which are reported to remain active in dental plaque and saliva (Scully, 1980; Newman, 1990).
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.
The main etiological agent in occlusal and pit and fissure caries is the S. mutans. Deep dentinal caries is commonly associated with lactobacilli, certain gram-positive anaerobes and filaments such as Eubacterium and Actinomyces.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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).
Figure 4 The early stages of a proximal carious lesion. The surface of the enamel reveals a bluish-black hue with no discontinuity of the enamel surface. Courtesy: Department of Oral Medicine and Radiology, MCODS, Mangalore
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.
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).
• Any carious lesion usually an incipient one may become arrested, if there is a change in oral environment. Arrested caries, clinically appears as a dark brown pigmentation with smooth surface, referred to as ‘eburnation’, which is a Latin word that means arrested caries.
Nursing bottle caries: A type of acute carious lesion, which occurs among those children who take milk or fruit juice by the nursing bottle, for a considerably longer duration of time, preferably during sleep.
The predominant group of microorganism is streptococci. Among these strains S. mutans is responsible. These are gram-positive organisms which are round or ovoid. These may appear rod shaped, non-sporulating and non-motile. These can be cultured on blood agar with formation of refractory colonies measuring 0.5–1.5 mm at 37°C. These are pathogenic to human beings.
The three common organisms seen to be associated with secondary caries are S. mutans, lactobacilli and Actinomyces viscosus. Fontanna et al (1996) observed a definite relationship of S. mutans and secondary caries. S. mutans is also present in saliva and in dental plaque in individuals with rampant caries due to xerostomia as well as in children nourished with bottle milk. S. mutans and lactobacilli have been found to increase in significant numbers in the plaque as well as dentin of teeth restored with amalgams having marginal defects wider than 40 μm.
Fitzergerald et al (1994) were of the view that in association with these three major microorganisms, others also played a role in secondary caries. They found S. mutans, S. sanguis and S. salivarius in 35%, 24% and 14% of growth positive samples respectively. Other isolates like S. gordonii, S. milleri, S. oralis and S. mitis were also recognized. Certain organisms, which occurred very frequently were Propionibacterium, Bifidobacterium, Eubacterium and Peptococcus. Actinomyces were found in 46% of the samples. A. viscosus and A. naeslundii were most prevalent followed by A. israelii and A. odontolyticus.
S. mutans can adhere to the tooth surface by glucan which is produced by utilization of dietary sucrose. These organisms ferment mannitol and lactose with the production of acid. These can take up dietary sucrose and breakdown into glucose and fructose by means of the enzyme, invertase. Finally glucose and fructose is broken down to lactic acid. These have the ability to store glucose and fructose from degradation for the synthesis of acids in the absence of dietary sucrose.