Dental caries are the result of progressive destruction of the mineralized tissues of the tooth. They are primarily caused by the acid products of glycolytic metabolic activity when the plaque bacteria are fed the right substrate. The basic characteristic of the carious lesion is that it progresses inward from the tooth surface, either the enamel-coated crown, or the cementum of the exposed root surface, involving the dentin and finally the pulp of the tooth (Figures 41–3 and 41–4). From there, infection can extend into the periodontal tissues at the root apex or apices.
Caries produced by plaque bacteria
Cariogenesis. A microscopic view of pellicle and plaque formation, acidification, and destruction of tooth enamel. (Reproduced with permission from Willey JM: Prescott, Harley, & Klein’s Microbiology, 7th edition. McGraw-Hill, 2008.)
Hemisected human tooth showing an advanced carious lesion on the right side of the crown and a much smaller lesion on the left side. Note the progression of the lesion through the enamel and dentin, pointing toward the pulp chamber in the center of the tooth.
The microbial basis of dental caries has been long established based on work first with Lactobacillus acidophilus and then S mutans. Although S mutans is now regarded as the dominant organism for the initiation of caries, multiple members of the plaque biofilm participate in the evolution of the lesions. These include other streptococci (S salivarius, S sanguis, S sobrinus), lactobacilli (L acidophilus, L casei), and actinomycetes (A viscosus and A naeslundii). The acid products produced by the interaction of S mutans with multiple species in the biofilm are the underlying cause of dental caries.
Members of biofilm produce acid
S mutans is most cariogenic
Dietary monosaccharides and disaccharides such as glucose, fructose, sucrose, lactose, and maltose provide an appropriate substrate for bacterial glycolysis and acid production to cause tooth demineralization. A possible edge for S mutans is its ability to metabolize sucrose more efficiently than other oral bacteria. It also has regulatory systems which stimulate the conversion of dietary carbohydrates to acid and intracellular storage polymers. Ingested carbohydrates permeating the dental plaque are absorbed by the bacteria, and are metabolized so rapidly that organic acid products accumulate and cause the pH of the plaque to drop to levels sufficient to react with the hydroxyapatite of the enamel, demineralizing it to soluble calcium and phosphate ions. Production of acid and the decreased pH are maintained until the substrate supply is exhausted. Upon exhaustion of the immediate source S mutans is able to survive long periods of sugar starvation. Obviously, foods with high sugar content, particularly sucrose, which adhere to the teeth and have long oral clearance times are more cariogenic than less retentive foodstuffs such as sugar-containing liquids. Once the substrate is exhausted, the plaque pH returns slowly to its more neutral pH resting level and some recovery can take place. This sets up a demineralization–remineralization cycle, which depends on carbohydrate refueling from the diet. With repeated snacking between meals, the plaque pH may never return to normal and demineralization dominates.
Demineralization is by acid production from dietary carbohydrate
Acid production facilitated by sticky carbohydrates
Demineralization–remineralization related to snacking
An additional factor with sucrose is that it is also used in the synthesis of extracellular polyglycans such as dextrans and levans by transferase enzymes on the bacterial cell surfaces. This polyglycan production by S mutans contributes to aggregation and accumulation of the organism on the tooth surface. Extracellular polyglycan may also increase cariogenicity by serving as an extracellular storage form of substrate. Certain microorganisms synthesize extracellular polyglycan when sucrose is available but then break it down into monosaccharide units to be used for glycolysis when dietary carbohydrate is exhausted. Some oral bacteria also use dietary monosaccharides and disaccharides internally to form glycogen, which is stored intracellularly and used for glycolysis after the dietary substrate has been exhausted; thus, the period of acidogenesis is again prolonged and the cariogenicity of the microorganism increased. These microorganisms can prolong acidogenesis beyond the oral clearance time of the substrate.
Extracellular polyglycans from sucrose important in adherence and carbohydrate storage
Acidogenesis prolonged by intracellular glycogen stores
The most common complications of dental caries are extension of the infection into the pulp chamber of the tooth (pulpitis), necrosis of the pulp, and extension of the infection through the root canals into the periapical area of the periodontal ligament. Periapical involvement may take the form of an acute inflammation (periapical abscess), a chronic nonsuppurating inflammation (periapical granuloma), or a chronic suppurating lesion that may drain into the mouth or onto the face via a sinus tract. A cyst may form within the chronic nonsuppurating lesion as a result of inflammatory stimulation of the epithelial rests normally found in the periodontal ligament. If the infectious agent is sufficiently virulent or host resistance is low, the infection may spread into the alveolar bone (osteomyelitis) or the fascial planes of the head and neck (cellulitis). Alternatively, it may ascend along the venous channels to cause septic thrombophlebitis. Because most carious lesions represent a mixed infection by the time cavities have developed, it is not surprising that most oral infections resulting from the extension of carious lesions are mixed and frequently include anaerobic organisms.
Extension to pulp and periapical locations complicate infections
Severe complications spread to bone or local fascia
Dental caries is the single greatest cause of tooth loss in the child and young adult. Its onset can occur very soon after the eruption of the teeth. The first carious lesions usually develop in pits or fissures on the chewing surfaces of the deciduous molars and result from the metabolic activity of the dental plaque that forms in these sites. Later in childhood, the incidence of carious lesions on smooth surfaces increases; these lesions are usually found between the teeth. The factors involved in the formation of a carious lesion are (1) a susceptible host or tooth, (2) the proper microflora on the tooth, and (3) a substrate from which the plaque bacteria can produce the organic acids that result in tooth demineralization.
Greatest cause of tooth loss in children and young adults
Require microflora and suitable substrates for organic acid production
The newly erupted tooth is most susceptible to the carious process. It gains protection against this disease during the first year or so by a process of posteruptive maturation believed to be attributable to improvement in the quality of surface mineral on the tooth. Saliva provides protection against caries, and patients with dry mouth (xerostomia) suffer from high caries attack rates unless suitable measures are taken. In addition to the mechanical flushing and diluting action of saliva and its buffering capacity, the salivary glands also secrete several antibacterial products. Thus, saliva is known to contain lysozyme, a thiocyanate-dependent sialoperoxidase, and immunoglobulins, principally those of the secretory IgA class. The individual importance of these antibacterial factors is unknown, but they clearly play some role in determining the ecology of the oral microbiota.
Saliva protects by mechanical flushing and multiple chemical actions
Proper levels of fluoride, either systemically or topically administered, result in dramatic decreases in the incidence of caries (50-60% reduction by water fluoridation, 35-40% reduction by topical application). In the case of systemic fluoridation, the protective effect is thought to result from the incorporation of fluoride ions in place of hydroxyl ions of the hydroxyapatite during tooth formation, producing a more perfect and acid-resistant mineral phase of tooth structure. Topical application of fluoride is believed to achieve the same result on the surface of the tooth by initial dissolution of some of the hydroxyapatite, followed by recrystallization of apatite, which incorporates fluoride ions into its lattice structure. Another important mode of action, namely, the inhibition of demineralization, and the promotion of remineralization of incipient carious lesions by fluoride ions in the oral fluid, has more recently been proposed as an important anticaries mechanism of fluoride, perhaps more important than the other proposed mechanisms. In any event, fluoridation represents the most effective means known for rendering the tooth more resistant to the carious process.
Fluoride produces more acid-resistant mineral phase of tooth