PTHL 312b: Oral and Maxillofacial PathologyDental Caries, Inflammatory Pulp, and Periapical
Acid-producing bacteria are attached to teeth by plaque proteins that protect them.
Carrying Miller’s theory forward to modern times, scientists have found that microorganisms becomeattached to tooth surfaces by adhesive proteins in dental plaque where they are protected from theimmunologic properties of saliva. Thus, if plaque is allowed to form, microorganisms attach and metabolizefood debris forming decalcifying acids. Placed in the modern context, Miller’s acidogenic theory explainsthe development of smooth surface caries in which plaque becomes attached to the labial, lingual, mesial, or distal tooth surfaces.
The Proteolytic Theory
Another theory was developed presumably to explain the origin of caries of the occlusal surfaces (pit andfissure caries). The idea here is that bacteria first invade malformations commonly found in enamel. Themost common of these are incompletely calcified occlusal grooves and protein lamellae that extend throughenamel. As bacterial acids accumulate in these sites, surrounding protein is destroyed exposing calcifiedenamel to bacterial acids.
While bacterial acids are the initiating agent in both theories, the proteolytic theory starts with destruction of protein rather then calcified enamel. Actually both may be correct. Perhaps the acidogenic theory operates inthe etiology of smooth surface caries while the proteolytic theory better explains pit and fissure caries.
Histopathology of Dental Caries
Except in old people and those suffering from periodontal disease, the exposed surfaces of teeth are coveredwith enamel. As a consequence of this anatomic fact, most carious lesions must start by attacking the body’shardest tissue—enamel.
Smooth Surface Enamel Caries
On smooth surfaces, enamel decalcification produces cone-shaped lesions, the tips pointing at thedentinoenamel junction (DEJ) and the wide ends facing the external surface. Since most enamel rods areoriented perpendicular to the external surface and since destruction of rods follows them, the cariouslesion’s long axis is also perpendicular to the tooth surface.Eventually, the cone-shaped lesion contacts dentin along the DEJ. At first only a small spot of dentin isexposed to the action of carious microorganisms. At this early stage, before dentin caries is far along,removal of the lesion and restoration of the tooth can be accomplished with minimal tooth structuresacrifice.Microscopically, several zones have been identified. It is not important to recount them except to state thatin the early stages of enamel caries, while enamel is still intact, the lesion is darker than surroundingunaffected enamel. The lines of Retzius, are much more conspicuous here than in surrounding enamel.Incremental lines on individual enamel rods are also affected, a change indicating that rod dissolution is notfar away.There is an important clinical principle that is based on the microscopic changes summarized above: earlyenamel caries usually cannot be detected upon clinical examination; however, the disease can be detected onradiographs.
Pit and Fissure Enamel Caries
While the process is the same, the effect of pit and fissure caries is significantly different from that of smooth surface caries. Because enamel rods diverge at the base of occlusal pits and fissures, a carious lesionwill, when it reaches the DEJ, infect a large area of dentin. In pit and fissure caries, the small end of theinfecting cone is located at the occlusal surface while its broad end is located at the DEJ. Removal of theselesions and subsequent restoration of the tooth requires sacrifice of considerable tooth structure.