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PTHL 312b: Oral and Maxillofacial PathologyDental Caries, Inflammatory Pulp, and Periapical Diseases

139

Topic 9:

Teeth and Jaws: Dental Caries, Inflammatory Pulp, andInflammatory Periapical Conditions

Dental Caries

IntroductionIncidence of Dental CariesEtiology and Pathogenesis of Dental CariesHistopathology of Dental Caries

Inflammatory Pulp Diseases

IntroductionInflammatory Diseases of the PulpPulp HyperemiaAcute PulpitisChronic PulpitisChronic Hyperplastic PulpitisPulp Necrosis

Inflammatory Periapical Diseases

General FeaturesAcute Inflammatory Periapical DiseasesChronic Inflammatory Periapical Diseases

ReferencesLearning Guide

ObjectivesDefinitionsWorkbook

Web Site

ImagesStudy QuestionsTerms and Definitions “Flash Cards”Disease Features “Flash Cards”Web Reader with ImagesReader and Learning Guides PDFs

PTHL 312b: Oral and Maxillofacial PathologyDental Caries, Inflammatory Pulp, and Periapical

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Dental Caries

Introduction

Dental caries has afflicted humans longer than any other disease. Dental caries was not prominent in theearliest humans; it appeared around 12,000 B.C. or about 14,000 years ago. From that time to the present,dental caries has afflicted almost all human populations, all socioeconomic levels, and all ages. The pain andother suffering this disease has caused has been chronicled in literature, art, and movies.Understanding dental caries has stimulated much research. The first studies were published in the 1870’sand have continued uninterrupted to the present. As the result of these efforts, control of dental caries ismore promising that at any time. Prevention of dental caries has spawned an industry with sales of over $20 billion each year. While this attention has decreased the incidence of this disease in United States’ young people, its incidence remains high in the 50% of the U.S. population and in most of the world’s under developed countries.

Incidence of Dental Caries

The incidence of dental caries has been studied most in American white populations. The results showdental caries to be most prevalent chronic disease in this population. The disease affects all regardless of location, sex, age, or social stratum. The disease starts in young people just as soon as teeth erupt. About90% of youngsters are affected by age 14. As mentioned earlier however, the incidence of caries isdecreasing in this young population in the U.S. and in other Western countries. This downward trend isexplained by increased fluoridation of community water supplies and by increased attention to regular careat dental offices and at home.Isolated populations who have not adopted eating habits of the West have long been known to decreaseincidence of dental caries. Inuits, some African natives, and inhabitants of rural India are examples of such“immune” populations. Examination of teeth shows considerable abrasion of the occlusal surfaces indicatingconsumption of a coarse, abrasive diet. It is not uncommon to observe teeth abraded down to the contact points between adjacent teeth. This no doubt explains the fact that dental caries in these “primitive” populations is restricted to the interproximal areas below contact areas where food impaction may occur.While decreased incidence has been observed in the U.S. young, caries rates are increasing in Third Worldcountries as they adopt Western diets. It is also increasing in the U.S. elderly. In this population, retention of teeth into old age with accompanying exposure of root surfaces, has led to an increase in “cemental caries.”

Etiology and Pathogenesis of Dental Caries

From the earliest days of dental caries research, the role of acids and microorganisms in its development wasappreciated. Carious lesions were produced in extracted teeth by exposing their crowns to acid. Themicrobial source of acid soon followed. A quotation from a past standard pathology text said it all whendental caries was described as “…a microbial disease of the calcified tissues of the teeth, characterized bydemineralization of the inorganic portion and destruction of the organic substance of the tooth.” While thisdescription accurately summarizes the etiology of dental caries, the emergence of two theories led to thisunified concept.

Acidogenic Theory

In 1882, a pioneer in caries research, Willoughby Miller promulgated the acidogenic theory of dental caries,a theory that has survived pretty much unchanged until today. In it Miller, recognized two stages in thecarious process: decalcification of enamel and dissolution of protein interrod substances. Decalcification of enamel, the first step in the process, was, Miller believed, caused by metabolism of carbohydrate foodresidues by microorganisms. In the early days, Lactobacillus acidophilus was thought to be the primeculprit. More recently, Streptococcus mutans and other microorganisms have been implicated as well.Whatever organisms are involved, the calcified portion of enamel is dissolved exposing the protein rodsheaths to degradation as well.

PTHL 312b: Oral and Maxillofacial PathologyDental Caries, Inflammatory Pulp, and Periapical

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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.

Combination Theory

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

Enamel 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.