Challenge 2010

propound

Dental Caries Out-Line

Lecture Title : Etiology of Dental Caries Prof name : Dr. Ghada Maghaireh

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Etiology of Dental Caries Dr.Ghada Maghaireh BDS,MS,ABOD

Caries Mechanisms Through History Worms Humor Vital Chemical Parasitic Chemo-parasitic Proteolytic Proteolysis-chelation

Worms Probably the earliest reference to tooth decay and toothache came from the ancient Sumerian text known as the 'Legend of the W orm'. The text refers to the creation of the Heavens, the Earth, the Marshes and the latter created the Worm. The early history of India, Egypt, and the writing of Homer also make reference to the worm as the cause of toothache. The great surgeon of the Middle Ages, Guy de Cahuliac (13001368) still espoused the belief that worms cause dental caries.

Humoral Theory The legend of the worm faded over the early centuries as the Greek physicians advanced the humoral theory of disease. The four elemental humors of the body were blood, phlegm, black bile and yellow bile. According to Galen, the ancient Greek physician and philosopher, dental caries is produced by internal action of acrid and corroding humors. An imbalance in these humors resulted in disease. Hippocrates, the 'Father of Medicine', while favoring the concept of humoral pathology also referred to the accumulated debris around teeth and to their corroding action. He, also, stated that stagnation of juices in the teeth was the cause of toothache. Vital Theory

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A vital theory of tooth decay was advanced, towards the end of the 18th century, which postulated that tooth decay originated, like bone gangrene, from within the tooth itself. A forerunner to this theory may have been the observation that internal resorption occurs in some teeth, or from the presence of deep, undermining carious lesions with but pinpoint surface involvement of a pit or fissure. Chemical (Acid) Theory In the 17th and 18th centuries, paralleling new insights into chemistry, there emerged the concept that teeth are destroyed by acids formed in the oral cavity. One suggestion was that putrefaction of protein gave rise to ammonia which was subsequently oxidized to nitric acid; another was that food in saliva decomposed to form sulfuric, nitric or acetic acids. Robertson in 1835 proposed that dental decay was caused by acid formed by fermentation of food particles around teeth. Since fermentation was at this time considered to be a strictly non-vital process, the possibility that microorganisms were involved was not, as yet, recognized. Parasitic (Septic) Theory Long before the demonstration of the germ theory of disease, the possibility that microorganisms can have toxic and destructive effects on tissue was postulated. These postulations spelled the end of the vital theory and gave rise to the idea that chemicals can destroy teeth. Early microscopic observations of scrapings from teeth and of the carious lesions, by Antoni van Leeuwenhoek (1632 1723), maker of the first powerful microscopes, indicated that microorganisms were associated with the carious process. In 1843, Erdl described filamentous parasites in the membrane removed from teeth. A few years later in 1847 Ficinus, a physician, also observed filamentous organisms in the enamel cuticle (surface protein membrane of teeth) and in carious lesions. Dental caries was thought to develop as a result of the infiltration and decomposition of the enamel cuticle, the interprismatic substance of enamel and finally dentin. Ficinus may have been one of the first to recognize the presence of an organic matrix in enamel. An explanation of the mechanism by which microorganisms caused decay was not attempted until later. Miller's Chemicoparasitic Theory
A synthesis of the ideas that acid and microorganisms were involved in the

etiology of dental caries did not occur until 1889 through a work by Miller.

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 Miller was able to assign to oral microorganisms the role of acid formation and

thus assigned a chemical role to flora which is the basis of his chemicoparasitic theory of dental caries.

The essential features of the chemicoparasitic theory are as follows: That the microorganisms of the mouth, by secretion of enzymes or by their own metabolism, degrade the fermentable carbohydrate food material so as to form acids. Carbohydrate food material lodged between and on surfaces of teeth is the source of the acid which demineralizes the lime salts of the tooth. He believed that starchy foods were more effective than soluble sugars. Thus, the enamel is destroyed by the acid of fermentation and the disintegrated enamel is subsequently mechanically removed by forces of mastication. After penetration of the enamel, the dissolution of dentin is brought about in the same manner with the organisms penetrating along the dentinal tubes. The final breakdown of dentin results from the secretion of proteolytic enzymes that digest the organic part of dentin and form a cavity. Critique of Chemoparasitic Theory Miller's chemoparasitic theory is the backbone of current knowledge and understanding of the etiology of dental caries but, Miller's chemoparasitic theory was unable to explain the predilection of specific sites on a tooth to dental caries. The initiation of caries on smooth surfaces was not accounted for by this theory. Miller worked with mixed cultures from saliva and with techniques that did not attempt to ascertain types of organisms present. Miller believed that dental caries was caused by a multiple species of bacteria. Miller's theory does not explain why some populations are cariesfree. The phenomenon of arrested caries is not explained by the chemico-parasitic theory. Miller believed that in some systemic conditions the inorganic salts within a tooth could be withdrawn and that the organicinorganic bonds would be weakened. He did not produce any experimental evidence that the adult tooth is subject to such systemic influences. The concept of tooth resistance while logical did not have any experimental support. Proteolytic Theory The surface coverings found on the tooth, in grooves and pits, are organic in nature; also, enamel contains small but significant amounts of organic material. These observations and the fact that carious lesions are characterized histologically by pigmentation, a phenomenon that was interpreted, without

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evidence, as being indicative of proteolysis, led to the development of the proteolytic theory. It described carieslike lesions that were initiated by proteolytic activity at a slightly alkaline pH, and considered that the process involved depolymerization and liquification of the organic matrix of enamel. To date no one has, under physiological conditions, successfully demonstrated significant loss of enamel tissue through proteolytic activity. Enamel is a highly structured tissue and the accessibility of organic material to enzymatic action before decalcification is restricted.

Enamel can be dissolved under physiological conditions only by demineralization with acids, chelating or complexing agents.

Proteolysis-Chelation Theory This theory proposed by Schatz et al. implies a simultaneous microbial degradation of the organic components (hence, proteolysis), and the dissolution of the minerals of the tooth by the process of chelation. According to the proteolyticchelation theory, dental caries results from an initial bacterial and enzymatic proteolytic action on the organic matter of enamel without preliminary demineralization. Such action, the theory suggests, produces an initial caries lesion and the release of a variety of complexing agents, such as amino acids, polyphosphates and organic acids. The complexing agents then dissolve the crystalline appetite. Less than 1% of mature enamel is organic in nature and the suggestion that this material upon degradation can give rise to a significant concentration of chelator sufficient to dissolve up to 96% mineral matter has no experimental support. Also, there is no substantial experimental evidence that the initial caries lesion stems from a breakdown of organic matter, i.e. due to proteolytic action. W hile proteolysischelation is an important biological phenomenon, its primary role in the etiology of dental caries has not been corroborated. Current Concept
Dental caries is a multifactorial disease. The term multifactorial is used to denote the interaction between the factors.

This model of viewing a disease process is applicable to dental caries.

PRIMARY (ESSENTIAL) FACTORS IN THE ETIOLOGY OF DENTAL CARIES Interaction between three primary factors is essential for the initiation and progression of caries:

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Microflora: Acidogenic bacteria that colonize the tooth surface. Host: Quantity and quality of saliva, the quality of tooth, etc. Diet: Intake of fermentable carbohydrates, especially sucrose. Time: Total exposure time to inorganic acids produced by the bacteria of the dental plaque.

Essentiality of Oral Bacteria

As early as in 1946 it was demonstrated that penicillin administered in the diet and drinking water to rats significantly reduced experimentally induced caries. This study provided concrete evidence for the earlier assumption that bacteria are involved in caries. Also, since the antimicrobial spectrum of penicillin primarily encompasses grampositive bacteria, this study narrowed the range of species suspected of causing dental caries. The study also provided a direction for studies in caries prevention in humans. The hypothesis that bacteria are a prerequisite for the initiation and progression of dental caries was clinched by Orland et al. [1954] in their classical germfree animal studies. Germ-free animals obtained by Cesarean delivery and directly transferred to a sterile isolator were fed sterile food. Twentytwo rats which were fed a cariogenic diet, and maintained in a germfree environment, were caries free.

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Of the 39 control rats fed the same diet but maintained in a conventional laboratory environment, and with no interference with their normal microflora, 38 developed carious lesions. This study laid to rest debates extending over a century about the role of bacteria in dental caries. Dental caries is a disease caused by oral bacteria. Esentiality of a Local Substrate

The study which indicated that a local substrate is essential for the oral flora to initiate dental caries was the tube feeding experiment of Kite et al. [1950]. Animals that were fed a cariogenic food via a stomach tube, unlike the controls that were fed the same diet ad libitum, did not develop caries. These studies proved that a local food supply for bacteria, ingested ad libitum by the host, is essential for the initiation of dental caries, and that blood plasma constituents cannot mediate this role systematically via salivary secretions or by other mechanisms.

SECONDARY FACTORS THAT AFFECT DENTAL CARIES A secondary or predisposing factor is the factor that control the rate of progress of a disease. Many secondary factors, such as salivary composition and flow rate, oral hygiene and diet influence the caries process. Secondary factors affect one or a combination of the following: increase or reduce the tooth (host) resistance to dental caries; increase or decrease the quantitative and qualitative nature of the oral microflora involved in dental caries; increase or reduce the cariogenicity of the local substrate. Saliva has many functions: cleansing effect, buffering capacity, provision of an environment saturated with calcium and phosphate, antibacterial action. These characteristics influence the rapidity at which caries develops. However saliva is not a prerequisite for caries initiation in the same sense that organisms, substrate, and the tooth are essential. Fluoride is an important trace element that affects the resistance of mineral of enamel to the caries process and enhances remineralization of incipient lesions. Fluoride deficiency potentiates caries since the host factor (tooth) cannot attain its maximum resistance to caries on a suboptimal intake. Other examples of secondary factors that influence dental caries are oral hygiene and dental plaque control. Meticulous oral hygiene may completely prevent caries (a perfectly clean tooth does not decay), but perfect oral hygiene cannot be attained. Oral hygiene affects caries but it is not a primary factor in caries.

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