Presentation on theme: "PREVENTION II “CARIOLOGY’. HISTORICAL OVERVIEW General understanding of cause of dental caries has not changed since Miller developed the chemoparasitic."— Presentation transcript:
PREVENTION II “CARIOLOGY’
HISTORICAL OVERVIEW General understanding of cause of dental caries has not changed since Miller developed the chemoparasitic theory over 100 years ago: –Acid is produced by metabolism of dietary carbohydrates by oral bacteria. –Acid dissolution of the mineral phase of the tooth. –Secondarily, the organic phase of enamel and dentin is broken down.
KEY FEATURES Dental caries has a multi-factorial causation. Dental caries is an oral infection. Dental caries is a dynamic process. Dental caries can be modified by protective factors.
MULTI-FACTORIAL PROCESS Involves the interaction of host factors (tooth surface, saliva, acquired pellicle), diet, and dental plaque (biofilm). Caries does not occur in the absence of either plaque or dietary fermentable carbohydrates. Therefore, caries must be considered a dietobacterial disease. Dental caries can be conceptualized as an interaction between genetic and environmental factors, in which the biopsychosocial components are expressed in a highly complex, interactive manner.
CARIES IS AN ORAL INFECTION Germ free rats that were fed high sucrose containing diets do not develop dental caries. When the same animals were infected with specific strain of micro-organisms, caries developed. Experiments also document that micro-organisms could be recovered from a carious lesion, isolated, cultured, and used to infect caries- free animals, resulting in caries. Antibiotics have been shown to reduce the incidence and severity of caries in experimental animals.
GENETICS In the past the importance of genetic factors has been minimized primarily because the disease was essentially present in the entire population, thus not allowing genetic differences among individuals to manifest themselves. Genetic factors relate to: –tooth composition and structure –tooth morphology –arch form –tooth alignment – saliva flow rate and composition –oral physiology –endogenous microflora –food preferences –personality traits
TEETH Location, morphology, composition, ultra-structure, and post-eruptive age of the tooth. Teeth have a high resistance to caries, as evidenced by the low caries prevalence in primitive humans. Modern humans have challenged this natural resistance by modifying our diets.
ENAMEL SOLUBILITY Theoretically, if one could decrease the acid solubility of enamel, this would decrease the caries susceptibility of a tooth. However, studies have shown that even pure fluorapatite, which is the least acid-soluble form of calcium-phosphate species, demineralizes in the presence of a strong acid challenge. While enamel is composed mostly of mineral in the form of hydroxyapatite, it also contains other inorganic and organic components.
MAJOR COMPONENTS OF ENAMEL
ENAMEL COMPOSITION Enamel composition reflects the composition of the physiologic fluid surrounding the developing tooth. Enamel composition at the surface also reflects the fluids of the oral environment as well. Evidence suggests that trace element composition in enamel, such as the amount of fluoride present as fluorapatite, is of relatively minor importance in the clinical expression of dental caries.
ENAMEL STRUCTURE Factors other than enamel composition affecting enamel solubility are crystal size and shape, and the proximity of the crystals. Enamel is composed of long, thin, crystallites (approximately 40 nm in diameter) that are bundled together to form enamel rods or prisms (approximately 4 microns in diameter) running from the dentin to the outer enamel surface. An organic matrix surrounds the prism, forming the prism sheath; this organic material composes about 5% of the tooth enamel by volume.
STRUCTURAL RESISTANCE The larger and more uniform the crystals, the less the specific surface area and reactivity (solubility). The more closely packed the crystals, the less space for water and thus diffusion pathways between crystals. Because of the spaces between crystals, enamel is a micro-porous material. Water between the crystals serves as a diffusion channel in which acids can diffuse into those spaces to attack the crystals. Therefore, the more closely packed the crystals, the less soluble the enamel.
POST-ERUPTIVE MATURATION Caries susceptibility is greatest immediately subsequent to eruption, and tends to decrease with age. Teeth undergo a post-eruptive maturation process that involves changes in the composition of the surface enamel. This is related to the demineralization-remineralization dynamic which will be discussed subsequently. During the demineralization process, the more soluble carbonate-rich apatite is preferentially lost and replaced by apatite lower in carbonate and higher in fluoride, assuming fluoride exists in the oral environment. These reprecipated crystals eventually grow to be larger than the original crystals, creating hypermineralized areas of enamel. This response of the enamel explains the decreased susceptibility to caries that occurs with age. The effectiveness of fluoride in caries prevention can be largely attributed to its ability to enhance the remineralization process.
SALIVA Salivary flow rate and composition are well recognized as important host factors that modify the caries process. Salivary tooth protection mechanisms include mechanical cleansing action, dilution and buffering plaque acids, anti-microbial properties, and providing inorganic and organic components that inhibit tooth demineralization and assist in the remineralization and repair process. Reduced or loss of salivary function is associated with dramatic increases in caries activity.
ACQUIRED PELLICLE The acquired pellicle, which is an acellular, essentially bacteria-free organic film of mucopolysaccrides that is deposited on teeth, occupies a critical position between the enamel surface and the biofilm which we refer to as the dental plaque. The formation of biological films, such as the pellicle, is ubiquitous in nature and precedes the formation of all biofilms. The pellicle is formed mainly by selective adsorption of salivary glycoproteins and proteins. These organic components of saliva have a high affinity for the enamel surface and rapidly adsorb to a clean (pumiced) enamel surface. The pellicle adheres to the enamel and acts as a diffusion barrier to protect the enamel from acid exposures of short duration, as in ingestion of acidic foods.
ACQUIRED PELLICLE If removed (by dental polishing) the pellicle requires a maturation period (7 days) before it becomes maximally protective against acids. The use of abrasive toothpastes and whitening products, as well as the abrasion from rubber cup prophylaxis, removes the pellicle, and can have an adverse effect on exposed tooth surfaces in increasing the probability of loss of tooth enamel by demineralization.
DIET The frequency of eating fermentable carbohydrates has been strongly associated with dental caries. Factors associated with diet and dental caries include the relative retentiveness of the food; the presence of protective factors in food, such as calcium, phosphate, and fluoride, and the type of carbohydrate. Complex carbohydrates (starches) are less cariogenic than simple carbohydrates (sucrose, glucose, and fructose).
SUCROSE The cariogenicity of sucrose is partly attributed to its contribution to the plaque bacteria’s ability to synthesize extracellular polysaccharides, which favors the accumulation of more bacteria. In studies using mutans Streptococci, plaque prepared from sucrose-containing cultures was found to have a markedly enhanced demineralization potential compared with glucose- grown plaque. The effect was attributed to an alteration of the diffusion properties of plaque due to the water-insoluble extracellular matrix (the glucan) synthesized from sucrose. The glucan permits greater penetration of dietary carbohydrates into the plaque.
THE PROCESS DIAGRAMMATICALLY
PLAQUE A number of endogenous oral microorganisms found in dental plaque can contribute to the caries process: –mutans streptococci (S. mutans, and S. sobrinus –S. sanguis and salivarius, and other non-mutans species –Lactobacilli species –Actinomyces species –yeast It is important to remember that even in a caries free mouth, 1 ml of saliva contains ,000 endogenous microorganisms.
PLAQUE Initial colonization of the plaque biofilm on a tooth surface is predominately S. sanguins and S. salivarius. Shortly after initial adherence to the tooth, Streptococcus mutans becomes a major component of the biofilm. Streptococcus mutans is generally considered the most virulent of the organisms that participate in dental caries. Through time there is a maturation of the plaque characterized by a shift from a predominated aerobic Gram positive cocci to anaerobic Gram negative rods. If a lesion progresses to cavitation, and particularly as it advances into the dentin, lactobacilli seem to be favored because they thrive in this sheltered, highly acidic environment. Thus the process of enamel demineralization and eventual cavitation is related to bacterial succession, in which one organism initiates or pioneers the plaque, while subsequently another organism takes over.
PLAQUE pH The pH of dental plaque is normally close to neutrality. When a fermentable carbohydrate (such as sucrose) is ingested, the plaque bacteria produce acids which causes a drop in the pH level. pH levels lower than 5.5 can initiate demineralization and after a sucrose rinse, the pH value can fall to as low as 4.0. At these low pH levels, calcium and phosphate ions begin to dissolve out of the enamel and will continue to do so as long as the environment remains sufficiently acidic.
STEPHAN CURVE Approximately twenty minutes after ingestion of sucrose, and once the supply of fermentable nutrients is exhausted, the bacterial will cease to produce acids and the plaque pH will gradually return to a slightly alkaline resting level.
DYNAMIC NATURE OF CARIES The earliest macroscopic evidence of caries of a smooth enamel surface is a small opaque white region; referred to as a white spot lesion. Its presence is an indication that there is a localized decrease in mineral content of the enamel, although the surface is still hard when examined with a dental explorer. In ground section of a white spot lesion, viewed under polarized light microscopy, four different zones can be identified.
PHOTOMICROGRAPH OF WHITE SPOT LESION
RADIOMICROGRAPH OF WHITE SPOT LESION
WHITE SPOT LESION #1 SURFACE ZONE One of the the fascinating features of this initial lesion of caries is that most of the demineralization begins to occur at a subsurface level, leaving the surface zone relatively unaffected.
WHY SUBSURFACE? It is theorized that the mineral dissolved from this subsurface zone is pumped toward the surface and acts to remineralize the surface zone by precipitation of minerals from this underlying layer. The surface layer of enamel is also more highly mineralized than the subsurface layer to begin with, and thus may be more resistant to acid attack. Although the surface layer is relatively unaffected, it is more porous at this stage than it was before the lesion was initiated.
WHITE SPOT LESION #2 BODY OF THE LESION This is the largest portion of carious enamel in the white spot lesion. It has often lost one-quarter of its original mineral content.
WHITE SPOT LESION #3 DARK ZONE This zone is very porous, and has experienced a mineral loss of about 6%.
WHITE SPOT LESION #4 TRANSULENT ZONE This is the advancing front of the enamel lesion. It is more porous than sound enamel but less porous than the dark zone.
DEMINERALIZATION:REMINERALIZATION Eventually, the relatively unaffected surface zone becomes demineralized and the rate of the progress of the lesion increases rapidly. This surface zone appears to control, to a large extent, the rate of progression of a lesion. If the surface layer above a lesion can be ‘strengthened’ through fluorides or mineralizing solutions, the lesion can become arrested, and the process reversed. Or if the surface area becomes and remains plaque-free, then the saliva itself, being supersaturated with regard to calcium and phosphate, can remineralize the initial lesion as well. The average time for the dynamic carious process to proceed from the stage of a white spot lesion to clinical detectable caries is approximately two years. A high frequency of exposure to sucrose could greatly accelerate the process of demineralization, while exposure to fluorides may favor remineralization.
DEMINERALIZATION:REMINERALIZATION The enamel surface is in a state of dynamic equilibrium with its local oral environment (plaque fluid and saliva) that involves the constant movement of ions in and out. As the pH of plaque drops, a point is reached where the mineral phase of enamel begins to dissolve. This critical point is estimated to be between 5.0 and 6.0
IMPLICATIONS FOR RADIOGRAPHIC DIAGNOSIS Laboratory studies demonstrate that histologically the lesion must penetrate just into the dentin before evidence of a carious lesion is observed on a routine bite- wing radiograph At this stage the lesion is observed on the radiograph as a small triangular region of radiolucency in the outer enamel.
RADIOGRAPH VERSUS HISTOLOGY
PRIMARY TEETH In the primary dentition, this understanding of the carious process suggests a significant problem. Primary molars tend to have broad, flat contact areas in contrast to the contact ‘points’ in the permanent dentition. This exposes a large interproximal area of primary teeth to stagnation which favors bacterial colonization. Additionally, primary enamel thickness is about one-half that of permanent enamel, and the pulp chamber is relatively larger. Studies indicate that the rate of progression of a lesion through primary enamel is much faster compared with an equal distance through permanent enamel.
CLINICAL IMPLICATIONS FOR CARIES DIAGNOSIS A carious lesion which could not be detected by explorer or radiographically, has already penetrated halfway through the enamel. A lesion which can be observed on a bite- wing radiograph has probably already advanced into the dentin. This is especially true in the primary dentition.
CARIES PROGRESSION Although the enamel surface is clinically intact when the lesion reaches the enamel-dentin junction, acids can diffuse into the dentin via carious enamel and, together with other clinical stimuli, can cause the dentin and pulp to respond. Lateral spread along the enamel-dentin junction produces a broad-based lesion that follows the curvature of the dentinal tubules so its narrow apex approaches the pulp. In the dentin there is a zone of sclerosis walling off the lesion from the surrounding normal dentin. The pulp also reacts to the advancing lesion by laying down a region of reparative dentin.
CARIES PROGRESSION The body of the dentinal lesion may at first be uninfected, since bacteria cannot gain access until a cavitation forms in the surface enamel. At this stage, if preventive measures are instituted, the lesion can remain static or even regress. Once the enamel lesion becomes cavitated, bacteria can penetrate into the tissue, and the rate of progression of the dentin lesion increases. At this time, proteolytic enzymes of the bacteria destroy the organic collagenous matrix of the enamel and dentin, and the characteristic dental cavity exists.
CARIES PROGRESSION IN A FISSURE
SUMMARY Dental caries has a multi-factorial causation. Dental caries is an oral infection. Dental caries is a dynamic process. Dental caries can be modified by protective factors.