Tooth Decay Treatment in Hyannis, MA

Teeth are essentially indestructible under the correct conditions. However in the living person the teeth are continuously being assaulted by microbial challenges which make dental caries and other dental infections, primarily gingivitis and periodontitis, rank as the most universal affliction of man. The discomfort caused by these infections, and their enormous cost (ranking third in medical costs, only behind heart disease and cancer in the United States), give dental diseases this status despite their non-life-threatening nature. Even though these diseases are not life-threatening, they can drastically diminish quality of life, diet and nutrient intake, and systemic health.

Dental Caries and Genetic Profile
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Genetic factors can predispose the teeth to a higher incidence and severity of dental caries by affecting tooth morphology, resistance to infection, dental plaque retention and utilization, and sucrose metabolism. In the past, several inbreeding and inter-racial breeding studies have suggested no genetic effect on caries susceptibility [defined as the number of decayed, missing and filled teeth (DMFT)]. However, more recently, a genetic predisposition for dental caries has been reported.

Dental Caries and Twin Studies

Twin studies have provided evidence for genetic susceptibility to dental caries. Monozygotic (MZ) twins showed more similarities than dizygotic (DZ) twins in relation to caries incidence, especially for the lower anterior teeth and smooth surface lesions. The Minnesota Study of Twins Reared Apart (MSTRA) has provided the most persuasive evidence for genetic conditions and dental caries. In this study, caries susceptibility was more highly associated in MZ when compared to DZ twins. Similar heritability patterns were also observed for periodontal disease, IQ, religion, values and attitudes, personality, and interests. Nevertheless, some environmental factors, such as fluoride use, can overshadow genetic influences.


Dental Caries Diagnoses

Clinically, a dental caries lesion (also called a cavity) occurs when a hole appears on the tooth surface. However, when this is observed, dental caries has proceeded to the late stage. A clinically noticeable lesion, termed a white spot (which may not be detectable to the naked eye), may precede the carious lesion. Not all visible white spots are due to the initiation of the decay process. In addition, interproximal (between) tooth surfaces may only be visible with the use of a dental X-ray (radiograph), and the decay can go unnoticed in these areas until it is too late in the caries process .


Symptoms of Dental Caries

Pain is the chief complaint of the patient that causes them to seek dental treatment. This usually occurs when the decay in the dentin layer of the tooth approaches the innervated tooth pulp. Pain can be intermittent or continuous and dull or excruciating.


Diagnostic Tests
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Diagnostic tests for dental caries are non-invasive. This is due to the fact that the teeth are exposed to the environment and can be visualized by looking into oral cavity (mouth). During a clinical examination, a dental explorer is used by dental professionals to help diagnose dental caries. When the explorer is placed into a cavity it will usually stick into the decayed area. Dental radiographs (X-rays) are used to help the dental professional diagnose caries that cannot be viewed by the naked eye. Microbiologic diagnoses for Strep.mutans/lactobacilli infections are rarely sought. Primarily, it is acute pain that brings the patient to the dentist, which is almost always relieved by a dental restoration or extraction. Conventional dental therapy is based on response to symptoms; therefore knowledge of an underlying Sm infection would not change the treatment. The most accurate way to confirm a diagnosis of dental caries is by a histological examination; however this would require tooth extraction.


Dental Caries and Sugar

Dental decay is due to the irreversible solubilization (demineralization) of tooth mineral by acid, predominantly lactic acid, formed by plaque bacteria that adhere to teeth surfaces, after the consumption of foods that contain fermentable carbohydrates. When sucrose is ingested during meals, sufficient saliva is secreted to buffer the plaque pH and decay does not occur. In fact, studies show that as much as one-half of a pound of sucrose consumed daily at meals for two years was not associated with an increase in dental decay; however, when the same or lesser amounts of sucrose were ingested between meals, subjects developed new decay at the rate of about 3-4 tooth surfaces per year. Frequent sucrose ingestion increases the lengths of time that sucrose is available for fermentation and acid formation by plaque. Thus, eating frequency, the amount of sugar retained in the mouth particularly on the tooth surface, and the length of time that sugar is retained in critical areas, are more important than the total amount of sugars consumed.

Sucrose is required for the metabolism of caries-related Sm and many other acid-forming organisms. Almost immediately following exposure of these microorganisms to sucrose, they produce:

  1. Acid
  2. Intracellular polysaccharides, that provide a reserve source of energy for each bacterium, much like glycogen does for human cells
  3. Extracellular polysaccharides including glucans (dextrans) and fructans (levans)

Glucans are viscid substances that help anchor and stabilize the plaque onto the tooth. Fructans can act as an energy source for any bacteria having the enzyme levanase. Quantitatively, the glucans constitute up to approximately 20% of plaque by weight, levans about 10%, and bacteria the remaining 70 to 80%. The glucans and fructans are the major contributors to the intercellular plaque matrix.
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Sucrose fermentation produces a rapid drop in the pH, to 5.0 or lower, at the interface between plaque and enamel. When sucrose is consumed frequently, Sm, which has been distinctively linked to the initiation of dental decay, begins to flourish and become the principal bacterial organism in plaque. When the plaque pH value falls below 5.0-5.2, the salivary buffers are overwhelmed and lactic acid, which is an end-product of Sm metabolism, diffuses into the tooth and the enamel begins to dissolve, releasing calcium and phosphate ions from sites beneath the surface enamel. This low pH is derived from acid-producing bacterial organisms, and favors demineralization over a period of time, resulting in a cavity.

The tooth enamel (hydroxyapatite, Ca10(P04)6(0H)2) is permanently dissolved from these acids, particularly lactic acid, when these bacteria adhere to the tooth surface and form bacterial colonies or communities called “plaque”. Sm and other bacteria, such as lactobacilli, store sugars and continue to secrete acid long after the food has been swallowed. Dental plaque will continue to build up on the tooth surface, unless it is adequately removed.


White Spots on Teeth/White Lesions

Small lesions, called white lesions, may appear on the tooth. When white lesions were microbiologically sampled, a proportional and absolute increase in Sm levels were observed on both the white lesion and in the saliva of the individuals sampled. When these lesions advance to the cavity stage, Sm is seen infiltrating into the enamel crystals. Eventually, enough minerals are lost so that a cavitation occurs in the enamel, and if this enlarges so that it extends into the dentin, a partially enclosed system is then formed in which the pH value drops below 5.0. Under these acidic conditions, growth of a different microorganism called lactobacilli is favored, and these organisms succeed as the predominant flora in the carious lesion. Lactobacilli are the most acid tolerant of the plaque bacteria, but these organisms only predominate when the carious lesion has extended into the dentin layer of the tooth. This process provides the bacteria access to the inorganic elements (e.g., calcium and phosphate) needed for their nutritional requirements. This same search for nutrients may explain the extension of bacteria from the exposed crown of the tooth into the gingival sulcus (the area between the tooth and the gum tissue).