Dental Caries

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Tooth Pain Causes and Treatment

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The first step in the origination of caries is the formation of a dental plaque (2). An increase in the amount of plaque is responsible for the ultimate development of gingivitis. A variety of factors interact in the generation of dental plaque and subsequent emergence of caries. These include the presence of a susceptible tooth surface, the proper microflora, and a suitable nutritional substrate for that flora. Several oral acid producing aerobic and anaerobic bacteria, including Streptococcus mutans, Lactobacillus acidophilus, and Actinomyces viscosus, are capable of initiating the carious lesion. However, S. mutans is consistently the only organism recovered from decaying dental fissures and is isolated in greater quantities from carious teeth than in non-carious ones (9). The overwhelming majority of microorganisms isolated from carious dentin are obligate anaerobes (10). The predominant organisms are Propionibac-terium, Eubacteria, Arachnia, Lactobacillus, Bifidobacteria, and Actinomyces. Some microorganisms also contribute to caries generation through synthesis of extracellular polysaccharides that adhere to the tooth surface (11). Fermentable carbohydrates are substrates for the microbial enzyme systems that produce organic acids (primarily lactic acid); sucrose is the optimum substrate for extracellular polysaccharide synthesis. In addition to providing a source of fermentable carbohydrate for conversion to acid, these extracellular polysaccharides greatly increase the bulk of the dental plaque and heighten its capacity as an area of bacterial proliferation.

TABLE 1 Microorganisms Associated with Periodontal Infections

Aerobic and facultative anaerobic

Anaerobic

I. Gram-positive cocci

I. Gram-positive cocci

Streptococcus spp.

Peptostreptococcus spp.

Beta-hemolytic streptococci

Peptostreptococcus micros

Streptococcus millerigroup (viridans)

II. Gram-negative cocci

Streptococcus mutans group

Veillonella spp.

II. Gram-positive bacilli

III. Gram-positive bacilli

Rothia dentcocariosa

Actinomyces spp.

Lactobacillus spp.

Eubacterium spp.

III. Gram-negative coccobacilli

Propionibacterium spp.

Actinobacillus spp.

Lactobacillus spp.

Actinobacillus actinomycentemcomitans"

IV. Spirochetes

Campylobacter spp.

Treponema denticola

Campylobacter rectus

Treponema sokranskii

Capnocytophaga spp.

V. Gram-negative rods

Eikenella spp.

Prevotella spp.

IV. Gram-negative rods

Prevotella intermedia

Pseudomonas spp.b

Prevotella nigrescens

Enterobactericeaeb

Porphyromonus spp.

Porphyromonus gingivalis

Bacteriodes spp.

Bacteriodes forsythus

Fusobacterium spp.

Fusobacterium nucleatum

Selemenomas sputigena

a Common in juvenile periodontitis. b Rare.

a Common in juvenile periodontitis. b Rare.

Ingestion of dietary carbohydrates plays a major role in caries initiation. The types of carbohydrates and the frequency of their ingestion are more important than the total quantity that is consumed. Frequent between-meal snacks, especially of sucrose-containing foods, enhance the carious process; sticky foods linger in the mouth and are potentially more harmful than non-sticky foods. Mechanisms that can shield the teeth include the cleaning action of the tongue, the buffering and protective activity of the saliva and its secretory immunoglobulin (IgA) (11).

Although caries can be arrested, none of the destroyed tooth structure will regenerate. Treatment involves removal of all affected tooth structure and proper replacement with a restorative material. Prophylaxis of caries includes ingestion of proper amounts of fluoride (about 1 mg/day) or local application of fluoride compounds. The fluoride forms a complex with the apetite crystals in enamel, as it replaces the hydroxyl group. It strengthens and increases acid resistance and promotes remineralization of carious lesions, and has also mild bacteriostatic properties. Daily brushing and mechanical removal of plaque, and adhering to proper diet that contains fewer carbohydrates are also important.

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