Oral diseases and cariogenicity

Oral refers to the mouth, and includes the teeth and gums (gingival) and their supporting tissues, the hard and soft palate, the mucosal lining of the mouth and throat, the lips, salivary glands, chewing muscles, and upper and lower jaw bones. Digestion begins in the oral cavity, and there are numerous supporting structures for the mouth including the nervous, vascular, and immune systems. Humans contract oral diseases for a number of reasons including genetics, poor hygiene, poor nutrition, alcohol and tobacco use, drug abuse (Shaner et al., 2006), and complications from other diseases such as diabetes (Sandberg et al., 2000, Twetman et al., 2002), cancer (Woo et al., 1993), obesity (Ritchie and Kinane, 2003), and osteoporosis (Norlen et al., 1993). Oral infections themselves may play a role in progressing pathogenesis of many systemic diseases in healthy individuals, ill patients, and those immunocompromised (Ridker et al., 1998). The theory is that oral infections, specifically periodontitis, elicit a hyper-inflammatory response. Indirect damage to the heart is caused by a release of inflammatory mediators eliciting different host-related reactions including release of C-reactive protein. This section reviews the two most common oral diseases - dental caries and periodontitis.

7.2.1 Dental caries

Dental caries has caused a great deal of discomfort and pain for the majority of mankind. This ubiquitous disease is usually not a fatal condition but has extolled tremendous costs to its victims including monetary and personal appearance. Untreated dental caries leads to periodontal disease, tooth loss, and potentially jawbone deterioration. Patients that ignore their dental cavities present symptoms of having difficulty to eat, swallow, speak, and possess a different social personality.

Human teeth are highly vascularized, calcified structures coated with a biofilm of indigenous and endogenous microorganisms (Fig. 7.1). This very nutritional substrate becomes the primary focus for dental caries. Caries lesions result from interactions of odontopathogenic bacteria that colonize the tooth surface (Fig. 7.2). In Fig. 7.2 oral microbial flora embedded in the plaque biofilm utilize dietary sugars to produce mutans and organic acids. The organic acids demineralize calcium and other cations from the tooth's hydroxyapatite crystals. The body counteracts demineralization by the salivary protein statherin binding calcium to remineralize the tooth's surface. Dental caries worsen if odontopathogenic bacteria overcome the body's ability to remineralize the tooth. Dairy proteins, especially caseinophosphopeptides, have a role similar to statherin. Severe periodontitis, an anaerobic infection in the gingival crevice and crevicular fluid, elicits an inflammatory reaction in gum tissue. Interaction with dietary constituents, especially sugar, enables the bacteria to form a plaque layer on the tooth's enamel surface. This microecological niche is colonized by millions of bacteria that secrete glycosyltransferases to metabolize carbohydrates consumed by the host and trapped in plaque matrix (Fig. 7.3). Odontopathogenic bacteria secrete glucans as constituents of their outer layer and this contributes to plaque build-up. The plaque layer reportedly contains over 20% carbohydrate by dry weight (Bowen et al., 1977).

The function of bacteria in causing dental caries is a source of continual controversy. The debate has been whether a specific bacterial species or a

Enamel

Gingival sulcus (space between gum and tooth)

Mandibular bone

Fig. 7.1 Tooth anatomy.

Enamel

Gingival sulcus (space between gum and tooth)

Gum (gingiva)

Mandibular bone

Fig. 7.1 Tooth anatomy.

Fig. 7.2 Exaggerated representation of the oral environment illustrating dental caries mechanisms.

Fig. 7.2 Exaggerated representation of the oral environment illustrating dental caries mechanisms.

Fig. 7.3 Dental plaque formation by mutans streptococci (SM). Dietary sugars are transported into SM by glucosyl transferases to be metabolized and excreted as polysaccharides (mutans). The plaque layer thickens as mutans accumulate on the tooth surface.

Fig. 7.3 Dental plaque formation by mutans streptococci (SM). Dietary sugars are transported into SM by glucosyl transferases to be metabolized and excreted as polysaccharides (mutans). The plaque layer thickens as mutans accumulate on the tooth surface.

non-specific mixed bacterial flora is the agent responsible. Also debated is whether dental caries is an infectious bacterial disease in the classical sense or an ecological overgrowth (Kleinberg, 2002). Frequent isolation and identification of Lactobacillus acidophilus and Streptococcus mutans with caries activity gave credibility to them being specific cariogens. There does not seem to be as much question whether these bacteria are responsible for dental plaque formation. When genes responsible for glucan production by mutans streptococci are deleted, the organisms lose their virulence to induce dental caries in experimental animals (Yamashita et al., 1993). However, many other indigenous oral bacteria are capable of producing substantial amounts of organic acid from fermentable carbohydrates providing arguments for non-specificity. Numerous studies have shown some indigenous bacteria are capable of remineralizing tooth enamel to prevent dental caries.

Dental cavity formation results from a complex series of interactions occurring on the tooth enamel surface inside of the plaque biofilm. Generally, cariogenic bacteria produce organic acids that demineralize the calcified surface (Fig. 7.4). Once cavitation has begun, the tooth is continually under siege due to the different metabolic rates of cariogenic bacteria. Organic acid penetrates through the plaque biofilm to the tooth's enamel surface and begins diffusing into hydroxyapatite through water-filled interprismatic spaces. Loss of apatite crystals in the enamel is demineralization. The first visible change in tooth enamel is a translucent zone, and represents approximately 1 to 2% mineral loss from the enamel (Fig. 7.5). Tooth cavity formation is still reversible at this stage by calcium (or other minerals) and phosphate diffusing into the subsurface lesion and remineralizing the tooth. If further demineralization occurs to approximately 25% of a lesion in the enamel a visible cavitation occurs. Robinson et al. (2000) present a thorough review on enamel cavitation and dental caries.

Although dental sealants have reduced dental caries incidence in children, tooth decay affects more than 20% of American children aged 2 to 4 years, 50% of those aged 6 to 8, and nearly 60% of those aged 15 years old

Fig. 7.4 The chemical reaction of dental caries formation. Hydroxyapatite is hydrolyzed from the tooth's enamel by organic acids secreted from mutans streptococci and other cariogenic bacteria to solubilize calcium and phosphate.

Ca10(PO4)6(OH)2 + 11H+^-► 10Ca2+ + 6(HPO4)2- + 2H2O

Ca10(PO4)6(OH)2 + 11H+^-► 10Ca2+ + 6(HPO4)2- + 2H2O

Hydroxyapatite Ca10 Po4

Fig. 7.4 The chemical reaction of dental caries formation. Hydroxyapatite is hydrolyzed from the tooth's enamel by organic acids secreted from mutans streptococci and other cariogenic bacteria to solubilize calcium and phosphate.

Fig. 7.5 Stages of dental caries formation. Caries usually begin in pits and crevices in the tooth enamel surface (a). This stage is known as the initial surface zone. Odontopathogenic bacteria colonize in crevices and pits to begin demineralizing the tooth. A loss of approximately 1% mineral (usually as magnesium and carbonate) occurs during stage the translucent zone (b). Enamel erosion progresses at an irregular pace as the body attempts to counteract demineralization using its own defenses (immune response and statherin), dietary factors (e.g., milk and other dairy products), and oral hygiene (various dentifrices and other products) to remineralize the carious lesion. In the positively birefringent zone (c) calcium phosphates are precipitated deeper in the tooth often reaching into the dentin layer. Surface remineralization can still occur if the salivary pellicle is saturated with minerals (especially calcium and fluoride), but the tooth has lost approximately 5-10% of mineral at this stage, and cavity formation may not be reversible. Visible cavitation (d) occurs when demineralization exceeds 25%, and is referred to as the body of the lesion zone.

(Carmona, 2005). Children's teeth become infected with potential odontopathogenic bacteria between the middle of the second year and the end of the third year of life - the 'window of infectivity' (Caufield et al., 1993). The primary infection source for infants is maternal, but certain environmental conditions, such as infants born into a high caries-prone population, can also favor non-familial infection (Mattos-Graner et al., 2001). Children not infected by a high maternal dose by three years of age remain minimally colonized by odontopathogenic bacteria until secondary teeth eruption.

7.2.2 Periodontal disease

The gingival sulcus environment provides a selective habitat for establishment of a mixed, predominantly anaerobic, microflora. Periodontal disease is a chronic infection of tissues (gums) supporting the teeth. The infectious vector for chronic periodontitis is predominantly opportunistic Gram-negative anaerobic bacteria that colonize in crevices below the gum line. Specifically, the etiology in adults is caused by Bacteroides forsythus and Porphyromonas gingivalis. Juvenile patients are infected by Actinobacillus actinomycetemcomitans that results in a localized, aggressive periodontitis (Moore and Moore, 1994). The organisms utilize a variety of virulence factors to colonize and cause periodontium infection. Although periodontitis etiology is bacterial, the pathogenesis of periodontal disease is progressed by host response associated with increased production of reactive oxygen species and other inflammatory factors to anaerobic bacteria in gingival spaces below the teeth (Moore and Moore, 1994). If these reactive oxygen species are not buffered, damage to the host cells and tissues occurs (Moynihan, 2005). For more information on periodontal inflammatory response consult Van Dyke and Serhan (2003).

Periodontitis is diagnosed by observing loss of gum attachment to teeth and probing periodontal pocket depth along the tooth and gum line. The prevalence and severity of periodontal disease in different age groups have been measured in several global populations. Although periodontal disease is observed in all populations in varying degrees, severity is 10 to 20% higher in industrialized nations especially America (Petersen and Ogawa, 2005). Periodontal disease prevalence and severity is higher in older age groups as compared to younger age groups (Petersen, 2003). The disease is also more prevalent in lower socio-economic classes. Poor oral hygiene is a high risk factor for disease progression, but other risk factors contribute to severe periodontal disease including tobacco use, excessive alcohol consumption, drug abuse, stress, malnutrition, and diabetes mellitus (Genco et al., 1999, Nishida et al., 2000, Shaner et al., 2006, Tezal et al., 2001). Al-Zahrani (2006) utilized data collected from the Third National Health and Nutrition Examination Survey (NHANES III) to correlate dairy product intake with reduced periodontitis prevalence. Individuals in the highest quintile of dairy product consumption were 20% less likely to have periodontitis.

Diabetes patients exhibit a very high prevalence of periodontal symptoms, and the disease is much more aggressive (Grossi et al., 1996). Periodontitis is recognized as the sixth complication of diabetes. If a diabetic does not maintain very high oral hygiene and consistently regular visits to their dentist, the disease will rapidly deteriorate the gum structure resulting in tooth loss and an impaired quality of life.

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