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Lactobacillus counts have been used to predict the incidence of new carious lesions.

29-03-2010
Evidence
Lactobacillus counts have been used to predict the incidence of new carious lesions.
 
Crossner (1981) studied a group of children, who had been given dental treatment at baseline so that no open lesions were present at the bacterial sampling. Two subgroups in this material are of special interest: those with very low or very high lactobacillus counts. Very few individuals in the low lactobacillus group developed new carious lesions over a 64-week period. In the high lactobacillus group, many, but not all, developed new lesions.
 
Some studies have shown that caries incidence is significantly increased when MS and lactobacilli occur in the same individual: During a 3-year longitudinal study, Alaluusua et al (1990) showed that teenagers with high salivary values for both MS and lactobacilli developed several times more new carious surfaces than did those with lower counts of either. The percentages of children who developed 0, 1 to 3, and more than 3 new carious surfaces were correlated to the total scores of MS and lactobacilli (Fig 37). Similar findings were reported by Stecksen-Blicks et al (1985).
 
In a 2-year study by Crossner et al (1989), samples from saliva, the tongue, and 276 interdental spaces were obtained from 23 7 year olds to (1) relate the presence of lactobacilli at various oral sites to the occurrence of lactobacilli in saliva, and (2) relate the presence of mutans streptococci and various types of lactobacilli interdentally to the development of proximal carious lesions. The results showed that the number of interdental samples containing lactobacilli increased as the number of salivary lactobacilli increased. Furthermore, lactobacilli were never found
interdentally without the presence of mutans streptococci, and lactobacilli proved to be the more suitable microorganism for prediction of proximal carious lesions.
 
Neither the number nor the differentiation into different species of interdental lactobacilli seemed to be of importance, merely their presence or absence. The presence of lactobacilli probably reflects a caries-inducing environment (etiologic microflora plus fermentable carbohydrates), thus explaining their high predictive ability despite their rather limited etiologic importance in the initiation of caries. 
 
Lactobacilli are also implicated in root surface caries. Fure and Zickert (1990a) studied a group of 208 randomly selected 55, 65, and 75 year olds. To estimate the number of root caries lesions, an index, DFS%(R), was used, indicating the number of decayed and filled root surfaces as a percentage of the exposed root surfaces. The mean DFS%(R) was 13 for the 100 subjects with low lactobacillus counts (less than104), and 23 for the 52 subjects with high counts (more than 105). In crosssectional and longitudinal studies, it has been demonstrated that lactobacillus counts
are among the factors with a significant correlation to the development of root caries lesions (Ravald and Birkhed, 1991, 1994; van Houte et al, 1990). Ellen et al (1985) also showed that root surfaces harboring both MS and lactobacilli are most likely to develop root caries.
 
A number of studies have tried to clarify the prevalence of lactobacilli in various populations, eg, two Swedish studies, one comprising 646 9 to 12 year olds (Klock and Krasse, 1977) and the other a group of 101 13 to 14 year olds (Zickert et al, 1982b). About 50% showed low salivary counts (less than 10,000 CFUs/mL of saliva) and 10% to 20% had high counts (100,000 to 1 million CFUs/mL of saliva). 
 
Generally the MS counts were 10 times greater than the lactobacillus counts. Most children with low mutans streptococci levels also had low numbers of lactobacilli, but there were situations where one type of bacterium was high and the other low.
 
In a dentate Swedish population of 80 and 85 year olds, Kohler and Persson (1991) found that 95% of the subjects had detectable salivary lactobacilli counts and 35% very high levels (more than 100,000 CFUs/mL of saliva). Almost 90% were MS positive, and 30% had more than 1 million CFUs/mL of saliva.
 
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Comments
Гость:
Please read Dr. Ellie’s book kiss your dentist gobodye . Goofy title but really interesting book written by a dentist. She also has a blog and tons of info about xylitol and a home care system to have great oral health. Our whole family began the program and our mouths have never felt cleaner. If this helps just 1 person it is worth this post. Brushing and flossing alone WILL NOT keep you cavity free if you have the bacteria in your mouth. Must control the bacteria. Also WATCH OUT for products that are not 100% sweetened with xylitol. They are a scam if xylitol is just 1 of the sweetners won’t work. Should be 1st ingedient. Sorbitol & other fake sweetners worse than sugar. Sugar doesn’t give cavities it feeds the bacteria already in mouth which create acid. Acid & dry mouth are the worst for teeth. Unfortunately xylitol very expensive compared to other sweetners which is why not used a lot.

Гость:
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Гость:
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Гость:
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Гость:
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Гость:
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Гость:
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Articles for theme “caries”:
29-03-2010
Cariogenicity of lactobacilliAccording to the specific plaque hypothesis, some strains of lactobacilli are considered to be major caries pathogens along with S mutans and S sobrinus. Lactobacilli are acidogenic and even more aciduric than MS. Mutans streptococci are strongly correlated to the etiology of initial enamel and root surface lesions, because they can adhere to and colonize the tooth surfaces. Lactobacilli are more dependent on retentive sites for heavy colonization: Mutans streptococci are regarded as the pioneers, followed by lactobacilli in the succession toward more cariogenic plaque.
29-03-2010
Methods of samplingAs mentioned earlier, the correlation between salivary MS counts and the number of MS-colonized tooth surfaces is relatively good (Lindquist et al, 1989), and simple salivary sampling methods are a more convenient and realistic means of assessing the severity of MS infection than sampling from individual tooth surfaces. Laboratory methods. Saliva is collected, mixed with a proper transport medium, and forwarded to a microbiologic laboratory. After incubation using a selective medium, mutans colonies are counted and the results are expressed as the number of colonyforming units per milliliter of saliva.
29-03-2010
Cariogenicity of mutans streptococciMutans streptococci are acidogenic as well as aciduric and can adhere to tooth surfaces (Gibbons et al, 1986). Mutans streptococci can produce extracellular and intracellular polysaccharides from sucrose. Intracellular polysaccharides in particular can be degraded during periods of low nutrient supply, indicating that these polysaccharides increase the virulence of some MS species (S mutans and S sobrinus).  Because the microbial ecology of the mouth is highly complex, strains of the same species could vary considerably in virulence (Bowden and Edwardsson, 1994).
29-03-2010
Role of Specific Cariogenic MicrofloraIntroductionMicroorganisms implicated in the etiology of dental caries must be acidogenic as well as aciduric. To initiate carious lesions in enamel, the microorganisms must also be able to colonize the tooth surface and survive in competition with less harmful species, forming biofilms¾the so-called dental plaque. As early as 1960, Fitzgerald and Keyes showed that certain microorganisms isolated from human dental plaque, when inoculated in germ-free rodents on a high-sucrose diet, resulted in the spread of rampant caries.
29-03-2010
Strategies for prevention and control of caries based on plaque ecology hypothesis According to the plaque ecology hypothesis, low pH (less than 5) will promote overgrowth of aciduric microorganisms, such as the cariogenic mutans streptococci and lactobacilli, at the expense of less acid-tolerant plaque microorganisms, such as S oralis, which are associated with healthy tooth surfaces.  Therefore the treatment strategy would be to increase plaque pH and thereby promote reestablishment of the harmless normal microflora of the tooth surfaces.