Objective To examine whether long term consumption of a probiotic milk could reduce gastrointestinal and respiratory infections in children in day care centres. Design Randomised, double blind, placebo controlled study over seven months. Setting 18 day care centres in Helsinki, Finland. Participants 571 healthy children aged 1-6 years: 282 (mean (SD) age 4.6 (1.5) years) in the intervention group and 289 (mean (SD) age 4.4 (1.5) years) in the control group. Intervention Milk with or without Lactobacillus GG. Average daily consumption of milk in both groups was 260 ml. Main outcome measures Number of days with respiratory and gastrointestinal symptoms, absences from day care because of illness, respiratory tract infections diagnosed by a doctor, and course of antibiotics. Results Children in the Lactobacillus group had fewer days of absence from day care because of illness (4.9 (95% confidence interval 4.4 to 5.5) v 5.8 (5.3 to 6.4) days, 16% difference, P = 0.03; age adjusted 5.1 (4.6 to 5.6) v 5.7 (5.2 to 6.3) days, 11% difference, P = 0.09). There was also a relative reduction of 17% in the number of children suffering from respiratory infections with complications and lower respiratory tract infections (unadjusted absolute % reduction − 8.6 ( − 17.2 to − 0.1), P = 0.05; age adjusted odds ratio 0.75 (0.52 to 1.09), P = 0.13) and a 19% relative reduction in antibiotic treatments for respiratory infection (unadjusted absolute % reduction − 9.6 ( − 18.2 to − 1.0), P = 0.03; adjusted odds ratio 0.72 (0.50 to 1.03), P = 0.08) in the Lactobacillus group. Conclusions Lactobacillus GG may reduce respiratory infections and their severity among children in day care. The effects of the probiotic Lactobacillus GG were modest but consistently in the same direction.

Lactobacillus rhamnosus GG, ATCC (LGG), has shown antagonism to many bacteria including mutans streptococci. This randomized, double–blind, placebo–controlled intervention study was designed to examine whether milk containing LGG has an effect on caries and the risk of caries in children when compared with normal milk. 594 children, 1–6 years old, from 18 municipal day–care centres were included. The children received the milk with meals from coded containers 5 days a week in the day–care centres for 7 months. The children’s oral health was recorded at baseline and at the end, using WHO criteria. The caries risk was calculated based on clinical and microbiological data, comprising mutans streptococcus levels from dental plaque and saliva. The risk was classified as high if the child had a dmft/DMFT or initial caries score >0, and a mutans streptococcus count ≧10⁵ CFU/ml. The results showed less dental caries in the LGG group and lower mutans streptococcus counts at the end of the study. LGG was found to reduce the risk of caries significantly (OR = 0.56, p = 0.01; controlled for age and gender, OR = 0.51, p = 0.004). The effect was particularly clear in the 3– to 4–year–olds. Thus, milk containing the probiotic LGG bacteria may have beneficial effects on children’s dental health.

Dental erosion is caused by acidic solutions which come into contact with the teeth. Because the critical pH of dental enamel is approximately 5.5, any solution with a lower pH value may cause erosion, particularly if the attack is of long duration, and repeated over time. Saliva and salivary pellicle counteract the acid attacks but if the challenge is severe, a total destruction of tooth tissue follows. Ultrastructural studies have shown that erosive lesions are seen in prismatic enamel as characteristic demineralization patterns where either the prism cores or interprismatic areas dissolve, leading to a honeycomb structure. In aprismatic enamel the pattern of dissolution is more irregular and areas with various degrees of mineral loss are seen side by side. In dentin the first area to be affected is the peritubular dentin. With progressing lesions, the dentinal tubules become enlarged but finally disruption is seen also in the intertubular areas. If the erosion process is rapid, increased sensitivity of the teeth is the presenting symptom. However, in cases with slower progression, the patient may remain without symptoms even though the whole dentition may become severely damaged. Regarding the role of causative agents, present data does not allow the ranking of different acids with regard to their potential of causing erosion. Neither is there consensus as to how effective fluorides are in preventing the progression of erosive lesions, or how the chemical and structural factors of tooth tissue in general might modify this pathological process.

During the last two decades, there has been an increasing interest in the impact of oral health on atherosclerosis and subsequent cardiovascular disease (CVD). The advent of the inflammation paradigm in coronary pathogenesis stimulated research in chronic infections caused by a variety of micro-organisms-such as Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus-as well as dental pathogens, since these chronic infections are thought to be involved in the etiopathogenesis of CVD by releasing cytokines and other pro-inflammatory mediators (e.g., C-reactive protein [CRP], tumor necrosis factor [TNF-␣]) that may initiate a cascade of biochemical reactions and cause endothelial damage and facilitate cholesterol plaque attachment. Yet, due to the multi-factorial nature of dental infection and CVD, confirming a causal association is difficult, and the published results are conflicting. The main deficit in the majority of these studies has been the inadequate control of numerous confounding factors, leading to an overestimation and the imprecise measurement of the predictor or overadjustment of the confounding variables, resulting in underestimation of the risks. A meta-analysis of prospective and retrospective followup studies has shown that periodontal disease may increase the risk of CVD by approximately 20% (95% confidence interval [CI], 1.08-1.32). Similarly, the reported risk ratio between periodontal disease and stroke is even stronger, varying from 2.85 (CI 1.78-4.56) to 1.74 (CI 1.08-2.81). The association between peripheral vascular disease and oral health parameters has been explored in only two studies, and the resultant relative risks among individuals with periodontitis were 1.41 (CI 1.12-1.77) and 2.27 (CI 1.32-3.90), respectively. Overall, it appears that periodontal disease may indeed contribute to the pathogenesis of cardiovascular disease, although the statistical effect size is small.

The pathogenetic mechanisms behind alcohol-associated carcinogenesis in the upper digestive tract remain unclear, as alcohol is not carcinogenic. However, there is increasing evidence that a major part of the tumour-promoting action of alcohol might be mediated via its first, toxic and carcinogenic metabolite acetaldehyde. Acetaldehyde is produced from ethanol in the epithelia by mucosal alcohol dehydrogenases, but much higher levels derive from microbial oxidation of ethanol by the oral microflora. In this study we investigated factors that might alter the composition and quantities of the oral microflora and, consequently, influence microbial acetaldehyde production. Information about dental health, smoking habits, alcohol consumption and other factors was obtained by a questionnaire from 326 volunteers with varying social backgrounds and health status, e.g. oral cavity malignancy. Paraffin-induced saliva was collected and the microbial production of acetaldehyde from ethanol was measured. Smoking and heavy drinking were the strongest factors increasing microbial acetaldehyde production. Whether poor dental status may alter local acetaldehyde production from ethanol remained unanswered. Bacterial analysis revealed that mainly gram-positive aerobic bacteria and yeasts were associated with higher acetaldehyde production. Increased local microbial salivary acetaldehyde production due to ethanol among smokers and heavy drinkers could be a biological explanation for the observed synergistic carcinogenic action of alcohol and smoking on upper gastrointestinal tract cancer. It offers a new microbiological approach to ethanol-associated carcinogenesis at these anatomic sites.