Oral bacterial levels of 46 mother-child pairs were monitored from infant birth up to five years of age so that the acquisition of mutans streptococci (MS) by children could be studied. The initial acquisition of MS occurred in 38 children at the median age of 26 months during a discrete period we designated as the "window of infectivity". MS remained undetected in eight children (17%) until the end of the study period (median age of 56 mo). The levels of both MS and lactobacilli in saliva of mothers of children with and without MS were not significantly different. Comparisons between a caries-active cohort colonized by MS (nine of 38) and children without detectable MS revealed similar histories in terms of antibiotic usage, gestational age, and birth weight. Interestingly, half of the children between the ages of one and two years who were not colonized by MS were attended by caretakers other than the mother, while all of the caries-active children during this same time period were cared for by their mothers; the difference was statistically significant. Here we report for the first time that MS is acquired by infants during a defined period in the ontogeny of a child. Support for the notion of a discrete window of infectivity comes from other sources, including animal models.

The molecular and cellular mechanisms responsible for the etiology and pathogenesis of Alzheimer's disease (AD) have not been defined; however, inflammation within the brain is thought to play a pivotal role. Studies suggest that peripheral infection/inflammation might affect the inflammatory state of the central nervous system. Chronic periodontitis is a prevalent peripheral infection that is associated with gram-negative anaerobic bacteria and the elevation of serum inflammatory markers including C-reactive protein. Recently, chronic periodontitis has been associated with several systemic diseases including AD. In this article we review the pathogenesis of chronic periodontitis and the role of inflammation in AD. In addition, we propose several potential mechanisms through which chronic periodontitis can possibly contribute to the clinical onset and progression of AD. Because chronic periodontitis is a treatable infection, it might be a readily modifiable risk factor for AD.

In both developed and developing countries, low birth weight (LBW) has a tremendous impact on both the health care system and the individual families affected. This warrants the continuous search for risk factors for LBW that are amenable to prevention. Can poor oral health of the pregnant woman be one such factor? In a 1:1 matched case-control study (N = 55 pairs), we evaluated the hypothesis that poor oral health of the pregnant woman is a risk factor for LBW. The effect of periodontal and dental caries status of the woman at the time of delivery on the birth weight of the infant was evaluated by using conditional logistic regression analyses, while controlling for known risk factors for LBW. Mothers of LBW infants were shorter, less educated, married to men of lower occupational class, had less healthy areas of gingiva and more areas with bleeding and calculus, and gained less weight during the pregnancy. Conditional logistic regression analyses indicated that mothers with more healthy areas of gingiva (OR = 0.3, 95% CI = 0.12 - 0.72) and those who were taller (OR = 0.86, 95% CI = 0.75 - 0.98) had a lower risk of giving birth to an LBW infant. Risk of LBW was higher in mothers who had no or late prenatal care (OR = 3.9, 95% CI = 1.24 - 12.2). We conclude that poor periodontal health of the mother is a potential independent risk factor for LBW.

The associations of inflammation/immune responses with clinical presentations of Alzheimer’s disease (AD) remain unclear. We hypothesized that TNF-α and elevated antibodies to periodontal bacteria would be greater in AD compared to normal controls (NL) and their combination would aid clinical diagnosis of AD. Plasma TNF-α and antibodies against periodontal bacteria were elevated in AD patients compared with NL and independently associated with AD. The number of positive IgG to periodontal bacteria incremented the TNF-α classification of clinical AD and NL. This study shows that TNF-α and elevated numbers of antibodies against periodontal bacteria associate with AD and contribute to the AD diagnosis.