Faculty Bibliography

The heterogeneous group of oral bacteria within the sanguinis (sanguis) streptococci comprise members of the indigenous biota of the human oral cavity. While the association of Streptococcus sanguinis with bacterial endocarditis is well described in the literature, S. sanguinis is thought to play a benign, if not a beneficial, role in the oral cavity. Little is known, however, about the natural history of S. sanguinis and its specific relationship with other oral bacteria. As part of a longitudinal study concerning the transmission and acquisition of oral bacteria within mother-infant pairs, we examined the initial acquisition of S. sanguinis and described its colonization relative to tooth emergence and its proportions in plaque and saliva as a function of other biological events, including subsequent colonization with mutans streptococci. A second cohort of infants was recruited to define the taxonomic affiliation of S. sanguinis. We found that the colonization of the S. sanguinis occurs during a discrete "window of infectivity" at a median age of 9 months in the infants. Its colonization is tooth dependent and correlated to the time of tooth emergence; its proportions in saliva increase as new teeth emerge. In addition, early colonization of S. sanguinis and its elevated levels in the oral cavity were correlated to a significant delay in the colonization of mutans streptococci. Underpinning this apparent antagonism between S. sanguinis and mutans streptococci is the observation that after mutans streptococci colonize the infant, the levels of S. sanguinis decrease. Children who do not harbor detectable levels of mutans streptococci have significantly higher levels of S. sanguinis in their saliva than do children colonized with mutans streptococci. Collectively, these findings suggest that the colonization of S. sanguinis may influence the subsequent colonization of mutans streptococci, and this in turn may suggest several ecological approaches toward controlling dental caries.

The aim of this investigation was to evaluate the relationship between MHC alleles at the HLA-DRB1, DQB1 and TNFa microsatellite loci and levels of oral bacteria that play a role in the etiology of dental caries, and the DMFS index in 186 AA primparous women. The average age of the cohort was 20.8+/-3.7 years. The median DMFS index was 9 (range 0-68). High levels of S. mutans were positively associated with DRB1*3 and DRB1*4 presence (p < or = 0.005). DRB1*8 was positively associated with higher levels of S. mutans as a percentage of total Streptococci (p = 0.04). DRB1*1 was positively associated with high levels L. casei (p = 0.04). DQB1 alleles were not observed associated with oral bacterial levels. TNFa allele 103 was negatively associated (p = 0.04), and TNFa 117 was positively associated (p = 0.007), with high levels of L. acidophilus. No significant associations were observed between any DRB1, DQB1 or TNFa allele and the DMFS index. These results support an hypothesis of an association between host HLA class II and TNFa genetic profile and colonization of S. mutans, L. casei, and L. acidophilus thought to be pathogens involved in the etiology of dental caries.

Due to the greater range of lengths available to the third complementarity determining region of the heavy chain (HCDR3), the Ab repertoire of normal adults includes larger Ag binding site structures than those seen in first and second trimester fetal tissues. Transition to a steady state range of HCDR3 lengths is not complete until the infant reaches 2 mo of age. Fetal constraints on length begin with a genetic predilection for use of short DH (D7-27 or DQ52) gene segments and against use of long DH (e.g., D3 or DXP) and JH (JH6) gene segments in both fetal liver and fetal bone marrow. Further control of length is achieved through DH-specific limitations in N addition, with D7-27 DJ joins including extensive N addition and D3-containing DJ joins showing a paucity of N addition. DH-specific constraints on N addition are no longer apparent in adult bone marrow. Superimposed upon these genetic mechanisms to control length is a process of somatic selection that appears to ensure expression of a restricted range of HCDR3 lengths in both fetus and adult. B cells that express Abs of an 'inappropriate' length appear to be eliminated when they first display IgM on their cell surface. Control of N addition appears aberrant in X-linked agammaglobulinemia, which may exacerbate the block in B cell development seen in this disease. Restriction of the fetal repertoire appears to be an active process, forcing limits on the diversity, and hence range of Ab specificities, available to the young

Due to the greater range of lengths available to the third complementarity determining region of the H chain (HCDR3), the human antibody repertoire includes larger antigen binding site structures than those seen in first and second trimester fetal tissues. Transition to a steady state range of HCDR3 lengths is not complete until the infant reaches two months of age. Fetal constraints on length result from a genetic predilection for use of short DH and JH gene segments, and from DH-specific limitations in N addition. Superimposed upon these genetic mechanisms is a process of somatic selection that appears to ensure expression of a restricted range of HCDR3 lengths. A similar selection for a restricted range of HCDR3 intervals occurs in the neonatal mouse. Human cells expressing antibodies with "inappropriate" lengths appear to be eliminated when they first express IgM on their cell surface. Modeling studies suggest that increasing the length of HCDR3 creates "knob-like" antigen binding site structures not seen in the mouse. In human, the restriction in the range of HCDR3 lengths serves as a marker for an immature antibody repertoire and may contribute to the immunodeficiency state of the neonate.

The purpose of this study was to establish age- and sex-specific normative data for Caucasians and African Americans in Birmingham, Ala. Subjects (136) between 6 and 18 years old were included in the study. Chang's method (AF-BF) and 12 other measurements were used as determinates of the skeletal sagittal jaw relationship. All subjects had acceptable facial profiles and Class I occlusion. Subjects were divided into eight subgroups based on race, gender, and age. Differences of mean cephalometric values were tested using parametric and nonparametric statistical tests. Compared with Caucasians, African Americans had greater mean values for all measurements except AFB and AF-BF. More negative values were found for the African Americans in the Wits appraisal. Most measurements were found to decrease with age. These findings support our hypothesis that cephalometric norms should be based on racial, sex, and age differences

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