The initial infection of children by Streptococcus mutans, the main pathogen of dental caries, depends on the ability of S. mutans to adhere and accumulate on tooth surfaces. These processes involve the adhesin antigen I/II (AgI/II), glucosyltransferases (GTF) and glucan-binding protein B (GbpB), each a target for anticaries vaccines. The salivary immunoglobulin A (IgA) antibody responses to S. mutans antigens (Ags) were characterized in 21 pairs of 5-to 13-month-old children. Pairs were constructed with one early S. mutans-infected and one noninfected child matched by age, racial background, number of teeth, and salivary levels of IgA. Specific salivary IgA antibody response and S. mutans infection levels were then measured during a 1-year follow-up. Robust responses to S. mutans were detected from 6 months of age. Salivary IgA antibody to AgI/II and GTF was commonly detected in salivas of all 42 children. However, GbpB-specific IgA antibody was seldom detected in the subset of infected children (38.1% at baseline). In contrast, most of the subset of noninfected children (76.2%) showed GbpB-reactive IgA antibody during the same period. Frequencies of GbpB responses increased with age, but differences in intensities of GbpB-IgA antibody reactions were sustained between the subsets. At baseline, GbpB-reactive IgA antibody accounted for at least half of the total salivary IgA S. mutans-reactive antibody in 33.3 and 9.5% of noninfected and infected children, respectively. This study provides evidence that a robust natural response to S. mutans Ags can be achieved by 1 year of age and that IgA antibody specificities may be critical in modulating initial S. mutans infection.

Alloxan damages insulin-producing cells and has been used as an inducer of experimental diabetes in several animal species. In this study, administration of alloxan (40 mg/kg, i.v.) to rats was followed by a selective and time-dependent reduction in the number of pleural mast cells (50±2.2%, p<0.01; mean ± SEM), while mononuclear cell and eosinophil counts were not altered. As compared to naive rats, the reduction in mast cell numbers was first noted 48 h following alloxan administration and remained unaltered for at least 60 days. It is noteworthy, that the depletion in the mast cell population was not accompanied by alterations in the total amount of histamine stored per cell. Sensitized rats turned diabetic by alloxan treatment performed 72 h before challenge showed a less pronounced antigen-induced mast cell degranulation compared to nondiabetic rats. Moreover, rats injected with alloxan 72 and 48 but not 24 h before challenge, reacted to allergenic challenge with 50% reduction in the number of eosinophils recruited to the pleural cavity within 24 h. We found that the less pronounced eosinophil accumulation did not relate to an intrinsic cell locomotor abnormality since eosinophils from diabetic rats presented similar chemotactic responses to LTB4 and PAF in vitro as compared to matching controls. Insulin (3 IU/rat) restored basal levels of mast cells and reversed the subsequent inhibition of allergen-induced pleural eosinophilia, suggesting a causative relationship between these phenomena. Treatment with insulin also significantly increased the number of mast cells in the pleural cavity of naive rats (from 637±57 to 978±79 × 10³ cells/cavity, p<0.001). Consistently, previous depletion of mast cells by means of local treatment with compound 48/80 significantly reduced the antigen-induced eosinophil recruitment in sensitized animals. We conclude that the reduction in the pleural mast cell population noted in alloxan-treated rats could be directly implicated in the diminished pleural eosinophil influx following allergen challenge. This hyporesponsiveness is independent of an intrinsic abnormality of cell chemotaxis, but can be imitated by local mast cell depletion.

Transmission of Streptococcus mutans, a major dental caries pathogen, occurs mainly during the first 2.5 years of age. Children appear to acquire S. mutans mostly from their mothers, but few studies have investigated non-familial sources of S. mutans transmission. This study prospectively analysed initial S. mutans oral colonization in 119 children from nursery schools during a 1.5-year period and tracked the transmission from child to child, day-care caregiver to child and mother to child. Children were examined at baseline, when they were 5-13 months of age, and at 6-month intervals for determination of oral levels of S. mutans and development of caries lesions. Levels of S. mutans were also determined in caregivers and mothers. A total of 1392 S. mutans isolates (obtained from children, caregivers and mothers) were genotyped by arbitrarily primed PCR and chromosomal RFLP. Overall, 40.3 % of children were detectably colonized during the study, and levels of S. mutans were significantly associated with the development of caries lesions. Identical S. mutans genotypes were found in four nursery cohorts. No familial relationship existed in three of these cohorts, indicating horizontal transmission. Despite high oral levels of S. mutans identified in most of the caregivers, none of their genotypes matched those identified in the respective children. Only 50 % of children with high levels of S. mutans carried genotypes identified in their mothers. The results support previous evidence indicating that non-familial sources of S. mutans transmission exist, and indicate that this bacterium may be transmitted horizontally between children during the initial phases of S. mutans colonization in nursery environments.

A.; PUGLIESE, L. S.; REIS, S. R. de A. Contribuição ao estudo da cárie dentária em crianças de 0-30 meses. Pesqui Odontol Bras, v. 15, n. 3, p. 215-222, jul./set. 2001. Este estudo avaliou as condições de saúde bucal de 340 crianças de 0-30 meses de idade (21,3 ± 5,6), sendo 54,4% meninos, 45,6% meninas, de 20 creches de Salvador, considerando lesões incipientes e relacionando-as a alguns fatores determinantes da cárie. Os exames foram realizados por um único examinador utilizando-se espelho, sonda e lanterna. Os dentes foram limpos, secos com gaze e as lesões classificadas de acordo com o grau de severidade em cinco ní-veis (C0-C4; ativa/inativa). Um questionário avaliou o conhecimento sobre a cárie, fatores de risco, instrução, renda familiar e uso de flúor. Foram incluídos 229 questionários (67,35%). A análise dos dados foi realizada no Epi-info 6.02. Observou-se uma prevalência de cárie de 55,3% quando todos os estágios da lesão foram considerados: 25% entre 0-12 meses; 51,18% entre 13-24 meses; 71,03% entre 25-30 meses (χ 2 = 25,31; p < 0,01). Avaliando-se apenas manchas brancas ativas, 49,7% das crianças mostraram-se afetadas e 17,6%, apenas com lesões cavitadas. Das crianças afetadas, 90,96% apresentavam apenas dentes anteriores afetados: 80% das lesões eram incipientes e 20%, cavitadas. Não foi observada diferença significante entre sexos. O aumento da quantidade de biofilme dental mostrou associação positiva com a cárie nesta faixa etária (χ 2 = 67,61; p < 0,01) e a porcentagem de crianças afetadas mostrou-se maior na presença de aleitamento noturno (χ 2 = 0,24; p = 0,62). Foi observado um aumento da prevalência de cárie com a idade (χ 2 = 25,31; p < 0,01) e com o número de dentes irrompidos ( χ 2 = 122,95; p < 0,01). Sugere-se atenção precoce à saúde bucal para o diagnóstico de lesões incipientes e adoção de medidas educativas e preventivas, incentivando mudanças na higiene bucal e dieta.UNITERMOS: Cárie dentária; Dieta cariogênica; Saúde bucal. INTRODUÇÃOA cárie rampante relacionada ao hábito do aleitamento (peito ou mamadeira) durante o sono foi descrita pela primeira vez em 1862 pelo pediatra americano Jacobi 11,13 . Inicia-se com uma discreta desmineralização em mais de um dos incisivos superiores, progredindo de seis meses a um ano para lesões cavitadas 23 , podendo causar dor, infecção e perda prematura dos dentes decíduos 2,17 . O padrão característico inicial da cárie de aleitamento, segundo RIPA 13 (1978), é o quadro contrastante observado na mesma criança, com cárie severa nos incisivos superiores e incisivos inferiores intactos. A distribuição e severidade das lesões entre maxila e mandíbula estão relacionadas a 4 fatores: cronologia de erupção, duração e severidade de hábitos deletérios, fluxo salivar e padrão muscular de sucção 8,13 . Os incisivos estão expostos por um período mais prolongado ao aleitamento noturno e à higiene bucal deficiente do que os demais dentes. A continuidade destes hábitos acaba por envolver os outros dentes na seqüência de sua erupção 13 . O fluxo salivar e a f...