A study into the prevention of fissure caries using an antimicrobial varnish.

The aim of this study, performed in Bangkok, was to evaluate the possibility of reducing fissure caries development using an antimicrobial varnish, Cervitec. Children aged 7-8 years and 12-13 years, 251 in each age group, with at least 2 sound contra-lateral permanent molars, were selected. A split mouth method was used with one test and one control tooth within the same jaw. At baseline and after two years all children were investigated for DMFS and DMFT. In addition, the size of any cavities was estimated. From 200 children, plaque samples of test and control occlusal surfaces were collected at baseline and after one year and processed to estimate the number of mutans streptococci. Mutans streptococci in saliva were estimated by the Strip mutans method. Cervitec varnish, containing 1 per cent chlorhexidine and thymol was applied at baseline, after 3-4 and after 8-9 months. The results showed that: Cervitec varnish reduced fissure caries development significantly; the levels of salivary mutans streptococci at baseline were significantly correlated with caries status at baseline and with total caries increment over the two-year period; caries development in a fissure was significantly correlated to the level of plaque mutans streptococci at that same site; three months after the last varnish application, a certain reduction of mutans streptococci in plaque could be seen in the test teeth; comparing the size of the lesions, more large cavities were found in the untreated teeth. It is concluded that varnishes should be considered as further options for prevention of fissure caries, possibly in more individualised programmes or in combination with already established methods.

Host metabolites that phenotypically increase the resistance of Haemophilus influenzae type b to clearance mechanisms.

Unidentified low-molecular-weight factor(s) in serum or nasopharyngeal secretions were known to phenotypically increase the resistance of Haemophilus influenzae type b (Hib) to bactericidal and opsonic antibodies, and resistance was attributed to two hypothetical mechanisms. Serum components generating resistance were studied. Mechanism 1, present in some Hib strains and their capsule-deficient mutants and accompanied by apparent increases in lipopolysaccharide content, was reproduced with a mixture of glucose, lactate, urea, and bicarbonate. Mechanism 2, present only in capsulated Hib and accompanied by increased capsulation, was reported with a mixture of Ca++ and lactate. Hib incubated with these compounds in buffer or grown in serum filtrate was resistant, but Hib grown in conventional media containing the metabolites in serum filtrate was resistant, but Hib grown in conventional media containing the metabolites was not. The resistant phenotype, which resembles Hib in vivo, may depend on nutrient balance as well as the specific factors. Lactate apparently is an important energy source for Hib.

[Inhibitory effect of mouthwashes on Streptococcus mutans growth].

The efficacy of 10 mouthwashes available in Bangkok in inhibiting Streptococcus mutans growth in vitro was studied. After one-minute incubation with the bacterium, most mouthwashes, at concentrations recommended by the manufacturers, demonstrated the antimicrobial effect; three exhibited a complete while five a partial but varying degree of inhibition. Only two mouthwashes were found that did not significantly show any detrimental effect on the bacterial viability.

Multiple mechanisms in serum factor-induced resistance of Haemophilus influenzae type b to antibody.

Incubation of Haemophilus influenzae type b at less than or equal to 10(7) CFU/ml with serum ultrafiltrate induces a phenotypic conversion in which complement-mediated bactericidal activity by somatic antibodies decreases while killing by capsular antibody is unchanged. Conversion had been shown to occur in a capsule-deficient (b-) mutant of strain Eag (thus appearing independent of capsulation), to include an increase in lipopolysaccharide content, and to be inhibited by chloramphenicol or puromycin. In the present study, in several strains not previously examined, conversion was not inhibited by the drugs and the corresponding b- mutants did not convert. Incubation in ultrafiltrate was also found to increase capsulation, as detected by radioassay, only 1.6-fold in Eag but 4.5-fold in DL26, the strain with the largest increase in resistance; moreover, complement-mediated opsonization by capsular antibody was greatly decreased. Thus, multiple mechanisms, capsule dependent as well as independent, appear to contribute to the serum factor-induced resistance of H. influenzae type b to antibody.

Sources of low-molecular-weight host factors that phenotypically increase the resistance of Haemophilus influenzae type b to bacteriolysis: non-identity with a factor active in gonococci.

Both gonococci and Haemophilus influenzae type b (Hib) in response to incubation with low-molecular-weight components of blood are converted to a relative resistance to killing by antibody and complement in vitro. Recently, cytidine 5'-mono-phospho-N-acetylneuraminic acid (a sialyl donor present in mammalian tissues) was found to convert gonococci. Here we report that this compound was inactive in Hib. In further contrast, the Hib-converting activity of serum was not retained by 500-M, filters, not sensitive to pH 2, and not active in the presence of growth media. Thus the phenotypic resistance in Hib and gonococci appear to have a different metabolic basis. The low-Mr serum factors active in Hib remain to be identified. Filtrates of human nasopharyngeal washes were also active, further suggesting that the converted form resembles the phenotype of Hib in vivo.