The short and long-term fluoride release of 16 products (seven conventional glass-ionomers, five light-activated glass-ionomers, two polyacid-modified resin composites and two resin composites) commercialized as fluoride-releasing materials were measured. A potential link between the material type and its level of fluoride release was researched. The fluoride release was evaluated after different time intervals. Initial fluoride release from all materials was highest during the first 24 h and decreased sharply over the first week. Some groups of materials appeared to be significantly different after, respectively, 7 and 91 days. However, it was impossible to correlate the fluoride release of the materials by their type (conventional or resin-modified glass-ionomers, polyacid-modified resin composite and resin composite) except if we compared the products from the same manufacturer. The link between fluoride release and an acid-base reaction seems to be confirmed. The glass-ionomer composition (glass particles and polyacid's type, powder/liquid ratio) should have more influence on fluoride release than material type.

Agar diffusion testing was used with four different media to evaluate the antibacterial activity of six products (one conventional glass-ionomer cement (GIC), two light-activated glass-ionomers, two polyacid-modified resin composites and one resin composite) on Streptoccoccus mutans. Their respective antibacterial activities were also compared during and after setting. The relationship between product acidity and antibacterial activity was evaluated. All the GICs demonstrated antibacterial properties in contrast to the polyacid-modified resin composites and resin composite which did not shown any antibacterial effects. Vitrebond GIC exhibited higher antibacterial action, probably because of a cytotoxic photo-initiator diphenyliodoniumchloride. A direct relationship between material acidity and growth inhibition of S. mutans was observed.

We describe a patient who had four relapses of Miller Fisher syndrome over a period of 20 years. The classical triad – ophthalmoparesis, ataxia and areflexia – was present during the first two attacks; ataxia was not observed during the third episode. The final recurrence was characterized by signs suggestive of a central involvement of the oculomotor pathways, subclinical slowing of the visual-evoked potentials, and peripheral vestibular hyporeactivity. Brain imaging was normal, but high levels of anti-GQ1b IgG antibodies were detectable during the second relapse and persisted after the fourth recurrence despite complete clinical recovery.

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