Faculty Bibliography

BACKGROUND:Some encephalitides or seizure disorders once thought idiopathic now seem to be immune mediated. We aimed to describe the clinical features of one such disorder and to identify the autoantigen involved. METHODS:15 patients who were suspected to have paraneoplastic or immune-mediated limbic encephalitis were clinically assessed. Confocal microscopy, immunoprecipitation, and mass spectrometry were used to characterise the autoantigen. An assay of HEK293 cells transfected with rodent GABA(B1) or GABA(B2) receptor subunits was used as a serological test. 91 patients with encephalitis suspected to be paraneoplastic or immune mediated and 13 individuals with syndromes associated with antibodies to glutamic acid decarboxylase 65 were used as controls. FINDINGS/RESULTS:All patients presented with early or prominent seizures; other symptoms, MRI, and electroencephalography findings were consistent with predominant limbic dysfunction. All patients had antibodies (mainly IgG1) against a neuronal cell-surface antigen; in three patients antibodies were detected only in CSF. Immunoprecipitation and mass spectrometry showed that the antibodies recognise the B1 subunit of the GABA(B) receptor, an inhibitory receptor that has been associated with seizures and memory dysfunction when disrupted. Confocal microscopy showed colocalisation of the antibody with GABA(B) receptors. Seven of 15 patients had tumours, five of which were small-cell lung cancer, and seven patients had non-neuronal autoantibodies. Although nine of ten patients who received immunotherapy and cancer treatment (when a tumour was found) showed neurological improvement, none of the four patients who were not similarly treated improved (p=0.005). Low levels of GABA(B1) receptor antibodies were identified in two of 104 controls (p<0.0001). INTERPRETATION/CONCLUSIONS:GABA(B) receptor autoimmune encephalitis is a potentially treatable disorder characterised by seizures and, in some patients, associated with small-cell lung cancer and with other autoantibodies. FUNDING/BACKGROUND:National Institutes of Health.

Following ingestion of dietary fluoride, microquantities of fluoride return to the mouth in saliva, but in quantities large enough to facilitate the maintenance and reparative functions of enamel. Dietary fluoride supplements alone are unlikely to be the cause of the reported increase in fluorosis. Compliance continues to be extremely poor and few children use supplements for more than a year and a half. The amount of background fluoride resulting from dietary fluoride supplements appears to be very small. Considering the almost ubiquitous presence of fluoride dentifrice and the strong possibility of additional unintentional fluoride ingestion from many sources, the present fluorosis data is too amorphous to use as a basis for making reasonable risk/benefit evaluations. Very mild and mild fluorosis is not a serious problem for either the clinician or the patient. By altering the present recommended dosage we may deprive children from receiving a proven effective dose. One cannot make a risk/benefit decision concerning an esthetic problem without involving the patient's perception as well as the caries score. The apparent severity of the milder forms of fluorosis lessens with age and a community fluorosis index should be used only on populations who are older than 15 years.

Tooth enamel erosion occurs only in susceptible individuals regardless of food and beverage consumption patterns, that is, consumption of an acidic drink or food alone is highly unlikely to cause erosion. Susceptibility is highly variable from person to person and multifactorial in nature, as are the causes of erosion itself. Tooth enamel erosion is relatively rare and is easily misdiagnosed. A thorough differential diagnosis that eliminates the many other possible causes of enamel loss must be conducted. It is important to distinguish dental erosion from dental caries. Although the end result is similar, these two pathologies rarely occur simultaneously at the same site. In cases of true erosion, the tooth enamel is demineralised by direct contact with acids, while caries is a disease that occurs by the action of acids produced by plaque biofilm micro-organisms. It should also be stressed, clinically speaking, that erosion is primarily a surface phenomenon, while caries generally begins as a subsurface demineralisation of enamel structure that eventually leads to a pit in the tooth surface. As tooth enamel erosion is relatively rare, and the result of many factors, further research is needed to determine why susceptibility to erosion differs so widely from person to person.

Oral carbohydrate clearance and acid production were monitored over a two hour time period following the ingestion of six foods (chocolate bar, potato chip, oreo cookie, sugar cube, raisin and jelly bean). Each food was evaluated intra-orally in eight volunteers. Oral fluid samples were obtained from each volunteer at 30 min intervals at five different tooth sites using absorbent paper points. The oral fluid samples were analyzed qualitatively and quantitatively for carbohydrates and organic acids using high performance liquid chromatography. Data obtained for each food were averaged and subjected to statistical analysis. The quantity of lactic acid produced 30 min after ingestion was found to be in the following order: (highest) raisin > chocolate bar > sugar cube > jelly bean > oreo cookie > potato chip (least). Two hours after food intake the order had changed significantly: potato chip > jelly bean > sugar cube > chocolate bar > oreo cookie > raisin. A direct linear relationship existed between lactic acid production and the presence of glucose. In foods containing cooked starch prolonged clearance occurs via the intermediate metabolites maltotriose, maltose and glucose. Results indicated that the term 'stickiness', when used to label certain foods such as jelly bean and chocolate bar, should be used cautiously. Foods containing only cooked starch or cooked starch and sugars can be considered as 'sticky', since glucose arising from their intra-oral degradation contributed to acid production over prolonged periods of time.

Moisture contamination is a major factor in sealant application, often determining clinical success or failure. A new enamel conditioner using HNO3 (2.5%) has been introduced that does not require a water rinse after etching. The aim of this study is to compare etching characteristics using sealant retention from shear bond strength tests for traditional etch conditioning using H3PO4 (37%) and the HNO3 (2.5%) conditioner with and without a water rinse. We used 28 crown-intact extracted human teeth. We evaluated eight shear bond strength tests per group, on cylindrical sealant stubs (3.24 mm diameter x 3 mm height) for 12 groups (three etch conditions, two prophylactic methods, and two enamel surface type). The highest mean values of shear bond strength of 22.0 MPa was measured for H3PO4, and the lowest of 12.7 MPa for HNO3 (2.5%) without water wash. No significant differences (P < 0.05) were found between water rinse and air blast post-treatment groups after HNO3 conditioning.

The rate of early loss of preventive resin restoration and single application of pit and fissure sealant was determined by a clinical survey. The rate of partial and complete sealant loss on the observed surfaces was 14.4% (43/299) at the 3-month recall, with a further loss of 7.0% (12/171) between the 3- and 6-month recalls. Typically, a complete loss of sealant was observed on maxillary molars and on the buccal surface of mandibular molars, while partial loss caused on the occlusal surface of mandibular molars. Scanning electron microscopic observation of in vivo tooth replicas revealed partial gap formations and small fractures of sealant indicating failure or degradation of adhesion. The presence of unetched areas after routine cleaning and acid etching, especially in and around pits and fissures could be a major cause of early sealant loss.