Special Care Dentistry: attitudes of Specialists in Paediatric Dentistry practising in the UK to the creation of a new specialty.

OBJECTIVES: This study was designed to examine the attitudes of Specialists in Paediatric Dentistry (SPDs) practising in the UK towards the creation of a specialty of Special Care Dentistry (SCD). DESIGN: Data were collected by postal questionnaire. Sample and methods. Two hundred and eleven dentists whose names were entered on the General Dental Council's Specialist List in Paediatric Dentistry, and who were resident and practising in the UK, were asked to complete a questionnaire consisting of both open and closed questions. RESULTS: Questionnaires were returned by 167 (79.2%) of the eligible SPDs. One hundred and sixty respondents (95.8%) expressed an opinion in relation to the creation of a specialty of SCD. One hundred and forty-three respondents (85.6%) stated that they supported such a proposal. However, slightly fewer (n = 149) respondents were prepared to indicate what they considered to be the remit of the proposed specialty. Ninety-two respondents (55.1%) considered that it should be restricted to the provision of specialist care for adults with 'special needs'; the remaining 57 respondents felt that it should provide specialist care across the entire age spectrum. CONCLUSIONS: Among SPDs, there is overwhelming support for the creation of a specialty of SCD, the majority view being that this should be dedicated to the provision of specialist care for adults with 'special needs'.

Management of molar teeth with periodontal disease.

Over the years patients' attitudes towards maintaining a functional and aesthetic masticatory apparatus have improved, and their expectations of delivery of care by the dental professional have risen. With the advance of new techniques and materials, the periodontist can now offer an ever-expanding range of treatments in the management of molar teeth with periodontal disease. This paper considers such treatment in relation to the levels of disease present and within the overall context of adult restorative dental healthcare.

The effect of multiple anticonvulsant therapy on the expression of phenytoin-induced gingival overgrowth.

The potential effect of co-medication with phenobarbitone, primidone and carbamazepine on plasma and saliva concentrations of 5-(4-hydroxyphenyl)-5-phenylhydantoin (4-HPPH), the major metabolite of phenytoin in man and on the incidence of phenytoin-induced gingival overgrowth was investigated in a group of 36 adult epileptic patients. There were no significant differences in plasma or saliva concentrations of 4-HPPH or phenytoin in patients prescribed phenytoin alone, compared to those who received phenytoin with either phenobarbitone, primidone, or carbamazepine. In addition, the extent and the incidence of gingival overgrowth were similar in the 2 groups. The results suggest that chronic co-medication with other anti-convulsant drugs which induce phenytoin metabolism, does not affect the plasma or saliva 4-HPPB steady-state levels, nor the degree of gingival overgrowth in adult epileptic patients on therapy with phenytoin.

Phenytoin metabolism to 5-(4-hydroxyphenyl)-5-phenylhydantoin (HPPH) in man, cat and rat in vitro and in vivo, and susceptibility to phenytoin-induced gingival overgrowth.

Interspecies differences in phenytoin (PHT) metabolism to 5-(4-hydroxyphenyl)-5-phenylhydantoin (HPPH) were examined in human, cat and rat hepatic microsomes in vitro. Rat liver microsomes were 25 and 650 times more efficient at the conversion of PHT to HPPH than human and cat liver microsomes, respectively. Sulphaphenazole (83%) and tolbutamide (TOL) (64%) were the most potent inhibitors of HPPH formation in human liver microsomes, while ciprofloxacin (27%), enoxacin (27%) and TOL (26%) produced the greatest inhibition in cat liver microsomes. TOL was tested for its effect on HPPH formation and gingival overgrowth in cats in vivo. Eight cats received PHT sodium (4 mg/kg/d) and another 8 cats received PHT sodium together with TOL (20 mg/kg/d) for 10 wk. Six cats (75%) in the PHT group and 4 cats (50%) in the PHT & TOL group developed significant gingival overgrowth by the end of the study. However, the extent and incidence of the overgrowth were similar in the 2 groups. There were no significant differences in mean AUC 0-10 weeks for plasma PHT (552.90 +/- 29.6 micrograms.d/mL [PHT alone] vs. 582.41 +/- 24.49 micrograms.d/mL [PHT & TOL]) and unconjugated HPPH (1016.4 +/- 295.5 ng.d/mL [PHT alone] vs. 1174.5 +/- 397.2 ng.d/mL [PHT & TOL]) concentrations between the 2 groups of cats. Neither PHT nor HPPH were detectable in the plasma of 8 rats which received PHT (4 mg/kg/d) over a 10-wk period. The rats showed no sign of gingival inflammation (mean gingival index = 0) or gingival overgrowth (mean gingival overgrowth index = 0). Thirty-six adult epileptic patients on chronic PHT therapy were examined; 17 (47%) of the patients demonstrated clinically significant overgrowth. The mean steady-state plasma PHT concentration was comparable to, and the mean plasma unconjugated HPPH concentration 5-fold greater than, that observed in the cats. The results suggest that the rapid metabolism and elimination of PHT and HPPH in the rat may enable it to become more resistant towards developing gingival overgrowth, compared to the cat and man.

Plasma and saliva concentrations of phenytoin and 5-(4-hydroxyphenyl)-5-phenylhydantoin in relation to the incidence and severity of phenytoin-induced gingival overgrowth in epileptic patients.

This study examined the relationships between plasma and saliva concentrations of phenytoin and 5-(4-hydroxyphenyl)-5-phenylhydantoin (HPPH), the major metabolite of phenytoin in man, and the prevalence and severity of gingival overgrowth. Thirty-six adult epileptic patients who had been receiving phenytoin for greater than 6 months without a recent change in dosage were assessed for signs of periodontal disease and gingival overgrowth. Plasma and saliva samples were analyzed by high performance liquid chromatography for the determination of phenytoin and HPPH concentrations. Seventeen patients demonstrated clinically significant gingival over-growth (responders; overgrowth index > or = 30%). There were significant correlations between the gingival overgrowth index and both the papillary bleeding index (r = 0.495; P < 0.005) and probing depth (r = 0.632; P < 0.005). The plaque index correlated with the papillary bleeding index (r = 0.420; P < 0.05) and the probing depth (r = 0.301; P < 0.005), but not with the gingival overgrowth index. The extent of gingival overgrowth did not correlate significantly with either plasma or saliva concentrations of phenytoin or HPPH. Mean plasma and saliva concentrations of phenytoin and HPPH did not differ significantly between non-responders and responders, nor did the mean plaque index. The mean papillary bleeding index (32.5 +/- 21.2 vs. 63.8 +/- 37.7; P < 0.01) and mean probing depth (12.4 +/- 14.4% vs. 35.9 +/- 25.3%; P < 0.02) were significantly greater in the responders. This study found no evidence of a relationship between phenytoin or HPPH concentrations in plasma or saliva and the extent, or prevalence of phenytoin-induced gingival overgrowth. Further studies with larger populations may be necessary to establish the relationship, if any, between phenytoin or HPPH levels and gingival overgrowth.

Human gingival crevicular fluid keratin at healthy, chronic gingivitis and chronic adult periodontitis sites.

The present study was designed to determine, in a cross-sectional study, whether there was any relationship between the keratin-positive material in gingival crevicular fluid and the clinical periodontal status. Keratins were selected as putative indicators of degradation of epithelial cells cytoskeletal proteins. Keratin positive material was determined by enzyme-linked immunosorbent assay in 42 subjects exhibiting clinical sites of health, chronic gingivitis and chronic periodontitis. The concentration of keratin in parotid saliva was also measured for each subject. Keratin concentration in gingival crevicular fluid samples was significantly greater at sites exhibiting signs of gingivitis and periodontitis compared with healthy sites. No differences were detected between sites exhibiting gingivitis and periodontitis. No differences were found between the 3 groups for the saliva keratin-positive material which was significantly less than that detected in gingival crevicular fluid. These results suggest that gingival crevicular fluid keratin concentration may serve as a marker of gingival damage.

The pharmacokinetics of phenytoin in gingival crevicular fluid and plasma in relation to gingival overgrowth.

The aim of this study was to determine whether phenytoin (PHT) could be detected in gingival crevicular fluid (GCF), and to relate its concentration to both plasma level and degree of gingival overgrowth. 23 patients medicated with phenytoin for at least 6 months were clinically examined for signs of periodontal disease and gingival overgrowth. 12 patients out of these demonstrated clinically significant overgrowth and their plaque scores and gingival inflammation were greater than for the non-overgrowth group (p < 0.001). Phenytoin concentrations were determined by high performance liquid chromatography, and was detected in GCF. There was a significant correlation between the GCF and plasma phenytoin concentrations (p < 0.05), but it was not related to the extent of gingival overgrowth. Inflammation increased the GCF volume, but was not a determinant of GCF phenytoin concentration. It is concluded that effusion of phenytoin into GCF is regulated by the plasma levels of the drug, but its concentration in GCF is not related to the incidence of gingival overgrowth.

The immediate effects of smoking on gingival fluid flow.

The aim of the present study was to examine the immediate effect of smoking a cigarette on gingival crevice fluid (GCF) flow-rate. The study involved 17 healthy volunteers (6 male, 11 female) aged 19-57 years (mean 34.5 years) who regularly smoked cigarettes. All were periodontally healthy. GCF was collected at the mesio-buccal aspects of the right and left maxillary 2nd premolar teeth, using filter-paper strips left in place for 3 min. Samples were taken at baseline and subsequently at 10 min intervals for 70 min. Each subject sham smoked an unlit standard cigarette for 7 min after the 20 min recording, and smoked the same cigarette for 7 min to within 1 cm of the filter, following the 40 min recording. The results showed that following sham smoking (30 min recording) GCF volume increased by a mean of 16.7% (p = 0.057), and following smoking (50 min recording) GCF volume increased by a mean of 89.7%, over the previous recording (p < 0.0001). The increase following smoking was greater than that following sham smoking (p < 0.0001). Flow-rate returned to near resting levels within the experimental period. The results indicate that smoking produces a marked transient increase in GCF flow-rate, which might reflect changes in blood flow known to be produced by nicotine.

Congenital absence of all primary and permanent lateral incisors in a carrier of X-linked hypohidrotic ectodermal dysplasia.

A case report is presented of congenital absence of all primary and permanent lateral incisors in a female patient who was a carrier of X-linked hypohidrotic ectodermal dysplasia. Congenital absence of all lateral incisors is extremely rare.