Notes: We analyze the mechanism by which positive ions and neutral species desorb from surfaces as a result of photon- or electron-beam induced electronic transitions. The system fluorine on aluminum is used as a prototype. We first present results of ab initio density-functional calculations of the potential energy curves of several charge states of fluorine on aluminum. We find that fluorine adsorbs as F−(2s22p6) and is strongly bound in the ground state. Valence (i.e., 2s22p5) and core (e.g., 2s12p6)-ionized states are, however, repulsive. F+(2s22p4) ions form bound states on Al but their adsorption energies are much smaller and their equilibrium distance is further out from the surface than those of F− ions. The difference in the bonding of positive and negative ions is ascribed to differences in the corresponding screening mechanisms. Screening of negative ions proceeds only by an image mechanism, while screening of positive ions can proceed by both image and charge–transfer mechanisms in which charge from the metal occupies the large-radius 3s and 3p orbitals of F. The resulting partially neutralized positive-ion states have reduced image attraction and increased electron kinetic energy (Pauli) repulsion. Franck–Condon transitions from the ground state populate the repulsive part of F+ potential energy curve and lead to efficient F+ desorption. F++ states are strongly bound and do not desorb. The same conclusions are reached by a more general analysis of the desorption of electronegative atoms from any metallic substrate, based on the concepts of effective medium theory. Finally, we discuss the applicability of our conclusions regarding the desorption of neutral and ionic fluorine to desorption of molecular adsorbates and also desorption from nonmetallic substrates.

Notes: A 3-month clinical trial was conducted to compare the effects of two concentrations of a chlorhexidine mouthrinse on gingivitis and plaque accumulation. Six hundred (600) adults were divided into three treatment groups matched for age, sex, and initial gingivitis severity. Following a thorough examination and prophylaxis at baseline, subjects were given a mouthrinse containing either 0.12% or 0.20% chlorhexidine gluconate or a placebo mouthrinse. Subjects were evaluated after 6 weeks and 3 months of mouthrinse use. After 3 months, both chlorhexidine groups showed significantly less gingivitis and plaque than the placebo group. The group using the 0.12% chlorhexidine gluconate mouthrinse demonstrated 27–27 % less gingivitis occurrence and 28–28% less gingivitis severity than the placebo group. The 0.12% chlorhexidine gluconate group also had 48–48% less gingival bleeding and 36% less plaque than the placebo group. There were no significant advantages for the 0.20% mouthrinse over the 0.12% mouthrinse. It is therefore concluded that a 0.12% chlorhexidine gluconate mouthrinse offers the same clinical benefits as a 0.20% chlorhexidine gluconate mouthrinse.

Notes: After prophylaxis, 5 dental hygienists performed optimal oral hygiene under supervision for 6 months. At months 0, 1, 4 and 6, Plaque Index, Gingival Exudate Flow Rate and Gingival Index were assessed, and a buccal biopsy of their gingiva taken. Point counting procedures were performed at 2 different levels of magnification to estimate the volume densities of epithelium, infiltrated and non-infiltrated connective tissue, and collagen. The percentages of fibroblasts, polymorphonuclear neutrophilic granulocytes, lymphocytes, plasma cells and macrophages were estimated by counting the number of profiles of these cells in the connective tissue area close to the apical end of the junctional epithelium. All the changes inside the tissue occurred slowly. During the 6-month period there was a continuous increase of the volume density of the epithelium in the gingiva. An increase in the percentage of fibroblasts was observed between months 1 and 4 together with a decrease in the percentage of lymphocytes and in the volume density of the infiltrated connective tissue. Between months 4 and 6 an increase of the volume density of the collagen was found together with a further increase in the percentage of fibroblasts and a further decrease in the percentage of lymphocytes. After 6 months of perfect oral hygiene no more plasma cells were visible. This study has shown that, even in presence of clinically healthy gingiva, subclinical changes may take place. It appears realistic to accept the presence of a very mild gingivitis localized in an area adjacent to the attachment as compatible with gingival health.

Notes: The purpose of this investigation was to study stereologically the histopathologic alterations occurring during a human experimental gingivitis, and to establish a relationship between clinical parameters and histologic findings. Eight dental students volunteered for the study. After a prophylaxis they performed optimal oral hygiene for 3-4 weeks to reach mean plaque and gingival indices approaching zero. They then abandoned all oral hygiene procedures for a period of 21 days. At d 0, 4, 7, 14 and 21, Plaque Index (PII), Gingival Index (GI) and Gingival Exudate Flow Rate (GEFR) were assessed, and a buccal biopsy of their gingiva was taken. Point counting procedures were performed at 2 different levels of magnification to estimate the volume densities of epithelium, infiltrated and non-infiltrated connective tissue, and collagen. The percentages of polymorphonuclear neutrophilic granulocytes, lymphocytes, plasma cells, macrophages and fibroblasts were estimated by counting the number of profiles of these cells in the connective tissue area close to the apical end of the junctional epithelium. The histological picture during the entire experiment was one of an early lesion (Page & Schroeder 1976). The clinically healthy gingiva did not correspond to a histologically healthy gingiva containing only a few inflammatory cells, probably because the 3-4 wk of perfect oral hygiene were not sufficient to generate histological health. Furthermore, no chronic inflammation of the gingiva, as characterized by a predominance of plasma cells, was observed after 3 wk without oral hygiene. Thus, more than 3 wk of no oral hygiene are necessary to obtain an established gingival lesion. With increasing gingivitis scores between GI = 0 and GI = 2 there was a significant increase in the percentages of lymphocytes and a significant decrease in the percentages of fibroblasts. With increasing GEFR similar trends in percentages were observed for lymphocytes and fibroblasts. It was concluded that GI scores and GEFR reflect histologic changes in tissue and, hence, are valid indicators of gingivitis development.

Notes: The experimental gingivitis model was used to compare the antigingivitis, antiplaque, and antimicrobial efficacies of two commercially available (a phenolic and a plant alkaloid) compounds used as mouthrinses with those of a mouthrinse containing chlorhexidine digluconate. Thirty-one male and female volunteers with healthy gingivae and clean teeth ceased all oral hygiene procedures for 21 days during which they rinsed twice daily with: a) a phenolic compound (Listerine®), b) sanguinarine (Viadent®), c) 0.12% chlorhexidine digluconate, or d) a placebo mouthrinse. After 21 days of rinsing, virtually no signs of clinical gingivitis were observed in the chlorhexidine group. Subjects rinsing with Listerine, Viadent, or placebo developed clinical signs of gingivitis as measured by gingivitis occurrence, severity, and the proportion of gingival bleeding sites. At the same time, plaque accumulation was only slightly higher than at baseline in the chlorhexidine group, while the Listerine, Viadent, and placebo groups had significantly greater plaque accumulations, particularly during the initial period of treatment between day 0 and day 7. Microbiological enumeration of supragingival plaque collected at the end of the treatment period showed that chlorhexidine digluconate reduced plaque bacteria by 62–62% compared to the placebo group. No significant reductions in plaque bacteria were found among subjects using Listerine or Viadent.This study demonstrated that 0.12% chlorhexidine digluconate was superior to Listerine and Viadent in its ability to maintain optimal gingival health during the entire three weeks of mouthrinse use. It was of particular interest to note these effects during the final 14 to 21-day period of extreme challenge in this experimental model when gingivitis severity and bleeding site occurrence are most pronounced in the placebo group.

Notes: Two clinical studies were performed to evaluate the safety and efficacy of an intracoronal device for the controlled release of SnF2. SnF2-polycarboxylate cement, containing approximately 72mgF−, was placed in subjects' molars requiring two-surface restorations.In the trial for safety, eight subjects had the restoration in place for 34 days. The salivary fluoride levels were elevated to a mean of 0.3/106. over the experimental period. Urinary fluoride levels were only above baseline levels during the first few days. The restoration's physical properties were adequate; however, subjects experienced gingival irritation in areas where the restoration was contacted with gingiva.In the trial for efficacy, fourteen subjects had either a SnF2-polycarboxylate or a placebo restoration placed in a molar tooth during a 2 week period of no oral hygiene. During the experimental period, the control subjects had higher levels of salivary total CFU, Streptococcus sanguis and Streptococcus mutans: while the subjects with the SnF2 restoration had increased S. sanguis and decreased S. mutans levels. No differences in G.I. or PL 1 scores were noted between groups.Further development of this controlled release system should include using the SnF2-polycarboxylate restoration in more than one tooth per subject to increase the fluoride reservoir, and not allowing the restoration to contact gingival tissues.

Notes: Abstract The aim of the present study was to investigate stereologically the histologic alterations occurring during gingival healing after experimental gingivitis and to compare clinical parameters with histological findings. 8 dental students volunteered for the investigation. After a prophylaxis, they performed optimal oral hygiene to reach mean plaque and gingival indices approaching zero. They then abolished all oral hygiene procedures for a period of 21 days. After this experimental gingivitis phase, they again performed optimal oral hygiene for 8 days to restore gingival health. At days 0. 1, 2, 4, and 8 after experimental gingivitis, the plaque index (PII), the gingival index (GI) and the gingival exudate flow rate (GEFR) were assessed and their buccal gingiva was biopsied. Point counting procedures were performed at 2 different levels of magnification on light microscopic sections to estimate the volume fractions of epithelium, infiltrated and non-infiltrated connective tissue, and collagen. The relative numbers of fibroblasts, polymorphonuclear neutrophils. lymphocytes, plasma cells and macrophages were estimated by counting the number of profiles of these cells in a specific connective tissue area adjacent to the apical end of the junctional epithelium. A rapid drop in the PII was noted with increasing time after oral hygiene, followed by a slower decrease in the GI and GEFR scores. The histological picture during the entire experiment was that of an initial gingival lesion. At day 0, no chronic inflammation of the gingiva characterized by a predominance of plasma cells was observed. After resumption of oral hygiene when the relative cell numbers at day 0 and day 8 were compared, only an increase in the PMN population was observed. As GI and GEFR scores decreased no significant changes were noted in the relative numbers of the various cell types. These observations suggest that the “physiogenesis during experimental health” appears first clinically and then histologically, and hence, it may take more than 8 days to observe significant variations in cell populations.

Notes: Abstract In association studies, micro-organisms can only be recognized as suspects for playing a major rôle in the development of a pathological environment, if their destructive action goes along with a marked proportional increase of their numbers or if their first detection can be related to the clinical onset of the disease. Limitations in the reproducibility of repeated samples have lo be taken into account, when changes of the microbial composition of subgingival environments are to be studied, and when local clinical changes are to be related to shifts in the composition of the pertaining microbiological compartment. To study reproducibility, a total of 109 sites was sampled repeatedly with sterile paperpoints at an interval of 7 to 10 days in 24 patients suffering from periodontal disease and 12 edentulous patients wearing successful and failing osseointegrated titanium implants. Using continuous anaerobic techniques, the samples were cultured on nonselective and selective media and were studied by darkfield microscopy. Both the intertest-agreements of frequencies of detection (x-statistics) as well as the discrepancies of proportions of bacterial groups and selected bacterial species were determined. The standard deviation of proportional differences between first and second samples ranged between 6.4% (fusiform organisms) and 17.2% (coccoid cells) for darkfield parameters, between 4.3% (B. melaninogenicus on ETSA/Kana.) and 14.0% (B. gingivalis on ETSA/Kana.) for selected bacterial species and between 6.9% (gram-negative anaerobic cocci) and 24.0% (gram-positive facultative cocci) for bacterial groups classified according to gram stain characteristics and atmospheric growth conditions. As the magnitude of deviation depended upon the mean value, coefficients of variation (cv) were also determined. The lowest cv values (0.25) were found for the proportions of spirochetes in the darkfield microscope, for the proportions of the gram-positive facultative rods (0.29) for gross bacterial groups and for Fusobacterium spp. (0.60) for selected bacterial species. The intertest-agreement of the frequencies of detection were best for spirochetes in the microscope and for B. intermedius with selected cultivated species. The results did not indicate a general bias of the results of second samples due to the previous sampling (McNemar's x2). Methodological proposals for estimation and comparison of proportions of bacteria are made and discussed in an appendix.

Notes: Abstract The purpose of this investigation was to follow the development of the gingival conditions during puberty and to correlate oral clinical parameters with chronological age as well as with parameters used for the determination of the pubertal development. In 22 boys and 20 girls pubertal and skeletal development, as well as plaque index (PII) and gingival index (GI) were monitored at 1-year intervals between the ages of 11 and 15 years. During this time, the papillary bleeding index (FBI) was assessed 10 times in all interdental spaces of the dentition. The bleeding tendency, represented by whole mouth mean FBI values, as well as the % of bleeding interdental sites, was found to increase significantly with the start of the pubertal phase. It reached a peak value after 1–5 years in 35% of the children. A significant trend of decrease was noted after the age of 14 years in boys and girls. In boys, mean FBI and the % of interdental sites with bleeding were correlated with testes growth, in girls with the Tanner index for secondary sex characteristics (breast development). PII and GI. which were only recorded annually, did not show a significant trend of increase or decrease.

Notes: Abstract The cleavage of complement may be an important immunopathologic mechanism in the development of gingival inflammation. Utilizing the experimental gingivitis model, cleavage of C3, C4 and B was assessed in gingival fluid following abstention from oral hygiene. 4 male dental students performed stringent oral hygiene measures until the gingival index approached 0, then refrained from any oral hygiene for 21 days. Gingival fluid, sampled with filter paper strips from the mesial surface of all maxillary premolars at 0, 7, 14, and 21 days, was assayed for C3, C4 and B cleavage by multilayer crossed-immunoelectrophoresis. Clinical indices were assessed following gingivat fluid sampling. The subjects, who were plaque-free (PI=0) at the beginning of the study, showed significant plaque accumulation at day 21 (87% of sites with PI ≥ 2). Approximately 90% of the sites were free from clinical inflammation (GI = 0) at the start, but gingivitis increased with time such that 25% of the sites had GI scores of 2 at day 21. Bleeding on probing to the base of the pocket was not observed at day 0, but was observed at 62% of sites by day 21. Statistical analyses showed that all 3 indices significantly increased with time. The %C3 cleavage increased from a mean of 24% at day 0, to 35%, 45% and then 57% at days 7, 14 and 21, respectively, and both days 14 and 21 demonstrated significantly greater C3 conversion than that seen at day 0. The Spearman rank-order correlation coefficient for %C3 conversion versus time was p-0.52, significant at the p 〈 0.0001 level. B cleavage to Bb was commonly seen, but C4 cleavage to C4c was never observed. Thus, during experimental gingivitis, %C3 cleavage significantly increased with plaque accumulation and resultant gingivitis, correlating with gingivitis at p= 0.64. These results suggest that cleavage of complement may be an important factor in the initiation of gingival inflammation.