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The purpose of this study was to clarify the effect of covering gingival sulcus with denture base on periodontal tissue. Six subjects participated in this study. An experimental denture was inserted to a test tooth of each subject that was prepared for a full crown. Each experimental denture was designed to cover the gingival sulcus around the tooth. All subjects used them for two weeks. The parameters were as follows: 1) pH in gingival sulcus, 2) amount of gingival crevicular fluid, 3) tooth mobility, 4) temperature in gingival sulcus, 5) probing depth, 6) GI, and 7) P1I. Measurements were performed during the following periods: 1) pre-examination, 2) after cementation of provisional restoration, 3) during insertion of experimental denture, 4) after cementation of final restoration. A repeated-measures ANOVA was used for statistical analysis. The results were as follows: 1. pH value and amount of GCF increased after insertion of the experimental denture, and returned to same level as pre-examination after cementing of the final restoration. 2. Tooth mobility decreased during insertion of the experimental denture. 3. The changes of the other parameters were not significant. These results suggested that subclinical inflammatory change occurred in periodontal tissue in an early stage accompanied with covering of the gingival sulcus.
The objective of this study was to quantitatively compare the bacterial population structure in plaque from the gingival margin of two groups of 21 Chinese patients with gingivitis or necrotizing ulcerative gingivitis (NUG). Subjects were recruited in four dental clinics in Eastern China. Samples were quantitatively assessed by immunofluorescence and fluorescent in situ hybridization for taxa known to be associated with periodontal diseases. The analyses showed that the fusiform taxa (Fusobacterium nucleatum/Fusobacterium periodonticum, Leptotrichia buccalis, Tannerella forsythensis, and Capnocytophaga sp.), Campylobacter rectus, Prevotella intermedia, Prevotella nigrescens, Selenomonas sputigena, and treponemes were present in both groups with high prevalence. Porphyromonas gingivalis and Actinomyces gerencseriae were much more prevalent in the NUG group. Quantitatively, most taxa, including P. gingivalis, F. nucleatum and the treponemes, accounted, on average, for < 3% of the total bacterial cell number. Only P. intermedia/P. nigrescens, P. gingivalis, S. sputigena, A. gerencseriae, and the sum of all monitored suspected periodontal pathogens were significantly increased in the NUG group. The present study demonstrates for both groups a highly diverse plaque composition and suggests that, etiologically, the overall concentration and the concerted effects of the entire group of opportunistic pathogens thriving in NUG-associated plaque are of prime importance.
BACKGROUND: The aim of this study was to assess the prevalence and extent of gingival recession, gingival bleeding, and dental calculus in United States adults, using data collected in the third National Health and Nutrition Examination Survey (NHANES III). METHODS: The study group consisted of 9,689 persons 30 to 90 years of age obtained by a stratified, multi-stage probability sampling method in 1988 to 1994. The weighted sample is representative of U.S. adults 30 years or older and represents approximately 105.8 million civilian, non-institutionalized Americans. Gingival recession, gingival bleeding, and dental calculus were assessed at the mesio-buccal and mid-buccal surfaces in 2 randomly selected quadrants, one maxillary and one mandibular. Data analysis accounted for the complex sampling design used. RESULTS: We estimate that 23.8 million persons have one or more tooth surfaces with > or = 3 mm gingival recession; 53.2 million have gingival bleeding; 97.1 million have calculus; and 58.3 million have subgingival calculus; and the corresponding percentages are 22.5%, 50.3%, 91.8%, and 55.1% of persons, respectively. The prevalence, extent, and severity of gingival recession increased with age, as did the prevalence of subgingival calculus and the extent of teeth with calculus and gingival bleeding. Males had significantly more gingival recession, gingival bleeding, subgingival calculus, and more teeth with total calculus than females. Of the 3 race/ethnic groups studied, non-Hispanic blacks had the highest prevalence and extent of gingival recession and dental calculus, whereas Mexican Americans had the highest prevalence and extent of gingival bleeding. Mexican Americans had similar prevalence and extent of gingival recession compared with non-Hispanic whites. Gingival recession was much more prevalent and also more severe at the buccal than the mesial surfaces of teeth. Gingival bleeding also was more prevalent at the buccal than mesial surfaces, whereas calculus was most often present at the mesial than buccal surfaces. CONCLUSIONS: Dental calculus, gingival bleeding, and gingival recession are common in the U.S. adult population. In addition to their unfavorable effect on esthetics and self-esteem, these conditions also are associated with destructive periodontal diseases and root caries. Appropriate measures to prevent or control these conditions are desirable, and this may also be effective in improving the oral health of the U.S. adult population.
OBJECTIVES: The purpose of this study, conducted on patients with gingivitis and periodontitis, was twofold: to find out the serum and gingival crevicular fluid concentration of ciprofloxacin, which is a common drug used effectively against Actinobacillus actinomycetemcomitans and to determine the effects of ciprofloxacin administration on clinical parameters. METHOD: A total of 32 adult patients, consisting of 16 subjects with gingivitis and 16 subjects with untreated chronic periodontitis, were included in the study. The subjects were divided into four groups: group I included eight subjects with chronic gingivitis who had not previously received any ciprofloxacin; group II included eight subjects with chronic gingivitis to whom three doses of ciprofloxacin were administered (Siprosan 500 mg) to establish adequate gingival crevicular fluid and serum concentrations of the agent; group III consisted of eight subjects with chronic periodontitis who had not received any ciprofloxacin; group IV included eight subjects with chronic periodontitis to whom three doses of ciprofloxacin were administered to establish adequate gingival crevicular fluid and serum concentrations of the agent. All patients were systemically healthy, free of pain and reported no current medication usage. Each patient was treated with scaling and/or root planing using specific hand instruments under local anesthesia. Gingival index, plaque index and clinical attachment levels of the teeth were used to determine the clinical condition of the subjects and findings were recorded at the beginning, seventh day, 21st day and third month of the study. Serum ciprofloxacin level was measured in venous blood. Approximately 5 ml of venous blood was drawn from subjects in groups II and IV using a standard venipuncture technique. Gingival crevicular fluid samples were sampled from six interproximal sites with six paper strips in the posterior region of upper jaw (excluding third molar) and all gingival crevicular fluid and serum samples were evaluated by high-performance liquid chromatography. RESULTS: The serum concentrations of ciprofloxacin at the first and 72nd hour were not significantly different in subjects with periodontitis compared to subjects with gingivitis. But the gingival crevicular fluid concentrations of ciprofloxacin at the same hours were significantly high in subjects with periodontitis compared to subjects with gingivitis. Both subjects with gingivitis and periodontitis had significantly higher ciprofloxacin levels in the gingival crevicular fluid than in serum. The application of ciprofloxacin did not have any positive or statistically significant effect upon the clinical parameters of the subjects with gingivitis. On the other hand, a significant decrease in the clinical attachment level scores of the subjects with periodontitis (group IV) was observed compared to group III in the 21st day and third month. CONCLUSION: According to these results, the use of ciprofloxacin as an alternative drug in subjects with periodontitis but not gingivitis can be recommended. However, long-term studies are also needed to assess the effects of ciprofloxacin on clinical parameters.
A recently reported six-month gingivitis study demonstrated that in subjects with gingivitis, a triclosan/pyrophosphate dentifrice provided supragingival plaque control. The level of plaque reduction was comparable with that reported for other triclosan-containing dentifrices; however, no reductions in gingivitis were observed for triclosan/pyrophosphate relative to the negative control. One possible explanation of this result is that the Hawthorne effect in the study was too great to allow the detection of a treatment benefit for the triclosan product. In order to further explore the relevance of these results, three independent clinical studies were undertaken utilizing designs based on a 21-day experimental gingivitis model in which Hawthorne effects are minimized, in part due to the absence of toothbrushing. In each model, a pre-study prophylaxis was followed by a three-week period of oral hygiene instruction to establish optimum baseline gingival health in study participants. The studies varied in enrollment; 120, 33 and 32 subjects completed treatment on studies 1, 2, and 3, respectively. In study 1, test articles were dentifrice products (0.28% triclosan/5% pyrophosphate/0.145% sodium fluoride, 0.2% triclosan/0.5% zinc citrate/0.112% sodium fluoride, 0.145% sodium fluoride and 0.15% sodium monofluorophosphate) applied neat and undiluted via a performed tooth shield (that prevents mechanical tooth-brushing at the test sites in the oral cavity) in a partial mouth design. In study 2, test articles were also dentifrice products (0.28% triclosan/5% pyrophosphate/0.243% sodium fluoride, 0.3% triclosan/2% Gantrez copolymer/0.24% sodium fluoride and 0.243% sodium fluoride) but administered to subjects in the form of 1:3 aqueous slurry rinses. Lastly, in study 3, test articles were all mouthrinses (0.12% chlorhexidine, 0.045% triclosan in ethanol plus respective vehicle placebos). Clinical assessments to quantify the test articles' effects on the development of plaque and gingivitis were conducted at baseline (studies 1, 2 and 3), day 7 (studies 2 and 3), day 14 (studies 2 and 3) and day 21 (studies 1, 2 and 3). In study 1, no statistically significant treatment effects were observed between the test articles and controls for plaque or gingivitis development. In study 2, no statistically significant treatment effects were observed at any time point between test products for the development of gingivitis. At days 7 and 14, there were no significant differences between test products and control for plaque development as well. At day 21, the group rinsing with the triclosan/pyrophosphate/sodium fluoride slurry had significantly less plaque accumulation than the group rinsing with the triclosan/copolymer/sodium fluoride slurry (p < 0.05); however, neither of the groups using test products containing triclosan was significantly different for plaque development from the group using the sodium fluoride control test article. In addition, aspartate aminotransferase activity in gingival crevicular fluid was assayed at days 0 and 21; no between-group differences were found at either of these time points, though day 21 AST activities were higher than those at baseline. In study 3, statistically significant treatment differences in plaque regrowth and gingivitis were observed at day 21 for the chlorhexidine rinse versus all other rinses (p < 0.05). No other statistically significant treatment effects were observed between test compounds at any other time points. The results benchmark the anti-plaque and anti-gingivitis benefit for a range of triclosan-based product forms against positive and negative controls in a three different experimental gingivitis models, a design considered predictive of clinical efficacy in longer-term investigations. It is concluded that dentifrice products containing triclosan do not possess sufficient antimicrobial activity to suppress plaque and gingivitis development in the absence of normal oral hygiene, and that relative to chlorhexidine, triclosan itself offers only modest efficacy for the prevention of plaque accumulation and therefore the delayed onset of gingivitis.
Short-chain carboxylic acids (SCCA; C < or = 5; e.g., lactic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which accumulate in the gingival crevice, and exhibit significant biological activity, including the ability to alter gene expression. It has been hypothesized that among the activities of SCCAs are their ability to contribute to gingival inflammation. This concept complements the notion that specific periodontal pathogens are the causative agents of gingival inflammation. To begin testing these 2 hypotheses, we examined the relationship between SCCA concentrations, specific putative periodontal pathogens, and gingival inflammation in medically healthy periodontally diseased subjects. We reasoned that if SCCAs and/or specific periodontal pathogens were causative gingival inflammatory agents, gingival inflammation should increase with increasing concentration of the inflammatory mediator. We also recognized that other clinical variables needed to be controlled for, and an objective quantitative assessment of gingival inflammation used. To accomplish these tasks, sites within subjects were stratified by location and pocket depth, and the following quantified: bacterial presence; SCCA concentration; and gingival inflammation. The results indicated that gingival inflammation directly and significantly correlated with SCCA concentrations in the maxillary and mandibular molars, incisors and canines (all r > or = 0.47; all p < or = 0.015; too few bicuspids were available for complete analysis). The relationship between gingival inflammation and SCCA concentration was best described by a natural log relationship. Gingival inflammation did not, however, correlate positively with either the total number of specific putative periodontal pathogens, or the sum of subsets of these pathogens (-0.31 < or = r < or = 0.39; 0.08 < or = p < or = 0.75) for any of the locations. Finally, the SCCA concentration did not correlate with the level of individual or groups of pathogens. These data, together with historical work and other preliminary data, support the hypothesis that SCCA, rather than specific putative periodontal pathogens, may be a causative agent in gingival inflammation. This work may, in part, begin to explain the apparent lack of a direct relationship between current gingival inflammation and the prediction of bacterially mediated periodontal attachment loss.
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The purpose of the present study was to compare the bleeding tendency as elicited by probing the marginal gingiva (BOMP) and probing to the bottom of the pocket (BOPP) in smokers and non-smokers in natural gingivitis and during experimental gingivitis. 11 smokers (sm) and 14 non-smokers (nsm) were recruited. When they had less than 20% approximal bleeding sites, they entered a 14-day trial period of 'experimental gingivitis'. Subjects returned 30 days later, after resuming normal oral hygiene procedures, for a final gingival assessment. A split-mouth design was chosen using 2 contra-lateral quadrants for each index (being either BOMP or BOPP). A consistently higher bleeding score of approximately 10% was observed by probing to the bottom of the pocket. At day 14 with both indices, a significant difference between smokers and non-smokers was detected (BOMP: sm=15%, nsm=30%; BOPP: sm=27%, nsm=44%). The increment between gingival health and experimental gingivitis was significantly higher in non-smokers than in smokers but comparable for both indices (BOMP: sm=8%, nsm=23%; BOPP: sm=9%, nsm=26%). Probing to the bottom of the pocket results in significantly more bleeding in gingival health and gingivitis as compared to probing of the marginal gingiva. This shows that evaluation of the gingival condition with BOMP, the method of choice with respect to gingivitis, can be used as a parameter for inflammation when comparing smokers and non-smokers. The suppressed inflammatory response to plaque accumulation, as observed in smokers, indicates that they should be identified as a separate group when they participate as panelists in (experimentally induced) gingivitis studies.
The objective of this study was to determine the cytocompatibility of three different extracts of gingival retraction cords and to compare the cytotoxic effect of these materials on human gingival fibroblasts. Gingival retraction cords impregnated with aluminium sulphate (Gingi-Aid), dl-adrenaline HCl (Gingi-Pak) and non-drug-impregnated cord (Gingi-Plain) were eluted with culture medium for 10 min and 24 h. Cytotoxicity was judged using a tetrazolium bromide reduction assay. Our data demonstrated that gingival retraction cords applied alone almost completely inhibited cell viability (P < 0.05). In addition, the results also showed that the eluates from aluminium sulphate-impregnated cord, dl-adrenaline HCl-impregnated cord and non-drug-impregnated cord were cytotoxic to primary human gingival fibroblast cultures (P < 0.05). The cell viability of incubation of gingival fibroblasts containing 10-min eluates of aluminium sulphate, dl-adrenaline HCl and non-drug-impregnated cord was 61, 21 and 70%, respectively. The cell viability of incubation of gingival fibroblasts containing 24 h eluates of aluminium sulphate, dl-adrenaline HCl and non-drug-impregnated cord was 68, 58 and 72%, respectively. It was found that dl-adrenaline HCl-impregnated gingival retraction cord was the most toxic gingival retraction cord among the materials tested in all cultures (P < 0.05). The cytotoxicity decreased in an order of dl-adrenaline HCl-impregnated cord > aluminium sulphate-impregnated cord > non-drug-impregnated cord. The extent or degree of the cytotoxicity depended on the materials tested. Gingival retraction cords have significant potential for gingival toxicity. Careful management of gingiva retraction cords would lower the risk of potential gingival tissue damage during clinical application procedure and thus increase the success of prosthodontic procedures.
The prevalence and distribution of gingivitis and gingival recession were studied in 820 Nigerians aged 15, 19, 20 and 21 years sampled from Lagos educational establishments. The prevalence of gingivitis was relatively high at all ages. There was a high degree of correlation between the prevalence of gingivitis affecting mouths, papillae and margins. It therefore would appear that in those mouths with gingivitis, the proportion of affected papillae or margins to those not affected varies only within narrow limits. Although the peak prevalance of gingivitis was observed in the 15-year olds, the prevalence of gingival recession was higher in the 21-year-old students than in those aged 15 years. Gingival recession may be a sequel of gingivitis resulting from apical proliferation of the epithelial attachment with destruction of the subjacent periodontal tissues. Hence gingivitis should be distinguished from gingival recession in its prevalence and distribution.
The present study concerns an investigation carried out to determine the effects of gingival stimulation on the resolution of a human experimental gingivitis. 10 young male dental students participated in the experiment. Following the baseline examination (day 0), the participants were instructed to abstain from all oral hygiene procedures during a 21-day period. Heavy plaque accumulation and gingivitis developed during the 21-day induction period. On the evening of the 21st day, active oral hygiene measures were reinstitued, for an 8-day period, using 2 different methods. For the left side of the maxillary arch, a hygiene procedure including gingival stimulation was prescribed. On the other hand, for the right side, a hygiene method without gingival stimulation was instituted. On both sides of the upper arch, the gingival condition was assessed by means of the gingival index, and soft deposits were assessed by the plaque index (selected teeth: 13, 14, 15, 23, 24, 25). Measurements were performed on days 0, 21, 22, 23, 24, 25, 26, 27, 28, 29. On day 29, ideal oral hygiene conditions and gingival health were re-established on both sides. However, a statistical analysis of the data collected during the recovery period revealed that gingival index scores were temporarily, but significantly, higher on the side where mechanical stimulation was performed, although plaque deposits there decreased more rapidly. Thus the present work supports the idea that gingival stimulation does not in any way improve recovery from experimental gingivitis.
OBJECTIVES: Cyclosporin A (CsA) is a potent immunosuppressive drug used in organ transplant patients to prevent graft rejection. CsA-induced gingival overgrowth is one of the side effects of this drug and its pathogenesis is still unclear. The present study was planned to comparatively analyse total proteoglycan (PG) and chondroitin-4-sulphate (C4S) levels in CsA-induced overgrown gingival tissue samples obtained before and after initial periodontal treatment and to compare these findings with the situation in healthy gingiva. MATERIAL AND METHODS: Gingival tissue samples were obtained from nine patients with CsA-induced gingival overgrowth before and 4 weeks after initial periodontal treatment including oral hygiene instruction and scaling and also from 10 healthy control subjects. Total PG and C4S levels were determined by biochemical techniques. PG levels were analysed using modified Bitter and Muir method. C4S assay was carried out using chondroitin sulphate lyase AC and chondroitin-6 sulphate sulphohydrolase enzymes. The results were tested statistically using non-parametric tests. RESULTS: All clinical measurements in the CsA-induced gingival overgrowth group demonstrated significant reductions 4 weeks after initial periodontal treatment (p<0.05). There was no significant difference between the levels of baseline total PG in CsA-induced gingival overgrowth and healthy control groups (p>0.05). The gingival tissue levels of PG in CsA-induced gingival overgrowth group decreased significantly 4 weeks after treatment (p=0.043). Gingival tissue C4S levels in the overgrowth group were significantly higher than the healthy control group at baseline (p=0.000). C4S levels of the overgrowth group were significantly reduced after treatment (p=0.033), but these levels were still significantly higher than the healthy control group (p=0.000). CONCLUSION: The observed prominent increase in gingival tissue C4S levels may be interpreted as a sign of an increase in C4S synthesis in CsA-induced gingival overgrowth. Furthermore, remission of clinical inflammation by means of initial periodontal treatment had a positive effect on tissue levels of these extracellular matrix molecules.
The plaque flora isolated from discrete dentogingival sites during a human gingivitis experiment was analyzed as a function of the plaque score and of the gingivitis score. When the gingivitis score was plotted as a function of the plaque score, a nonbleeding gingivitis was associated with a proportional increase in the Actinomyces sp. at the expense of the Streptococcus sp. In particular, the percentage of Actinomyces israelii increased significantly, while the percent Streptococcus sanguis decreased significantly. A. israelii also increased significantly when a bleeding gingivitis developed. When the plaque score was plotted as a function of the gingivitis score, A. israelii increased significantly as the nonbleeding gingivitis developed, but A. viscosus and Bacteroides melaninogenicus increased significantly when the bleeding gingivitis developed. The availability of a sufficient number of plaques with a plaque score of 2.0 permitted the examination of the interrelationship of gingivitis and flora minus the effect of plaque biomass. The bacteriological profile showed that when bleeding occurred, the levels and proportions of A. viscosus and B. melaninogenicus increased significantly. These findings raise the possibility that proportional changes in the gingival plaque flora may uniquely contribute to the development of gingival inflammation in this experimental model.
BACKGROUND: We explore the possible association between the extent of gingivitis or periodontitis and an index of gingival microvascular perfusion response to compression of alveolar mucosa, called the gingival perfusion index (GIPI). METHODS: A cross-sectional analytical study was done in a sample of 60 adults, including healthy and non-insulin-dependent diabetic subjects of either gender, with teeth in the anteromandibular sextant with or without gingivitis and with or without periodontitis at the lower-left lateral incisor (LLLI). A sample was selected by convenience non-probability sampling. Gingival perfusion was evaluated at labial LLLI attached gingiva. Two perfusion recordings were done 5 minutes apart, each one consisting of a 40-second control phase, a 22-second compression phase, and a 40-second postcompression phase. LLLI alveolar mucosa was compressed with a wood-mounted cotton swab until reaching about one-fifth of the control perfusion value. GIPI was used as response dependent variable. The gingival index and probing depth were used as measures of the extent of gingivitis and periodontitis, respectively. RESULTS: By analysis of covariance and multiple regression analysis, it was found that only the probing depth (negatively) and gingival index (positively) predicted GIPI (R(2) adjusted = 0.5194, P <0.0001). CONCLUSIONS: The data strongly suggest that, at least in the studied sample, gingivitis and periodontitis operate as antagonistic modulators of gingival perfusion. The major practical implication of our findings is that an increase or decrease in this index (GIPI) at a given attached gingiva site could indicate, respectively, the clinical predominance of gingivitis or periodontitis in such a site.