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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.
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.
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 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.
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.
This parallel-group, double-blind, placebo-controlled clinical trial directly compared the efficacy of two antimicrobial dentifrice formulations for the control of plaque, gingivitis and gingival bleeding during six months of use following a pre-test randomization period. Test antimicrobial dentifrices for the study included: a stabilized stannous fluoride formulation (Crest Plus Gum Care-currently marketed in U.S.) comprised of 0.454% SnF2 in a stabilized silica abrasive base; and a formulation containing triclosan (Colgate Total, currently marketed outside the U.S. in numerous countries) comprised of 0.30% triclosan. 2.0% Gantrez co-polymer and 0.243% NaF in a silica abrasive base. The control dentifrice was a conventional fluoride dentifrice comprised of 0.243% NaF in a silica abrasive base. Clinical evaluations included Turesky et al. plaque, Löe-Silness gingivitis and gingival bleeding, and Meckel stain. The stabilized stannous fluoride dentifrice exhibited significant efficacy in the reduction of both gingivitis (20.5%) and gingival bleeding (33.4%) after six months relative to the placebo control (p < 0.05). In direct comparison, the stabilized stannous fluoride dentifrice reduced gingivitis and gingival bleeding significantly relative to the triclosan/copolymer dentifrice (p < 0.05). These results establish: 1) the superior clinical efficacy of a stabilized stannous fluoride dentifrice relative to a triclosan/copolymer dentifrice in the chemotherapeutic control of gingivitis and gingival bleeding; 2) the important contribution of clinical test design/sensitivity in assessing the therapeutic efficacy of antimicrobial agents; and 3) the value of head-to-head comparative studies in establishing the therapeutic relevance of clinical effects of formulations for the reduction of gingivitis.
One adverse effect of nifedipine, a long-acting vasodilator, is gingival overgrowth. Preexisting gingival inflammation and/or dental plaque has been suggested to be responsible for the progression of this side effect, but the precise mechanism is uncertain because of a lack of suitable animal models. A study was therefore done to establish an experimental model of gingival overgrowth in rats and to investigate the possible involvement of gingival inflammation and/or dental plaque in its development. Specific pathogen-free Fischer rats (male, 14 days old) were used. Gingival inflammation and dental plaque accumulation were induced by infection with Streptococcus mutans MT8148R. The nifedipine-treated rats (experimental group) were fed a caries-inducing diet containing nifedipine either with or without infection, while the nifedipine-untreated rats (control group) were fed the same diet, similarly with or without the infection. Marked gingival overgrowth was induced in the mandibular molar region of nifedipine-treated rats regardless of S. mutans infection, although the infection resulted in a further increase in the degree of gingival overgrowth. Histological examination of the gingival overgrowth revealed the presence of redundant subepithelial connective tissue in the treated rats, and inflammatory cell infiltration was apparent only in the tissue of the S. mutans-infected rats regardless of the nifedipine administration. These findings suggest that nifedipine induces gingival overgrowth in rats either in the presence or absence of gingival inflammation and/or dental plaque, although these factors can augment the effect of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
Triclosan is a broad-spectrum antimicrobial agent widely used in oral care products. In recent studies, a triclosan/pyrophosphate dentifrice has shown efficacy against dental plaque but not gingivitis. Further, experimental gingivitis studies on triclosan itself and in combination with other dentifrice ingredients demonstrate only moderate antimicrobial activity. In contrast, there are a number of other studies in the literature reporting the antigingivitis efficacy of triclosan/copolymer and triclosan/zinc citrate dentifrices. These dentifrices possess similar effects on dental plaque to triclosan/pyrophosphate, thus the lack of effect on gingivitis from triclosan/pyrophosphate was unexpected since comparable effects on dental plaque from similar formulations may infer similar antimicrobial activity and duration of action within the oral cavity. Therefore, the objective of this research was to understand the clinical variables important to observe the reported effects for triclosan dentifrice so this clinical model could in turn be used to test the effects of the triclosan/pyrophosphate dentifrice on gingivitis. To achieve this objective, it was determined that a suitable approach was to duplicate the methodology of previous successful clinical trials on triclosan/copolymer dentifrice in order to better understand the study design used to demonstrate the antigingivitis efficacy of triclosan-containing dentifrices. To this end, a prospective trial was conducted employing the same active product, clinical site, investigator and gingivitis/plaque examiner previously used. The study was a randomized, blinded, placebo-controlled, parallel group 3-month trial, which recruited subjects with Löe-Silness Gingival Index (GI) scores > or = 1.0 and Turesky Plaque Index (PI) scores of > or = 1.5. The study population consisted of 160 adults who brushed twice daily with either triclosan/copolymer or placebo control (containing copolymer) following a prophylaxis. Gingivitis and plaque were measured using the GI and PI, respectively, and scores were analyzed using a one-way analysis of covariance. There was no evidence that 3-month gingivitis or plaque scores (whole mouth or severity index) for the triclosan/copolymer group were different from the placebo group. Additional analyses were conducted on study population subgroups with increasing intervals of baseline GI bleeding sites to gauge the effect of baseline bleeding on the treatment effect. For subjects in the > or = 40 bleeding sites subset, triclosan/copolymer demonstrated a 4.2% GI and 15% gingivitis severity index reduction versus placebo at 3 months (0.10 < p < 0.20). These findings suggest that a study design which includes subjects with greater numbers of gingival bleeding sites at baseline may have the required sensitivity to demonstrate treatment benefits for triclosan/copolymer. However, additional experimental parameters remain to be fully articulated in order to replicate previously successful trials. The overall results of this trial are consistent with the experimental gingivitis results, and indicate that, even when formulated with the copolymer, triclosan as an oral antimicrobial agent possesses limited activity as an antigingivitis ingredient.
In both cross-sectional and longitudinal studies of young adults with plaque-induced gingivitis it has been observed that bleeding upon probing is only weakly associated with supragingival plaque. It has been speculated that gingival bleeding may be influenced by several independent factors other than plaque. Great intra- and interindividual variation of gingival thickness and width has been reported. Based on respective observations, the existence of different gingival phenotypes has been suggested. The aim of the present study was to investigate the possible influence of gingival thickness and width on bleeding on probing. Forty young adults with mild, plaque-induced gingivitis, 24 non-smokers and 16 smokers, participated in this cross-sectional study. In addition to periodontal probing depth, clinical attachment loss, width of gingiva, bleeding on probing, and presence of plaque, gingival thickness was measured with an ultrasonic device. Multivariable models were separately calculated for buccal, mandibular lingual, and palatal surfaces and generally adjusted for tooth type. Generalised Estimation Equation methodology was employed in order to adjust for correlated observations. Plaque was significantly associated with bleeding upon probing only at buccal sites (odds ratio 1.80, 95% confidence interval 1.19-2.72) An influence of similar magnitude was identified for smoking (odds ratio 1.76; 1.07-2.89). At lingual sites in the mandible, bleeding was influenced by smoking (odds ratio 2.25; 1.18-4.25) and gingival thickness (odds ratio for thick gingiva >1 mm of 1.93; 1.02-3.65), but not plaque. At palatal sites, only periodontal probing depth had an influence (odds ratio 1.89; 1.25-2.84). It was concluded that, apart from supragingival plaque, smoking was an independent risk factor for gingival bleeding on probing. Thin and vulnerable gingiva of insufficient width was not more likely to bleed after probing than thicker tissue.
Changes in the permeability of the underlying vasculature of the gingival crevice region may occur either as part of an inflammatory response during gingivitis or as a response to trauma during collection of gingival crevicular fluid IgM was selected as a marker of permeability and the concentration in gingival crevicular fluid was determined immunochemically by dot blotting, using rabbit antihuman IgM specific for mu chain. Gingival crevicular fluid samples were derived from experimental (non-cleaning) and control (cleaning) sites in six individuals participating in a 28-day experimental gingivitis study using a split-mouth protocol. The fluid was collected by a filter-paper method. At each site, four gingival crevicular fluid samples were collected for 5 s each over a 3-min period and a fifth sample was collected after a further 6 min. IgM was detected in 7/30 experimental strips at baseline (after intensive professional prophylaxis) and this increased to 21/30 by 24 days: control values were 13/30 and 12/30, respectively. The data indicate that IgM was detected with greater frequency as gingivitis becomes evident, suggesting increased permeability in response to plaque accumulation. IgM was detected in 17/120 of the first strip samples, collected over the 66-day study period, whereas in the fifth strip samples IgM was detected in 68/120, and the concentration of IgM in gingival crevicular fluid also increased, indicating that sequential collection induced permeability. It is concluded that the permeability of the gingiva changes in response to both an inflammatory stimulus and trauma due to collection.