Development Of Experimental Gingivitis Research Articles

Effect of guava and vitamin C supplementation on experimental gingivitis: A randomized clinical trial

To study the effect of guava and synthetic vitamin C on the development of gingival inflammation during experimental gingivitis. Participants were randomly assigned to three groups supplemented daily with either 200g guava, 200mg synthetic vitamin C or water. The study included a 14days pre-experimental period with oral hygiene instructions, scaling, prophylaxis and supplementation. Thereafter, experiment gingivitis was initiated, while continuing supplementation. At baseline, Day 7 and Day 14 of experimental gingivitis, Plaque Index (PlI) and Gingival Index (GI) were assessed. During the entire study, dietary fruit/vegetables intake was minimal. PlI increased in guava, vitamin C and control group (ΔPlI: 1.30, 1.61 and 1.79, respectively). However, the guava group developed significantly less plaque compared to the control group. The GI increase in both guava and vitamin C group was significantly less than the increase in the control group (ΔGI: 0.10, 0.24 and 0.87, respectively). In a population of young nonsmoking adults, consumption of either 200g guava/day or 200mg synthetic vitamin C/day, prior to and during the oral hygiene abstention period, has a preventive effect on the development of experimental gingivitis as compared to the control group that developed the usual amount of experimental gingivitis.

Salivary cytokine levels in early gingival inflammation

ABSTRACTSalivary protein levels have been studied in periodontitis. However, there is lack of information on salivary cytokine levels in early gingival inflammation. The aim of this study was to determine salivary levels of vascular endothelial growth factor (VEGF), interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1, IL-1β, and IL-1 receptor antagonist (IL-1Ra) in gingival inflammation. Twenty-eight systemically and orally healthy nonsmokers abstained from oral hygiene protocols for 10 days. After that, self-performed cleaning was resumed for 14 days. Plaque and gingival indexes were measured, and saliva samples were collected at days 1, 4, 7, 10, and 24. Salivary cytokines were detected with Luminex®-xMAP™. Salivary IL-1β, IL-1Ra, and VEGF levels decreased after 10 days’ development of experimental gingivitis and reached baseline levels at the end of the 2-week resolution period. Salivary IL-8 levels decreased and remained low during development and resolution of experimental gingivitis. Initial inflammation in gingival tissues is associated with a decrease in inflammatory cytokines in saliva. Further studies are needed to evaluate if inflammatory cytokines bind to their functional receptors within the gingival tissue during early gingivitis, which may limits their spillover to the gingival crevice and ultimately saliva.

Inhibition of Experimental Gingivitis in Beagle Dogs With Topical Mercaptoalkylguanidines

Nitric oxide is a free radical produced in host tissues by constitutive and inducible forms of the enzyme nitric oxide synthase. Nitric oxide plays physiological roles, but it is also involved in the pathophysiology of several inflammatory conditions, including arthritis, ulcerative colitis, and circulatory shock. Local increases in inducible nitric oxide synthase (iNOS) and reactive nitrogen products have also been demonstrated in humans and animals with periodontal disease. This masked, randomized, placebo-controlled preclinical investigation examined the effect of two mercaptoalkylguanidines, mercaptoethylguanidine (MEG) and guanidinoethyldisulfide (GED), which are iNOS inhibitors and reactive nitrogen scavenging compounds, on the development of experimental gingivitis in beagle dogs. Fifteen female, 1-year-old beagles first completed a 2-week dose-escalation experiment during which a maximum tolerated dose was determined for MEG and GED gels. Thereafter, all animals were brought to optimal gingival health by mechanical scaling, followed by rigorous daily toothbrushing over a 4-week washout period. Experimental gingivitis was then induced, with cessation of plaque control and institution of a soft diet over 8 weeks. Beagles randomly received 0.3% MEG, 0.3% GED, or placebo (vehicle) gels, topically applied twice daily to premolar teeth. Gingival inflammation, bleeding tendency, and supragingival plaque were clinically measured at baseline and at 2, 3, 4, 6, and 8 weeks. Comparisons among groups and between group pairs (active versus placebo) were made using Kruskal-Wallis tests. From baseline to day 7, all groups expressed similar indices. Thereafter, significant and time-dependent increases in the plaque index (PI), gingival index (GI), and percentage of bleeding on probing (%BOP) were observed in placebo-treated beagles. Mean GI scores for beagles treated with GED or MEG gels remained at or below baseline levels for the entire treatment period. At weeks 2, 3, 4, and 8, GI scores were significantly lower for MEG and GED groups compared to the placebo group (P<0.05). In addition, MEG and GED gels significantly reduced gingival bleeding responses by 8 weeks (P<0.05). Although placebo-treated beagles demonstrated %BOP scores of 43% at week 8, GED- and MEG-treated beagles exhibited %BOP scores of 21% and 26%, respectively. Since no statistical difference among PI scores was noted for any of the time points, neither mercaptoalkylguanidine appeared to affect supragingival plaque levels. The data from this preclinical study indicate that mercaptoalkylguanidines, topically administered, may significantly reduce experimental gingivitis in the beagle dog.

Longitudinal changes in TCRB variable gene expression and markers of gingival inflammation in experimental gingivitis.

The aim of this study was to gain information of the cellular and molecular events which occur during the development of experimental gingivitis and to determine whether such changes occur in the presence or absence of alveolar bone resorption. Clinical, radiographic, biochemical and immunological variables were monitored in a 3-week, single-centre, experimental gingivitis study of 10 healthy volunteers. Following screening and professional prophylaxis to achieve visibly healthy gingival status, subjects abstained from all oral hygiene practises in one maxillary (test) quadrant for a period of 21 days. At days 0 and 21, in test and (contralateral) control quadrants, % bleeding on controlled pressure probing (% BOP) was calculated, and radiographic alveolar bone status was assessed using bilateral standardised vertical bite-wing radiographs and digital subtraction radiography (DSR) analysis. In test quadrants, gingival crevicular fluid (GCF) was sampled from 4 sites per subject with Periopaper strips, and prostaglandin E2 (PGE2) levels measured using an enzyme immunoassay (EIA) kit. At days 0, 7 and 21, one interdental papilla was surgically excised from the test quadrant, and the expression of T cell receptor B variable (TCRBV) genes was investigated using a reverse transcription-polymerase chain reaction (RT-PCR) procedure. At days 0, 7 and 21, peripheral blood lymphocytes (PBL) were isolated and additionally investigated for TCRBV gene expression. Following 21 days of plaque accumulation in test quadrants, a statistically significant increase in % BOP scores confirmed the presence of gingival inflammation (p<0.001). DSR analysis revealed that there were no significant alveolar bone changes in either the test or control quadrants between days 0 and 21 (p>0.05). EIA analysis of GCF samples identified a significant decrease in mean GCF PGE2 concentrations from day 0 to day 21 (p<0.05). RT-PCR analysis indicated that genes from all 3 TCRBV families studied (TCRBV-2, -6, -8) were expressed in the PBL samples at all time points and in healthy gingival tissues at day 0. A restriction in the expression pattern of TCRBV genes similar to those which have previously been reported in chronic periodontitis was noted at gingivitis sites. It is possible that such an event may identify susceptibility to periodontal disease independently of other positive predictive markers such as GCF-PGE2.

Experimentally induced peri‐implant mucositis. A clinical study in humans.

The purpose of this study was to compare the clinical and microbiological (microscopic) parameters during the development of experimental gingivitis and experimental peri-implant mucositis. Twenty partially edentulous patients were treated for moderate to advanced periodontal disease. Following active periodontal therapy consisting of motivation, instruction in oral hygiene practices, scaling and root planing and periodontal surgery where indicated, IMZ oral implants were incorporated in posterior edentulous areas. After 3 months of healing, the prosthetic abutments were connected, and the patients were closely supervised for another 2 months of healing. At this time, baseline data were obtained. Re-examinations were scheduled at 3 and 6 months. Following this, the patients were asked to refrain from oral hygiene practices for 3 weeks. At all examinations including the end of the period of no oral hygiene, the following clinical parameters were obtained: Plaque Index, Gingival Index and Sulcus Bleeding Index, all modified by Mombelli et al. (1987), probing pocket depths and recession in mm. Furthermore, submucosal/subgingival plaque samples were obtained and analyzed using phase contrast microscopy. At the end of the 3-week period of plaque accumulation, optimal oral hygiene was reinstituted. There were no statistically significant differences between the mean values of all parameters at implant compared to tooth sites at any observation periods. The period of no oral hygiene demonstrated a similar cause-effect relationship between the accumulation of bacterial plaque and the development of peri-implant mucositis as established for the gingival units by the experimental gingivitis model.

Microcirculatory dynamics in experimental human gingivitis.

The purpose of this study was to determine the changes that occur in the gingival microcirculation during the development of experimental gingivitis in humans. There have been no studies published to date combining videomicroscopy and laser Doppler flowmetry to study vascular dynamics in experimental gingivitis. Alterations occurring in the microcirculation of the marginal gingiva in 10 (18-30-year-old), healthy male humans when they suspended oral hygiene procedures in a proscribed area for 12-16 days were monitored. A partial mouth, experimental gingivitis model was employed. Gingival health was evaluated before and after the experimental period by assessing gingival and plaque indices and gingival crevicular fluid volume. Gingival vascular monitoring included measurement of red blood cell velocity in individual gingival microvessels via videomicroscopy and measurement of regional gingival blood flow using laser doppler flowmetry. The number of vessels visible in a given microscopic field in a given subject and the number of vessels exhibiting flow were also determined from the videotapes. Systemic cardiovascular and respiratory parameters were monitored to ensure that gingival vascular changes were not secondary to systemic changes. Gingivitis developed in all subjects; significant increases (Student t-test, p < 0.05) were seen in plaque index, gingival index, bleeding on probing and crevicular fluid volume. No change in superficial capillary blood velocity and a significant decrease in gingival regional blood flow were seen with gingivitis. A significant increase in the number of vessels visible in microscopic fields and a decrease in the % of vessels exhibiting flow were observed. Gingival microcirculation exhibited a dramatic, dynamic change in response to the development and progression of gingivitis.

Changes in crevicular fluid levels of interleukin-1 beta, leukotriene B4, prostaglandin E2, thromboxane B2 and tumour necrosis factor alpha in experimental gingivitis in humans.

We conducted a study to determine the sequence of cytokine and lipid mediator activation within the periodontium during the development of experimental gingivitis in humans. Crevicular fluid samples were collected from 7 previously cleaned, healthy patients at baseline, 1, 2, 3 and 4 weeks following the cessation of all oral hygiene measures. Gingival and plaque scores were taken at each visit to follow the development of gingivitis and plaque retention. Crevicular fluid samples were assayed in quadruplicate for prostaglandin E2 (PGE2), thromboxane B2 (TxB2), leukotriene B4, interleukin-1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF alpha) by RIAs or ELISAs, maintaining site pairing to examine temporal changes. Redness scores (expressed as mean percentage of sites with redness present) increased almost linearly from a baseline value of zero to approximately 40% at 1 week, 59% at 2 weeks, 83% at 3 weeks and 100% at 4 weeks. The mean % of sites with bleeding on probing increased gradually from zero at baseline to 5% at 3 weeks and then rose abruptly to 25% at 4 weeks. CF-PGE2 and CF-TxB2 levels remained fairly stable at baseline levels for the first 3 weeks then rose sharply by 2.5- and 2-fold, respectively, at 4 weeks. CF-LTB4 levels increased 2-fold by 1 week and 4-fold by 4 weeks. The CF levels of IL-1 beta increased abruptly from mean baseline values of 16.5 +/- 9.3 ng/ml to 131 +/- 76.0 ng/ml at 1 week and remained at this level for the duration of the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of cigarette smoking on the development of experimental gingivitis.

The aim of this investigation was to study the influence of cigarette smoking on the development of gingivitis. Experimental gingivitis was induced in the mandibular anterior region by abstention from oral hygiene for 28 days. The study group consisted of 20 healthy dental students, 10 of whom were regular smokers. The clinical parameters studied were gingival bleeding on probing (60 g), gingival redness and gingival exudate. The results showed that the plaque formation rate was similar in both groups. However, smokers displayed a less pronounced gingival inflammatory reaction as compared with non‐smokers. Concerning gingival bleeding and gingival redness, the reaction in smokers was significantly less elevated from d 14 through d 28 and concerning the amount of gingival exudate it was significantly less elevated from d 21 through d 28. The differences between groups tended to increase with time. These results suggest that the inflammatory gingival response to accumulating plaque may be suppressed under the influence of cigarette smoking.

Development of a biochemical profile for gingival crevicular fluid. Methodological considerations and evaluation of collagen-degrading and ground substance-degrading enzyme activity during experimental gingivitis.

The potential application of gingival crevicular fluid (GCF) analysis to periodontal diagnosis has been examined for more than 25 years. Unfortunately, the information available has not provided the clinician with a more sensitive means of diagnosing periodontal disease or an effective means of monitoring periodontal therapy. A careful review of the literature on GCF, however, suggests that discrepancies occur in the method of GCF collection, the use of GCF for analysis from pooled or isolated crevicular locations, the method of analyzing the samples and the way in which the data is reported. Studies in our laboratory have suggested a technique for GCF analysis that collects GCF from individual crevices with a filter paper strip inserted for a standard time, determines the volume of GCF collected with a calibrated electronic meter and elutes the material into a larger volume of diluent. This approach allows for detection of site-to-site and patient-to-patient differences in GCF volume while providing sufficient samples to analyze GCF for multiple constituents. We have used this approach to evaluate GCF for vertebrate forms of the enzymes collagenase (latent and active forms), beta-glucuronidase and arylsulfatase during the development of experimental gingivitis in man. Interproximal and midradicular areas were studied. Our results indicate that during the 4 weeks of the gingivitis, the absolute amount of active collagenase in GCF increased 550% at the interproximal sites and 190% in the midradicular sites, and the per cent of active collagenase increased from 15 to 71% at the interproximal sites, and from 16 to 36% at the midradicular sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies of host responses during experimental gingivitis in humans

The aim of the study was to find out whether autologous supragingival plaques collected at various times during the development of experimental gingivitis in men differ in their potential to induce PMN responses in vitro. Ten subjects refrained from all oral hygiene for a period of 21 days. At day 0, Day 3 and Day 21 after cressation of oral hygiene clinical indices (plaque index, gingival index, gingival crevicular fluid flow) were assessed plaque was collected at day 3 and Day 21 after cessation of Oral hygiene clinical indices (plaque index, gingival index, gingival crevicular fluid flow) were assessed plaque was collected at Day 3 and Day 21. PMNs, isolated from peripheral blood 1–2 months after the non‐brushing period were incubated with the various autologous plaques in the presence or the absence of autologous serum. Supernatants of cell cultures were monitored for extracellular release of lysosomal constituents, viz. lysozyme, myeloperoxidase and lactoferrin. There was no difference in the amounts of lysozyme, myeloperox dase and lactoferrin. There was no difference in the amounts of lysozyme or myeloperoxidase released by PMNs. The inclusion of fresh serum enhanced PMN release reactions but there was no significant differences in the relative capacity of Day 0, Day3 and Day 21 sera to modulate PMN responses. A statistically significant positive correlation was established betwen the magnitude of lactoferrin release from PMNs exposed to Day 3 plaque and the gingival fluid flow recorded on Day3. Lactoferrin is segregated in the specific granules of the PMNs which also contain other cationic proteins, collagenases and neutral proteinases. These data suggest that a possible causal relationship may exit between the release of PMN constituents and the development of inflammation during the early phases of gingivitis.

Development of experimental gingivitis in the juvenile and adult beagle dog

Abstract. In a previous paper a lower tendency to develop gingivitis was reported among preschool children compared to adults. The aim of the present study was to clarify if the same age‐dependent difference exists in dogs.Six beagle dogs from the same litter were used. two periods of discontinued oral hygiene were studied, one period when the dogs were 3 months old and the other at 12 months. Prior to and between the experimental periods the animals were subjected to meticulous toothcleaning. During the experimental periods the Gingival and Plaque Index scores as well as the amounts of gingival exudate and crevicular leukocytes were determined on days 0, 4, 7, 14, 21 and 28.During the juvenile period the development of dental plaque was lower compared with the adult period. The frequency of gingival units with high Gingival Index scores was lower at every registration interval during the juvenile period. The amounts of gingival exudate and crevicular leukocytes increased to high values during the adult stage but only small increments were found in the juvenile stage. An intraindividual comparison of the increase in the amount of gingival exudate from day 0 to day 28 in areas with the same amount of dental plaque accumulation showed a lower increase in gingival exudate during the juvenile stage in all dogs.

Cell mediated immune responses to plaque antigens during experimental gingivitis in man.

The purpose of the present investigation was to evaluate the ability of antigens of human dental plaque microorganisms to stimulate peripheral blood lymphocytes (PBL) from humans during the development and recovery from experimental gingivitis.Eleven healthy dental students (22–36 years) participated in the study. At the start of the experiment, they exhibited clean teeth and clinically healthy gingivae. They then abstained from all oral hygiene measures for four weeks according to the model proposed by Löe et al. (1965). At the start, after 1, 2, 3 and 4 weeks of abolished oral hygience and 2 weeks following reinstitution of oral hygiene, the oral conditions were assessed, using the critieria of the Plaque Index system (Löe &amp; Silness 1964) and the Gingival Index system (Löe &amp; Silness (1963).At each examination triplicate microcultures, each containing 2 × 105 viable PBL in .2 ml TC 199 with glutamine and antibiotics containing 10% fetal calf serum, were stimulated with four concentrations of sonicates from V. alcalescens, F. nucleatum, B. melaninogenicus, A. viscosus, A. naeslundii, S. sanguis and pooled dental plaque all obtained from the previsouly performed experimental gingivitis. The cultures were incubated for 78 hours at 37°C in 5% CO2. 3H‐thymidine was added for the final 8 hours.Only A. viscosus was able to stimulate PBL to undergo blastogenesis during the development of experimental gingivitis. A. viscosus stimulated the PBL of 3 subjects after one week but all subjects after 2 weeks of abolished oral hygiene. The stimulation indices (SI) remained &gt;2.5 for the rest of the experimental period. Following 2 weeks of reinstituted oral hygiene, the SI reached preexperimental levels.These results suggest that A. visocus is capable of inducing a specific cellular immune response during the development of experimental gingivitis and may be important as a causative plaque constituent. Further research is indicated to study this association.

Experimental gingivitis in young and elderly individuals.

The development of experimental gingivitis was studied in young elderly humans during a 21-d period of oral hygiene abstention. The state of the gingiva was assessed by the Gingival Index and by measurements of the amount of gingival exudate on filter paper strips placed at the entrance of the gingival sulcus of the lower lateral incisors and cuspids. Soft deposits were assessed by the Plaque Index and by differential counts of microorganisms in gram stained smears od ento-gingival plaque. At the end of the plaque growth period, the patients were given a thorough dental prophylaxis. Gingival condition and plaque were assessed at regular intervals during a subsequent period of controlled oral hygiene. The development of gingivitis during the oral hygiene abstention period was more rapid and more severe in old than in young individuals. Plaque accumulation was greater in the older persons. A definite difference in plaque consistency was alos observed. However, microscopic counts of various types of microorganisms did not reveal any differences throughout the period of plaque accumulation. When active oral hygiene was reinstituted, the state of the gingiva rapidly returned to pre-experimental levels in both groups. The findings of this study indicate that with age ther is an altered host response to the microorganisms of the plaque.