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PubMed1997

A comparison of stabilized stannous fluoride dentifrice and triclosan/copolymer dentifrice for efficacy in the reduction of gingivitis and gingival bleeding: six-month clinical results.

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.

Adult↗
PubMed2006

Plasma and gingival crevicular fluid phenytoin concentrations as risk factors for gingival overgrowth.

BACKGROUND: Gingival enlargement is one of the side effects associated with the administration of phenytoin. The mechanism by which phenytoin induces gingival enlargement is not well understood. This study was conducted to investigate the relationship between plasma and gingival crevicular fluid (GCF) phenytoin concentrations and the degree of gingival overgrowth in patients with similar gingival and plaque indices and also to determine the risk factors for gingival enlargement. METHODS: Eighteen patients taking phenytoin in regular doses > or =6 months prior to the investigation participated in the study. Gingival enlargement was evaluated with two indices to score vertical and horizontal overgrowth. The gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), probing depth (PD), and clinical attachment level (CAL) were also evaluated. GCF and plasma phenytoin concentrations were determined by using high-performance liquid chromatography (HPLC). RESULTS: There was no significant difference between responders and non-responders for PD, CAL, PI, GI, and GBTI. Phenytoin was detected in all of the GCF and plasma samples using the HPLC analysis method. The mean concentration of phenytoin in GCF was significantly greater than the concentration of phenytoin in plasma. No significant difference was observed for the concentration of GCF phenytoin between responders and non-responders. However, the concentration of plasma phenytoin was significantly higher in responders than non-responders. CONCLUSION: This study showed that plasma phenytoin level appeared to be a risk factor for phenytoin-induced gingival overgrowth.

Adult↗
PubMed1993

Nifedipine-induced gingival overgrowth in the presence or absence of gingival inflammation in rats.

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)

Analysis of Variance↗
PubMed2002

Effects of triclosan/copolymer dentifrice on dental plaque and gingivitis in a 3-month randomized controlled clinical trial: influence of baseline gingivitis on observed efficacy.

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.

Adult↗
PubMed2002

The influence of gingival dimensions on bleeding upon probing in young adults with plaque-induced gingivitis.

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.

Adult↗
PubMed1997

Permeability of the gingival tissues to IgM during an experimental gingivitis study in man.

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.

Adult↗
PubMed2006

Interleukin-1beta, interleukin-12 and interleukin-18 levels in gingival fluid and serum of patients with gingivitis and periodontitis.

INTRODUCTION: Cytokines are of major importance in periodontal disease progression. Interleukin-12 (IL-12) stimulates interferon-gamma production by T helper type 1 (Th1) cells while IL-18 induces Th1 responses when present with IL-12 but Th2 responses in the absence of IL-12. IL-1beta has been correlated with periodontal disease destruction. This study determined the local concentrations of these cytokines in sites of gingivitis and periodontitis. METHODS: Gingival crevicular fluid was collected from two sites in each of 10 gingivitis patients and from two gingivitis sites and two periodontitis sites from each of 10 periodontitis patients. Serum samples were also collected. IL-1beta, biologically active IL-12 p70, the IL-12 p40 subunit and IL-18 concentrations were determined by enzyme-linked immunoabsorbent assay. RESULTS: IL-1beta and IL-18 concentrations were higher in the gingival crevicular fluid from periodontitis patients than in that from gingivitis patients; IL-18 concentrations were higher than those of IL-1beta. Very little IL-12, either p40 or p70, was detected in the gingival crevicular fluid samples. In the serum, very low levels of cytokines were found. The level of serum IL-12 p40, however, was higher than in the fluid from periodontitis sites of periodontitis patients. CONCLUSION: The local production of IL-1beta and IL-18 in the gingival crevicular fluid increased with increasing inflammation and IL-18 was the predominant cytokine at both gingivitis and periodontitis sites. Very little IL-12 was detected with levels decreasing with increasing inflammation. These results suggest that there is an association between severity of periodontal disease and levels of IL-1, IL-12 and IL-18.

Adult↗
PubMed1995

The clinical effect of a stabilized stannous fluoride dentifrice on plaque formation, gingivitis and gingival bleeding: a six-month study.

The effects of a stabilized 0.454% stannous fluoride dentifrice, currently marketed as Crest Gum Care, on supragingival plaque, gingivitis, gingival bleeding and oral soft tissue condition were studied in 328 adult male and female subjects who completed a six-month, double blind clinical study. Following initial examinations, subjects presenting with a minimum of five gingival bleeding sites received a thorough dental prophylaxis and were instructed to brush at least twice a day for three months with a commercially available fluoride dentifrice, packaged in such a way as to blind its identity to the study subjects. This constituted the three-month pre-test period. At the end of this period, subjects were again examined, given a second oral prophylaxis, and randomly assigned to brush with one of the following dentifrices: 1) stabilized 0.454% stannous fluoride, 2) 0.243% sodium fluoride control, or 3) one of three experimental dentifrices. Subjects were instructed to brush their teeth as they normally would, at least twice a day for one minute per brushing. Follow-up examinations after three and six months of dentifrice use evaluated supragingival plaque, gingivitis, gingival bleeding, extrinsic tooth stain and oral soft tissue status. After six months, the stabilized stannous fluoride dentifrice significantly reduced gingivitis and gingival bleeding by 20.5% and 33.4% compared to the sodium fluoride control group. However, the stabilized stannous fluoride dentifrice group was not significantly different from the control dentifrice group with respect to supragingival plaque scores. As expected, accumulation of extrinsic tooth stain was greater in the stabilized stannous fluoride group than the control group. No unexpected nor clinically significant oral soft tissue health effects were associated with the use of the test dentifrices. The results from this clinical study demonstrate that over a six-month period, twice-daily use of a dentifrice containing 0.454% stabilized stannous fluoride significantly reduced gingivitis and gingival bleeding, relative to a 0.243% sodium fluoride control dentifrice.

Adult↗
PubMed1998

Expression of the peptide antibiotic human beta-defensin 1 in cultured gingival epithelial cells and gingival tissue.

Human beta-defensin-1 (hBD-1) is a member of the family of small cationic antimicrobial peptides that have been identified in several mucosal epithelia. Because human gingival epithelium is a site that is constantly challenged by oral microorganisms, we examined the expression of hBD-1 in human gingival epithelial and fibroblast cell cultures and tissue samples. Cell cultures were challenged with cell wall extracts of Porphyromonas gingivalis or Fusobacterium nucleatum, Escherichia coli lipopolysaccharide, tumor necrosis factor alpha, or phorbol myristate acetate. hBD-1 mRNA was detected in unstimulated and stimulated cultures by reverse transcription (RT)-PCR using several primer sets specific for hBD-1. Gingival epithelial cells, but not gingival fibroblasts, expressed a product of the predicted size for hBD-1 mRNA. The sequence of the PCR product was identical to that of hBD-1. hBD-1 mRNA expression was not significantly modulated by any of the stimulants tested. Human gingival tissues from noninflamed and inflamed sites were also analyzed by RT-PCR. hBD-1 mRNA was expressed in all tissue samples. The relative expression of hBD-1 mRNA was similar in noninflamed and inflamed tissues obtained from each of four patients undergoing treatment for periodontitis. However, the relative expression of hBD-1 mRNA varied in gingival biopsies obtained from 15 different normal individuals, and the relative hBD-1 expression was unrelated to interleukin-8 expression. Our findings show the constitutive expression of hBD-1 mRNA in cultured epithelial cells and gingival tissues but not gingival fibroblasts. These findings suggest that expression of hBD-1 may play a role as part of the innate host defenses in maintaining normal gingival health.

Adult↗
PubMed1990

Langerhans cells in human chronic gingivitis and phenytoin-induced gingival hyperplasia.

Langerhans cell numbers in oral epithelium increase as dental plaque accumulates. The anti-convulsant drug phenytoin predisposes to gingival hyperplasia in certain patients who take this medication for epilepsy and who also have poor oral hygiene. In this study 7 patients with phenytoin-induced gingival hyperplasia were compared with 5 subjects with chronic marginal gingivitis. On initial examination and on completion of the hygiene phase of periodontal therapy (a period ranging from 3.0 to 4.25 months), clinical indices of plaque and gingivitis were recorded and biopsies were taken from the lower anterior labial gingiva. Frozen sections were stained by an immunoperoxidase technique using the monoclonal antibody OKT6, and the number of Langerhans cells in a defined cross-sectional area was counted. In phenytoin-induced gingival hyperplasia there was a marked increase in Langerhans cells (13.8 +/- 0.45) when compared with chronic gingivitis (7.7 +/- 0.31; p less than 0.05). Both groups showed marked reductions in their plaque and gingival indices and numbers of Langerhans cells once treatment had been completed. However, levels of Langerhans cells in the drug-induced hyperplasia remained significantly higher (3.5 +/- 0.26) than in chronic gingivitis (1.5 +/- 0.22; p less than 0.05).

Adult↗
PubMed1996

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

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

Adult↗
PubMed1996

Chemiluminescent assay of alkaline phosphatase in human gingival crevicular fluid: investigations with an experimental gingivitis model and studies on the source of the enzyme within crevicular fluid.

The purpose of this study was to investigate how levels of gingival crevicular fluid (GCF) alkaline phosphatase (ALP) change in relation to levels of plaque and gingival inflammation in 20 adults during a 21 day period of experimental gingivitis. The source of ALP within GCF was also investigated using a repeat sampling protocol; by determining enzyme levels derived from 30 putative periodontal pathogenic and non-pathogenic species; and by examining inhibition profiles from a variety of host and bacterial ALP isoenzymes. Total 30-s GCF ALP levels increased significantly (p < 0.002) during experimental gingivitis and preceded an increase in gingival index (GI) by approximately 7 days. Enzyme levels correlated with GCF volume (R = 0.7; p < 0.0001), but repeat sampling indicated that entry of ALP into the gingival crevice was independent of the rate of fluid flow. Only 5 of the bacterial species investigated produced clearly detectable levels of ALP in culture supernatants, these were P. gingivalis (381), P. intermedia (581), P. nigrescens (8944), Dentin P. gingivalis (TW 471: clinical isolate) and C. ochracea (25). Levamisole inhibition and studies on suspensions of washed plaque demonstrated that host-derived ALP contributed to > 80% of the enzyme in GCF. We conclude that elevated 30-s GCF ALP levels measured using the chemiluminescent assay reported, are detectable before increases in gingival indices and appear to be a better marker of gingival inflammation than ALP concentrations. The major source of ALP within GCF is host derived and in early inflammatory disease is likely to be of polymophonuclear leukocyte origin.

Adult↗
PubMed1996

Aggravation of gingival inflammatory symptoms during pregnancy associated with the concentration of plasminogen activator inhibitor type 2 (PAI-2) in gingival fluid.

Gingival inflammatory symptoms are aggravated during pregnancy. In vitro studies suggest a hormonal influence on the plasminogen activator inhibitor type 2 (PAI-2), and a disturbed balance of the fibrinolytic system could help to explain pregnancy gingivitis. Gingival crevicular fluid (GCF) was sampled in 14 women in pregnant and post-pregnant states. The gingival condition was assessed by the gingival index of Løe & Silness (GI) and the amount of bacterial plaque by the plaque index of Silness & Løe (PI). The ratio of sites with gingivitis to sites with bacterial plaque was calculated (G/P-ratio). Antigen levels of tissue plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), plasminogen activator inhibitors type 1 (PAI-1) and PAI-2 in GCF were determined with ELISAs and 17 beta-oestradiol and progesterone in serum with radioimmunoassays. For each individual the differences (delta) in hormone levels and PAs and PAIs between pregnancy and post-pregnancy were calculated. Based on differences in G/P-ratio between pregnancy and post-pregnancy, subgrouping was done into a high-reacting and a low-reacting group. For the total group, the mean G/P-ratio was 2.0 during and 1.2 after pregnancy (p = 0.064). A statistically significant correlation between delta progesterone and delta PAI-2 was noted: the higher delta progesterone, the lower delta PAI-2. No other significant correlations between hormone levels and components of the fibrinolytic system were found. For the total group of women, the concentrations of PAI-2, PAI-1 and t-PA were significantly higher during than after pregnancy. The individuals in the high-reacting group, however, showed a lower or unchanged production of PAI-2 during pregnancy, while those in the low-reacting group showed a greatly increased production. The lower inhibitory capacity in terms of a low production of PAI-2 during pregnancy in women with a higher inflammatory reaction indicates that the components of the fibrinolytic system may be involved in the development of pregnancy gingivitis and implies that PAI-2 serves as an inhibitor of importance for tissue proteolysis. The present finding contributes to the explanation of pregnancy gingivitis.

Adult↗
PubMed2001

Occurrence of Prevotella intermedia and Prevotella nigrescens in relation to gingivitis and gingival health.

AIM: The occurrence of Prevotella intermedia (Pi) and Prevotella nigrescens (Pn) in relation to natural gingivitis, gingival health and 14-day experimental gingivitis was investigated in 25 non-dental students. MATERIALS AND METHODS: Samples were taken from the dorsum of the tongue, the tonsils (or tonsillar area), and the supra- and subgingival plaque. RESULTS: The microbiological results show that 73% of the samples were positive for the bacterial species presumed to be Pi and/or Pn. In natural gingivitis, gingival health and in experimental gingivitis 25, 23 and 25 subjects were found to be positive for Pi and/or Pn, respectively. The results of the 889 isolates that were successfully purified and differentiated, show that almost all subjects were colonized with Pn whereas approximately half of the study population harboured Pi. These 2 species were isolated from both dental plaque and mucosal sites and were found to colonize the oral cavity simultaneously. CONCLUSION: In natural gingivitis, at the start and after 14 days of experimental gingivitis, Pn was the predominant micro-organism.

Adolescent↗
PubMed2005

Analysis of changes in gingival contour from three-dimensional co-ordinate data in subjects with drug-induced gingival overgrowth.

OBJECTIVES: This aim of this study was to develop and assess a technique that could be used to assess accurately the gingival volume changes seen in drug-induced gingival overgrowth by the analysis of data obtained from an entire gingival surface by means of three-dimensional imaging. MATERIAL AND METHODS: Stone dental models of patients before and after gingivectomy procedures were digitized with a laser scanner and then regenerated as computer models constructed from the acquired three-dimensional co-ordinate data. A comparison of superposed "before" and "after" surfaces was undertaken to assess and accurately quantify changes in gingival contour. RESULTS: The mean vertical tissue reduction varied from 1.58 to 2.56 mm in the four study subjects and individual differences are shown. The maximum thickness of removed buccal gingival overgrowth was found to range between 1.20 and 3.40 mm. The volume of tissue removed from each inter-dental papilla ranged from 4.2 to 46.1 mm3 and the mean volume of the papilla removed from each subject+/-SD values was 24.8+/-13.1 mm3. CONCLUSION: This method will measure changes in gingival tissues to within 60 microm in one plane, making it ideal for the assessment of longitudinal changes in gingival contour as seen in the development of gingival overgrowth, its recurrence after surgery or the changes in volume brought about by surgery.

Gingiva↗
PubMed1998

Immunohistochemical demonstration of the plasminogen activator system in human gingival tissues and gingival fibroblasts.

The relative distribution of urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) was studied in cultured human gingival fibroblasts, healthy gingival tissues and inflamed gingival tissues by immunohistochemistry. In cultured gingival fibroblasts t-PA, u-PA and PAI-1 were expressed in cytoplasm; u-PA and PAI-1 were more intensely stained than t-PA; PAI-2 was not detectable in gingival fibroblasts. Following interleukin 1 beta (IL-1 beta) stimulation, the intensity of intracellular staining for t-PA was increased and a number of cells staining strongly for PAI-2 were seen; no difference in the intensity of immunostaining level was noted for the expression of u-PA and PAI-1 between IL-1 beta stimulated cells and unstimulated cells. In healthy gingival tissues, u-PA and PAI-1 displayed a wide distribution throughout all the connective tissue and epithelium; t-PA localized mainly in the connective tissue while PAI-2 showed little association with the connective tissue but did faintly stain in the epithelial layer. In inflamed gingival tissues, staining for t-PA was significantly increased in the extracellular matrix of the connective tissue, whereas staining for u-PA, PAI-1 and PAI-2 was found to be slightly increased, but no significant difference was noted for staining when compared with the healthy gingival tissues. A granular distribution of t-PA, u-PA, PAI-1 and PAI-2 was noted around areas of inflammatory cell infiltration. These immunohistochemical findings indicate that the plasminogen activator system produced by fibroblasts may be influenced by the presence of the inflammatory mediator IL-1 beta. In addition, the significant increase of t-PA in inflamed connective tissue and the wide expression of these components around inflamed cells may contribute to connective tissue degradation and may relate to the migration and localization of monocytes/macrophages in inflamed tissue.

Antibodies, Monoclonal↗
PubMed1989

Assessment of complement cleavage in gingival fluid during experimental gingivitis in man.

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 gingival 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 greater than or equal to 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 less than 0.0001 level.(ABSTRACT TRUNCATED AT 250 WORDS)

Complement Activation↗