Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The plasminogen activator (PA)-plasmin proteolytic system has recently received considerable attention because of its participation in a wide variety of biological activities and in pathological conditions involving tissue destruction. Excessive mechanical stress such as occlusal trauma is associated with alveolar bone loss in severe periodontitis. Therefore, mechanical stress may involve degradation of the extracellular matrix by occlusal trauma through activation of the PA-plasmin proteolytic system. We examined the effects of mechanical stress on PA activity, gene expressions of tissue type (t) PA, urokinase type (u) PA and PA inhibitor-1 (PAI-1) in human PDL cells. Human PDL cells were cultured on flexible-bottomed culture plates and placed on a Flexercell Strain Unit. The cells were flexed at 6 cycles (5 s strain, 5 s relaxation) at 9% and 18% elongation for 5 d. Application of tension-force induced significantly higher PA activity in stressed PDL cells than in non-stressed controls, and did so in a time- and magnitude-dependent manner (p < 0.001, ANOVA). Western-blot analysis revealed that the high level of activity was due to tPA and not uPA. Gene expression of tPA mRNA in stressed PDL cells, as examined by RT-PCR, increased on d 5. These findings suggest that tPA may be involved in periodontal metabolism in response to mechanical stress.
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PMID:Effect of tension-force on plasminogen activator activity from human periodontal ligament cells. 913 97

Systemic and topical administration of non-steroidal anti-inflammatory drugs (NSAIDs) has been shown to reduce periodontal disease progression in both animal models and human subjects. Our present research focuses on single enantiomers of these agents to examine whether enantiospecific therapy will be efficacious in slowing periodontitis. The purpose of this study was to evaluate the inhibitory effects of (S)-ketoprofen on experimentally induced alveolar bone loss in beagle dogs. 16, 18-month-old, female beagles were brought to optimal periodontal health over a 2-week pretreatment period. Experimental periodontitis was then induced by placing silk ligatures around premolar and molar teeth and by instituting a soft, plaque-promoting diet. At baseline, animals were randomized to 1 of 4 groups, consisting of 2x daily administration of (1) placebo dentifrice, (2) 0.3% (S)-ketoprofen dentifrice, (3) 3.0% (S)-ketoprofen dentifrice, or (4) 10.0 mg (S)-ketoprofen capsules (p.o.) over a 60 day treatment period. Standardized, periapical radiographs exposed at days 1 and 60 were analyzed by computer-assisted digital radiography in order to assess the rate of alveolar bone loss. Secondary outcomes included technetium 99m-tin-diphosphonate (99mTc-Sn-MDP) uptake and the gingival index. At baseline, no differences were observed among the groups for linear bone height or 99mTc-Sn-MDP uptake ratios. From days 1 to 60, cohorts differed significantly in terms of bone loss rates (p < 0.001). In particular, beagles treated with systemic or topical (S)-ketoprofen (0.3% or 3.0% dentifrices) exhibited significantly lower mean rates of bone loss compared to placebo treated beagles (p < 0.05). Group differences in mean radiopharmaceutical uptake ratio changes approached significance (ANOVA, p = 0.07), where animals treated with topical 0.3% (S)-ketoprofen demonstrated a reduction and other groups demonstrated elevations over the 60-day dosing period. Treatment cohorts did differ significantly with respect to changes in mean gingival indices (p < 0.05). Animals treated with 0.3% or 3.0% (S)-ketoprofen dentifrice exhibited significantly reduced elevations in gingival index scores as compared to placebo treated animals. These data provide evidence that enantiospecific therapy with (S)-ketoprofen, topically or systemically delivered, may alter the progression of periodontal disease in the beagle dog model.
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PMID:Enantiospecific inhibition of ligature-induced periodontitis in beagles with topical (S)-ketoprofen. 926 37

This study compared the intra-examiner and inter-examiner error of 2 constant force probes to the reading of a conventional manual probe. 3 examiners made repeated examinations of attachment level using a modified Florida probe and a manual North Carolina probe (read to 1 mm or 0.5 mm); relative attachment level measurements were made using a Florida disk probe. One probe was used in each quadrant in 8 subjects with moderate to advanced periodontitis. Error was calculated as the mean of the absolute value of the difference between each examination, and the correlation between values at each examination calculated. Statistically-significant differences between probe type, examiners, and sites were detected using a repeated measures ANOVA accounting for the nesting within subjects. There was a significant difference in error by probe type (modified Florida probe 0.62 +/- 0.03 mm, r = 0.86; Florida stent probe 0.55 +/- 0.05 mm, r = 0.82; manual probe to 1 mm 0.39 +/- 0.02 mm, r = 0.88; manual probe to 0.5 mm 0.40 +/- 0.02 mm, r = 0.89; (p < 0.001). Significant differences were observed by examiners (p < 0.01). These data indicate that both manual and controlled-force probes can provide measurement within less than 1 mm of error; however, individual calibration of examiners remains important in the reduction of error.
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PMID:A comparison of manual and controlled-force attachment-level measurements. 944 30

The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) secretion by peripheral blood mononuclear cells (PBMC, consisting of monocytes and lymphocytes) and gingival mononuclear cells (GMC). Both peripheral blood and gingival tissue adjacent to the alveolar crest were taken from non-smoking adult periodontitis patients. Gingival tissue was treated with collagenase and deoxyribonuclease and GMC and PBMC were isolated by Ficoll-Hypaque centrifugation. GMC and PBMC (100,000 cells/200 microl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1% ST, 100 microg/ml nicotine, 1 microg/ml Porphyromonas gingivalis LPS, or 1 microg/ml P. gingivalis LPS and either 100 microg/ml nicotine or 1% ST. Enzyme immunoassays were used to quantify PGE2 and IL-1beta. Treatments were compared by repeated measures ANOVA. 100 microg/ml nicotine (7-fold, p<0.02) and 1% ST (3.5-fold, p<0.004) significantly increased secretion of PGE2 by PBMC relative to control cultures. 100 microg/ml nicotine and 1% ST, however, had no effect on IL-1beta secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+ 100 microg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 microg/ml nicotine significantly downregulated IL-1beta secretion by GMC relative to medium alone (p<0.008) and had no effect on PGE2 secretion by GMC. These data indicate that while nicotine and ST can stimulate PBMC to secrete PGE2, they cannot activate further mononuclear cells extracted from gingiva, possibly due to maximal previous stimulation in the periodontitis lesion.
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PMID:Nicotine and smokeless tobacco effects on gingival and peripheral blood mononuclear cells. 954 95

The objective of this study was to compare the efficacy of a systemic antibiotic (doxycycline) and a non-steroidal anti-inflammatory drug (ibuprofen), administered either separately or combined, as an adjunctive treatment of scaling/root planing (SRP). Thirty-two subjects diagnosed with generalized moderate adult periodontitis and having at least 2 teeth with > or =5 mm probing depth were randomly divided into 4 groups. Each group was treated with oral doxycycline and/or ibuprofen for 6 weeks as follows: group 1, doxycycline 200 mg the first day followed by 100 mg per day; group 2, ibuprofen 800 mg per day; group 3, doxycycline plus ibuprofen scheduled as in groups 1 and 2; group 4, one placebo capsule/day (control). A split mouth design was utilized in each subject such that half of the teeth received one session of scaling/root planing (SRP), while the other half received no SRP. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) using a customized acrylic stent were recorded at baseline and at 3, 6, 12, and 24 weeks following SRP. Analysis using ANOVA and Student t-test showed statistical significance (P< or =0.05) from baseline data in: 1) gains of 0.4 mm and 0.5 mm of CAL for groups 1 and 3, respectively; 2) reduction of 0.7 mm PD for group 3; 3) reduction of 0.4 and 0.1 GI scores for groups 1 and 3, respectively; and 4) gain of 0.5 mm CAL and reductions of 0.4 mm PD and 0.2 GI score for the SRP group when compared to the no SRP group at 24 weeks. It may be concluded that the adjunctive use of systemic doxycycline alone or in combination with ibuprofen results in a statistically significant, yet modest clinical, improvement beyond that obtained by scaling/root planing.
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PMID:Clinical evaluation of systemic doxycycline and ibuprofen administration as an adjunctive treatment for adult periodontitis. 970 54

A randomized, double-blind, clinical study was done to assess the microbiological and clinical effects of metronidazole plus amoxicillin (M+A) as the only therapy in 46 patients with moderate to advanced progressive adult periodontitis. Patients were included in the study after at least 2 sites showed > or =2 mm clinical attachment loss. Bleeding on probing, probing depth, and clinical attachment level were measured using on automated probe. The percentage of surfaces with plaque was recorded at day 0, and at 2 and 4 months after therapy. No effort was made to change the oral hygiene habits of patients. Identification of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia was assessed utilizing DNA technology at day 0 and 2 months after therapy. Twenty-three patients received metronidazole 250 mg plus amoxicillin 500 mg, 3 times/day for a week and 23 a placebo. Two patients in the placebo group were dropped at 2 months because they had taken antibiotics for medical reasons. Statistical analyses of differences between groups was done using the Mann-Whitney test, and the differences within each group were tested with ANOVA. There were no significant changes in surfaces with plaque in either group after therapy. The percentage of bleeding sites decreased significantly from baseline to 2 and 4 months in the M+A group (P = 0.001), and increased in the placebo group. Differences in bleeding on probing between groups were significant at 2 (P = 0.018), and 4 months (P = 0.005). The mean attachment level values at 2 and 4 months post-therapy improved significantly in the M+A group compared to the placebo group (P = 0.001). Treatment with M+A resulted in a significant mean reduction in probing depth at 2 and 4 months compared to baseline values (P = 0.001). The M+A group showed a significant reduction of sites with high levels of Pg (P = 0.001) at 2 months compared with baseline values, and there was a significant reduction of sites with Pg and Pi in the M+A group compared with the placebo group. The results showed that a combined M+A treatment as the only therapy changes the proportion of some subgingival microorganisms and allows a significant improvement in clinical conditions.
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PMID:Effects of metronidazole plus amoxicillin in progressive untreated adult periodontitis: results of a single 1-week course after 2 and 4 months. 984 40

Cigarette smoking is a potential risk factor which has recently been associated with periodontal disease progression. The objective of this study was to compare the microbial profile of smokers and non-smokers in a group of patients with early onset periodontitis. The study population consisted of 60 healthy individuals, 40 males and 20 females aged 22 to 35 yr, exhibiting early onset periodontitis. Thirty patients were smokers (30.9 cigarettes/d) and 30 non-smokers. Smokers had a higher proportion of deep pockets (PD >5 mm), especially in the maxilla anterior and premolar regions (p < 0.001) and presented a significantly greater mean probing depth and attachment loss (p <0.05) in diseased sites and a significantly greater alveolar bone loss (p <0.01) compared to non-smokers. Two pooled bacterial samples were obtained from each patient. Samples were collected from the deepest periodontal pockets of each quadrant. The samples were cultured anaerobically and in 10% CO2 plus air for bacterial isolation using selective and non-selective media. Isolates were characterized to species level by conventional biochemical tests and various identification kits. Smokers harboured a greater number of bacteria in total. Analysis of bacterial counts using the ANOVA (Mann-Whitney U-test) showed that Staphylococcus aureus, Peptostreptococcus micros, Campylobacter concisus, Escherichia coli, Bacteroides forsythus, C. gracilis, C. rectus, Porphyromonas gingivalis, Selenomonas sputigena, Candida albicans and Aspergillus fumigatus were found in significantly higher numbers and more frequently in smokers while Streptococcus intermedius, A. naeslundii, A. israelii and Eubacterium lentum were detected more frequently and in significantly higher proportions in non-smokers. The isolation of bacteria belonging to the exogenous flora such as E. coli, C. albicans, A. fumigatus and S. aureus in smokers' microbiota underscores the importance of the host that is adversely affected by cigarette smoking.
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PMID:Clinical and microbiological characteristics of smokers with early onset periodontitis. 1008 83

Histological periapical healing of infected roots obturated in one-step or with prior calcium hydroxide (Ca(OH)2) disinfection was compared. Seventy-two roots of vital dog teeth were instrumented to ISO size 45. Sixty roots were infected with dental plaque and closed. Six weeks later, apical periodontitis was radiographically confirmed in the infected roots. The teeth were divided into the following groups: group 1, one-step (n = 24)-roots were irrigated with 10 ml of saline, obturated, and permanently restored; group 2, Ca(OH)2 (n = 24)-roots were treated as in group 1, except that after saline irrigation, Ca(OH)2 dressing was placed in the canal for 1 wk before obturation; group 3, positive control (n = 12)--the roots were irrigated with saline, but the canals were not obturated; and an additional group, group 4, served as a negative control (n = 12)--these teeth that were not infected with plaque were aseptically obturated. The dogs were sacrificed after 6 months. The roots and surrounding apical tissues were prepared and histologically examined by two independent evaluators blinded to the treatment groups. A two-way ANOVA test demonstrated that the four treatment groups were significantly different from one another. The positive control showed the most inflammation, the negative control the least, and the Ca(OH)2 group had significantly less inflammation than the one-step group (p < 0.05). It is concluded that Ca(OH)2 disinfection before obturation of infected root canals results in significantly less periapical inflammation than obturation alone.
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PMID:Histological periapical repair after obturation of infected root canals in dogs. 1053 Feb 63

The purpose of this study was to evaluate the attachment loss around teeth and implants by clinical and microbiological analysis. The mandibular premolars were extracted in 5 mongrel dogs and, 3 months later, two titanium implants were installed on each side of the mandible and, after another 3 months, abutment connection was performed. Plaque control in the implants and maxillary premolars was maintained for two weeks prior to the start of the main experiment. On day 0 and 30 days after ligature placement, microbiological samples were obtained and relative attachment level was measured for the teeth and implants. The presence of Porphyromonas gingivalis, Bacteroides forsythus, Actinobacillus actinomycetemcomitans, Prevotella intermedia and Prevotella nigrescens was evaluated by polymerase chain reaction technique on day 0 and 30 days after ligature placement. None of the above bacteria were detected on day 0. Thirty days after ligature placement, P. gingivalis was present in 95% and 85% and B. forsythus was present in 80% and 85% of the implants and teeth sites, respectively. Statistical analysis (one-way RM-ANOVA) showed a significant difference (P<0.01) between pre- and post-induction measurements around teeth and implants. However, there was no significant difference (P=0.41) in the rate of attachment loss, between periodontitis and peri-implantitis. It can be concluded that: (1) P. gingivalis and B. forsythus were strongly associated with induced peri-implantitis and periodontitis, and (2) induced peri-implantitis and periodontitis presented a similar rate of attachment loss.
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PMID:Clinical and microbiological evaluation of ligature-induced peri-implantitis and periodontitis in dogs. 1148 57

The present study investigated the effect of nicotine administration on periodontal breakdown resulting from ligature-induced periodontitis in rats. Twenty adult male Wistar rats were used. After anesthesia, a mandibular first molar was randomly assigned to receive a cotton ligature in the sulcular area while the contralateral tooth was left unligated. The animals were randomly assigned to one of the following treatments. of daily intraperitoneal injections: A - saline solution, B -0.37 mg of nicotine kg, C -0.57 mg of nicotine kg and D -0.73 mg of nicotine/kg. Thirty days later, the animals were sacrificed and the specimens routinely processed for serial decalcified sections. Statistical analysis (ANOVA) revealed greater bone loss (p<0.05) in the ligated teeth of animals which received nicotine (groups B/C D) than in the ligated teeth of animals which received saline solution (group A). In addition, a dose-dependent response was observed among the nicotine groups. A negative effect of nicotine was observed in the unligated teeth of the experimental groups (p<0.05). Therefore, daily administration of nicotine enhanced, in a dose-dependent manner, the effects of local factors in producing periodontal breakdown. Furthermore, the nicotine seemed to have a direct deleterious effect on the periodontal tissues.
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PMID:Histometric evaluation of the effect of nicotine administration on periodontal breakdown: an in vivo study. 1176 71


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