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 purpose of this study was to examine and evaluate the short-term (six months) effects of clinical trials of nonsurgical periodontal therapy. The subjects studied included consisted of 34 patients, 24-52 years of age (836 teeth), with various degrees of advanced periodontitis. Following a baseline examination which included assessments of the gingival index (GI), plaque index (PlI), calculus index (CI), probing depth, and attachment level, the patients were subjected to nonsurgical therapy. Differences between various treatment intervals for the pockets initially measuring 1-3 mm, 4-6 mm, and 7 mm or more were analyzed by using the paired Students t-test. Following meticulous debridement of periodontal pockets with ultrasonic instrumentation, routine pocket irrigation with hydrogen peroxide (2.5-3.0%) and chlorhexidine gluconate solutions (0.12%) was performed by the authors as well as by the patients at sites with moderate to deep pockets and furcation involvement. Furthermore, the patients were supervised under a maintenance care program which provided patient motivation, the teaching of oral hygiene procedures, and offered regular recall for six months. The results demonstrated that non-surgical therapy resulted in a prominent reduction of gingival inflammation, dental plaque and calculus formation, and finally increased gingival recession. Also, for sites with an initial probing depth of 1-3 mm, there was a slight loss (0.1 mm) of the attachment level, 3 and 6 months after therapy. For sites with an initial probing depth of 4-6 mm, there was some attachment gain (0.31 mm and 0.69 mm) at 3 and 6 month post-treatment intervals. For pockets 7 mm or more in depth, a pronounced gain (0.49 mm and 1.00 mm) of attachment was noted following 3 and 6 month intervals. Generally, an obvious reduction of probing depth was constantly observed after nonsurgical treatment in each of the three initial pocket groups mentioned above. The changes of probing depths between baseline and at 3 or 6 months after treatment were 0.17 and 0.23, 1.23 and 1.75, and 1.83 and 2.63 mm, respectively. With the exception of attachment loss for the pockets initially measuring 1-3 mm, the difference of GI, PlI, CI, probing depth, and attachment level between baseline and 3 or 6 months after treatment were found statistically significant in each of the three initial pocket groups when analyzed individually by ANOVA.
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PMID:Clinical observations of the effects of nonsurgical periodontal therapy on human periodontal disease. II. Ultrasonic scaling and root planing for 6 months. 265 13

Juvenile diabetics have been shown to have an increased susceptibility to gingivitis and periodontitis following puberty. However, little data are available on changes in the microbial flora that occur at the onset of puberty. This study was performed to determine if antibacterial antibody titers to selected periodontal disease-associated microorganisms might be helpful in revealing changes in plaque flora at the onset and conclusion of puberty. Sera was obtained from 35 subjects (ages 7 to 18 years) selected from a population of insulin-dependent diabetics. The subjects were given a thorough medical examination which included an assessment of sexual maturation and a dental examination which included the recording of onset and magnitude of bleeding according to the papillary bleeding score. Antibody titers to A. naeslundii (AN), B. intermedius (BI), B. gingivalis (BG), F. nucleatum (FN), A. actinomycetemcomitans (AA), C. ochracea (CO) and T. denticola (TD) were determined using the microELISA. Stratification of antibody titers by age groups (less than or equal to 12 years, 12 to 15 years, greater than 15 years) revealed that titers to AN increased significantly (P less than 0.025, ANOVA) and progressively (P less than 0.05, regression analysis) with increasing age. In contrast, the titers to FN were maximal in the under 12 year group and decreased with age (ANOVA, P less than 0.05; regression analysis, P less than 0.05). There were no significant variations in titers observed for the other microorganisms. Stratification by sexual maturity revealed a similar progressive decrease of the titer to FN (ANOVA, P less than 0.05; regression analysis, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Humoral immune response to selected subgingival plaque microorganisms in insulin-dependent diabetic children. 272 33

Systemic non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce alveolar bone loss in periodontitis. This study assesses the efficacy of a topical NSAID rinse, containing ketorolac tromethamine as the active agent. Adult periodontitis patients (n = 55) were studied in this 6-month randomized, double blind, parallel, placebo and positive-controlled study. Each patient had a least 3 sites at high risk for bone loss as assessed by low dose bone scan. Groups, balanced for gender, were assigned to one of three regimens: bid ketorolac rinse (0.1%) with placebo capsule; 50 mg bid flurbiprofen capsule (positive control) with placebo rinse; or bid placebo rinse and capsule. Prophylaxes were provided every 3 months. Monthly examinations assessed safety, gingival condition, and gingival crevicular fluid PGE2. Standardized radiographs were taken at baseline and at 3 and 6 months for digital subtraction radiography. A significant loss in bone height was observed during the study period in the placebo group (-0.63 +/- 0.11; P < 0.001), but not in the flurbiprofen (-0.10 +/- 0.12; P = 0.40) or ketorolac rinse (+0.20 +/- 0.11 mm; P = 0.07) groups. Nested ANOVA revealed that ketorolac and flurbiprofen groups had less bone loss (P < 0.01) and reduced gingival crevicular fluid PGE2 levels (P < 0.03) compared to placebo. ANOVA suggests (P = 0.06) that ketorolac rinse preserved more alveolar bone than systemic flurbiprofen at the dose regimens utilized. These data indicate that ketorolac rinse may be beneficial in the treatment of adult periodontitis.
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PMID:A comparison of topical ketorolac, systemic flurbiprofen, and placebo for the inhibition of bone loss in adult periodontitis. 762 51

This 6-month, double-blind, controlled clinical trial determined the efficacy of the non-steroidal anti-inflammatory drug, meclofenamate sodium (Meclomen), as an adjunct to scaling and root planing in the treatment of rapidly progressive periodontitis (RPP). 22 subjects (7 male, 15 female) aged 36.5 +/- 7.88 years with RPP and disease-active sites as determined by pretreatment bone scan had standardized radiographs at baseline and 6 months, and clinical measurements at baseline, 3 and 6 months. Following full-mouth scaling and root planing, subjects were randomly assigned to either a placebo, 50 or 100 mg meclofenamate sodium bid group. Bone change over the 6-month period as assessed by subtraction radiography was the primary efficacy determinant. Specialized software was used to isolate the lesion from the subtraction image and to measure bone change along the root surface. ANOVA using the subject as the unit of analysis revealed a significant dose response (p < 0.001) with the placebo group having a mean bone loss of 0.42 +/- 0.06 mm and the low and high dose groups having mean bone gains of 0.07 +/- 0.05 and 0.20 +/- 0.07 mm, respectively. These findings indicate that meclofenamate sodium may be a useful adjunct in the treatment of rapidly progressive periodontitis.
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PMID:Efficacy of meclofenamate sodium (Meclomen) in the treatment of rapidly progressive periodontitis. 822 50

The purpose of this study was to compare the effectiveness of polylactic acid (PLA) granules as an alloplastic grafting material to that of decalcified freeze-dried bone allograft (DFDBA) and a flap procedure for debridement without graft (FPD) when treating periodontal intrabony defects. Ten patients presenting with advanced adult periodontitis, including at least 3 similar periodontal osseous defects (2- and 3-walled), comprised the study group. After completion of a hygienic phase of treatment, measurements were made with calibrated periodontal probes and stents to determine soft tissue recession, probing pocket depths, and probing attachment levels. Each defect was surgically exposed and hard tissue measurements were obtained. Defects were treated with one of the 3 methods above chosen randomly prior to the surgical appointment. Six months postsurgery, soft tissue measurements were repeated and all sites were surgically reentered to obtain hard tissue measurements. All surgical sites healed without clinical complication. The initial pocket depths and initial depth of osseous defects were compared between the groups using ANOVA and no significant differences were found. A mean osseous defect fill of 0.4 mm (11.2%) occurred with the flap procedure for debridement, 3.0 mm (65%) with DFDBA, and 0.1 mm (2.2%) with PLA. Mean crestal bone loss was 1.30 mm for FPD, 0.60 mm for DFDBA, and 1.55 mm for PLA. No statistically significant differences were found in soft tissue recession between groups or in the osseous defect measurement between PLA and FPD. A statistically significant improvement (P < 0.001) was found in the fill of the osseous defects when using DFDBA compared to the initial defect depth and to the other 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of polylactic acid granules and decalcified freeze-dried bone allograft in human periodontal osseous defects. 843 49

This clinical study evaluated the reinfection incidence by Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), and Prevotella intermedia (Pi) in periodontal pockets following scaling and root planing (SRP) and intra-pocket irrigation with antimicrobial agents in a patient population who did not receive supportive maintenance therapy. The number of target organisms was determined utilizing DNA probes. Forty-one (41) inflamed pockets > or = 5 mm with attachment loss and containing at least one target species were selected in 6 adult patients. Following a baseline clinical and bacterial examination, all patients received thorough SRP. In addition, 1 to 2 teeth in each patient were randomly assigned to each of the following 4 treatment modalities: 1) control group, no irrigation; 2) saline group, irrigation with 2 cc of 0.85% saline; 3) tetracycline group, irrigation with 2 cc of aqueous tetracycline HCl, 50 mg/ml (5%); and 4) chlorhexidine group, irrigation with 2 cc, respectively. All selected sites were non-adjacent. No additional therapy was rendered during the entire 1-year observation period. Clinical parameters and microbial analyses were recorded again at 1 week, and 1, 3, 6, 9, and 12 months post-treatment. The effect of antimicrobial irrigation on the reinfection rate of sites by Aa, Pg, and Pi was compared with that of the control groups (1 and 2) by ANOVA. No statistically significant differences were observed among the irrigation treatment groups with regard to any of the clinical or bacterial parameters studied. Therefore, the 4 treatment groups were combined into a single group whereby the rate of bacterial repopulation following extensive scaling and root planing could be ascertained. The infection incidence of sites at baseline (of total sites), 1 week and 12 months (of sites originally infected at baseline) was 14/41, 3/14, and 7/14 for Aa; 33/41, 6/33, and 12/33 for Pg; and 37/41, 3/37, and 12/37 for Pi, respectively. Thus, half or fewer of the originally infected sites became reinfected at 12 months despite lack of maintenance therapy. The results suggest that 1) a single episode of pocket irrigation with antimicrobial agents following thorough scaling and root planing did not affect the rate of repopulation of periodontal pockets by the tested pathogens; 2) thorough scaling and root planing has a lasting suppressive effect on selected periodontal pathogens for the majority of sites in patients with adult periodontitis; 3) pre-operative probing depth, the amount of gingival fluid flow and the composition of the subgingival microflora may serve as predictors for reinfection in the absence of maintenance care; and 4) reinfection of the treated sites by Aa, Pg, and/or Pi may constitute a risk factor that diminishes the effect of therapy in the absence of supportive maintenance care.
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PMID:Repopulation of periodontal pockets by microbial pathogens in the absence of supportive therapy. 866 33

Cigarette smoking is a major risk factor in the development and further progression of periodontitis. However, little is known regarding the pathogenesis of smoking-related periodontal diseases. The purpose of this study was to examine the effects of nicotine, alone and in combination with lipopolysaccharide (LPS), on monocyte secretion of bone-resorbing factors, PGE2 and IL-1 beta. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy, non-smoking donors. PBM were incubated for 24 h in RPMI 1640 containing nicotine (0, 50 ng/ml, 1 microgram/ml, 10 micrograms/ml and 100 micrograms/ml) with or without 10 micrograms/ml Porphyromonas gingivalis LPS or Escherichia coli LPS. Culture supernatants were assayed for PGE2 and IL-1 beta by ELISA. None of the nicotine preparations resulted in significant PBM secretion of PGE2 and IL-1 beta above that of unstimulated cultures. However, PGE2 release was potentiated 1.7-fold by the combination of P. gingivalis LPS and 10 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.05, one-way ANOVA). Prostaglandin E2 release also was potentiated 3.5-fold by P. gingivalis LPS and 100 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.00001, one-way ANOVA) and 3.1-fold by E. coli LPS and 100 micrograms/ml nicotine relative to E. coli LPS alone (p < 0.00001, one-way ANOVA). IL-1 beta secretion was lower for either LPS plus 100 micrograms/ml nicotine relative to LPS alone, although not significantly. These data demonstrate upregulation of LPS-mediated monocyte secretion of PGE2 by nicotine and suggest a potential role for nicotine in periodontal disease pathogenesis.
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PMID:Nicotine effects on PGE2 and IL-1 beta release by LPS-treated human monocytes. 870 46

The aim of the study was to evaluate the adjunctive effect of systemic tetracycline (250 mg qds for 14 days) in sequential root planing and surgical phases of treatment in a randomised, double-blind controlled trial. 38 patients who were under 26 years of age, in good general health and with localised (15 test/15 control) or generalised (4 test/4 control) early onset periodontitis completed the non-surgical phase. Data were analysed by ANOVA using baseline covariates and transformations where appropriate. Improvements in probing depth, probing attachment level and bleeding on probing were significantly better in the group treated with adjunctive tetracycline, at 3 months post-treatment. 26 patients (13 test/13 control) subsequently completed the surgical phase (modified Widman flap surgery with adjunctive tetracycline or placebo as before) and were re-examined at 6 months and 12 months. In the test group, 58% of the originally affected teeth required surgery compared to 75% in the control group. Surgery produced further reductions in mean probing depths but no further gains in probing attachment. There were no further statistically significant differences between test and control groups for any of the clinical measures, although the tetracycline group appeared to maintain an advantage. In conclusion, systemically administered tetracycline is a useful adjunct in the management of early onset periodontitis, particularly in non-surgical treatment.
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PMID:A double-blind trial of tetracycline in the management of early onset periodontitis. 884

A painful and rapidly progressive form of periodontitis--involving both soft tissue and bone, with gingival bleeding and loss of teeth--was observed in HIV-patients in the mid-80's. Today, there are few reports regarding the real incidence of periodontitis in HIV populations: however, it seems not as high as first supposed on discovering the disease, and bacterial plaque is moderate, compared with "conventional" periodontitis. Since there are few radiologic studies, the Authors report on the clinical-radiographic patterns of periodontitis in 20 HIV patients, compared to 20 normal controls. All the subjects were submitted to clinical-instrumental investigations (clinical tests, periodontal sampling, DMF index), and panoramic radiography. To assess periodontal disease severity, bone pocket depth is investigated radiographically, defined as the distance between the highest point of alveolar bone and root apex, at the mesial and distal aspects of all the teeth. We measured four alveolar quadrants, from the first premolar to the second molar. Statistical analysis was carried out with one way ANOVA test and non-parametric Kruskal-Willis's test; statistical significance is accepted at the probability level p < 0.05. Clinical-radiographic results demonstrated minimal bone loss and little teeth mobility, in the early stage of disease; involvement of total gingival attachment with partial bone sequestration at muco-gingival line, in the moderate stage; severe bone loss with soft tissue necrosis and risk of teeth exfoliation, in the advanced stage. Gingival tartar was also found. A significant statistical difference was demonstrated between the two examined populations. HIV-related periodontitis may represent one of the various features of the clinical picture of HIV infection, which must not be underestimated and mistaken for "conventional" adult periodontitis. If the diagnosis of periodontic disease is essentially clinic, radiography remains nevertheless important, because it yields data on bone status, integrity of lamina dura and morphology of roots, which data help make diagnosis and prognosis more reliable.
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PMID:[Periodontal disease in patients with HIV infection. Radiographic study]. 903 46

The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. Diabetics were divided into group A (gingivitis or mild periodontal disease) and group B (moderate to severe periodontal disease). In addition, 17 non-diabetic individuals with various degrees of periodontal disease served as control patients. Diabetics as a group had a significantly higher monocytic TNF alpha production in response to increasing Porphyromonas gingivalis A 7436 lipopolysaccharide concentrations (0, 0.003, 0.03, 0.3 and 3.0 micrograms/ml) as compared to non-diabetic patients with gingivitis or adult periodontitis (p < 0.05). A significant difference in the dose response was also noted in the level of TNF alpha secreted as a function of P. gingivalis LPS concentrations between group A and B diabetics, as determined by two-way repeated measurements ANOVA (p < 0.05). Furthermore, there was no significant difference in the mean HbA1C between the two diabetic groups, and the TNF alpha level was not significantly associated with the HbA1C level within diabetic patients. These data suggest that the diabetic state results in an upregulated monocytic TNF alpha secretion phenotype (4.6-fold increase) which, in the presence of Gram-negative bacterial challenge, is associated with a more severe periodontal disease expression. In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients.
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PMID:Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases. 904 92


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