SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
This work concerns a retrospective study of prevalence records and the clinical characteristics of localised aggressive periodontitis in the breast of consultants in the periodontitis service in Dental Medicine Faculty of Rabat (Morocco) from 1997 to 1999.
BACKGROUND: Enhanced neutrophil responses play a critical role in the activation of the innate immune system and causation of aggressive periodontitis (AgP). The hypothesis that comprehensive periodontal treatment expedites resolution of amplified leukocyte activity and facilitates the reconstitution of periodontal health was tested. METHODS: Four different gingival crevicular fluid (GCF) markers from 14 patients were characterized prior to and at 3, 6, 12, 24, and 36 months after periodontal therapy. GCF myeloperoxidase (MPO), beta-N-acetyl-hexosaminidase (beta-NAH), and beta-glucuronidase (beta-G) were determined spectrophotometrically, and cathepsin D (CD) by liquid scintillation counting using [14C] hemoglobin as substrate. The primary outcome was long-term stability of periodontal health. RESULTS: In untreated AgP, GCF markers were significantly amplified (MPO: 1.9-fold; beta-NAH: 1.3-fold; beta-G: 1.7-fold; CD: 4.7-fold). Following periodontal therapy, the leukocyte activity was significantly dampened (0.3- to 0.5-fold), and paralleled with a sustained improvement of periodontal health (P < 0.05). Thereafter and at 3 years, GCF leukocyte responses remained on a physiologic low level compatible to normal immune function. CONCLUSIONS: Comprehensive treatment of AP induces a downregulation of amplified crevicular neutrophil activity. The release of the innate immune system from exacerbating damage elicits a successful reconstitution of long-term periodontal health with no setbacks seen after 3 years.
BACKGROUND: Polymorphisms in FcgammaR have been associated with different forms of periodontitis. This study determined the frequency of FcgammaRIIa and FcgammaRIIIb alleles/genotypes in patients with generalized aggressive periodontitis (GAgP). METHODS: Thirty-one GAgP and 49 periodontally healthy Brazilian subjects participated in the study. Full-mouth periodontal examinations were carried out, and mouthwash samples were collected for human DNA isolation. FcgammaR genotyping was performed by polymerase chain reaction and hybridization with allele-specific oligonucleotide probes. Significant differences between groups were sought by Mann-Whitney, chi2, and Fisher exact tests and configural frequency analysis. RESULTS: FcgammaRIIa-H131 (53.8%) and FcgammaRIIIb-NA1 (75%) were the most prevalent alleles in this sample population. A significant overrepresentation of FcgammaRIIIb-NA2 was observed in the GAgP group, whereas FcgammaRIIIb-NA1 was detected more often in healthy individuals (odds ratio, 32.5; 95% confidence interval [CI], 10.6 to 99.8; P<0.001). No significant differences in the distribution of the FcgammaRIIa genotypes were observed between the groups. The prevalence of FcgammaRIIIb-NA2/NA2 was higher in GAgP patients, whereas FcgammaRIIIb-NA1/NA1 was predominant in the healthy group (chi2=45.1; P<0.001). The combination of the genotypes FcgammaRIIIb-NA2/NA2 plus FcgammaRIIa-H/H131 was observed more frequently in GAgP subjects than expected from marginal frequencies (chi2=12.5; P<0.001). CONCLUSIONS: The data suggest that the FcgammaRIIIb-NA2 allele and/or FcgammaRIIIb-NA2/NA2 genotype and the composite genotype FcgammaRIIIb-NA2/NA2 plus FcgammaRIIa-H/H131 may be associated with GAgP, whereas FcgammaRIIIb-NA1 and/or FcgammaRIIIb-NA1/NA1 may be related to periodontal health in this sample of the Brazilian population.
AIM: The aim of this study was to characterize the gingival inflammatory response to de novo plaque accumulation in subjects treated for aggressive periodontitis (AP). The gingival inflammatory response of the AP subjects was retrospectively compared with that of periodontally healthy individuals (PH) matched for exposure to plaque and of periodontally healthy subjects previously identified as "high responders" (HR) and "low responders" (LR). MATERIALS AND METHODS: 13 AP subjects and 26 matched PH subjects participated in a 21-day experimental gingivitis trial. Plaque index (PlI), Gingival index (GI), gingival crevicular fluid volume (GCF) and angulated bleeding score (AngBS) were recorded at days 0, 7, 14 and 21. Cumulative plaque exposure (CPE), i.e. PlI over time, was also calculated. RESULTS: GCF was significantly higher in AP compared with PH group at each observation interval (p< or =0.001). In addition, GCF was significantly higher in AP group compared with either LR or HR groups at each observation interval (p<0.001). CONCLUSIONS: These results suggest that susceptibility to gingival inflammation in response to de novo plaque accumulation may be related to susceptibility to periodontitis.
Host defense mechanisms are impaired in patients with congenital neutrophil (polymorphonuclear neutrophils (PMN)) defects. Impaired PMN chemotaxis is observed in localized aggressive periodontitis (LAP), a familial disorder characterized by destruction of the supporting structures of dentition. In the present studies, we sought evidence for molecular events underlying this aberrant human PMN phenotype. To this end, PMN transendothelial migration and superoxide anion generation were assessed with LAP patients and asymptomatic family members, as well as patients with other chronic mucosal inflammation. PMN from LAP patients showed decreased transmigration across vascular endothelial monolayers (18 +/- 12% of control, n = 4) and increased superoxide anion generation (358 +/- 37%, p = 0.003). Gene expression was analyzed using oligonucleotide microarrays and fluorescence-based kinetic PCR. cDNA microarray and kinetic-PCR analysis revealed diminished RNA expression of leukocyte-type diacylglycerol (DAG) kinase alpha in PMN from LAP patients (4.6 +/- 1.7 relative units, n = 6, p = 0.007) compared with asymptomatic individuals (51 +/- 27 relative units, n = 7). DAG kinase activity was monitored by DAG phosphorylation and individual DAG molecular species were quantified using liquid chromatography and tandem mass spectrometry-based lipidomics. DAG kinase activity was also significantly decreased (73 +/- 2%, p = 0.007) and correlated with increased accumulation of 1,2-diacyl-sn-3-glycerol substrates (p = 0.01). These results implicate defects in both PMN transendothelial migration and PMN DAG kinase alpha signaling as disordered functions in LAP. Moreover, they identify a potential molecular lesion in PMN signal transduction that may account for their aberrant responses and tissue destruction in this disease.
The genetic association of interleukin-1 (IL-1) with periodontitis has been investigated in different populations. Failure to detect an association with IL-1 genotypes in European Caucasians with aggressive periodontitis (AGP) has recently been reported. No data from Central American Hispanics are available. The purpose of this explorative study was to study the association between IL-1 genotypes and AGP in two populations. Ninety-one subjects, 28 North European patients and 33 controls together with 16 Central American patients and 14 controls were included in the study according to validated radiographic and clinical criteria. Two polymorphisms, IL-1alpha G(+4845)-T and IL-1beta C(+3954)-T were analysed by means of polymerase chain reaction-restriction fragment length polymorphism. The association between presence of specific genotypes and disease status was estimated by the odds ratio. A logistic regression was also used in order to investigate whether the occurrence of the disease depends upon the combination of the IL-1A and IL-1B alleles in the population. A similar distribution of genotypes between patients and controls in both populations was detected. The frequency of allele 1 of the IL-1A gene was higher in patients of both populations compared with controls, however, no statistical significant differences were found between patients and controls.
Several studies have shown a role for the involvement of interleukin (IL)-1 gene cluster polymorphisms in the risk of periodontal diseases. In the present study, we tested polymorphisms, derived from genes of the IL-1 cluster, for association with generalized aggressive periodontitis (GAP) through both allelic association and by constructing a linkage disequilibrium (LD) map of the 2q13-14 disease candidate region. The IL-1RN (VNTR) genotype distribution observed was significantly different in GAP and control subjects (P=0.019). We also observed some evidence for an association between GAP and the IL-1B(+3953) polymorphism (P=0.039). The pattern of association in the region, represented as an LD map, identifies a recombination hot area between the IL-1B(+3953) and IL-1B(-511) polymorphisms. Multilocus modelling of association with disease gives a location for the peak association at the IL-1B(+3953) marker, although support for the peak is not significant. Haplotype analysis identifies a IL-1B(+3953)-IL-1B(-511) haplotype as having the lowest P-value in the region. Recognition of the presence of a recombination hot area between the IL-1B(+3953) and IL-1B(-511) polymorphisms will have an important bearing on future efforts to develop higher resolution SNP analysis in this region for both this and other diseases for which this cluster is implicated.
OBJECTIVES: Recently, interleukin (IL) 4 gene polymorphisms have been analyzed in association with periodontitis. Genetic differences between Caucasian and Japanese patients with periodontitis have previously been detected. The aim of the present study was to analyze IL-4 genotypes in Caucasian and Japanese patients with aggressive periodontitis (AgP). MATERIAL AND METHODS: One hundred and twenty-four subjects were included in the study, 31 Japanese and 30 Caucasian patients with generalized AgP, plus 30 Japanese and 33 Caucasian healthy controls. IL-4 polymorphisms were determined by polymerase chain reaction. A logistic regression was used to investigate the possible association of the genotypes with the disease in both populations. Odds ratio (OR) estimates were analyzed for allele frequencies. RESULTS: No significant association of IL-4 polymorphisms with the risk of AgP was determined in either population. However, the allele frequencies showed different results between populations. The carriage of the polymorphism in intron 2 was higher in Caucasian patients compared with controls (OR: 2.0, 95% confidence interval: [1.0;4.2]. Furthermore, the frequency of the IL-4 promoter/intron 2 composite genotype (PP+/IP+) in patients and controls, respectively, was found to be approximately 25% and 60% higher in the Japanese population than in the Caucasian population. CONCLUSION: There was no evidence of an association of IL-4 genotypes and AgP in either population, although the frequencies of the IL-4 genotypes in the Japanese and the Caucasians were different.
HLA antigens have been considered as risk factors for periodontitis. Differences in prevalence and in the extent of attachment loss between males and females have suggested that gender-dependent HLA deviations could play a role in individual predisposition to periodontitis. The aim of the present study was therefore to investigate the incidence of gender-dependent HLA associations in 50 patients with generalized aggressive periodontitis (AP) and 102 patients with chronic periodontitis (CP) in comparison to 102 probands without any attachment loss caused by periodontitis. HLA typing was carried out using a microlymphocytotoxic test and a polymerase chain reaction with sequence-specific primers (PCR-SSP). Female AP patients showed an increase in the frequency of HLA-A*68/69 and a decrease in the frequency of DRBblank* (non-DRB3/4/5*) and DQB1*05-positive probands. Only in female CP patients was HLA-DQB1*0303 absent, whereas HLA-DQB1*06 homozygosity increased significantly. With regard to the (AP + CP) periodontitis group as a whole, the increased frequency of HLA-DQB1*06 homozygosity in females was similar to the findings obtained in the AP group. Evidently, gender is a confounding variable, which should be considered in further studies of HLA and periodontitis.
BACKGROUND: The objective of this study was to assess the adjunctive clinical effect of the administration of systemic amoxicillin and metronidazole in the non-surgical treatment of generalized aggressive periodontitis (GAP). METHODS: Forty-one systemically healthy subjects with GAP were included in this 6-month double-blind, placebo-controlled, randomized clinical trial. Patients received a course of full-mouth non-surgical periodontal treatment delivered over a 24 h period using machine-driven and hand instruments. Test subjects received an adjunctive course of systemic antibiotic consisting of 500 mg amoxicillin and 500 mg metronidazole three times a day for 7 days. Clinical parameters were collected at baseline, and at 2 and 6 months post-treatment. RESULTS: In both the test and the placebo groups, all clinical parameters improved at 2 and 6 months. In deep pockets (> or =7 mm), the test treatment resulted in an additional 1.4 mm (95% confidence interval 0.8, 2.0 mm) in full-mouth probing pocket depth (PPD) reduction and 1 mm (0.7, 1.3 mm) of life cumulative attachment loss (LCAL) gain at 6 months. In moderate pockets (4-6 mm), the adjunctive benefit was smaller in magnitude: PPD reduction was 0.4 mm (0.1, 0.7 mm) and LCAL gain was 0.5 mm (0.2, 0.8 mm). In addition, the 6-month data showed LCAL gains > or =2 mm at 25% of sites in test patients compared with 16% in placebo (p=0.028). Similarly, PPD reductions of 2 mm or more were observed in 30% of sites in test and 21% of sites in placebo patients. Seventy-four percent of pockets with PPD > or =5 mm at baseline were 4 mm or shallower at 6 months in the test group. This compared with 54% in the placebo group (p=0.008). Disease progression at 6 months was observed at 1.5% of test and 3.3% of sites in test and placebo, respectively (p=0.072). CONCLUSIONS: These data indicate that a 7-day adjunctive course of systemic metronidazole and amoxicillin significantly improved the short-term clinical outcomes of full-mouth non-surgical periodontal debridement in subjects with GAP.
BACKGROUND: It has been suggested that hyper-responsiveness of monocytes to the products of dental plaque, especially the endotoxin of Gram-negative bacteria and the secretion of high levels of pro-inflammatory cytokines, may have a role in the pathogenesis of aggressive periodontitis (AP). To investigate this possibility, IL-6 production by cultured peripheral blood monocytes before and after stimulation by E. coli lipopolysaccharide (LPS) in AP patients was evaluated. MATERIAL/METHODS: Fifteen patients with AP were compared with 15 periodontally healthy controls in a case control study. Monocytes were obtained from peripheral blood samples and cultured. The reaction of monocytes was studied by their IL-6 production using ELISA before and six hours after stimulation by 0.1 microg/ml E. col. LPS. The Wilcoxon and Mann-Whitney U tests were used to compare the groups. RESULTS: There was no significant difference in IL-6 production levels before LPS stimulation between patients and controls. Upon LPS stimulation, IL-6 levels increased in both the patient and control groups compared with their IL-6 levels before stimulation. IL-6 production after LPS stimulation in the patients was higher than controls, but this was not statistically significant. However, the increase in IL-6 production as a result of LPS stimulation was significantly higher in patients than in controls. CONCLUSIONS: Increased monocyte responsiveness may play a potential role in the pathogenesis of AP. However, whether this is an intrinsic characteristic of the monocyte/macrophage cells of AP patients or just a priming effect as a result of the periodontal disease remains to be investigated.
OBJECTIVES: The objective of the present randomized controlled trial was to evaluate the efficacy of a mouthrinse containing a combination of AmF/SnF2 in controlling supragingival plaque accumulation and gingival inflammation during a 12-week period in patients affected by generalized aggressive periodontitis (GAP). METHODS: Eighteen subjects, six males and 12 females, mean age: 32.2 years, were evaluated. One-half of the patients was either prescribed an AmF/SnF2-containing mouthrinse (test mouthrinse) or a control mouthrinse in addition to mechanical plaque control for 12 weeks. After a 2-week wash-out period, the patients received the alternative mouthrinse. Before and after treatment plaque index (PlI), gingival index (GI), angulated bleeding index (AngBI), tooth stain (GMSI), and tongue stain were recorded. RESULTS: Test mouthrinse resulted in a statistically significant decrease in PlI (p = 0.029) and GI (p = 0.017). After treatment, PlI was significantly lower in test compared to control mouthrinse (p = 0.027). GMSI significantly increased post-treatment for both mouthrinse regimens (p < 0.001), a significantly higher score being observed for the test compared to control mouthrinse (p = 0.002). CONCLUSIONS: The 12-week use of a AmF/SnF2-containing mouthrinse as an adjunct to conventional mechanical oral hygiene procedures in GAP patients was effective in controlling the amount of supragingival plaque deposits.
AIMS: Erythromycin (ERY) and spiramycin (SPI) are the most frequently prescribed macrolides by dentists. However, the emergence of resistant anaerobic subgingival bacteria imposes an increased vigilance. This study aims to compare these macrolides efficacy on principal periopathogens. MATERIALS AND METHODS: Twenty adult patients with aggressive periodontitis were selected and a total of 60 samples were taken from subgingival flora. Bacterial strains of Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Peptostreptococcus micros and Actinobacillus actinomycetemcomitans were isolated according to J. Slots's rapid identification method. The susceptibilities to ERY and SPI were studied using disk diffusion susceptibility test and minimum inhibitory concentration test (MIC test). RESULTS: The efficiency variability of ERY and SPI on the 50 isolated anaerobic periopathogens was present either interindividually (between different patients) and intra-individually (within the same patient). While 68% of the tested anaerobic bacteria were sensitive to SPI (22% resistant), only 54% were sensitive to ERY (34% resistant). Although moderate, the efficacy of SPI seemed more regular in general than ERY: it's variation coefficient (40%) is lower than the ERY one (53%). The 7 A. actinomycetemcomitans tested showed all a high resistance. CONCLUSION: In a general way, the spectre of activity of SPI is stacked in that of ERY. However, this study shows a better and regular activity of SPI on the main tested periopathogens. These results are in favour of the use of SPI in periodontology when penicillins and doxycycline are not useful because specific problems are identified (allergy, pregnancy...).
BACKGROUND: Eosinophilic granuloma (EG) is the mildest and mainly localized form of the clinicopathologic spectrum of Langerhans' cell histiocytosis. It is a destructive osseous lesion characterized by a vast number of eosinophils and histiocytes. The etiology remains unknown. In this paper, a case of EG is presented that was initially diagnosed and treated as aggressive periodontitis (AP). METHODS: Despite treatment procedures, the EG continued to expand very quickly, destroying the lingual cortical bone and the neighboring soft tissues and exhibiting periosteal reaction. Diagnosis of EG was established on the basis of histopathologic and immunohistochemical evaluation. Moreover, certain manifestations in the skeletal and respiratory system were observed. RESULTS: Surgical curettage of the lesions was effective; however, corticosteroids and low-dose radiation were used as adjunctive therapy. CONCLUSION: The rapid progress of eosinophilic granuloma, the diagnostic problems, and the consequences of late diagnosis and treatment are discussed.
BACKGROUND: Periodontal bacteria are known to invade the systemic circulation. Chronic low-level bacteremia and a systemic inflammatory response have been suggested as a pathogenetic link between periodontal disease and atherosclerosis. The purpose of this study was to examine the systemic effect of a non-surgical therapy on white blood cell count (WBC count) and differential blood count in smoking and non-smoking generalized aggressive periodontitis (GAP) patients. METHODS: 27 adult periodontitis patients (13 smokers and 14 non-smokers) with previously untreated GAP were subjected to 3 sessions of oral hygiene procedure. Afterwards, the patients were treated by scaling and root planing under local anaesthesia. Periodontal examinations were performed after supragingival pretreatment and three months after subgingival therapy. Pocket probing depth (PPD) and relative attachment level (RAL) were measured with Florida probe and disc probe. Accompanying clinical evaluation venous blood samples were taken to analyse the WBC counts and differential blood counts. For statistical analysis non-parametric tests were utilized. RESULTS: No clinical or demographic differences were found between smokers (n=13) and non-smokers (n=14). PPD, bleeding on probing (BoP) and suppuration improved significantly after therapy both in smokers and non-smokers. Following periodontal treatment WBC counts, neutrophil and platelet counts decreased significantly in non-smokers (p< or =0.004), while in smokers only platelet counts were significantly reduced (p=0.006). Non-smokers showed a significantly higher reduction of WBC counts (p=0.005) and neutrophils (p=0.001) compared to smokers. CONCLUSION: The results indicate that a therapeutical intervention may have a systemic effect on the blood count in GAP patients. This effect seems to differ between smokers and non-smokers.
BACKGROUND: The genes encoding the human leukocyte antigens (HLAs; major histocompatibility complex [MHC]) have been considered candidate markers for periodontitis because they are involved in regulating immune responses. Several studies have examined this association, and despite the inconclusive results, the antigens HLA-A9 and HLA-B15 have been found to be consistently associated with the destructive forms of periodontitis in many populations. Ethnic factors are considered to be a major variable for evaluating the predisposition to the disease. The purpose of the present study was to: 1) assess the association of HLA-A*9 and HLA-B*15 with generalized aggressive periodontitis (GAgP) and 2) evaluate the role of these genetic risk factors in influencing the severity of GAgP in a South Indian population. METHODS: Forty GAgP patients (cases) and 80 periodontally and systemically healthy subjects (controls) participated in this study. HLA-A*9 and HLA-B*15 typing was carried out using the polymerase chain reaction with sequence specific primers (PCR-SSP)-based molecular method. RESULTS: HLA-B*15 was a significant risk factor for GAgP and was positively correlated with the disease severity, whereas HLA-A*9 had no association with the disease. The haplotype of HLA-A*9:B*15 did not impart any additional risk for GAgP compared to that imparted by HLA-B*15 alone. CONCLUSIONS: To our knowledge, this is the first report on HLA-B*15 association with GAgP in an Indian population. The finding of HLA-B*15 as a risk factor may have potential use in the future management of GAgP. The precise disease-causing mechanism of this HLA disease association and whether this association is "causal" or "casual" need to be evaluated further.
BACKGROUND: Genetic polymorphisms for interleukin (IL)-1alpha and -1beta have been proposed as potential genetic markers for periodontal diseases. Since the prevalence of these polymorphisms could be race-related, and no data exist about the frequency of these polymorphisms in the Chilean population, the aim of the current study was to investigate the association of the interleukin-1 gene polymorphisms with aggressive periodontitis (AgP). METHODS: Thirty-six patients with AgP, 75 healthy controls, and 75 subjects of unknown periodontal status (reference population) were genotyped for the IL-1A -889 and IL-1B +3954 loci, by polymerase chain reaction (PCR) amplification followed by restriction enzyme digestion and gel electrophoresis. Data were analyzed using the chi-square test, calculating odds ratios (OR) and confidence intervals (CI). RESULTS: The prevalence of the positive composite IL-1 genotype was higher in patients (25%) than in healthy controls (12%), but the difference was not significant (P= 0.14). The IL-1B +3954 homozygous for allele 1 frequency was higher in controls than in patients suggesting a protective factor for AgP. The heterozygous for allele 2 of the IL- 1B showed a significant association with AgP (OR = 2.86, 95% CI 1.06 to 7.71, P= 0.030). No association was observed in localized AgP and generalized AgP between the extent of disease and the presence of the composite positive genotype. Because the number of smokers was too small in patients and in controls, no other analyses were performed. CONCLUSION: The results of the present study support a positive association between AgP and the presence of the IL-1B +3954 allele 2 polymorphism.
Immunoglobulin A Fc receptor (FcalphaRI) has been implicated in the pathogenesis of periodontitis, because increased IgA responses and FcalphaRI-bearing neutrophils are observed in the disease lesions. Inter-individual differences in susceptibility to periodontitis may be attributable to genetic variability in FcalphaRI-mediated immunity. We here identified an FcalphaRI novel polymorphism (nt 324 A-to-G transition) in the membrane-distal extracellular domain encompassing the ligand-binding site, not resulting in an amino acid change. We compared the FcalphaRI genotype distributions among 46 Japanese aggressive periodontitis (AGP) patients, 80 race-matched healthy controls (HCs), and 59 Caucasian HCs. No ethnic differences were observed in the FcalphaRI genotype distributions between Japanese and Caucasian HC. Notably, we observed a difference in the genotype distribution between the AGP and HC groups. Carriage rate of the nt 324 A allele was higher in the AGP (65.2%) than that in the HC group (42.5%) (odds ratio 2.54). Polymorphonuclear neutrophils from peripheral blood and gingival crevicular fluid exhibited a decreased phagocytosis of periodontopathic bacteria (Porphyromonas gingivalis) in the nt 324 A/A patients as compared with the nt 324 G/G patients. These results document a genetic polymorphism at the FcalphaRI ligand-binding site to be associated with susceptibility to AGP.