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PubMedDate not supplied

The -308 polymorphism in the promoter region of the tumor necrosis factor-alpha (TNF-alpha) gene and ex vivo lipopolysaccharide-induced TNF-alpha expression in patients with aggressive periodontitis and/or type 1 diabetes mellitus.

Several single-nucleotide polymorphisms (SNPs) have been identified in the TNF-alpha gene promoter. The transition G-->A at position -308 generates the TNF-alpha1 (G/G) and TNF-alpha2 (G/A or A/A) alleles, where the polymorphic TNF-alpha2 allele is associated with a high, in vitro TNF-alpha expression and an increased susceptibility to diverse illnesses. Here we study the association of the -308 TNF-alpha SNP with the susceptibility for developing aggressive periodontitis (AP), AP combined with type 1 diabetes mellitus (DM) and DM. We also explore the TNF-alpha capability expression and the presence of the -308 polymorphism. For this purpose we recruited 27 individuals with AP (AP+ group), 27 individuals with AP combined with DM (AP+/DM+ group), and 27 individuals with DM without signs of periodontitis upon clinical examination (DM+ group). The control group was comprised of 30 subjects. Genotyping for TNF-alpha promoter was performed by PCR-RFLP analysis. For TNF-alpha expression we used a blood culture system.

Adult↗
PubMed2002

Fc gamma receptor genes as risk markers for localized aggressive periodontitis in African-Americans.

BACKGROUND: Receptors for the Fc fragment of immunoglobulin G (Fc gammaRs) play a crucial role in host defense against bacterial infection by linking humoral and cell-mediated immune responses. Allelic variants of certain Fc gammaRs have been shown to differ relative to their biologic activity. Thus, genes encoding allotypes with diminished activity have been suggested as potential risk factors for infectious diseases. The goal of this study was to determine whether specific Fc gammaRIIa, Fc gammaRIIIa, and Fc gammaRIIIb alleles and/or genotypes could be used to predict susceptibility to localized aggressive periodontitis (LAgP) in an African-American population. METHODS: Whole blood or saliva was obtained from 48 LAgP and 67 periodontally-healthy African-American subjects. DNA was prepared from each sample. Fc gammaRIIa and Fc gammaRIIIa genotyping was analyzed by polymerase chain reaction (PCR) amplification of DNA with allele-specific primers followed by allele-specific restriction digestion of the products. Fc gammaRIIIb genotyping was done by allele-specific PCR. RESULTS: There was a statistically significant over-representation of the Fc gammaRIIIb-NA2 allele in LAgP patients compared to controls (P = 0.024). Relative to the Fc gammaRIIIb-NA1/NA2 and homozygous NA1/NA1 genotypes, the prevalence of the Fc gammaRIIIb NA2/NA2 genotype was higher in the LAgP group relative to the control population. Individuals expressing this genotype appeared at greater risk for developing LAgP (odds ratio 2.271, 95% confidence interval: 1.005 to 5.132). There were no significant differences in the distribution of the Fc gammaRIIa H/R or Fc gammaRIIIa-158 F/V genotypes nor their allelic frequencies between the LAgP patients and controls. CONCLUSIONS: These data suggest that the Fc gammaRIIIb NA2 allele and/or NA2/NA2 genotype may represent risk markers for susceptibility to LAgP in African-Americans.

Adolescent↗
PubMedDate not supplied

Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis.

Several studies have demonstrated that diabetes is a risk factor for developing periodontal disease, increasing its prevalence and severity. Furthermore, periodontitis may impair the metabolic control and adequate treatment of diabetic patients. LPS from Gram-negative bacteria penetrates the periodontal tissues and subsequently recruits and activates immune cells. Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). For this purpose we recruited 29 Type 1 diabetes mellitus (DM) patients, 14 with AP and 15 without AP. Fourteen healthy individuals formed the control group. For cytokine expression and PGE2 secretion, an ex vivo whole blood culture system was used. Cytokines and PGE2 were detected by commercial immunometric assays. A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. In both groups of patients, the means of LPS-induced IL-6 levels were higher than the controls but the differences observed were not significant (p = 0.07). However, the LPS-induced PGE2 levels varied significantly when all groups were compared (p = 0.007). The means of LPS-induced PGE2 levels for Type 1 diabetic patients with AP (p = 0.0009) and without AP (p = 0.024) were significantly higher than the levels observed for healthy controls. Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. However, the PGE2 levels released were significantly higher than those detected in controls.

Adult↗
PubMed2004

Locally produced anti-phosphorylcholine and anti-oxidized low-density lipoprotein antibodies in gingival crevicular fluid from aggressive periodontitis patients.

BACKGROUND: Sera from patients with periodontal attachment loss contain higher concentrations of IgG anti-phosphorylcholine (anti-PC) than sera from healthy subjects. Furthermore, a large proportion of plaque bacteria bear PC-containing surface antigens, implicating the oral flora as a source of immunogen for anti-PC. Additionally, anti-PC is cross-reactive with a variety of oral bacterial antigens and human antigens such as oxidized low-density lipoprotein (oxLDL). We hypothesized that, if the oral flora is a source of PC antigens, then we should be able to detect local anti-PC and anti-oxLDL production in gingival crevicular fluid (GCF). METHODS: To test this, we collected 66 GCF samples from 15 patients with aggressive periodontitis and examined both the GCF samples and serum samples for their content of IgG anti-PC, IgG anti-LDL, and IgG anti-oxLDL by enzyme-linked immunosorbent assay. We also determined levels of anti-tetanus toxoid (anti-TT) as a non-oral antigen control. Serum and GCF concentrations of serum albumin (HSA) were also determined for use as a dilution marker. A conservative GCF:serum antibody ratio of greater than 1.5 was considered to be evidence of local antibody production. RESULTS: For the non-oral antigen TT, only one out of 62 samples contained locally produced antibody. Eight out of 64 samples (7 from a single subject) demonstrated local production of anti-LDL. In contrast, 28 out of 66 samples demonstrated local production of anti-PC, and 47 out of 66 samples contained locally produced anti-oxLDL. It was observed that A. actinomycetemcomitans strains containing or devoid of PC could absorb anti-oxLDL from human sera. Although there was a correlation between the ratios of anti-PC and anti-oxLDL (Spearman's rho = 0.35, P = 0.0037), local production of both antibodies was found in only 17 out of 65 samples, indicating that these antibodies are not always reflective of reactivity to the same antigens. CONCLUSION: The local production of anti-PC and anti-oxLDL further implicates the oral flora as a source of antigen that may mediate immune reactions of relevance to cardiovascular and other systemic diseases.

Acute Disease↗
PubMed2003

Use of Emdogain enamel matrix proteins in the surgical treatment of aggressive periodontitis.

One of the ways of treating of the aggressive forms of periodontitis is the method of guided tissue regeneration using enamel matrix proteins included in Emdogain preparation. The aim of work was clinical evaluation of the complex treatment of those periodontolyses using the above mentioned material as the implant material. 35 intrabony pockets were operated in 11 patients aged 17-50. The treatment results were described with the use of clinical indices of API and SBI, indices of pockets depth PPD and the loss of the attachment CAL indices before and within the period of 8 to 12 months after the surgeries. The values of the examined features were submitted to statistical analysis using Shapiro-Wilks and Wilcoxon's tests. The treatment that was applied led to extremely statistically significant improvement of the examined parameters.

Adolescent↗
PubMed2002

Level of neopterin, a marker of immune cell activation in gingival crevicular fluid, saliva, and urine in patients with aggressive periodontitis.

BACKGROUND: Neopterin, a marker of cellular immune activation, is produced by human macrophages after induction by interferon gamma that is secreted by T lymphocytes. Neopterin concentrations in diverse body fluids have been reported to increase in parallel with bacteria in the clinical course of infections. Therefore, determination of neopterin in body fluids was thought to be useful for predicting the prognosis and diagnosis of aggressive forms of periodontal disease, in which the cell-mediated immune response plays an important role in immunopathogenesis. The aim of the present study was to observe the role of neopterin in the pathogenesis of aggressive periodontitis (AgP). METHODS: Thirteen individuals who were systemically and periodontally healthy and 16 systemically healthy individuals diagnosed with AgP were recruited for this study. Mixed saliva and urine samples were collected from each subject. Gingival crevicular fluid (GCF) samples were obtained from 6 teeth with > or =5 mm probing depth (PD). After evaluation of GCF amount from paper strips, enzyme-linked immunosorbent assay (ELISA) was employed to determine the amount of neopterin in urine, saliva, and GCF. RESULTS: The amount of neopterin in urine and saliva measured 235.77+/-405.31 micromol neopterin/mol creatinine and 9.85+/-7.66 nmol/l, respectively, for the AgP group and 225.45+/-100.72 micromol neopterin/mol creatinine and 5.25+/-5.76 nmol/l, respectively, for controls. The present data demonstrate that, while salivary neopterin levels were found to be significantly different between periodontitis and control subjects, there were non-significant differences in urine neopterin levels. The amount and concentration of neopterin in GCF measured was 18+/-12.75 nmol/l and 3.67+/-2.40 nmol/ml for the AgP group and 2.51+/-1.72 nmol/l and 3.88+/-4.50 nmol/ml for the control group. When total amounts of neopterin are taken into consideration, a significant difference between AgP and controls is shown; however, no significant difference in net concentration of neopterin was found between both groups. CONCLUSIONS: This study is the first report to evaluate the involvement of neopterin in AgP and this might be considered of value in understanding periodontal disease mechanisms.

Adolescent↗
PubMed2004

Cytokine profile in gingival crevicular fluid of aggressive periodontitis: influence of smoking and stress.

BACKGROUND: Cigarette smoking and stress are considered risk factors that have been associated with periodontal disease progression. Conflicting results have been reported concerning the direct influence of smoking on the subgingival microbiota of periodontitis patients. Cytokine production may also be influenced by smoking and stress leading to an imbalance that disturbs the host-parasite relationship. AIM: The objective of the present study was to evaluate the influence of cigarette smoking on the gingival crevicular fluid (GCF) levels of interleukin (IL)-1beta, IL-4, IL-6 and IL-8 in aggressive or early onset periodontitis (EOP) patients and in healthy controls (H), psychosocial stress being considered as modifying factor. MATERIAL AND METHODS: Sixty-five EOP and 35 periodontally healthy individuals participated in this cross-sectional study. All the participants were interviewed about their smoking habits and their stressful social events. Clinical examination included the assessment of plaque index (PI), bleeding on probing (BOP), clinical attachment level (CAL) and probing pocket depth (PPD). GCF was collected using durapore strips, from four sites per patient, randomly selected in each quadrant. The total amounts of IL-1beta, IL-4, IL-6 and IL-8 were measured in a total of 400 samples using commercially available enzyme-linked immunosorbent assays. RESULTS: All clinical parameters were significantly higher in the EOP group compared to the H group. There were no significant differences between EOP smokers and EOP non-smokers with regard to plaque accumulation, CAL and PPD of the sampling sites, whereas mean CAL and PPD of the diseased sites were greater in EOP smokers than in EOP non-smokers. In addition, EOP smokers seemed to have significantly less BOP and greater bone loss compared to EOP non-smokers. Significant interactions between "EOP" and "smoking" were present for total amounts of IL-1beta and IL-4. IL-1beta, IL-6 and IL-8 showed significant main effects with healthy smokers and healthy non-smokers, respectively. For IL-8, stress presented a statistically significant interaction with smoking status and EOP (F=4.742, p=0.030). More specifically EOP smokers were statistically affected by stress. CONCLUSIONS: Smoking influences host-related factors including cytokine network. The relative importance of smoking and stress-related alterations and their precise mode of action in increasing the risk of aggressive periodontitis remains to be elucidated.

Adult↗
PubMed2004

Gingival crevicular fluid monocyte chemoattractant protein-1 and RANTES levels in patients with generalized aggressive periodontitis.

BACKGROUND: Local and systemic inflammatory and immune mechanisms may be implicated in the pathogenesis of the aggressive forms of periodontal disease. Chemokines, monocyte chemoattractant protein-1 (MCP-1) and regulated on activation, normal T cells expressed and secreted RANTES (regulated on activation, normal T cells expressed and secreted), are involved in the activation and recruitment of inflammatory and immune cells to the infected sites and thereby mediating a variety of pathophysiological conditions. The aim of the present study was to examine the gingival crevicular fluid (GCF) levels of MCP-1 and RANTES in patients with generalized agressive periodontitis (G-AgP). METHODS: MCP-1 and RANTES levels were investigated in GCF samples of 10 patients with G-AgP and 10 periodontally healthy subjects. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing and plaque. In the G-AgP group, GCF samples were collected from the two approximal sites; from one single-rooted tooth and from one first molar tooth with > or =6 mm probing depth. In the healthy group, GCF samples were collected from one of the single-rooted teeth. GCF MCP-1 and RANTES levels were quantified by enzyme immunoassay. RESULTS: The G-AgP patients had significantly higher GCF MCP-1 and RANTES levels compared to the healthy group (p<0.05). GCF MCP-1 and RANTES levels were positively correlated with both probing depth and clinical attachment loss (p<0.05). There was no correlation between GCF MCP-1 and RANTES levels and the percentage of sites with bleeding (p>0.05). CONCLUSIONS: The results of the present study suggest that MCP-1 and RANTES could play key roles in both activation and recruitment of inflammatory and immune cells in periodontal environment of G-AgP patients. In conclusion, these CC chemokines may be considered in the biological mechanism underlying the pathogenesis and progression of G-AgP.

Adolescent↗
PubMed2002

Prevalence of aggressive periodontitis in school attendees in Uganda.

AIM: The prevalence and severity of early onset periodontitis (EOP) among students attending secondary schools in two regions of Uganda was studied. MATERIAL AND METHODS: 690 students (393 males and 297 females) aged 12-25 years (mean 17 years), representing a range of tribal groups, were recruited from six schools in the peri-urban Central and rural Western regions of Uganda. The study subjects were clinically examined in field conditions by a single calibrated examiner to measure gingival recession and probing depth at six sites per tooth, with subsequent calculation of clinical periodontal attachment level for each site. Subjects exhibiting >or= 4 mm of clinical periodontal attachment loss at approximal surfaces of one or more teeth were classified with EOP. A structured written questionnaire obtained demographic characteristics of the study subjects. RESULTS: 199 (28.8%) study subjects showed clinical features of EOP, of which 16 (2.3%) subjects exhibited generalized EOP, 29 (4.2%) localized EOP, and 154 (22.3%) incidental EOP. The percentage of EOP-affected males was significantly higher than females (33.8% vs. 22.2%, P < 0.001). EOP prevalence tended to increase with increasing age, but no association was found between EOP prevalence and socioeconomic status or residency in urban vs. rural areas of Uganda. Molars and mandibular incisors generally demonstrated the highest occurrence of >or= 4 mm attachment loss. Clinical periodontal attachment loss of >or= 5 mm was mainly seen at first molars and incisors, suggesting that these two tooth types are first affected with attachment loss. Approximal tooth surfaces showed greater probing depth and attachment loss than buccal and lingual surfaces. Gingival recession was most prevalent at mandibular anterior teeth, whereas gingival margin coronal to CEJ was most frequently observed at second molars and maxillary incisors. CONCLUSION: A relatively high prevalence of EOP (28.8%) was found in young Ugandan school attendees, with 6.5% of these showing severe disease. EOP in Uganda was significantly more prevalent in males than females, and most frequently characterized by approximal involvement of molars and mandibular incisors. Etiologic and predisposing factors associated with the high occurrence of EOP in Uganda, as well as therapeutic and preventive measures of the disease in this population, remain to be delineated.

Adolescent↗
PubMed2001

Heterogeneity of host immunological risk factors in patients with aggressive periodontitis.

BACKGROUND: The pathogenesis of early-onset periodontitis (EOP) can be explained by various host risk factors. Previous studies have focused on a single (among many possible) immunological risk factor and the association among the factors has not been assessed. We comprehensively investigated the associations among multiple host immunological risk factors in EOP patients to further elucidate their role in the pathogenesis of EOP. METHODS: Sixty-eight EOP patients (50 generalized EOP, 18 localized EOP), 51 EOP-suspected patients (S-EOP), 43 adult periodontitis (AP) patients, and 36 periodontally healthy subjects (HS) participated in this cross-sectional study. We examined peripheral neutrophil functions, phenotypic and functional characterization of peripheral lymphocytes (lymphocyte subsets, T-cell proliferative activity), cytokine productivity (interleukin [IL]-1, IL-2, tumor necrosis factor [TNF]-alpha, interferon [IFN]-gamma, IL-4 and IL-6), serum immunoglobulin G (IgG) antibody titers against 12 periodontal bacteria, and HLA class II genotypes. RESULTS: G-EOP, S-EOP, and AP patient groups showed significantly lower percentages of pan T cells and CD8-positive cells (P < 0.02) compared with the HS group. L-EOP patients showed depressed IL-4 and TNF-alpha productivity compared with the HS group (P < 0.02). The EOP group showed significantly elevated antibody levels against Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum compared with the HS group (P < 0.05). The frequency with DQB1*0503 was significantly higher in the EOP patient group than the HS group (P = 0.045) due to the higher frequency in L-EOP patients than the HS group (P = 0.035). There were wide interindividual variations in each of the tests among patient and HS groups; however, EOP patients showed wider intradiagnostic group variations in certain host defensive cell functions than the other groups. There were some EOP patients who showed extremely low or high values in some tests; the EOP patients could be further divided into subgroups according to their host defensive and immunological profiles. However, there was heterogeneity in some of the other host immunological tests even in the subgroups. CONCLUSIONS: The association of host immunological risk factors in EOP patients is widely varied and more complex than previously thought. These results indicate the difficulty of explaining the pathogenesis of EOP based on a single host risk factor and also emphasize the importance of critical assessment of not only EOP patient groups, but also individual patients.

Adult↗
PubMed2001

Aggressive periodontitis associated with Fanconi's anemia. A case report.

BACKGROUND: Fanconi's anemia is an autosomal recessive disease associated with chromosomal breakage as well as pancytopenia, skin pigmentation, renal hypoplasia, cardiac defects, microcephaly, congenital malformations of the skeleton, hypogonadism, and increased risk of leukemia. The present report describes the periodontal clinical and microbiological status of an 11-year old male having Fanconi's anemia. METHODS: Polymerase chain reaction analysis to detect human cytomegalovirus (HCMV), Epstein-Barr type 1 virus, and herpes simplex virus (HSV) was performed on paper-point samples pooled from either 3 periodontal sites with advanced attachment loss or 3 gingivitis sites with no clinical attachment loss. Anaerobic bacterial culture examination was performed on the pooled periodontitis sample. RESULTS: The patient suffered from pancytopenia, allergy, asthma, hearing impairment, and mental retardation. Dentition consisted of 7 primary teeth, 11 erupted permanent teeth, and 14 unerupted permanent teeth. Most erupted teeth showed severe gingival inflammation with some gingival overgrowth and various degrees of periodontal attachment loss. Genomes of HCMV and HSV were detected in the pooled periodontitis sample and HCMV in the pooled gingivitis sample. The periodontitis sample but not the gingivitis sample revealed HCMV mRNA of major capsid protein, suggestive of active viral infection. The periodontitis sample also yielded Actinobacillus actinomycetemcomitans (1.1% of total isolates), FusobActerium species (7.9%), Campylobacter species (2.2%), Peptostreptococcus micros (3.4%), and Candida albicans (0.3%). CONCLUSIONS: Oral features of Fanconi's anemia may include increased susceptibility to periodontitis. It is likely that underlying host defense impairment coupled with periodontal infection by HCMV and A. actinomycetemcomitans contribute to the severe type of periodontitis associated with Fanconi's anemia.

Actinobacillus Infections↗
PubMed2003

Localized aggressive periodontitis in primary dentition: a case report.

BACKGROUND: A 5-year-old Japanese boy presented with persistent gingival inflammation and severe mobility of the right lower primary incisors. Due to severe alveolar bone loss and a deep periodontal pocket (5 mm), the incisors were extracted at the second visit. METHODS: Clinical, radiographic, histological, and microbiological examinations were carried out. Then, the polymerase chain reaction (PCR) technique was employed to detect specific periodontal pathogens. The chemotactic activity of polymorphonuclear neutrophils was also measured. RESULTS: Tannerella, Capnocytophaga, Fusobacterium, and Eikenella sp. were recovered from the subgingival microflora around the right lower incisors, while A. actinomycetemcomitans, Tannerella forsythensis (formerly Bacteroides forsythus), Prevotella nigrescens, Campylobacter rectus, and Capnocytophaga gingivalis were detected using the PCR method. Further chemotaxis assay revealed that neutrophil function was depressed compared with that of healthy controls. CONCLUSIONS: Although inflammation remained around the right primary second molars, the bone loss was controlled by periodic professional mechanical teeth cleaning (PMTC), subgingival irrigation, and local antibiotic application. The probing depths of all teeth, including permanent incisors and molars, were within 2.5 mm.

Alveolar Bone Loss↗
PubMed2004

Intraosseous sarcoidosis of the jaws mimicking aggressive periodontitis: a case report and literature review.

BACKGROUND: Sarcoidosis is a relatively common systemic granulomatous disease of unknown etiology. The skeletal system is affected in up to 39% of patients, but intraosseous sarcoidosis affecting the maxilla and mandible is rare. Only 20 cases have been reported previously in the English literature. This paper presents a case of generalized intraosseous sarcoidosis of the jaw bones that mimicked rapidly progressive periodontitis. METHODS: A 46-year-old male patient presented with loose teeth for assessment of implants. He had been gradually losing his teeth since 1999. His past medical history was significant, with sarcoidosis diagnosed in 1998. A panoramic radiograph showed a bilateral cotton-wool appearance of the mandible. A soft tissue and bone biopsy was performed and sent for histological examination. RESULTS: Microscopic examination of hematoxylin and eosin-stained sections revealed non-caseating granulomatous inflammation consistent with skeletal sarcoidosis. CONCLUSIONS: Intraosseous sarcoidosis of the jaw bones is rare and presents commonly as progressive and rapid alveolar bone loss similar to periodontitis. Therefore, it is important for periodontists to be knowledgeable and able to diagnose this condition, as rapid alveolar bone loss may be the first sign of sarcoidosis.

Diagnosis, Differential↗