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PubMed2005

Simultaneous measurements of cytoplasmic Ca2+ responses and intracellular pH in neutrophils of localized aggressive periodontitis (LAP) patients.

In view of the reports that polymorphonuclear leukocytes (PMN) of patients with localized aggressive periodontitis (LAP) exhibit hyper-responsiveness to stimulation, it has been suggested that such abnormalities could lead to PMN-mediated tissue damage during inflammation. To determine whether these abnormalities include signal transduction, we compared cytoplasmic calcium concentration (Delta[Ca2+](i)) and cytoplasmic pH (DeltapH(i)) changes, early stimulus responses to chemotactic agents, of LAP versus control (C)-PMN and explored whether these could be modulated by sensitizing cytokines or calcium channel-blocking agents. PMN responses of LAP patients were compared with age- and gender-matched controls. Delta[Ca2+](i) and DeltapH(i) were measured fluorimetrically using 1H-indole-6-carboxylic acid, 2-[4-[bis[2-[(acetyloxy)methoxy]-2-oxoethyl]amino]-3-[2-[2-[bis[2-[(acetyloxy)methoxy]-2-oxoethyl]amino]-5-methylphenoxy]ethoxy]phenyl]-1 and 2',7'-bis-(carboxyethyl)-5(6)-carboxyfluorescein as respective probes. Not only was the maximal calcium response to chemoattractants higher in LAP-PMN, but also their subsequent intracellular calcium redistribution was significantly slower. The slower calcium redistribution of LAP-PMN, but not their higher maximal calcium response, was successfully mimicked in C-PMN treated with Nifedipine or 1-[b-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole-HCl, both known to be inhibitors of membrane-associated calcium influx, but this redistribution was not affected when inhibitors of other calcium influx mechanisms, Diltiazem or Verapamil, were used. Taken together, our findings indicate that certain early stimulus responses are aberrant in LAP-PMN, that internal redistribution of cytoplasmic-free calcium is compromised, and, additionally, that a membrane-associated Ca2+ transport defect may be present.

Aggressive Periodontitis↗
PubMed2003

Evidence of a substantial genetic basis for IgG2 levels in families with aggressive periodontitis.

IgG2 is elevated in localized but not in generalized aggressive periodontitis (AgP). Exposure to pathogenic bacteria is essential for disease. Immune responses are dominated by IgG2 reactive with bacterial surface carbohydrates. We used variance component analyses to assess IgG2 heritability and determine whether genes that influence IgG2 are the same genes that influence disease susceptibility. We studied 17 Caucasian and 43 African American families with two or more localized or generalized AgP-affected members (274 subjects with IgG2 measurements). Only 16% of the variance in IgG2 was attributable to age, race, and smoking. Even with the addition of localized AgP, the model still explained only 19% of IgG2 variance. By contrast, heritability of IgG2 levels was estimated to be 38% and highly significant (P = 0.0006), demonstrating a substantial genetic basis. Bi-trait variance component analyses of IgG2 and quantitative measures of AgP indicate that different genes appear to control IgG2 levels and disease susceptibility.

Adolescent↗
PubMed2005

Quantitative measures of aggressive periodontitis show substantial heritability and consistency with traditional diagnoses.

BACKGROUND: Aggressive periodontitis (AgP) research nearly always classifies subjects into traditional discrete categories of localized or generalized, based upon degree of attachment loss (AL) and types of affected teeth. Since AL is continuous and quantitative, however, useful information is lost. We developed quantitative measures of AgP, compared these to traditional methods, and estimated heritabilities in families. METHODS: We examined 237 healthy, 169 localized AgP, and 204 generalized AgP subjects. We used the site of maximum AL of each tooth to calculate means for each subject for different groups of teeth. We also applied principal components analysis (PCA) to condense variation among 28 teeth into three orthogonal (uncorrelated) variables. We used discriminant function analysis (DFA) to evaluate how well the quantitative measures match with traditional classifications. Quantitative trait heritabilities were estimated by variance components. RESULTS: PCA clustered first molars, incisors, and the other teeth into three groups. DFA showed that quantitative measures classified subjects consistent with traditional methods (87% to 94% agreement). Heritabilities ranged from 13.7% (P = 0.10) to 30.0% (P = 0.008) for quantitative measures, with highest values obtained for first molars. A combination of the principal component variables most heavily weighted on first molars and incisors gave the best model of disease susceptibility, with good separation of healthy versus diseased subjects, independent of disease extent or severity. CONCLUSIONS: Quantitative measures may provide improved precision and power for many kinds of periodontal research. Our finding of significant heritability supports their use in gene mapping studies of AgP susceptibility.

Acute Disease↗
PubMed2001

Localized aggressive periodontitis in a patient with type 1 diabetes mellitus: a case report.

BACKGROUND: Poor metabolic control of diabetes mellitus (DM) has often been associated with the severity of periodontal disease. The aim of this report is to present a 9-year-old female with localized aggressive periodontitis who had a history of type 1 DM and the outcome of her treatment. METHODS: The patient had received medical, clinical, and radiographic periodontal examinations. Peripheral blood analysis was done as well. She had non-surgical periodontal treatment, and medical management of her diabetes was performed at the same time. She was followed longitudinally for 5 years. RESULTS: Medical examination revealed no pathological findings except for growth retardation. Laboratory tests showed that she had poor metabolic control, with 497 mg/dl fasting blood glucose and 15.6% HbA1c. The random migration and neutrophil chemotaxis were significantly reduced. Periodontal treatment and metabolic control of her diabetes resulted in significant improvement in her periodontal condition. No incipient periodontal breakdown was observed around the teeth after 5 years from baseline. CONCLUSIONS: This report proves the efficiency of periodontal therapy in the prevention of future periodontal breakdown in a systemically compromised patient. It seems that in certain individuals who are predisposed to the aggressive forms of periodontitis, clinical and medical examinations and intervention to the systemic condition, in combination with periodontal treatment, are important in the management of these individuals.

Aggressive Periodontitis↗
PubMed2006

NADPH oxidase (CYBA) and FcgammaR polymorphisms as risk factors for aggressive periodontitis: a case-control association study.

INTRODUCTION: Neutrophils (PMN) in aggressive periodontitis (AgP) patients have been reported to be hyperactive especially with regards to superoxide production. Polymorphisms in genes influencing PMN function have been proposed as candidate risk factors for AgP. The aim of this study was to test the association of specific gene polymorphisms affecting PMN functions with AgP. MATERIALS AND METHODS: Two hundred and twenty-four patients with confirmed diagnosis of AgP and 231 subjects with healthy periodontium took part in the study. A blood sample was collected from subjects and genotypes for p22phox (CYBA) NADPH oxidase, FP, Fcalpha and Fcgamma receptors were analysed in a blind fashion. RESULTS: The C242T p22phox NADPH oxidase T allele was significantly associated with AgP in a multiple logistic regression model adjusting for confounders, and this was observed for all subjects [p = 0.002, odds ratio (OR) = 1.87, 95% confidence interval (CI) = 1.27-2.83] and Caucasians (p = 0.009, OR=2.07, 95% CI = 1.20-3.59). Concomitant presence of C242T p22phox NADPH oxidase T allele and FcgammaRIIIb NA1 homozygosity was associated with the generalized AgP phenotype in Caucasians (p = 0.001, OR = 30.35, 95% CI = 3.81-241.97). CONCLUSIONS: C242T p22phox NADPH oxidase and FcgammaR polymorphisms may predispose to AgP through a modulation of neutrophil superoxide production.

Adult↗
PubMed2004

Association analysis between interleukin-1 family polymorphisms and generalized aggressive periodontitis in a Chinese population.

BACKGROUND: It has been suggested that aggressive periodontitis (AgP) has a genetic basis, but this theory has not been confirmed. The intent of this investigation was to study whether specific interleukin (IL)-1 genotypes and/or alleles could be used to predict susceptibility to generalized AgP (GAgP) in Chinese. METHODS: The GAgP group consisted of 122 patients, and the control group included 95 healthy subjects. Single nucleotide polymorphisms at IL-1A (+4845) and IL-1B (-511, +3954) were analyzed by standard polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. The polymorphism of a variable number tandem repeat (VNTR) in intron 2 of IL-1RN was detected by PCR amplification and fragment size analysis. RESULTS: There was no significant association of IL-1 polymorphisms with GAgP in the unstratified subjects. However, when cases were stratified by gender, the frequencies of A2+ genotype and allele 2 at IL-1A +4845 were significantly increased in male patients compared to male controls (genotype: odds ratio [OR] 5.58, 95% confidence interval [CI]: 1.09 to 28.68, P = 0.039; allele: OR 4.97, 95% CI: 1.01 to 24.50, P = 0.049; adjusted for age and smoking status). The frequency of IL-1B -511 A1/A2 heterozygote was significantly increased in male GAgP group compared to male controls (adjusted OR 3.16, 95% CI: 1.01 to 9.89, P = 0.048). In females, no significant differences were found between patients and controls in corresponding analyses at all polymorphic loci. A possible combined effect of IL-1B -511 polymorphism and smoking on the elevated risk to GAgP was observed. The OR of GAgP for combined A2+ genotype and smoking was 12.45 (95% CI: 1.43 to 108.06, P = 0.022), and for combined allele 2 and smoking was 18.25 (95% CI: 2.32 to 143.86, P = 0.006). CONCLUSIONS: The polymorphisms of IL-1A +4845 and IL-1B -511 may play an important role in determining GAgP susceptibility in Chinese males. Furthermore, a possible combined effect of the polymorphism of IL-1B -511 and smoking on GAgP susceptibility was suggested.

Acute Disease↗
PubMed2002

Amplified crevicular leukocyte activity in aggressive periodontal disease.

Exaggerated neutrophil responses are a critical component in the pathogenesis of periodontal disease. We investigated whether leukocyte activity in aggressive periodontitis (AP) is increased compared with that in chronic periodontitis (CP) by gingival crevicular fluid (GCF) analysis of myeloperoxidase (MPO), beta-N-acetyl-hexosaminidase (beta-NAH), cathepsin D (CD), and elastase-alpha-1-proteinase inhibitor complex (alpha-1-EPI) before and 6 months after therapy. Initial AP neutrophil responses were significantly amplified compared with those in CP (MPO, 3.2-fold; beta-NAH, 37.5-fold; CD, 2.2-fold; alpha-1-EPI, 1.4-fold; p < 0.05). Surgical therapy resulted in a significant reduction of GCF markers compared with non-surgical treatment. However, the changes in clinical parameters were not different between AP and CP (P > 0.05). Analysis of the results suggests that the local inflammatory response in AP is characterized by increased release of inflammatory mediators of neutrophil origin into the GCF. Analysis of the data further suggests that surgical therapy is a more predictable method for removal of the pro-inflammatory etiology.

Adult↗
PubMed2004

Telomere length in leukocytes and cultured gingival fibroblasts from patients with aggressive periodontitis.

BACKGROUND: The association of genetic risk factors with the pathogenesis of aggressive periodontitis (AgP) has been a focus of attention. Telomeres, which are nucleoprotein complexes at the ends of chromosomes, could be a genetic marker for Down's syndrome and Hutchinson-Gilford progeria, in which patients' premature aging is involved in the pathogenesis. It has been reported that these patients tend to experience severe periodontitis. Therefore, we investigated the telomere length of peripheral blood leukocytes (PBL) obtained from patients with AgP and that in the patients' gingival fibroblasts undergoing cellular aging in vitro. METHODS: Twenty-one patients with AgP and 50 age-matched, periodontally healthy subjects (HS) participated in this study. Genomic DNA from PBL and from human gingival fibroblasts (HGF) was analyzed by Southern blotting for telomere length. The percentage of HGF positive for beta-galactosidase (beta-gal), a marker for cellular senescence, was also investigated. RESULTS: There was no significant difference in the telomere length (P = 0.20, Student's t test) between the two groups, and wide interindividual variation was found (5.93 to 11.4 kbp, average 8.35 +/- 1.19 kbp). The telomere length from PBL negatively correlated with donor age, but no significant difference in telomere loss between the two groups was observed. With HGF undergoing aging in culture, the mean telomere length of these cells from six patients with AgP and seven HS decreased an average of -67.5 bp and -81.0 bp, respectively. No association was found in the telomere length between PBL and HGF from the same donors (r = 0.56, P = 0.20). A significant association was found between the telomere length and the percentages of beta-gal-positive HGF during cell passages (r = 0.70, P < 0.001). CONCLUSIONS: These results indicate that patients with AgP do not have excessive telomere loss and thus do not support the notion of the occurrence of a generalized premature cellular aging in patients with AgP. Further studies are required to investigate the association between telomere length and beta-gal in HGF.

Acute Disease↗
PubMedDate not supplied

Clinical and immunological findings of two siblings in a family with generalized aggressive periodontitis.

PURPOSE: The clinical and immunological data from 2 siblings with generalized aggressive periodontitis in a family are presented. METHODS: Peripheral blood lymphocyte subpopulations were analyzed by dual color flow cytometry by using monoclonal antibodies for the lymphocyte receptors CD2, CD3, CD4, CD5, CD8, CD16, CD19, CD11b, CD11c, and HLA-DR. RESULTS: Both patients showed a higher increase in CD11b/CD18 expression. CONCLUSIONS: The evaluation of CD11b and CD11c receptors may be important in explaining leukocyte abnormalities in the pathogenesis of the disease. One of the patients showed decreased counts of natural killer cells while the other was normal. In both patients, the authors observed a slight elevation in Ts lymphocytes.

Antigens, CD19↗
PubMed2006

Aggressive periodontitis in a 16-year-old Ghanaian adolescent, the original source of Actinobacillus actinomycetemcomitans strain HK1651 - a 10-year follow up.

The highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans is strongly associated with periodontitis in adolescents. Availability of the DNA sequence of the complete genome of A. actinomycetemcomitans strain HK1651, a representative strain of the JP2 clone (http://www.genome.ou.edu/act.html), has provided new possibilities in basic research regarding the understanding of the pathogenesis of A. actinomycetemcomitans in periodontitis. This case report describes the periodontal treatment of the original source of A. actinomycetemcomitans HK1651, a 16-year-old Ghanaian adolescent girl with aggressive periodontitis. The bacterial examination involved polymerase chain reaction analysis for presence of JP2 and non-JP2 types of A. actinomycetemcomitans. The treatment, including periodontal surgery supplemented by antibiotics, arrested the progression of periodontitis for more than 10 years. Initially, infection by A. actinomycetemcomitans, including the JP2 clone, was detected at various locations in the oral cavity and was not limited to the periodontal pockets. Post-therapy, the JP2 clone of A. actinomycetemcomitans disappeared, while the non-JP2 types of A. actinomycetemcomitans remained a part of the oral microflora.

Adolescent↗
PubMed2004

Aggressive periodontitis of the primary dentition associated with idiopathic immune deficiency: case report and treatment considerations.

The present case, of a child with an idiopathic immune deficiency and aggressive periodontitis in the primary dentition, serves as an example for the treatment considerations in these cases. Extraction of all the primary teeth proved to be the most adequate treatment. It allowed the child to eat properly and prevented unwanted infections that could endanger the life of the child. The newly erupted permanent teeth have been subjected to careful oral hygiene, clorhexidine topical applications, and have mild gingival inflammation and no attachment loss.

Aggressive Periodontitis↗
PubMed2003

Identification of mRNAs for the various diacylglycerol kinase isoforms in neutrophils from patients with localized aggressive periodontitis.

BACKGROUND: Diacylglycerol kinase (DGK) metabolizes diacylglycerol (DAG), an endogenous activator of protein kinase C, to phosphatidic acid. We have previously reported increased DAG in neutrophils from patients with localized aggressive periodontitis (LAP) associated with reduced DGK activity. This reduction could be related to a mutation, post-translational modification, differential expression, or lack of expression of a particular isoform(s). OBJECTIVE: The aim of this study was to identify the mRNAs for DGK isoforms in normal and LAP neutrophils. METHODS: The alpha-, gamma-, and delta-isoforms of DGK were identified by polymerase chain reaction (PCR) using specific oligonucleotide primers for each isoform. The PCR products were isolated and sequenced for comparison to published sequences to confirm the validity of the PCR reaction. Total RNA was isolated from LAP and normal neutrophils, and northern blotting and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to examine the level of mRNA for each isoform. RESULTS: No major differences were found in the isoform pattern between resting normal and LAP neutrophils. However, the levels of mRNA for the alpha- and gamma-isoforms of DGK were increased in normal neutrophils while slightly decreased in LAP cells upon stimulation with N-formyl-methionyl-leucyl-phenylalanine (fMLP). CONCLUSION: These data suggest that alterations in the mRNAs for the various isoforms of DGK during cell stimulation and the involvement of DGK that is expressed in multiple forms are subject to a variety of regulatory/control mechanisms and these mechanisms may explain the role of the 'primed' neutrophil phenotype associated with LAP.

Adolescent↗
PubMed2006

Expression of caspase-3, p53 and Bcl-2 in generalized aggressive periodontitis.

BACKGROUND: Apoptosis, or programmed cell death is a form of physiological cell death. It is increased or decreased in the presence of infection, inflammation or tissue remodelling. Previous studies suggest that apoptosis is involved in the pathogenesis of inflammatory periodontal disease. The aim of the present study was to investigate the clinical features and known indicators of apoptosis (p53, Bcl-2, Caspase-3) in patients with generalized aggressive periodontitis (GAP) METHODS: Eight patients with GAP, who had sites with probing depths (PD) > 5 mm, and 10 periodontally-healthy persons were included in the study. Clinical examinations and PD were performed, and the plaque index and gingival index were recorded. Gingival tissues biopsies were obtained from active site of each patient and from healthy individuals. The expression of caspase-3, Bcl-2, and p53 was evaluated by immunohistochemistry RESULTS: There were no significant differences between GAP and control group with respect to levels of caspase-3 and p53 expression (P > 0.05). Contrary, the frequency of grade 3 expression of Bcl-2 was higher in GAP group than the control group. CONCLUSION: The higher frequency of Bcl-2 expression in GAP group indicates and delayed apoptosis can lead to increasing resident inflammatory cells in periodontal tissues and resulting in progressive periodontal destruction.

Adolescent↗
PubMed2006

C-reactive protein levels in patients with aggressive periodontitis.

BACKGROUND: Sera from patients with periodontal infections contain elevated levels of C-reactive protein (CRP) compared to periodontally healthy individuals. Most studies to date have included patients with chronic periodontitis, and few investigators have studied CRP levels in subjects with aggressive periodontitis (AgP). The purpose of this study was to determine the relative levels of serum CRP in AgP patients and periodontally healthy subjects and to examine patients' characteristics that might account for intergroup differences. METHODS: Serum samples were collected from 93 patients with generalized AgP (GAgP), from 97 patients with localized AgP (LAgP), and from 91 healthy controls (non-periodontitis [NP]). Periodontal examination consisted of plaque index, gingival index, probing depth, bleeding index, and attachment loss measurements. Current smoking was assessed by determination of serum cotinine levels by enzyme-linked immunosorbent assay (ELISA), and serum CRP levels were determined using a high-sensitivity ELISA assay. RESULTS: The three groups were significantly different from one another (P <0.0001). The 95% confidence interval for serum CRP concentrations were as follows: NP, 0.65919 (0.4901 to 0.8869); LAgP, 1.10138 (0.8265 to 1.468); and GAgP, 2.05318 (1.5313 to 2.7538) mg/l. CRP levels in both LAgP and GAgP subjects were significantly greater than those in NP subjects, and levels in GAgP were significantly greater than those in LAgP. Following adjustment of the data for periodontal and demographic variables and current smoking, both mean probing depth and periodontal diagnosis remained correlated with CRP levels. CONCLUSIONS: Patients with AgP have statistically significant elevations in serum CRP levels compared to subjects without periodontitis. Elevated CRP in these subjects might represent a contribution of periodontal infections to systemic inflammation in relatively young individuals.

Adult↗
PubMed2005

Altered lipoprotein subclass distribution and PAF-AH activity in subjects with generalized aggressive periodontitis.

In this study, we examined whether the documented increase of plasma triglycerides in patients with generalized aggressive periodontitis (GAgP) is associated with changes in lipoprotein subclass distribution and/or LDL-associated platelet-activating factor acetylhydrolase (PAF-AH) activity. Lipoprotein subclasses were analyzed in whole plasma samples using nuclear magnetic resonance methods. Compared with subjects without periodontitis (NP subjects; n = 12), GAgP subjects (n = 12) had higher plasma levels of large, medium, and small VLDL (35.0 +/- 6.7 vs. 63.1 +/- 9.6 nmol/l; P = 0.025), higher levels of intermediate density lipoprotein (24.8 +/- 11.6 vs. 87.2 +/- 16.6 nmol/l; P = 0.006), lower levels of large LDL (448.3 +/- 48.5 vs. 315.8 +/- 59.4 nmol/l; P = 0.098), and higher levels of small LDL (488.2 +/- 104.2 vs. 946.7 +/- 151.6 nmol/l; P = 0.021). The average size of LDL from NP and GAgP subjects was 21.4 +/- 0.2 and 20.6 +/- 0.3 nm, respectively (P = 0.031). Compared with NP subjects, GAgP subjects had a greater number of circulating LDL particles (961.3 +/- 105.3 vs. 1,349.0 +/- 133.2 nmol/l; P = 0.032). Differences in the plasma levels of large, medium, and small HDL were not statistically significant. NP and GAgP subjects had similar plasma levels of total LDL-associated PAF-AH activity; however, LDL of GAgP subjects contained less PAF-AH activity per microgram of LDL protein (1,458.0 +/- 171.0 and 865.2 +/- 134 pmol/min/microg; P = 0.014). These results indicate that, in general, GAgP subjects have a more atherogenic lipoprotein profile and lower LDL-associated PAF-AH activity than NP subjects. These differences may help explain the increased risk of GAgP subjects for cardiovascular disease.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2001

Polymorphonuclear neutrophils and their mediators in gingival tissues from generalized aggressive periodontitis.

BACKGROUND: Impaired polymorphonuclear neutrophil (PMN) functions were generally considered to be related to the onset of generalized aggressive periodontitis (GAgP). However, some research has indicated that the hyperreactivity of PMN seems to be involved in the inflammatory response of GAgP. The present study's main purpose was to provide more evidence about the role of PMN in the pathogenesis of GAgP by surveying PMN infiltration in gingiva and its relationship with the expression of their mediators including intercellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha). The inflammatory response in GAgP was also compared with that in adult periodontitis (AP) and periodontally healthy subjects. Since these PMN mediators were reported to be produced mainly by macrophages, the association between the expression of these PMN mediators and the distribution of macrophages was also investigated. METHODS: A total of 25 gingival specimens were obtained from 10 GAgP patients, 10 AP patients, and 5 periodontally healthy subjects. Serial sections were obtained from each specimen, and the following techniques were adopted to investigate the distribution and interrelation of different cells and cytokines. Infiltration of PMN was observed by using hematoxylin and eosin staining. Distribution of the macrophages, identified as CD68+, was shown by using immunohistochemistry. Immunohistochemistry and in situ hybridization were used to detect the expression of ICAM-1, IL-8, IL-1beta, and TNF-alpha in gingival tissues. These techniques were performed in serial sections from each individual specimen. RESULTS: Large numbers of infiltrating PMNs were observed in gingiva from GAgP. In gingiva from both GAgP and AP, the strongest protein and mRNA expression of IL-8, ICAM-1, IL-1beta, and TNF-alpha were located in pocket epithelium and adjacent connective tissue with large numbers of infiltrating PMNs. In tissues without abundant PMN infiltration, the appearance of positive cells expressing IL-8, ICAM-1, IL-1beta, and TNF-alpha was scattered. CD68+ was distributed sparsely in connective tissue and was hardly seen in pocket epithelium with large numbers of PMN infiltration. The degree of leukocyte infiltration and connective tissue destruction in gingiva from GAgP patients was not distinctly different from that in gingiva from AP. The gingival specimens with heavy PMN infiltration from both GAgP and AP patients presented strong expressions of IL-1beta and TNF-alpha; showed more extensive inflammatory cell infiltration; had severe connective tissue destruction; and presented severe elongation and ulceration of pocket epithelium. In gingiva from healthy subjects, inflammation was minor with visually no PMN, CD68+, or the positive cells of IL-8, ICAM-1, IL-1beta and TNF-alpha expression. CONCLUSIONS: Enhanced accumulation of PMN, which is associated with the upregulation of IL-8, ICAM-1, IL-1beta, and TNF-alpha expression, relates to the severity and activity of GAgP. In addition to macrophages, PMN and/or epithelial cells might also be important sources of IL-8, IL-1beta, and TNF-alpha production in gingiva.

Adult↗
PubMed2005

Concurrence between the gene expression pattern of Actinobacillus actinomycetemcomitans in localized aggressive periodontitis and in human epithelial cells.

Actinobacillus actinomycetemcomitans is a facultatively intracellular pathogen and the aetiological agent of localized aggressive periodontitis. Screening of the genome of A. actinomycetemcomitans for in vivo-induced antigen determinants previously demonstrated that the proteome of this organism differs in laboratory culture compared with conditions found during active infection. The aim of the present study was to determine whether the bacterial gene expression pattern inferred with in vivo-induced antigen technology (IVIAT) in human infections was consistent with the gene expression pattern occurring upon epithelial cell association. To this end, a real-time PCR method was developed and used to quantify absolute and relative bacterial gene expression of A. actinomycetemcomitans grown extra- and intracellularly in two human epithelial cell lines (HeLa and IHGK). The amount of template used in the assay was normalized using the total count of viable bacteria (c.f.u.) as a reference point and performed in duplicate in at least two independent experiments. Controls for this experiment included 16S rRNA and gapdh. Transcription of all eight ORFs tested increased significantly (P < 0.05) in HeLa and IHGK cells compared with bacteria grown extracellularly. The concurrence of gene expression patterns found in the two models suggests that these epithelial cells are valid in vitro models of infection for the genes tested. IVIAT is an experimental platform that can be used as a validation tool to assess the reliability of animal and other models of infection and is applicable to most pathogens.

Actinobacillus Infections↗