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PubMed2001

Treponema socranskii, Treponema denticola, and Porphyromonas gingivalis are associated with severity of periodontal tissue destruction.

BACKGROUND: The aim of the present study was to identify Treponema socranskii in addition to Treponema denticola and Porphyromonas gingivalis by polymerase chain reaction (PCR), and to clarify the relationship between the presence of these microorganisms and the severity of clinical periodontal parameters. METHODS: Saliva and subgingival plaque collected from 123 subjects (38 aggressive periodontitis patients, 65 chronic periodontitis patients, 20 healthy patients) were subjected to PCR to detect the aforementioned 3 microorganisms. RESULTS: Detection frequencies of T. socranskii, T. denticola, and P. gingivalis in plaque samples from aggressive periodontitis patients (71.1%, 73.7%, 84.2%, respectively) and chronic periodontitis patients (89.2%, 93.8%, 95.3%) were much higher than those from healthy subjects (30%, 5.0%, 10.0%). In aggressive and chronic periodontitis patients, these 3 species of bacteria were detected frequently at sites that showed deep periodontal pockets and severe attachment loss. The percentage of these bacteria-positive sites increased as the gingival index score of chronic periodontitis patients increased. T. socranskii was frequently detected together with T. denticola or P. gingivalis at the same sites, and coexistence of these microorganisms was frequently observed in deep periodontal pockets of aggressive periodontitis patients. CONCLUSIONS: T. socranskii, T. denticola, and P. gingivalis were frequently detected in periodontitis patients by PCR. The prevalence of these 3 microorganisms was correlated with various clinical parameters. Taken together, our findings suggest that T. socranskii, T. denticola, and P. gingivalis are associated with the severity of periodontal tissue destruction.

Adolescent↗
PubMed2002

Association of interleukin-1 receptor antagonist gene polymorphisms with early onset periodontitis in Japanese.

BACKGROUND/AIMS: Early onset periodontitis (EOP), newly 'aggressive periodontitis', is considered to have genetic basis, which have not been clearly defined. The interleukin-1 (IL-1) gene cluster polymorphism as one of genetic factors may influence the expression of several chronic inflammatory diseases. The aim of this study is to investigate the frequency of single nucleotide polymorphisms (SNPs) in the genes encoding IL-1alpha, IL-1beta and a variable number of tandem repeat (VNTR) polymorphisms in the IL-1 receptor antagonist gene (IL-1RN) in 47 generalized EOP (G-EOP) patients and 97 periodontally healthy controls. MATERIAL AND METHODS: All subjects were of Japanese descent and systemically healthy. They were identified according to established clinical criteria. SNPs in the IL-1alpha (+ 4845) and IL-1beta (- 511, + 3954) genes were analyzed by amplifying the polymorphic region using polymerase chain reaction (PCR), followed by restriction-enzyme digestion and agarose gel electrophoresis. IL-1RN (VNTR) polymorphisms were then detected by PCR amplification and fragment size analysis. RESULTS: There was no significant difference in the IL-alpha (+ 4845) and IL-1beta (- 511, + 3954) genotypes and allele frequencies between G-EOP patients and healthy controls. However, the frequency of IL-1RN (VNTR) polymorphic alleles was found to be significantly increased in G-EOP patients (chi2 test, P = 0.007; odds ratio = 3.40). Additionally, the carriage rate of IL-1RN (VNTR) polymorphisms was significantly higher in G-EOP patients than in healthy controls (chi2 test, P = 0.005; odds ratio = 3.81). CONCLUSION: These findings suggest that IL-1RN (VNTR) polymorphisms are associated with G-EOP in Japanese.

Adult↗
PubMed2003

Salivary IgA in response to periodontal treatment.

There is evidence that the quantity of antigen load is crucial for the activation of IgA immune responses. In order to investigate the relevance of these findings in aggressive periodontitis, salivary antibody responses were measured during non-surgical and antibiotic treatment. Twenty-one patients with generalized aggressive periodontitis were monitored for total salivary IgA and IgA reactive to Porphyromonas gingivalis in resting and stimulated whole saliva. Non-surgical treatment included full-mouth professional tooth cleaning and subgingival scaling and root planing (SRP) under local anesthesia. Patients were recalled at 3 months and 6 months following systemic antibiotic treatment. Non-parametric statistics showed significant improvements in the clinical parameters in all patients. Between baseline and 4 wk following SRP, median concentrations of total IgA decreased both in resting (-46%) and in stimulated (-33%) saliva. The P. gingivalis-specific IgA activity showed a twofold increase at 4 wk after SRP. In addition to these changes, periodontal treatment of aggressive periodontitis did not appear to affect salivary IgA, and there were no significant correlations of IgA to the clinical parameters. In conclusion, salivary IgA responses during periodontal treatment were not found to have a diagnostic or prognostic significance.

Adolescent↗
PubMed2005

The cytolethal distending toxin induces receptor activator of NF-kappaB ligand expression in human gingival fibroblasts and periodontal ligament cells.

Actinobacillus actinomycetemcomitans is associated with localized aggressive periodontitis, a disease characterized by rapid loss of the alveolar bone surrounding the teeth. Receptor activator of NF-kappaB Ligand (RANKL) and osteoprotegerin (OPG) are two molecules that regulate osteoclast formation and bone resorption. RANKL induces osteoclast differentiation and activation, whereas OPG blocks this process by acting as a decoy receptor for RANKL. The purpose of this study was to investigate the effect of A. actinomycetemcomitans on the expression of RANKL and OPG in human gingival fibroblasts and periodontal ligament cells. RANKL mRNA expression was induced in both cell types challenged by A. actinomycetemcomitans extract, whereas OPG mRNA expression remained unaffected. Cell surface RANKL protein was also induced by A. actinomycetemcomitans, whereas there was no change in OPG protein secretion. A cytolethal distending toxin (Cdt) gene-knockout strain of A. actinomycetemcomitans did not induce RANKL expression, in contrast to its wild-type strain. Purified Cdt from Haemophilus ducreyi alone, or in combination with extract from the A. actinomycetemcomitans cdt mutant strain, induced RANKL expression. Pretreatment of A. actinomycetemcomitans wild-type extract with Cdt antiserum abolished RANKL expression. In conclusion, A. actinomycetemcomitans induces RANKL expression in periodontal connective tissue cells. Cdt is crucial for this induction and may therefore be involved in the pathological bone resorption during the process of localized aggressive periodontitis.

Aggregatibacter actinomycetemcomitans↗
PubMed2001

Levels of platelet-activating factor in gingival crevicular fluid and gingival tissue in specific periodontal diseases.

BACKGROUND: Platelet-activating factor (PAF), a potent phospholipid mediator of inflammatory and immune reactions, is involved in a variety of biological responses seen in periodontal diseases. The aim of the present study was to examine the role of PAF in the pathogenesis of specific periodontal diseases. METHODS: PAF levels were investigated in gingival crevicular fluid (GCF) and gingival tissue (GT) samples of 12 patients with generalized aggressive periodontitis (GAgP), 6 patients with localized aggressive periodontitis (LAgP), 10 patients with chronic periodontitis (CP), 6 with gingivitis (G), and 6 periodontally healthy subjects (H). Periodontal status was evaluated by measuring probing depth, gingival index, papillary bleeding index, and plaque index. PAF was extracted from GCF samples passing through amberlit resin columns, purified by high performance liquid chromatographic method, and then analyzed by radioimmunoassay. RESULTS: GAgP, LAgP, and CP groups had significantly higher GCF PAF levels compared to the H group (P<0.005). Although statistically not significant, GCF PAF levels were also higher in the G group than those of the H group (P = 0.0784). GAgP, LAgP, and CP groups had similar GCF PAF levels (P>0.005). These groups had higher levels of GCF PAF than those of the G group, but the difference was significant only for the GAgP group (P<0.005). When the data were expressed as concentration, GAgP, LAgP, and CP groups were found to have higher concentrations of GCF PAF compared to the H group (P<0.005). GCF PAF concentration was similar in patient groups (P>0.005). All patient groups had significantly higher GT PAF levels compared to the H group (P<0.005). GAgP, LAgP, and CP groups had similar amounts of GCF and GT PAF (P>0.005). GAgP, LAgP, and CP groups had higher GT PAF levels than those of the G group, but the differences were only significant for LAgP and CP groups (P<0.005). No significant correlation was found between GCF and GT PAF levels and clinical parameters. CONCLUSIONS: The results of the present study indicate that PAF is likely to be an important mediator in regulating inflammatory responses in the human periodontal tissues. To our knowledge, this is the first report investigating PAF levels in GCF and GT in specific periodontal diseases. We believe that this potent phospholipid mediator may need to be considered in the pathogenesis of periodontal diseases.

Adult↗
PubMed2005

[Analysis of FcgammaRIIIb genotype of periodontal disease in the Han nationality in China].

PURPOSE: The purpose of the present study was to compare FcgammaRIIIb genotype of aggressive periodontitis (AgP) with chronic periodontitis (CP) and control group (Cont) in the Han nationality in China. METHODS: The classification, which was applied in this study, was presented and discussed at the 1999 International Workshop for the Classification of the Periodontal Disease organized by the American Academy of Periodontology (AAP). 23 patients with aggressive periodontitis, including 20 with chronic periodontitis according to the established clinical criteria, and 22 matched healthy controls was included in this study. Peripheral blood samples were taken from all patients and controls, then DNA was isolated from blood using DNA purification kit. And FcgammaRIIIb genotyping was determined by PCR and DNA sequencing. The different results of genotype in all three groups were analysed by chi(2) test. RESULT: FcgammaRIIIb-NA1, -NA2 (old definition) frequencies didn't equal 1.00 in all 3 groups, and also without -SH, -NA(NULL) genotype. At the same time, many new allele of NA1 and NA2 were found in all groups. However, there were no rules of new alleles in each group and between the groups, no statistical significance as well. The -NA1 of FcgammaRIIIb (new definition) frequency was 0.77, and that of -NA2 (new definition) was 0.23 in this study. CONCLUSION: Including FcgammaRIIIb-NA1 and -NA2, five alternate allele of -NA1 (-NA1*01b, -NA1*02a, -NA1*02b, -NA1*03a and-NA1*03b) and three alternate allele of -NA2(-NA2*02, -NA2*03 and -NA2*04) were described. The results suggest that FcgammaRIIIb may not be a risk indicator for the susceptibility of periodontitis in the Han nationality of China.

Aggressive Periodontitis↗
PubMed2005

Elevated serum IgG titer and avidity to Actinobacillus actinomycetemcomitans serotype c in Japanese periodontitis patients.

AIM: The purpose of this study was to characterize serum antibody responses to different serotypes of Actinobacillus actinomycetemcomitans strains in various forms of periodontitis and to determine whether any specific type of A. actinomycetemcomitans was associated with any specific form of periodontitis in a Japanese population. METHODS: Sonicated whole cell and autoclaved serotype antigens of A. actinomycetemcomitans were used. Serum IgG titer and avidity to A. actinomycetemcomitans were measured by enzyme-linked immunoabsorbant assay (ELISA) and ammonium thiocyanate-dissociation ELISA, respectively, in 46 aggressive periodontitis patients (8 localized, 38 generalized), 28 chronic periodontitis patients, and 18 periodontally healthy subjects. The presence of A. actinomycetemcomitans in plaque and saliva samples was determined using polymerase chain reaction. RESULTS: Generalized aggressive and chronic periodontitis patients exhibited significantly higher IgG titers than healthy subjects to both sonicated and autoclaved antigens of serotype c strains, while IgG titer to serotype b (Y4) was significantly higher in localized aggressive periodontitis patients compared to healthy subjects. No A. actinomycetemcomitans was detected in localized aggressive periodontitis patients. A. actinomycetemcomitans-positive patients exhibited significantly higher IgG titer and avidity to serotype c than A. actinomycetemcomitans-negative patients. In A. actinomycetemcomitans-positive patients, a significantly positive correlation was observed between antibody titer and avidity to serotype c. A. actinomycetemcomitans-positive patients with generalized aggressive periodontitis showed lower IgG avidities to serotype c than those with chronic periodontitis, though no statistically significant difference was found. CONCLUSION: A. actinomycetemcomitans serotype c may play a significant role in chronic and generalized aggressive periodontitis, while A. actinomycetemcomitans serotype b may be associated with localized aggressive periodontitis in a Japanese population.

Actinobacillus Infections↗
PubMed2006

[Expression of human beta defensin-2 in normal and various periodontitis-involved gingiva].

PURPOSE: To investigate the expression of HBD-2 peptides in normal and periodontitis-involved gingiva. METHODS: Immunohistochemistry were performed for detection of HBD-2 peptides expression in gingival tissues from 11 healthy subjects,18 patients with chronic periodontitis and 9 patients with aggressive periodontitis. The data were quantitatively analyzed with a computerized image processing system. And the data were analyzed by one-way ANOVA with SPSS11.5. RESULTS: HBD-2 peptides were expressed in all tissue samples. The expression of HBD-2 peptides were mainly confined to the granular and spinous layers of the gingival epithelium, in which HBD-2 was detected in the cytoplasm. Significantly higher levels of HBD-2 expression were found in healthy gingival epithelium as compared with that in chronic periodontitis among three groups(P<0.05). CONCLUSIONS: The results suggested that HBD-2 may play an important role as part of the innate host defenses in maintaining periodontal health.

Aggressive Periodontitis↗
PubMedDate not supplied

Lipoxin signaling in neutrophils and their role in periodontal disease.

Endogenous molecules involved in counterregulation of inflammatory responses provide an opportunity to explore new therapeutic approaches based on manipulation of new pathways that may reduce the possibility of unwanted toxic side effects. Lipoxins (LX) are trihydroxytetraene-containing eicosanoids that are generated within the vascular lumen during cell-cell interactions or at mucosa through leukocyte-epithelial cell interactions. Transcellular biosynthetic pathways are the major lipoxin biosynthetic routes where LX are formed in vivo during inflammation and serve as "stop signals" that regulate key steps in leukocyte trafficking. In this review, recent findings in lipoxin generation, impact on the resolution of acute inflammation, and organ protection from neutrophil-mediated injury are presented. Periodontitis, specifically localized aggressive periodontitis, which is recognized as an example of neutrophil-mediated tissue injury, is discussed as a disease model where LX and other endogenous pro-resolution pathway mediators could have potential value.

Animals↗
PubMed2006

Correlation between single nucleotide polymorphisms in a calprotectin subunit gene and risk of periodontitis in a Chinese population.

S100A8, the light subunit of calprotectin, has been known to be associated with periodontal inflammation. The present study looked to detect whether three polymorphisms in the upstream region of the S100A8 gene are correlated with periodontitis. Three hundred and twenty one subjects, including chronic periodontitis (CP) patients, aggressive periodontitis (AgP) patients and periodontally healthy controls, were recruited. The SNPs rs3795391, rs3806232 and rs3885688 were analyzed by PCR-RFLP analysis. No person carried the rs3885688 polymorphism in this cohort. For the other two polymorphisms, the combined effects of genotype/allele and gender were shown to be associated with the risk of periodontitis using multivariate logistic regression analysis. The G+ genotype/G allele may be considered to exert a significant protective effect in males against AgP (Genotype: rs3795391: P= 0.032, rs3806232: P= 0.017; Allele: rs3795391: P= 0.024, rs3806232: P= 0.013). Although the combined effects of genotype and gender on CP susceptibility were not observed for these two polymorphisms, there does seem to be increased risk of CP in males with allele A compared to females with allele A (rs3795391: P= 0.008; rs3806232: P= 0.009). Hence we found an important association between polymorphisms in the S100A8 gene and periodontitis in a Chinese population.

Adult↗
PubMed2003

Molecular pathogenicity of the oral opportunistic pathogen Actinobacillus actinomycetemcomitans.

Periodontitis is mankind's most common chronic inflammatory disease. One severe form of periodontitis is localized aggressive periodontitis (LAP), a condition to which individuals of African origin demonstrate an increased susceptibility. The main causative organism of this disease is Actinobacillus actinomycetemcomitans. A member of the Pasteurellaceae, A. actinomycetemcomitans produces a number of interesting putative virulence factors including (a) an RTX leukotoxin that targets only neutrophils and monocytes and whose action is influenced by a novel type IV secretion system involved in bacterial adhesion; (b) the newly discovered toxin, cytolethal distending toxin (CDT); and (c) a secreted chaperonin 60 with potent leukocyte-activating and bone resorbing activities. This organism also produces a plethora of proteins able to inhibit eukaryotic cell cycle progression and proteins and peptides that can induce distinct forms of proinflammatory cytokine networks. A range of other proteins interacting with the host is currently being uncovered. In addition to these secreted factors, A. actinomycetemcomitans is invasive with an unusual mechanism for entering, and traveling within, eukaryotic cells. This review focuses on recent advances in our understanding of the molecular and cellular pathogenicity of this fascinating oral bacterium.

Actinobacillus Infections↗
PubMed2002

Periodontitis in humans and non-human primates: oral-systemic linkage inducing acute phase proteins.

BACKGROUND: The acute phase response (APR) represents a systemic counterpart to the localized inflammatory response. This report describes patient-oriented and non-human primate model studies to determine the effect of periodontal disease on systemic acute phase proteins (APP). METHODS: Patient-oriented studies included comparison of the levels of APP, using enzyme-linked immunosorbent assay (ELISA), with the presence and severity of periodontitis in localized chronic periodontitis (LCP), generalized aggressive periodontitis (GAP), and Sjogren's syndrome (SS) patients. The non-human primate experiments evaluated the serum level of APPs under natural conditions, following mechanical hygiene, experimental gingivitis, and during ligature-induced periodontitis. RESULTS: Analysis of the LCP population showed what appeared to be a threshold of periodontal disease severity required for elevating the C-reactive protein (CRP) and haptoglobin (HG). The results demonstrated a significant elevation in CRP in the GAP versus the control groups, as well as lower levels of all mediators in healthy non-smokers (HNS) versus smokers (HS), suggesting that these systemic inflammatory markers were altered in response to challenge by noxious materials from smoking. Significantly different levels of CRP, HG, and alpha1-antiproteinase were noted in the SS patients suggesting that the autoimmune aspects of Sjögren's syndrome may impact upon oral health and systemic responses. Parallel evidence was also obtained from the primate studies. Providing mechanical oral hygiene, which significantly lowered clinical inflammation and bleeding of the gingiva, decreased the serum APP levels. Both CRP and fibrinogen were significantly elevated during progressing periodontitis, which also appeared to have an impact on serum lipids and lipoproteins. CONCLUSIONS: These findings supported results relating chronic oral infections and the inflammation of periodontitis as contributors to and/or triggers for systemic inflammatory responses. Finally, similarities in the clinical and microbiological parameters of gingival inflammation and periodontitis between humans and non-human primates was extended to identification of changes in serum APP in the non-human primates that appeared to be in direct response to the induction of progressing periodontitis. These systemic changes provide additional evidence for the biological plausibility of periodontal infections contributing to various systemic diseases.

Acute-Phase Proteins↗
PubMed2004

[The stages of comprehensive periodontal therapy--diagnosis-driven treatment planning].

The rationale and the stages of the comprehensive periodontal treatment are overviewed. The consecutive phases are logically following each other. Basically three major therapeutical categories can be established, such as: 1. absolutely healthy from periodontal point of view, 2. gingivitis, 3. periodontitis. Within the periodontitis group the basic principles and strategies are totally different for the management of chronic and aggressive periodontitis cases. Principally the comprehensive periodontal therapy can be divided into four main phases: phase I. initial or cause related therapy, phase II. surgical therapy, phase III. periodontal reconstruction, and phase IV. periodontal maintenance. The classic non-surgical and surgical techniques can cure inflammation, arrest the progression of periodontal destruction and restore gingival-periodontal health, and the outcome is quite predictable for gingivitis and chronic periodontitis. The long-lasting results are dependent on the patients' motivation and maintenance. The late therapeutical results and the maintenance of aggressive periodontitis cases are less predictable. Technically the vertical component of the bone loss can be fully corrected by regenerative surgical techniques. So far the horizontal bone loss should be considered as an irreversible feature as no periodontal regenerative techniques are available to restore the lost alveolar crest and interdental septa.

Chronic Disease↗
PubMed2003

Mutations of F110 and C126 of the formyl peptide receptor interfere with G-protein coupling and chemotaxis.

BACKGROUND: Localized aggressive periodontitis (LAgP) is a disease characterized by rapid loss of alveolar bone in teeth of otherwise healthy patients. Neutrophils from LAgP patients have been shown to exhibit diminished chemotaxis and low levels of formyl peptide receptor (FPR) surface expression. A recent study has associated LAgP with 2 polymorphisms in the FPR: 110Phe-->Ser and 126Cys-->Trp. METHODS: We transfected Chinese hamster ovary cells with wtFPR, FPR-110Phe-->Ser, FPR-126Cys-->Trp, or FPR-110Phe-->Ala and determined their surface expression of FPR, their ligand binding affinity, their G-protein coupling, and their chemotaxis toward N-formyl-methionyl-leucyl-phenylalanine (FMLP). RESULTS: FPR-110Phe-->Ser mutants failed to show any significant surface expression or chemotaxis toward FMLP. FPR-126Cys-->Trp mutants exhibited slightly lower than normal binding affinity, markedly lower G-protein coupling response, and markedly lower chemotaxis toward FMLP than that observed with wtFPR. We also analyzed another FPR-Phe110 mutant, FPR-110Phe-->Ala, to ascertain what the effect of mutating this residue might be in a mutant that could be expressed on the cell surface. The FPR-110Phe-->Ala mutant demonstrated markedly lower surface expression, normal ligand binding affinity, markedly lower G-protein coupling, and markedly lower chemotaxis toward FMLP. CONCLUSIONS: Our data substantiate the hypothesis that the chemotactic defects observed in LAgP patients are due at least in part to molecular alterations in the FPR. The FPR-110Phe-->Ser polymorphism appears to be more defective than the FPR-126Cys-->Trp polymorphism, indicating that patients with the former polymorphism might be expected to exhibit a more severe form of aggressive periodontitis.

Aggressive Periodontitis↗
PubMed2005

Epidemiology and risk factors of periodontal diseases.

Periodontal diseases are chronic inflammatory disorders encompassing destructive and nondestructive diseases of the periodontal supporting tissues of teeth. Gingivitis is a nondestructive disease ubiquitous in populations of children and adults globally. Aggressive periodontitis is characterized by severe and rapid loss of periodontal attachment often commencing at or after the circumpubertal age and is more prevalent among Latin Americans and subjects of African descent, and least common among Caucasians. Chronic periodontitis is a common disease and may occur in most age groups, but is most prevalent among adults and seniors world-wide. Approximately 48% of United States adults have chronic periodontitis, and similar or higher rates have been reported in other populations. Moderate and advanced periodontitis is more prevalent among the older age groups, and rates of 70% or more have been reported in certain populations. Chronic and aggressive periodontitis are multifactorial diseases caused primarily by dental plaque microorganisms, and with important modifying effects from other local and systemic factors. The study of the significance of demographic, environmental, and biologic variables is important for risk assessment and the control of periodontal diseases.

Adult↗
PubMed2005

Dendritic-NK cell interactions in P. gingivalis-specific responses.

Patients with localized aggressive periodontitis have type-1 cytokines in gingival crevicular fluid and high titers of IFN-gamma-dependent IgG2 reactive with P. gingivalis in gingival crevicular fluid and serum. Localized aggressive periodontitis monocytes spontaneously differentiate into dendritic cells that can stimulate IFN-gamma production by NK cells. These relationships prompted the hypothesis that P. gingivalis-dendritic cell-NK cell interactions might promote type-1 cytokine responses. Although P. gingivalis is not a potent inducer of Th1 responses, it stimulated strong IL-12 responses by monocyte-derived dendritic cells in the presence of IFN-gamma, and IFN-gamma was produced by NK cells within 24 hrs in the presence of dendritic cells. Anti-P. gingivalis IgG2 responses were enhanced by dendritic cells, and removal of NK cells reduced IFN-gamma- and P. gingivalis-specific IgG2. Thus, P. gingivalis-dendritic cell-NK cell interactions apparently resulted in reciprocal stimulation and increased type-1 cytokine production by both dendritic cells and NK cells, and increased P. gingivalis-specific IgG2.

Adult↗
PubMed2003

Patterns of chemokines and chemokine receptors expression in different forms of human periodontal disease.

Current knowledge states that periodontal diseases are chronic inflammatory reactions raised in response to periodontopathogens. Many cell types and mediators, including Th1 and Th2 lymphocytes, cytokines and chemokines, appear to be involved in the immunopathogenesis of periodontal diseases. Chemokines, a family of chemotactic cytokines, bind to specific receptors and selectively attract different cell subsets to the inflammatory site. They can also interact with classical cytokines and modulate the local immune response. In order to study the role of chemokines in periodontal diseases, we examined the expression of chemokines, chemokine receptors and cytokines by means of reverse transcription-polymerase chain reaction (RT-PCR) techniques. Characteristic patterns of such factors' expression were found in gingival biopsies from patients presenting with aggressive periodontitis and chronic periodontitis. The expression of the chemokines macrophage inflammatory protein-1 alpha (MIP-1alpha) and interferon-gamma inducible protein 10 (IP-10) and of their respective receptors, CCR5 and CXCR3, were more prevalent and higher in aggressive periodontitis, and associated with higher interferon-gamma (IFN-gamma) expression and lower interleukin-10 (IL-10) expression. In contrast, chronic periodontitis patients exhibited a more frequent and higher expression of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR4, and higher expression of IL-10. It is possible that chemokines, in addition to the classical cytokines, are involved in the immunopathogenesis of periodontal disease, driving the migration and the maintenance of several inflammatory cell types such as polymorphonuclear leukocytes, dendritic cells (DCs), natural killer cells, macrophages, and subsets of lymphocytes in the gingival tissues. These cells are thought to participate in the inflammatory and immune reaction that takes place in periodontal disease, killing pathogens, presenting antigens, and producing cytokines. The selective recruitment of polarized lymphocyte subsets could result in differential cytokine production at the site of response, which is supposed to determine the stable or progressive nature of the lesion. Besides, the role of chemokines as activators and chemoattracts of osteclasts may be involved in the determination of disease severity.

Adult↗
PubMed2001

Non-redundant roles for interleukin-1 alpha and interleukin-1 beta in regulating human IgG2.

BACKGROUND: Serum concentrations of immunoglobulin G2 (IgG2) are elevated in localized aggressive periodontitis (LAgP) patients, and secretory products of monocytes from LAgP patients enhance IgG2 responses of lymphocytes from healthy subjects. Furthermore, genes regulating production of interleukin (IL)-1 influence the risk for both aggressive periodontitis (AgP) and chronic periodontitis. These observations, and the fact that IgG2 dominates responses to carbohydrates from Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis, prompted the hypothesis that IL-1 alpha, IL-1 beta, and IL-RA may help regulate human IgG2 responses. METHODS: Human peripheral blood leukocytes (PBL) were stimulated in culture with pokeweed mitogen (PWM); the levels of available IL-1 gene products were manipulated; and the effect on IgG2 production was monitored. Manipulations of IL-1 were accomplished by adding specific neutralizing monoclonal antibodies or recombinant IL-1RA, IL-1 alpha, or IL-1 beta. RESULTS: Blocking the IL-1 receptor with IL-1RA or neutralizing IL-1 alpha or IL-1 beta with specific antibody dramatically suppressed IgG2 production (50% to 70%). Additionally IL-1 alpha did not compensate for neutralized IL-1 beta, and additional IL-1 beta did not compensate for neutralized IL-1 alpha, suggesting the 2 monokines have separate roles in promoting IgG2. Furthermore, combinations of anti-IL-1 alpha and anti-IL-1 beta were more inhibitory than either antibody alone, and IL-1 alpha and IL-1 beta in combination appeared to work additively in promoting IgG2. Moreover, PBL cultures from a group of LAgP patients with high IgG2 levels had elevated levels of IL-1 beta. CONCLUSION: IL-1 alpha and IL-1 beta appear to have critical and non-redundant roles in the generation and regulation of potent IgG2 responses, which appear to be important in human responses to carbohydrate-bearing bacteria.

Adult↗