1α,25-dihydroxyvitamin D3 promotes early osteogenic differentiation of PDLSCs and a 12-year follow-up case of early-onset vitamin D deficiency periodontitis.

Periodontitis is a chronic periodontal disease that contributes to tooth loss. In recent years, many animal studies have reported that vitamin D (VitD) deficiency results in chronic periodontitis. However, no studies have reported cases of early-onset periodontitis with VitD deficiency. This study reports a 5-year-old male patient with early-onset periodontitis, VitD deficiency and VitD receptor (VDR) mutation. The patient was treated with VitD and calcium, and received systematic periodontal treatment. During the 12-year treatment, the periodontal conditions of this patient were stable. Our in vitro study found that VitD could promote the expression of alkaline phosphatase (ALP), runt-related transcription factor 2 (Runx2), bone morphogenetic protein 2 (BMP2), bone gamma-carboxyglutamate protein (BGLAP), and VDR in the early osteogenic differentiation of periodontal ligament stem cells (PDLSCs). Meanwhile, VitD could downregulate mRNA expression levels of Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-1ß (IL-1ß) and protein levels of IL-6 in the tumor necrosis factor-α (TNF-α) -induced inflammation of PDLSCs. Therefore, sufficient VitD supply can be a potential treatment for VitD deficiency induced early-onset periodontitis.

Functional Polymorphisms of CTLA4 Associated with Aggressive Periodontitis in the Chinese Han Population.

BACKGROUND/AIMS: CTLA4 has been identified functioning as a protein receptor which functions as an immune checkpoint, downregulating the immune system. Susceptibility to aggressive periodontitis (AgP) is influenced by gene polymorphisms related to the immune response. In this study, we focused on SNPs in the 3'-UTR of CTLA4 among Chinese AgP patients, and investigated any further relationships between the SNPs and miRNAs. METHODS: This case-control study included 120 AgP patients and 150 healthy controls. Genotyping was used to detect allele distribution. Cell transfection and the dual luciferase reporter assay were performed to investigate the potential functions of SNPs located in the 3'UTR of CTLA4. RESULTS: The data show that patients with a history of smoking were more susceptible compared to controls, exhibiting deeper probing depth, greater attachment loss and more sites of bleeding on probing. The results of genotyping analysis revealed that individuals with the GA and AA genotypes, and with the A carrier had a decreased risk (P = 0.015, P = 0.03). Furthermore, patients with the G allele might be regulated by miR-105, which caused a down-regulation of CTLA4. The carriers of the GG genotype exhibited the worst results of attachment loss and bleeding on probing. CONCLUSION: These findings show that rs56102377 in the 3'-UTR of CTLA4 may act as a protective factor by disrupting the regulatory role of miR-105 in CTLA4 expression. Thus, our study highlighted a potential role of these polymorphisms as genetic susceptibility biomarkers of periodontitis in Chinese Han populations.

Comparative analysis of immune cell subsets in peripheral blood from patients with periodontal disease and healthy controls.

Periodontitis is a chronic inflammatory disease caused by the colonization of teeth by the bacterial plaque biofilm and the resultant host immune responses in adjacent periodontal tissues. Disease severity can vary dramatically between patients with periodontitis, with some subjects displaying inflammation without bony destruction (gingivitis), while others experience chronic progressive or rapidly aggressive gingival connective tissue damage and bone loss. To determine whether peripheral immune dysregulation is associated with periodontitis, we performed extensive analysis of immune cell subsets in peripheral blood from patients with chronic or aggressive periodontitis versus periodontally healthy control subjects. Peripheral blood mononuclear cells (PBMC) from patients with chronic periodontitis or aggressive periodontitis and from periodontally healthy controls were analysed by 8-10-colour flow cytometry for the frequencies of various lymphocyte subsets, including interleukin (IL)-17-, interferon (IFN)-γ-, tumour necrosis factor (TNF)-α- and IL-10-producing cells, and the frequencies and phenotype of monocytes. Cytokine levels in serum from the different groups were determined by Luminex assay. We found no significant differences in the frequencies of major immune cell populations [CD4+ T cells, CD8+ T cells, γδ T cells, CD4+ CD45RO+ CD25+ CD127low regulatory T cells (Tregs ), CD19+ B cells, CD14+ monocytes] or of cytokine-producing T cells, or in the phenotype of CD14+ monocytes in peripheral blood from these patient cohorts. Additionally, no significant differences were observed in serum levels of prototypical inflammatory cytokines. These results suggest that the local gingival inflammatory response is not reflected by obvious changes in major blood immune cell subset frequencies.

Nonincised Papillae Surgical Approach (NIPSA) in Periodontal Regeneration: Preliminary Results of a Case Series.

A new surgical approach has been developed to optimize the preservation of the gingival margin and papillae when treating periodontal defects. The flap is raised by one mucosal incision far away from the marginal tissues. This case series reports on the effectiveness of a nonincised surgical approach (NIPSA) in conjunction with a hydroxyapatite-based graft biomaterial and enamel matrix derivative in treating intrabony defects. Ten defects in 10 patients were treated. The follow-up period ranged from 6 to 18 months (mean: 10.8 ± 4.7 months). Probing pocket depth was 9.6 ± 2.3 mm before surgery and 2.3 ± 0.5 mm postsurgery. Clinical attachment level (CAL) decreased from 10.4 ± 2.7 mm to 3.1 ± 0.87 mm postsurgery. The gingival papilla height, keratinized tissue width, and buccal gingival margin remained stable over time. No wound dehiscence was recorded. Mean Early Healing Index was 1.5 ± 0.7. Results show a substantial CAL gain, limited postsurgical shrinkage, minimal morbidity, and early healing.

Outcomes After 25 Years of Periodontal Treatment and Maintenance of a Patient Affected by Generalized Severe Aggressive Periodontitis.

This report describes the long-term outcomes of nonsurgical periodontal therapy and supportive periodontal treatment (SPT) of a 21-year-old patient affected by generalized aggressive periodontitis at multiple teeth with a compromised prognosis. After 25 years of SPT, no teeth had been extracted and no periodontal pockets associated with bleeding on probing were present. Radiographic analysis showed an improvement in infrabony defects, demonstrating long-term improvement is possible with nonsurgical periodontal treatment provided that smoking is not present and the patient is included in a strict SPT.

Lack of association between the TNF-α-1031genotypes and generalized aggressive periodontitis disease.

Periodontal disease is one of the most prevalent inflammatory illnesses and is a main cause of tooth loss in human population. Tumor necrosis factor-α (TNF-α) gene is one of pro-inflammatory cytokines which has important role in pathogenesis of periodontal disease. The main purpose of this study is to determine genotype abundance of TNF-α-1031 gene in both groups of patients and controls, and also investigation of relation of single nucleotide polymorphism (SNP) these genotypes with periodontal disease risk. DNA was extracted from blood tissue of 31 patients and 54 controls. The TNF-α-1031 polymorphism was evaluated by polymerase chain reaction- confronting two-pair primer (PCR-CTPP) method. In the GAP group, the frequencies of TT, TC and CC genotypes were 35.48%, 61.29 and 3.23%, respectively. In controls the frequencies of TT, TC and CC genotypes were 22.22%, 72.22%, and 5.56%, respectively. Results of this study showed that there was no significant association between TNF-α (-1031 T/C promoter) gene polymorphisms and the risk of generalized aggressive periodontitis disease.

Platelet activation and platelet-leukocyte interaction in generalized aggressive periodontitis.

Generalized aggressive periodontitis (GAgP) is an inflammatory disease of host response to bacterial challenge. To explore the role of platelets in host-microbial interactions in patients with periodontitis, 124 patients with GAgP and 57 healthy subjects were enrolled. Reliable indicators of subclinical platelet functional status, platelet count (PLT), platelet large cell ratio (PLCR), and mean platelet volume (MPV), were significantly lower in the GAgP group than in the control group and were negatively correlated with clinical periodontal parameters. The levels of important cytosolic protein in neutrophils, calprotectin (S100A8/A9) in plasma, and gingival crevicular fluid (GCF) were significantly higher in patients with GAgP compared with healthy subjects. Moreover, the GCF calprotectin level was negatively correlated with PLCR and MPV values. To explore the possible mechanisms of changes in platelet indices in periodontitis, flow cytometry analysis was performed, and patients with GAgP were found to have a higher status of platelet activation compared with healthy controls. Porphyromonas gingivalis (P. gingivalis) and recombinant human S100A8/A9 (rhS100A8/A9) induced platelet activation and facilitated platelet-leukocyte aggregate formation in whole blood of healthy subjects. In response to P. gingivalis and rhS100A8/A9, platelets from patients with GAgP increased activation and increased formation of platelet-leukocyte aggregates compared with those from healthy subjects. Platelet aggregates and platelets attached to leukocytes were found on gingival tissues from patients with GAgP, suggesting that decreased platelet size and count in the circulation might be related to consumption of large, activated platelets at inflamed gingiva. Platelets may have a previously unrecognized role in host response to periodontal infection.

Clinical and histological characterization of an aggressive periodontitis case associated with unusual root canal curvatures.

The article presents the histological and clinical characteristics in a severe generalized aggressive periodontitis case associated with multiple root curvatures and the complex therapeutic approach of the severe periodontal destructions. The patient received a complex therapy, including periodontal non-surgical, regenerative and reconstructive approaches, and also endodontic and prosthetic treatments. Recall appointments were fixed at 3-month intervals. One year after the finalization of the active therapy, a hyperplasic, inflamed interdental papilla associated with a recurrent clinical attachment loss was diagnosed at the mesial aspect of the right maxillary second premolar. A biopsy was harvested for histological examination and the recurrent site was treated. The histological study revealed important modifications of the epithelial layer and of the connective tissue of the gingiva. An extremely accentuated pattern of the gingival rete ridges at the epithelial-connective tissue junction, the presence of inflammatory cells infiltrating the epithelial layer and lamina propria and the disorganization of the fascicules of collagen fibers were observed. The inflammatory infiltrate was dominated by plasma and monocytic-like cells as immunohistochemical analyses highlighted. The complex therapeutic approach led to a satisfactory aesthetic and functional outcome. The severe root curvatures may be an unusual trait in this generalized aggressive periodontitis case substantially increasing the amount and the costs of non-periodontal procedures. In this case, the cell make-up of the inflammatory infiltrate and the paucity of collagen in the infiltrated tissue portions are considered to correspond to a fully developed recurrent lesion.

Lipid subclasses profiles and oxidative stress in aggressive periodontitis before and after treatment.

BACKGROUND AND OBJECTIVE: Associations between dyslipidaemia, oxidative stress and periodontitis have emerged in recent years. However, there is a lack of studies investigating these associations in aggressive periodontitis (AgP) cases. The aim of this study was to investigate the lipid and oxidative stress profiles in patients with AgP, and to relate them to clinical variables and interleukin (IL)-6 genetic variants. MATERIAL AND METHODS: Twelve non-smoking Caucasian patients with AgP selected based on their IL6 haplotypes underwent periodontal non-surgical and surgical treatment. Peripheral blood samples taken at baseline and at six different time-points after treatment were processed to determine IL-6 circulating levels, lipid profiles (cholesterol, triglycerides, high-density lipoprotein [HDL] and low-density lipoprotein [LDL] subclasses) and oxidative stress markers (glutathione and total lipid hydroperoxide levels). RESULTS: HDLs were the most prevalent lipoproteins, followed by intermediate-density lipoprotein, very-low-density lipoprotein and LDL. The LDL subclasses consisted mainly of the less atherogenic large LDL. The lipid profile did not consistently change after treatment up to 3 mo after surgery. Periodontal disease severity was associated with LDL levels and size. The IL6 haplotypes were associated with total cholesterol, triglycerides, HDL and LDL subclasses after adjusting for confounders. IL-6 circulating levels were associated with both very-low-density lipoprotein and lipid hydroperoxide levels. CONCLUSION: Based on these data, we conclude that both periodontal disease severity and IL6 haplotypes may influence lipid profiles in AgP.

10-year survival rate and the incidence of peri-implant disease of 374 titanium dental implants with a SLA surface: a prospective cohort study in 177 fully and partially edentulous patients.

PURPOSE: This prospective cohort study evaluates the 10-year survival and incidence of peri-implant disease at implant and patient level of sandblasted, large grid, and acid-etched titanium dental implants (Straumann, soft tissue level, SLA surface) in fully and partially edentulous patients. MATERIAL AND METHODS: Patients who had dental implant surgery in the period between November 1997 and June 2001, with a follow-up of at least 10 years, were investigated for clinical and radiological examination. Among the 506 inserted dental implants in 250 patients, 10-year data regarding the outcome of implants were available for 374 dental implants in 177 patients. In the current study, peri-implantitis was defined as advanced bone loss (≧1.5 mm. postloading) in combination with bleeding on probing. RESULTS: At 10-year follow-up, only one implant was lost (0.3%) 2 months after implant surgery due to insufficient osseointegration. The average bone loss at 10 year postloading was 0.52 mm. Advanced bone loss at 10-year follow-up was present in 35 dental implants (9.8%). Seven percent of the observed dental implants showed bleeding on probing in combination with advanced bone loss and 4.2% when setting the threshold for advanced bone loss at 2.0 mm. Advanced bone loss without bleeding on probing was present in 2.8% of all implants. CONCLUSION: In this prospective study, the 10-year survival rate at implant and patient level was 99.7% and 99.4%, respectively. Peri-implantitis was present in 7% of the observed dental implants according to the above-mentioned definition of peri-implantitis. This study shows that SLA implants offer predictable long-term results as support in the treatment of fully and partially edentulous patients.

The pro-apoptotic and pro-inflammatory effects of calprotectin on human periodontal ligament cells.

Calprotectin, a heterodimer of S100A8 and S100A9 subunits, is associated with inflammatory disorders such as rheumatoid arthritis and cystic fibrosis. Although calprotectin levels are increased significantly in the gingival crevicular fluid (GCF) of periodontitis patients, its effects on periodontal ligament cells (PDLCs) remain largely unknown. The aim of this study was to evaluate calprotectin levels in the GCF of generalized aggressive periodontitis (AgP) patients and to investigate the effects of recombinant human calprotectin (rhS100A8/A9) and its subunits (rhS100A8 and rhS100A9) in PDLCs. Both the concentration and amount of crevicular calprotectin were significantly higher in the AgP group compared with healthy controls. In addition, the GCF calprotectin levels were correlated positively with clinical periodontal parameters including bleeding index, probing depth, and clinical attachment loss. rhS100A8/A9 promoted cell apoptosis, whereas rhS100A8 and rhS100A9 individually exerted little effect on apoptosis in PDLCs. rhS100A9 and rhS100A8/A9 increased the activation of nuclear factor-κB (NF-κB) by promoting the nuclear translocation of p65 in PDLCs, subsequently inducing expression of the pro-inflammatory cytokines IL-6, IL-8, TNFα, and COX2. Treatment with an NF-κB inhibitor partially reversed the rhS100A9- and rhS100A8/A9-induced upregulation of the pro-inflammatory cytokines. rhS100A9, and not rhS100A8, was mainly responsible for the pro-inflammatory role of calprotectin. Collectively, our results suggest that calprotectin promotes apoptosis and the inflammatory response in PDLCs via rhS100A9. These findings might help identify novel treatments for periodontitis.

Periodontitis agresiva infantil en un niño de 4 años / Aggressive infantile periodontitis in a 4-year-old boy

Se define a la periodontitis agresiva como una forma agresiva y rápidamente destructiva de enfermedad, caracterizada por la pérdida severa del ligamento periodontal y hueso alveolar. Si bien la mayor prevalencia se ubica en la población adulta, se han registrado casos en niños y adolescentes. Se reporta el caso clínico de un niño de 4 años de edad que concurre a la consulta en el año 2010 por pérdida prematura de piezas dentarias. La evaluación de los exámenes de rutina y las radiografías con las que acudió permitieron descartar una periodontitis como manifestación de una enfermedad sistémica. Se confirma el diagnóstico de periodontitis infantil agresiva, por medio de examen microbiológico y ténica PCR. El tratamiento indicado fue terapia básica, antibioticoterapia y controles periódicos. Luego de tre años no hay signos clínicos de la enfermedad. El diagnóstico preciso, sumado a la motivación constante y los controles periódicos, hacen posible la detención del avance de la enfermedad...

Apoptotic activity of gingival crevicular fluid from localized aggressive periodontitis.

INTRODUCTION: The aim of this study was to examine a potential link between apoptotic biomarkers in gingival crevicular fluid (GCF) and periodontal destruction in four cases of localized aggressive periodontitis (LAP), diagnostically enhanced by cone beam computed tomography. CASE SERIES: This study examined the GCF in four patients diagnosed with LAP (formerly localized juvenile periodontitis) at a routine periodontal examination. The LAP diseased sites had attachment loss ranging from 5-12 mm. Atotal of 62 samples of GCF were collected from diseased sites and from contralateral, matched healthy sites with minimal or no attachment loss. All samples were assayed for apoptotic markers, including Fas/FasL, DNAfragmentation, and nitric oxide. The GCF samples were analyzed utilizing enzyme-linked immunosorbent assays for DNA fragments and nitric oxide levels, whereas Western blotting was used for Fas/FasL analyses. Our results showed a significant increase in the apoptotic markers Fas/FasL and DNA fragmentation when comparing GCF from diseased versus non-diseased sites in patients with LAP. CONCLUSION: To our knowledge, this is the first report of apoptotic biomarkers associated with patients diagnosed with LAP. Finding significantly increased levels of these markers in localized areas may help us understand the pathophysiology associated with this specific form of periodontitis, and, furthermore, may provide a basis for a quantifiably prognostic test when attempting to treat this disease.

Elevated oral and systemic levels of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in periodontitis.

The Triggering Receptor Expressed on Myeloid cells 1 (TREM-1) is a cell-surface receptor of the immunoglobulin superfamily, involved in the propagation of the inflammatory response to bacterial challenge. Soluble (s)TREM-1 is released from the cell surface during the course of infection and is a useful inflammatory biomarker in the early diagnosis of systemic sepsis. The hypothesis of this study was that oral and systemic levels of sTREM-1 are elevated in periodontitis. Therefore, the aim was to investigate, by ELISA, the sTREM-1 concentrations in saliva and serum of individuals without periodontitis (control) and persons with chronic or generalized aggressive periodontitis. In saliva, sTREM-1 concentrations were higher in chronic and aggressive periodontitis than in the control group, by 3.3-fold and 5.6-fold, respectively. In serum, these differences were 1.7-fold and 2-fold, respectively. However, there were no significant differences between the two forms of periodontitis, neither in saliva nor in serum. Salivary and serum sTREM-1 levels positively correlated with full-mouth clinical periodontal parameters. In conclusion, the increased oral and systemic levels of sTREM-1 in periodontitis denote a value for this molecule as a biomarker for the disease and may also have implications in the association between periodontal infections and systemic inflammatory response.

Expression of peptidylarginine deiminase-2 and -4, citrullinated proteins and anti-citrullinated protein antibodies in human gingiva.

BACKGROUND AND OBJECTIVE: The presence of citrullinated proteins, and peptidylarginine deiminase types -2 (PAD-2) and -4 (PAD-4) in periodontal tissues, determine the presence of anti-cyclic citrullinated protein antibodies (anti-CCP) in gingival crevicular fluid (GCF) and compare the expression of these proteins between inflamed and non-inflamed sites. MATERIAL AND METHODS: Tissue sections were stained using antibodies against citrullinated proteins, PAD-2 and PAD-4. RT-PCR was performed to investigate PAD-2 and PAD-4 mRNA in inflamed and non-inflamed gingival tissues. Anti-CCP antibodies in gingival crevicular fluid were detected by ELISA. RESULTS: Citrullinated proteins, PAD-2 and PAD-4 were detected in gingiva. There was a correlation between inflammation and expression of these proteins. mRNAs for PAD-2 and PAD-4 were detected in both inflamed and non-inflamed gingival tissues. Antibodies to CCP were found mostly in the GCF of individuals with periodontitis. CONCLUSION: PAD-2 and PAD-4 (protein and mRNA) as well as citrullinated proteins are present in inflamed gingiva, and anti-CCP antibodies can be detected in the GCF of some patients. Tissue expression of citrullinated proteins and PAD increased with the severity of inflammation. The presence of anti-CCP antibodies in GCF was almost exclusive to a subset of patients with periodontitis. Increased expression of these proteins in inflamed gingiva lends support to the notion that periodontal inflammation contributes to the inflammatory burden in a similar way to rheumatoid arthritis.

Effects of cranberry components on human aggressive periodontitis gingival fibroblasts.

BACKGROUND AND OBJECTIVE: Aggressive periodontitis (AgP) causes rapid periodontal breakdown involving AgP gingival fibroblast production of cytokines [i.e. interleukin (IL)-6, a bone metabolism regulator], and matrix metalloproteinase (MMP)-3. Lipopolysaccharide upregulates fibroblast IL-6 and MMP-3, via transcription factors (i.e. NF-κB). Cranberry (Vaccinium macrocarpon) inhibits lipopolysaccharide-stimulated macrophage and normal gingival fibroblast activities, but little is known of its effects on AgP fibroblasts. Objectives of this study are to use AgP fibroblasts, to determine cytotoxicity of cranberry components or periodontopathogen (Fusobacterium nucleatum, Porphyromonas gingivalis) lipopolysaccharide ± cranberry components, and effects of cranberry components on lipopolysaccharide-stimulated NF-κB activation and IL-6 and MMP-3 production. MATERIAL AND METHODS: AgP fibroblasts were incubated ≤ 6 d with high molecular weight non-dialyzable material (NDM) (derived from cranberry juice (1-500 µg/mL) or lipopolysaccharide (1 µg/mL) ± NDM. Membrane damage and viability were assessed by enzyme activity released into cell supernatants and activity of a mitochondrial enzyme, respectively. Secreted IL-6 and MMP-3 were measured by ELISA. NF-κB p65 was measured via binding to an oligonucleotide containing the NF-κB consensus site. Data were analyzed using analysis of variance and Scheffe's F procedure for post hoc comparisons. RESULTS: Short-term exposure to NDM, or lipopolysaccharide ± NDM caused no membrane damage. NDM (≤ 100 µg/mL) or lipopolysaccharide ± NDM had no effect on viability ≤ 7 d exposure. NDM (50 µg/mL) inhibited lipopolysaccharide-stimulated p65 (P ≤ 0.003) and constitutive or lipopolysaccharide-stimulated MMP-3 (P ≤ 0.02). NDM increased AgP fibroblast constitutive or lipopolysaccharide-stimulated IL-6 (P ≤ 0.0001), but inhibited normal human gingival fibroblast IL-6 (P ≤ 0.01). CONCLUSION: Lack of toxicity of low NDM concentrations, and its inhibition of NF-κB and MMP-3, suggest that cranberry components may regulate AgP fibroblast inflammatory responses. Distinct effects of NDM on AgP and gingival fibroblast production of IL-6 (which can have both positive and negative effects on bone metabolism) may reflect phenotypic differences in IL-6 regulation in the two cell types.

Increased gingival crevicular fluid levels of soluble triggering receptor expressed on myeloid cells (sTREM) -1 in severe periodontitis.

AIM: This study was designed to evaluate the presence of a new regulator of innate immunity in periodontitis: the soluble form of triggering receptor on myeloid cells-1 (sTREM-1) in gingival crevicular fluid (GCF). MATERIAL AND METHODS: GCF was collected at four sites, three pathological and one healthy from 17 patients with periodontitis, and at one healthy site from 23 control patients. An enzyme-linked immunosorbent assay (ELISA) kit was used to quantify sTREM-1 levels in collected crevicular fluid. Recorded clinical parameters were probing pocket depth (PPD), bleeding upon probing, tooth mobility, plaque index (PlI), and gingival index (GI). RESULTS: The mean sTREM-1 level in collected fluid was significantly higher in pathological sites than in healthy sites from either periodontal or control patients: 353.9 pg/ml, 50.2 pg/ml and 25.4 pg/ml respectively. Soluble TREM-1 concentration was significantly correlated with PPD. The sTREM-1 levels increased with the augmentation of the PlI and GI scores and levelled off at score 2 for both indexes. In multivariate analysis, periodontal pocket depth and smoking status were statistically associated with highest sTREM-1 concentrations. CONCLUSION: sTREM-1 was detected in crevicular fluid and its concentration was higher in pathological sites. It could be a marker of periodontal tissue destruction.

Effects of periodontal therapy on GCF cytokines in generalized aggressive periodontitis subjects.

AIM: To examine changes in levels of gingival crevicular fluid (GCF) cytokines, after periodontal therapy of generalized aggressive periodontitis (GAgP). MATERIALS AND METHODS: Twenty-five periodontally healthy and 24 GAgP subjects had periodontal clinical parameters measured and gingival crevicular fluid (GCF) samples collected from up to 14 sites/subject. GCF samples were analysed using multiplex bead immunoassay for: GM-CSF, IFN-γ, IL-10, IL-1ß, IL-2, IL-6 and TNF-α. Aggressive periodontitis subjects were randomly assigned to either scaling and root planing (SRP) alone or SRP plus systemic amoxicillin (500 mg) and metronidazole (400 mg) 3 times a day for 14 days. Clinical parameters and GCF cytokines were re-measured 6 months after treatment. Differences over time were analysed using the Wilcoxon test and between groups using the Mann-Whitney test. RESULTS: Significant reductions in GCF GM-CSF, IL-1ß and the ratio IL-1ß/IL-10 and increases in GCF IL-6 were detected after therapy. The mean change in GCF cytokines did not differ significantly between groups. CONCLUSIONS: Periodontal therapy improved GCF cytokine profiles by lowering IL-1ß and increasing IL-10 levels. The reduction in GCF GM-CSF after therapy implicates this cytokine in the pathogenesis of GAgP. There was no difference between therapies in changes of GCF cytokines.

IL-1-polymorphism and severity of periodontal disease.

OBJECTIVE: To determine the association between the interleukin (IL)-1-polymorphism and the severity of periodontal disease prior to active periodontal therapy. MATERIALS AND METHODS: Two hundred and six patients with obtained baseline x-rays were tested for IL-1-polymorphism. Relative bone loss before active periodontal treatment was measured with a Schei ruler and classified in five groups. Descriptive statistics and backward stepwise linear regression analyses were performed. RESULTS: Forty-nine patients with moderate (mChP), 79 with severe chronic (sChP) and 78 with aggressive periodontitis (AgP) were included. Age correlated significantly with bone loss and number of teeth at baseline. Gender, smoking and IL-1-polymorphism were neither associated with bone loss nor with number of teeth prior to treatment. After adjusting for age as well as gender, AgP was significantly associated with more severe bone loss in untreated periodontal disease (p = 0.036). In non-smokers, mean number of teeth prior to active periodontal therapy correlated significantly with presence of IL-1 polymorphism. CONCLUSION: The IL-1-polymorphism is associated with lower number of teeth in non-smokers with untreated periodontal disease. Untreated AgP is associated with more severe bone loss than untreated ChP.