The relationship between periodontal status and peripheral levels of neutrophils in two consanguineous siblings with severe congenital neutropenia: case reports.

Congenital neutropenia is characterized by a severe reduction in absolute neutrophil counts, resulting in an almost total absence of neutrophils. It is well known that severe neutropenia affects periodontal status. Oral manifestations include ulcerations, gingival desquamation, gingival inflammation, attachment loss, and alveolar bone loss which may result in tooth loss. Treatment with granulocyte-colony stimulating factor (G-CSF) may improve this periodontal condition. This article reports the relationship between periodontal disease status and peripheral neutrophil levels in two consanguineous siblings with severe congenital neutropenia who did not receive routine G-CSF for 2 years prior to examination. Both siblings were given scaling, root planing, and periodontal prophylaxis in regular follow-up visits. This report demonstrates that periodontal therapy supported by adequate oral hygiene may result in restoration of neutrophil counts in siblings with congenital neutropenia.     

Clinical periodontal findings and microflora profiles in children with chronic neutropenia under supervised oral hygiene

BACKGROUND: This is the first known case report that used a polymerase chain reaction (PCR)-based method to help identify the oral microflora in patients with chronic neutropenia. In this study, we report clinical periodontal findings and microflora profiles of 2 children, 1 with severe congenital neutropenia (SCN, Kostmann type) and 1 with cyclic neutropenia (CN). METHODS: The SCN patient had severe gingivitis, whereas the patient with CN had mild gingivitis in the gingival margins. Monthly oral cleaning instruction and review were performed without subsequent periodontal therapy. Oral hygiene conditions remained satisfactory and visible plaque was scarce, despite the persistence of mild gingivitis. Under supervised oral hygiene, we examined the presence of periodontal pathogens from patient plaque samples. RESULTS: By a PCR-based method, Prevotella nigrescens, Bacteroides forsythus, Campylobacter rectus, and Capnocytophaga gingivalis were detected in the SCN patient and P. intermedia, C. rectus, C. gingivalis, and C. sputigena in the CN patient, suggesting the existence of periodontal pathogens. Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, and C. ochracea were not found in either patient. CONCLUSIONS: Use of 1% povidone iodine solution and local antibiotic application under supervised oral hygiene were helpful to improve gingival conditions in patients with chronic neutropenia.     

牙周炎症对牙龈组织巨噬细胞胞外诱捕网形成的影响

目的:探讨牙周炎症对牙龈组织中巨噬细胞胞外诱捕网(METs)形成的影响。方法:纳入基础治疗后,需进行牙周翻瓣手术的牙周炎患者29例,以牙周健康的牙冠延长术患者20例作为对照。术前记录菌斑指数(PLI)、牙龈指数(GI)、探诊深度(PD)、临床附着丧失(CAL)等牙周临床指标,收集龈沟液(GCF)样本,术中收集牙周炎患者牙周破坏最严重部位的牙龈组织及牙冠延长术患者的健康牙龈组织。采用激光共聚焦显微镜观察牙龈组织中METs的形成情况,采用ELISA技术检测GCF中TNF-α和IL-9表达水平,分析两组样本METs形成水平与各牙周临床指标、GCF中TNF-α、IL-9水平的相关性。结果:牙周炎组METs形成分数,PLI、GI、PD、CAL等牙周临床指标,以及TNF-α、IL-9水平均显著高于正常对照组(P<0.05)。METs形成分数与PD、CAL正相关(P<0.05)。结论:牙周炎症破坏可以促进牙龈组织中METs的形成。     

Correlations between pentraxin 3 or cytokine levels in gingival crevicular fluid and clinical parameters of chronic periodontitis

The gingival crevicular fluid (GCF) contains various biomarkers, such as interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α), and IL-10, among others. These cytokines have been reported to correlate with gingival inflammation and periodontal status. Therefore, the analysis of GCF may be useful for the diagnosis of periodontal status. Pentraxin 3 (PTX3) is the first identified long pentraxin, and is released by several cell types in response to proinflammatory signals. The aim of this study was to determine the levels of IL-1β, IL-6, IL-8, TNF-α, IL-10 and PTX3 in GCF from diseased and healthy sites in patients with chronic periodontitis. Cross-sectional clinical data were obtained from 50 patients with chronic periodontitis. GCF samples were collected with paper strips from one periodontal diseased site and one periodontally healthy site per subject. The levels of IL-1β, IL-6, IL-8, IL-10 and TNF-α were determined using a multiplexed bead immunoassay, and the PTX3 level was measured using an enzyme-linked immunosorbent assay. Mean clinical parameters were significantly higher at diseased sites (P < 0.01) as compared to healthy sites, and the mean levels of PTX3, IL-1β, IL-6, IL-8, IL-10 and TNF-α were higher in diseased sites (P < 0.01) than in healthy sites. There were strong correlations between PTX3 or IL-1β and periodontal status. These results suggest that GCF PTX3 levels might be useful as a diagnostic marker for periodontal disease.     

Effects of oral prophylaxis including tongue cleaning on halitosis and gingival inflammation in gingivitis patients—a randomized controlled clinical trial

Objective

The objective of this study was to assess the effect of oral prophylaxis including tongue scraping on level of halitosis, clinical periodontal parameters and local cytokine response in gingivitis patients.

Materials and methods

In this randomized controlled clinical trial, 36 gingivitis patients were randomly assigned into two subgroups after scaling and polishing. Group 1 received oral hygiene instructions including the use of tongue scraper; group 2 received oral hygiene instructions alone without tongue cleaning. Levels of volatile sulfur compounds (VSC), organoleptic and tongue coating scores, clinical periodontal parameters and gingival crevicular fluid (GCF) samples were collected at baseline and 7 days after oral prophylaxis. GCF samples were analyzed using multiplexing analysis for the simultaneous measurements of cytokines. The Chi-square, Mann-Whitney U, Wilcoxon, and Student’s paired and unpaired t tests were used for statistical analysis.

Results

Statistically significant reductions were found in terms of clinical periodontal parameters in both groups. However, significant improvements in VSC levels, organoleptic and tongue coating scores were observed just in tongue scraping group. Moreover, the GCF levels of IL-1β and IL-8 significantly decreased after the treatment in group 1 according to the baseline values.

Conclusion

The present study indicated that oral prophylaxis including tongue scraping was effective in improving intra-oral halitosis and pro-inflammatory cytokine response in GCF in gingivitis patients.

Clinical relevance

The results suggest that tongue scraping can be taken into consideration in order to manage gingival inflammation as well as VSC levels in gingivitis patients but further clinical studies are required to judge the clinical relevance.

     

Calprotectin in gingival crevicular fluid correlates with clinical and biochemical markers of periodontal disease

Clinical and biochemical markers of periodontal disease have been used for precise objective diagnosis of periodontal inflammation. Interleukin 1beta (IL-1beta) and prostaglandin E2 (PGE2), inflammatory factors, levels in gingival crevicular fluid (GCF) of patients with periodontal disease are elevated and have been studied as biochemical markers. The levels of calprotectin, a leukocyte protein, in body fluids of patients with some inflammatory diseases are raised. Recently, we detected calprotectin in GCF and its concentrations in periodontal pockets were higher than those in healthy gingival crevices. In this study, we investigated the correlations between GCF calprotectin levels and clinical indicators (probing depth and bleeding on probing, BOP), and the IL-1beta or PGE2 levels in GCE Probing depth and BOP at 130 sites of 110 subjects with periodontal or other oral diseases were examined, then GCF samples were collected and their calprotectin, IL-1beta and PGE2 were determined by ELISA. The calprotectin level correlated positively with the probing depth and was significantly higher at BOP-positive than BOP-negative sites. There were significant, positive correlations between the calprotectin and IL-1beta or PGE2 concentrations. These results indicate that the calprotectin level in GCF correlates well with clinical and biochemical markers of periodontal disease and suggest that calprotectin may be useful for evaluating the extent of periodontal inflammation.     

Relationship between IL-1A polymorphisms and gingival overgrowth in renal transplant recipients receiving Cyclosporin A

AIM: Levels of interleukin-1alpha (IL-1alpha) are elevated in periodontal inflammation. IL-1A gene polymorphisms are associated with inflammatory diseases. This study aimed to investigate IL-1A gene polymorphism in Cyclosporin A (CsA)-treated renal transplant patients and investigate the association between this polymorphism and gingival crevicular fluid (GCF) levels of several cytokines. MATERIALS AND METHODS: Fifty-one renal transplant patients on CsA treatment (25 with and 26 without gingival overgrowth) and 29 healthy controls were recruited for the study. Demographic, pharmacological and periodontal parameters were recorded and gingival overgrowth was assessed. RESULTS: Multiple regression analysis showed that genotype was significantly associated with gingival overgrowth (p=0.02). Carriage of the IL-1A (-889) T allele was strongly protective [95% confidence interval (CI): 0.046-0.77], although not significantly associated with IL-1alpha protein levels in GCF. IL-1alpha, IL-1beta and IL-8, but not IL-6, were detected in GCF of CsA-treated patients, but none of them was significantly associated with gingival overgrowth. CONCLUSIONS: This study is the first to associate a gene polymorphism as a risk factor for CsA-induced gingival overgrowth in renal transplant patients, demonstrating that IL-1A polymorphism might alter individual susceptibility to CsA. However, there was no association between GCF cytokine levels and the presence of gingival overgrowth or patient IL-1A genotype.     

Measurement of interleukin-1α and -1β in gingival crevicular fluid: Implications for the pathogenesis of periodontal disease

Samples of gingival crevicular fluid (GCF) were harvested from sites manifesting features characteristic of active disease including inflammation, periodontal attachment loss, and radiographic signs of alveolar bone destruction in untreated patients with advanced periodontitis. The presence and concentrations of interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) were measured using ELISAs specific for these cytokine molecules. IL-1 alpha and/or IL-1 beta were identified in the GCF of 15 of 15 patients having untreated periodontitis. Ninety percent (71 of 79) of the sites tested contained measureable amounts of IL-1, with IL-1 beta as the more frequently occurring form. IL-1 alpha levels ranged from 0.23 nM to 13.9 nM in the GCFs. IL-1 beta levels were between 0.04 nM and 5.28 nM. Marked reductions of total IL-1 levels were observed following effective treatment. Both forms of IL-1 messenger RNA (mRNA) were detected in 17 of 17 gingival tissue samples from 6 patients. These results demonstrate that IL-1 is produced and released locally in periodontal disease at concentrations sufficient to mediate tissue inflammation and bone resorption. IL-1 may serve as a marker of periodontal tissue destruction.     

Effects of scaling and root planing on the amounts of interleukin-1 and interleukin-1 receptor antagonist and the mRNA expression of interleukin-1beta in gingival crevicular fluid and gingival tissues

OBJECTIVE: The purpose of this study was to evaluate the relationship between the clinical changes after non-surgical periodontal therapy and interleukin 1 (IL-1) in gingival crevicular fluid (GCF) and gingival tissues from patients with chronic periodontitis. BACKGROUND: The inflammatory responses mediated by IL-1 play an important role in periodontal tissue destruction. Although numerous studies have attempted to elucidate the dynamic movement involved in chronic periodontitis, the results have often conflicted. Such discrepancies may have been due to the inability to determine clinical disease activity. METHODS: Seven patients with chronic periodontitis were examined. The severity of periodontal inflammation was expressed using clinical parameters before and after a scaling and root planing (SRP) procedure. The amounts and concentrations of IL-1alpha, IL-1beta and IL-1 receptor antagonist in GCF were measured by enzyme-linked immunosorbent assay (ELISA) and IL-1 activity index was calculated. A needle biopsy in matching gingival tissues was also performed before and after the SRP procedure. The localization and mRNA expression of IL-1beta were determined using histological methods. RESULTS: Clinical parameters improved slightly after the SRP procedure. Only the probing pocket depth (PPD) was reduced significantly (p < 0.05). However, the amount of IL-1beta in GCF was slightly increased. The localization and mRNA expression of IL-1beta could still be observed after the SRP procedure. Therefore, none of the clinical parameters showed a high sensitivity or specificity for evaluating subgingival inflammation. CONCLUSION: These observations suggest that IL-1 is effective for evaluating in detail the state of subgingival inflammation.     

Gingival crevicular fluid levels of interleukin-1beta and glycemic control in patients with chronic periodontitis and type 2 diabetes

BACKGROUND: Patients with diabetes have increased incidence and severity of periodontal disease not accounted for by differences in the subgingival microbial infection. Poor glycemic control has been consistently associated with periodontal disease severity. Also, recent evidence suggests that hyperglycemia may induce inflammatory cytokine production. Few studies, however, have examined local biochemical measures of periodontal inflammation in patients with type 2 diabetes. The aim of this study was to determine whether glycemic control was related to gingival crevicular fluid (GCF) levels of interleukin-1beta (IL-1beta). METHODs: GCF samples were collected from 45 patients with type 2 diabetes and untreated chronic periodontitis. Plaque index (PI), bleeding on probing (BOP), probing depth (PD), and attachment level (AL) were recorded at six sites per tooth. IL-1beta levels were determined from individual GCF samples by enzyme-linked immunoabsorbent assay (ELISA). Individual site and mean patient values were calculated. Glycated hemoglobin (HbA1c) levels were measured from anticoagulated whole blood using an automated affinity chromatography system. Serum glucose was also determined. RESULTS: Clinical periodontal measures (PD, AL, BOP) and measures of glycemic control (HbA1c, random glucose) were significantly correlated with GCF IL-1beta. Patients with greater than 8% HbA1c had significantly higher mean GCF IL-1beta levels than patients with less than 8% HbA1c. In a multivariate model adjusting for age, gender, PD, AL, BOP, and PI, HbA1c and random glucose were independent predictors of high GCF IL-1beta. CONCLUSIONS: Poor glycemic control is associated with elevated GCF IL-1beta. These data are consistent with the hypothesis that hyperglycemia contributes to an heightened inflammatory response, and suggests a mechanism to account for the association between poor glycemic control and periodontal destruction.     

Periodontal status in two siblings with severe congenital neutropenia: diagnosis and mutational analysis of the cases

BACKGROUND: Severe congenital neutropenia (SCN), also known as Kostmann syndrome, was originally reported as an autosomal recessive disease of neutrophil production. The disease is characterized by a maturation arrest of neutrophil precursors at the promyelocytic stage of differentiation and by extremely low levels of mature neutrophils in peripheral blood. METHODS: A 6-year-old male presented with a complaint of gingival swelling and bleeding, and swelling at the left side of his face. Upon clinical examination, severe inflammation of all gingival tissues was apparent, and a periapical abscess with mobility was noted on the left mandibular second molar. Medical and dental histories revealed numerous recurrent bacterial infections associated with oral and non-oral tissues. His medical history with recurrent infections led us to evaluate his 3-year-old sister to determine the status of her oral health. Inflammation of her oral tissues and recurrent bacterial infections were apparent. Their consanguineous parents were in good health. To assist in identifying possible systemic diseases underlying the inflammatory situation in the siblings, consultations were requested from the Pediatric Hematology Department at Selcuk University and Pediatric Oncology Department at Gulhane Military Medical Academy. RESULTS: Based on absolute neutrophil count (< or =200/mm(3)) and bone marrow aspiration findings consistent with early maturation arrest in myelopoiesis, the cases were diagnosed as SCN. No chromosomal abnormality was detected upon cytogenetic examination. Sequencing analysis also revealed no mutation in the neutrophil elastase or growth factor independent-1 (GFI-1) genes in these patients. Severe periodontal disease, attachment loss, and mobility for over 50% of the deciduous teeth were noted. Within 6 months, the male sibling lost all of his deciduous teeth due to periapical and periodontal infections. His sister presented with tooth mobility for all mandibular incisors. Monthly visits, including scaling, polishing, and 0.2% chlorhexidine digluconate irrigation were performed to support their oral hygiene and to avoid recurrent oral infections. We have been able to stabilize these patients' periodontal conditions during a 2-year follow-up period. CONCLUSION: This case report emphasizes the role of periodontists and pediatric dentists in the diagnosis of diseases linked with neutrophil and other systemic disorders and highlights the need to optimize the health of oral tissues with regular appointments.     

Effect of meloxicam on gingival crevicular fluid IL-1beta and IL1 receptor antagonist levels in subjects with chronic periodontitis, and its effects on clinical parameters

The aim of the present study was to determine the effects of meloxicam after initial periodontal treatment on interleukin-1beta (IL-1β) and IL-1 receptor antagonist (IL-1ra) in gingival crevicular fluid (GCF) and clinical parameters in the chronic periodontitis patients. Data were obtained from 30 patients with chronic periodontitis. Fifteen chronic periodontitis patients received 7.5 mg meloxicam, and 15 patients received placebo tablets in a 1×1 regimen for 1 month. All subjects were nonsmokers and had not received any periodontal therapy. The plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) were recorded. The GCF was collected using a paper strip: eluted and enzyme-linked immunoabsorbent assays (ELISAs) were performed to determine the cytokine levels. The clinical data and GCF samples were obtained after periodontal therapy and 1 month after periodontal therapy. The PI, GI, PD, and GCF IL-1ra decreased significantly (p<0.05) in meloxicam group at first month when comparing the initial levels. While decrease of the PI was statistically significant in control group (p<0.05), statistically significant changes were not determined in the other clinical parameters and GCF cytokine levels (p>0.05). There were no significant differences between two groups in any of the investigated parameters. Our observations did not reveal any influence of meloxicam on levels of IL-1β and IL-1ra in chronic periodontitis. Additional clinical studies are advisable to determine whether COX-2 selective drugs alter periodontal disease outcome with greater safety.     

Levels of interleukin-1 beta, -8, and -10 and RANTES in gingival crevicular fluid and cell populations in adult periodontitis patients and the effect of periodontal treatment

BACKGROUND: Various cytokines have been identified at sites of chronic inflammation such as periodontitis. Cytokines are synthesized in response to bacteria and their products, inducing and maintaining an inflammatory response in the periodontium. The purpose of the present study was to investigate the involvement of interleukin-1 beta (IL-1 beta), IL-8, and IL-10 and RANTES (regulated on activation, normally T cell expressed and secreted) and the cell populations associated with the immune response in destructive periodontitis, as well as the effect of periodontal therapy on cytokine levels in gingival crevicular fluid (GCF). METHODS: Data were obtained from 12 patients with moderate to advanced periodontitis and 6 healthy controls. Patients presenting at least 2 sites with > or =2 mm clinical attachment loss were included in the destructive periodontitis group. After monitoring for 4 months, only 6 patients showed destructive periodontitis and GCF samples and soft tissues biopsies were collected from these patients. GCF samples and biopsies were collected both from active (12 CGF samples and 6 biopsies) and inactive (12 CGF samples and 6 biopsies) sites. The comparison with healthy controls was carried out by collecting GCF samples from 6 healthy volunteers (12 samples) and biopsies during the surgical removal of wisdom teeth. In periodontal patients, clinical data and GCF samples were obtained prior to periodontal treatment (72 samples) and 2 months after periodontal therapy (72 samples). GCF was collected using a paper strip; eluted and enzyme-linked immunoabsorbent assays (ELISA) were performed to determine cytokine levels. The inflammatory infiltrate was analyzed by immunohistochemistry of gingival biopsy samples with monoclonal antibodies against CD3, CD8, CD4, CD11c, and CD19 antigens. RESULTS: Cellular components of the inflammatory infiltrate include B and T lymphocytes and monocyte/macrophages. Active sites contained a higher number of B lymphocytes and macrophages. IL-8 and IL-1 beta and RANTES in GCF were detected in the majority of sites from periodontal patients (100%, 94% and 87%, respectively); IL-10 was found in only 43%. IL-8 was the only cytokine detected in the GCF (75%) of the control group. Moreover, IL-1 beta levels were significantly higher in active sites versus inactive sites (P <0.05). IL-8 and IL-10 and RANTES were increased in active sites; however, differences were not significant (P>0.05). A positive correlation between the IL-8 and RANTES (r = 0.677, P<0.05) was observed in periodontitis patients. Periodontal therapy reduced the total amount of IL-1 beta, IL-8, and IL-10 and RANTES. Data showed a weak correlation between the clinical parameters and the total amount of cytokines in periodontitis. CONCLUSIONS: These data suggest that the amount of crevicular IL-1 beta, IL-8, and IL-10 and RANTES is associated with periodontal status. Removal of the bacterial plaque reduces the antigenic stimuli and consequently could modulate the chemokines present in GCF. We propose that the dynamic interactions between cytokines, their production rates, and their quantity could represent factors controlling the induction, perpetuation, and collapse of the cytokine network present in the periodontal disease.     

Localization of interleukin-1 (IL-1) mRNA-expressing macrophages in human inflamed gingiva and lL-1 activity in gingival crevicular fluid

The exact cell type and site(s) involved in interleukin-1 (lL-1) production during gingival inflammation was determined by combining immunohistochemistry and in situ hybridization. IL-1 messenger RNA (mRNA)-expressing cells in human inflamed gingiva were identified as macrophages. The rate of IL-α mRNA expression in these macrophages was the same as IL-1 β mRNA expression. The rate of IL-1 mRNA expression was higher in connective tissue furthest from the pocket epithelium, although more macrophages were present at the connective tissue subjacent to the pocket epithelium. The IL-1 activity in gingival crevicular fluid (GCF) obtained from inflamed gingiva was higher than that from healthy gingiva and decreased after periodontal therapy. The IL-1 activity in GCF was almost completely abolished by the addition of anti-IL-1α antibody but not by anti-IL-1 β antibody, indicating that IL-1α is the predominant form in GCF. However, the IL-1 activity in GCF was unrelated to the number of IL-1 mRNA-exprerssing macrophages in the same gingival site where the GCF was obtained at the same time. The results suggest that macrophages in the connective tissue subjacent to the oral epithelium contribute to the production of IL-1 but those in connective tissue subjacent to the pocket epithelium play a different role in the generation of gingival inflammation.     

Evaluation of periodontal disease and oral inflammatory load in adults with special needs using oral neutrophil quantification

The purpose of this study was to validate and assess the feasibility of using an assay of oral neutrophils to measure periodontal inflammation in uncooperative adults with special needs. Conventional periodontal measurements and neutrophil counts obtained from oral swabs were performed on patients having dental care under general anesthesia (GA) and at subsequent recall. Forty‐nine patients were assessed under GA and 30 (61%) returned for follow‐up. A high prevalence of gingival inflammation was found at baseline and oral neutrophil levels positively correlated with traditional periodontal parameters (p < 0.05). Neutrophils were acquired using swabs for 100% of patients examined at recall and a significant reduction in oral inflammatory load was noted after a single treatment session (p < 0.05), despite the persistence of poor oral hygiene and prolonged recall intervals. This study demonstrates that oral neutrophil quantification may serve as a novel and standardized method for clinical assessment of periodontal diseases in people with special needs.     

Levels of interleukin-17 in gingival crevicular fluid and in supernatants of cellular cultures of gingival tissue from patients with chronic periodontitis

BACKGROUND AND AIMS: Interleukin-17 (IL-17) is a T-cell-derived cytokine that may play an important role in the initiation or maintenance of the pro-inflammatory response and has recently been found to stimulate osteoclastic resorption. The purpose of the present study was to determine the presence of IL-17 in gingival crevicular fluid (GCF) samples and in the culture supernatants of gingival cells from patients with chronic periodontitis. METHOD: GCF samples were collected during 30 s from two sites in 16 patients from periodontally affected sites (probing depth > or =5 mm, attachment loss > or =3 mm). The comparison with healthy controls was carried out by collecting GCF samples from eight healthy volunteers. GCF was collected using a paper strip and ELISA was performed to determine the total amount of IL-17. Supernatant cellular cultures of gingival cells were obtained from periodontal biopsies taken from 12 periodontitis patients and from eight healthy control subjects during the surgical removal of wisdom teeth. Spontaneous and phytohaemagglutinin (PHA)-stimulated levels of IL-17 were determined by ELISA. RESULTS: The total amount of cytokine IL-17 was significantly higher in the periodontitis group than the control group (45.9 versus 35.6 pg, p=0.005). Significantly higher GCF volume and amount of total proteins were obtained from periodontitis patients as compared with control subjects (0.98 versus 0.36 microl, p=0.0005; 0.12 versus 0.05 microg, p=0.0005, respectively). A higher concentration of IL-17 was detected in culture supernatants from periodontitis patients compared with healthy subjects, either without stimulation (36.28+/-8.39 versus 28.81+/-1.50 microg/ml, p=0.011) or with PHA stimulation (52.12+/-14.56 versus 39.00+/-4.90 microg/ml, p=0.012). Treatment with PHA induced a significant increase in the production of IL-17 in healthy subjects and periodontitis patients (p=0.001 and 0.003). CONCLUSIONS: The total amount of cytokine IL-17 in GCF samples and in the culture supernatants of gingival cells are significantly increased in periodontal disease.     

慢性牙周炎患者牙周治疗前后龈沟液中白介素-10水平的变化

目的探讨慢性牙周炎患者牙周治疗前后龈沟液中抗炎性细胞因子白介素(IL)-10水平的变化。方法采集12例慢性牙周炎患者的12个健康牙位和36个炎症牙位于治疗前及治疗后6、122、4周的龈沟液,用酶联免疫吸附分析法(ELISA)检测龈沟液中IL-10的浓度。另外,分别记录治疗前、后的探诊深度(PD)、临床附着丧失(CAL)、牙龈指数(GI)和菌斑指数(PlI)。结果IL-10浓度在健康牙位明显高于炎症牙位(P<0.01),且于牙周治疗后明显升高。IL-10浓度与探诊深度(PD)、临床附着丧失(CAL)呈负相关(P<0.05)。结论IL-10浓度与牙周组织破坏程度呈负相关,在牙周炎中起抗炎作用。     

Effect of periodontal therapy on crevicular fluid interleukin-1beta and interleukin-10 levels in chronic periodontitis

OBJECTIVES: This study aimed to analyse the levels of the proinflammatory cytokine IL-1beta and the anti-inflammatory cytokine IL-10 in gingival crevicular fluid (GCF) of patients with chronic periodontitis prior to, and following, periodontal therapy for a period of 32 weeks. MATERIAL AND METHODS: GCF samples were obtained from 24 non-diseased and 72 diseased sites of 12 periodontal patients prior to as well as at 6, 16 and 32 weeks post-periodontal therapy. All sites received conventional periodontal treatment and IL-1beta and IL-10 levels (concentration and total amount) were determined by enzyme linked immunosorbent assay (ELISA). Additionally, probing pocket depth (PD), clinical attachment loss (CAL), gingival (GI) and plaque (PII) indices were evaluated pre-and post-therapy. RESULTS: IL-1beta was detected in 382 out of 384 samples, while IL-10 was detected in 337 out of 384 samples. The total amount of IL-1beta was significantly higher at diseased compared to non-diseased sites (p<0.01). Following therapy, IL-1beta total amounts were reduced, while IL-1beta concentration gradually increased. IL-10 total amounts (per 30 s sample) were similar in diseased and non-diseased sites, and following therapy they remained almost unchanged. By contrast, IL-10 concentration was significantly higher in non-diseased sites (p<0.01) and displayed a significant increase post-therapy. Moreover, IL-1beta concentration and total amount were significantly greater in smokers following therapy, while IL-10 total amount was significantly higher in non-smokers both prior to and following therapy. Total IL-1beta amounts were positively correlated with GI and Pll. A weak negative correlation between IL-1beta and IL-10 levels was noted (p<0.05). CONCLUSIONS: The data suggest that the total amount rather than the concentration of IL-1beta in GCF seemed to be closely associated with periodontal disease severity. Moreover, smoking status influenced IL-1beta and IL-10 levels. An inverse relationship between IL-1beta and IL-10 was evident.     

Gingival fluid IL-1 and IL-6 levels in refractory periodontitis

Abstract Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post-active treatment clinical attachment loss (>2% sites/year lost ≥ 3 mm) were compared to 10 age-, race-, and supragingival plaque-matched patients with low post-treatment clinical attachment loss (<0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus antinomycetemcomitans, Porphyromonas gingivalis. Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL-1 alpha, IL-1 beta, IL-6) as determined by two-site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patients produced significantly more IL-6 (30.1 ± 4.0 versus 15.4 ± 2.8 nM, p<0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL-1 concentrations. These data suggest that gingival IL-1 and IL-6 production is different in response to local and systemic factors associated with periodontitis, and that IL-6 may play a role in the identification and mechanisms of refractory periodontitis.