Higher elastase activity associated with lower IL-18 in GCF from juvenile systemic lupus patients.

PURPOSE: Our aim was to evaluate the expression of interleukin-18 (IL-18), interleukin-l-beta (IL-1beta) and the amount of elastase activity in gingival crevicular fluid (GCF) from inflamed gingival sites in patients with juvenile systemic lupus erythematosus (JSLE), and compare these to the expression in GCF from inflamed sites in generally healthy controls. In addition, the local inflammation in periodontal tissues was related to systemic inflammation by the assessment of IL-18 levels in plasma. MATERIALS AND METHODS: GCF from 16 patients with JSLE and 14 controls were collected using a washing device. Elastase activity was measured with a specific substrate, and IL-18 and 11-1 were measured by ELISA. RESULTS: The percentage of visible plaque index, gingival bleeding index and attachment level were similar in JSLE and controls, while the percentage of probing depth greater or equal to 3 mm was significantly higher in the controls. The total amount of IL-1beta and IL-18 in GCF were significantly decreased in JSLE, while the total amount and the percentage of free elastase activity were significantly higher in JSLE when compared with the controls. The plasma levels of I1-18 and the erythrocyte sedimentation rate were significantly higher in JSLE patients. CONCLUSION: We found more active elastase in GCF from inflamed sites in JSLE patients even in the presence of significantly lower levels of IL-18 and IL-13. The increased elastase activity suggests a hyperactivity of neutrophils in JSLE, possibly generated by a priming effect caused by the higher plasma levels of IL-18 found in these JSLE patients.

Decreased interleukin-1beta and elastase in the gingival crevicular fluid of individuals undergoing anti-inflammatory treatment for rheumatoid arthritis.

BACKGROUND: The primary aim of this study was to compare the inflammatory activity in the gingival crevicular fluid (GCF) in a group of patients with rheumatoid arthritis (RA) and a group of matched controls. Secondarily, we aimed to evaluate the effect of rheumatologic treatment on periodontal inflammation. METHODS: Seventeen individuals with RA with a mean duration of disease of 12.1 (+/- 9.9) years and the same number of systemically healthy individuals matched for age, gender, periodontal status, and tobacco use were selected. Medication data were registered, and GCF was collected by means of an intracrevicular washing method. Besides clinical registrations, periodontal inflammation was assessed by analysis of the cytokines interleukin (IL)-1beta and -18 and of elastase activity. RESULTS: Amounts of IL-1beta and total elastase were significantly lower in the patient group. IL-1beta and total elastase had a significant and strong correlation in the RA group (r(s) = 0.883). This correlation was not observed in the control group. CONCLUSION: The anti-inflammatory treatment taken by RA patients might influence the periodontal inflammation status represented by IL-1beta and elastase in the GCF.

Decreased Interleukin-1ß and Elastase in the Gingival Crevicular Fluid of Individuals Undergoing Anti-Inflammatory Treatment for Rheumatoid Arthritis.

BACKGROUND: The primary aim of this study was to compare the inflammatory activity in the gingival crevicular fluid (GCF) in a group of patients with rheumatoid arthritis (RA) and a group of matched controls. Secondarily, we aimed to evaluate the effect of rheumatologic treatment on periodontal inflammation. METHODS: Seventeen individuals with RA with a mean duration of disease of 12.1 (± 9.9) years and the same number of systemically healthy individuals matched for age, gender, periodontal status, and tobacco use were selected. Medication data were registered, and GCF was collected by means of an intracrevicular washing method. Besides clinical registrations, periodontal inflammation was assessed by analysis of the cytokines interleukin (IL)-1ß and -18 and of elastase activity. RESULTS: Amounts of IL-1ß and total elastase were significantly lower in the patient group. IL-1ß and total elastase had a significant and strong correlation in the RA group (rs = 0.883). This correlation was not observed in the control group. CONCLUSION: The anti-inflammatory treatment taken by RA patients might influence the periodontal inflammation status represented by IL-1ß and elastase in the GCF.

Changes in periodontal and rheumatological conditions after 2 years in patients with juvenile idiopathic arthritis.

BACKGROUND: The aim of this study was to monitor changes in periodontal inflammation in patients with juvenile idiopathic arthritis (JIA) for 2 years. We investigated the influence of rheumatic disease activity and antirheumatic medication on clinical and immunological parameters of periodontal inflammation in these individuals. METHODS: Two years after a baseline examination, the periodontal and rheumatological conditions of 18 adolescents with JIA and 14 control subjects were described. The clinical periodontal inflammation was monitored by registration of visual plaque, marginal bleeding, probing depth, and clinical attachment loss (AL). Periodontal inflammation was also assessed by analysis of the cytokines interleukin (IL)-1beta and IL-18 and the collagenase matrix metalloproteinase (MMP)-8 by enzyme-linked immunosorbent assay. RESULTS: The erythrocyte sedimentation rate and clinical rheumatological parameters were significantly improved at the 2-year follow-up. The number of sites with plaque decreased, and the number of pockets >/=4 mm increased, whereas bleeding levels and the extension of AL remained unchanged. IL-1beta in gingival crevicular fluid decreased significantly in the JIA group after 2 years. No differences were observed for IL-1beta, MMP-8, or IL-18 levels between groups after 2 years. CONCLUSION: Two years after the baseline examination, no clinical or laboratory differences in periodontal inflammation could be found between JIA patients and control subjects.

B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease.

Receptor activator of nuclear factor-kappaB (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in diseased gingival tissues than in healthy tissues. Double-color confocal microscopic analyses demonstrated less than 20% of both B cells and T cells expressing RANKL in healthy gingival tissues. By contrast, in the abundant mononuclear cells composed of 45% T cells, 50% B cells, and 5% monocytes in diseased gingival tissues, more than 50 and 90% of T cells and B cells, respectively, expressed RANKL. RANKL production by nonlymphoid cells was not distinctly identified. Lymphocytes isolated from gingival tissues of patients induced differentiation of mature osteoclast cells in a RANKL-dependent manner in vitro. However, similarly isolated peripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated in vitro to express RANKL; emphasizing the osteoclastogenic potential of activated RANKL-expressing lymphocytes in periodontal disease tissue. These results suggest that activated T and B cells can be the cellular source of RANKL for bone resorption in periodontal diseased gingival tissue.

Increased interleukin-18 in patients with juvenile idiopathic arthritis and early attachment loss.

BACKGROUND: Patients with juvenile idiopathic arthritis (JIA) have been shown to have incipient attachment loss (AL) more frequently than systemically healthy individuals. This study investigated neutrophil activity and proinflammatory cytokines in these patients and aged-matched controls. METHODS: Elastase activity, measured with a low molecular weight substrate (S-2484), and interleukin-1beta (IL-1beta), measured with the enzyme-linked immunosorbent assay (ELISA), were analyzed in the gingival fluid of 38 patients with JIA and 29 controls. IL-1beta and interleukin-18 (IL-18) were measured with ELISA in the serum of the same groups. Subgingival plaque was analyzed by DNA probes to detect 12 bacteria. RESULTS: Significantly elevated serum levels of IL-1beta and IL-18 were found in the JIA group. No differences were found in the gingival fluid levels of elastase and IL-1beta between groups, or in the frequency of subjects positive to most of the bacteria analyzed, except F. nucleatum, C. rectus, P. micros, and S. intermedius, which were significantly more frequent in the control group. When the JIA group was subdivided according to the presence/absence of AL, IL-18 was significantly increased in the JIA subgroup with AL compared to those without it. There were no differences in the subgingival microbiota between the subgroups. CONCLUSION: The findings of increased serum IL-18 and IL-1beta in patients with JIA accompanied by a similar subgingival microbiota suggest that the increased frequency of incipient attachment loss observed in these patients might be due to their altered systemic inflammatory response, making them more susceptible to periodontal disease.

Periodontal conditions in patients with juvenile idiopathic arthritis.

OBJECTIVE: Our aim was to compare the periodontal conditions in a group of juvenile idiopathic arthritis (JIA) patients with those in a control group of healthy subjects (CTR). MATERIAL AND METHODS: Thirty-two patients with JIA and 24 controls were selected. The measurements used to diagnose periodontal disease included plaque and bleeding scores, probing depths (PDs) and clinical attachment loss (CAL). Laboratory indicators of JIA activity included the erythrocyte sedimentation rate (ESR) and capsule-reactive protein (CRP). The Mann-Whitney test was used to evaluate the data (alpha = 0.05). RESULTS: The mean ages were 15.9 (+/- 2.7) years and 14.7 (+/- 2.3) years for groups JIA and CTR, respectively. The median ESR was 42 mm/h 13 mm/h in the CTR group (p = 0.032) and the median CRP was 1.9 and 0.4 mg/l, respectively (p = 0.001). The prevalence of patients with a proximal attachment loss of 2mm or more in the JIA group was 25% and in controls it was 4.2%. The mean percentages of visible plaque and marginal bleeding were similar in the JIA (54 +/- 22 and 30 +/- 16, respectively) and CTR groups (44 +/- 18 and 29 +/- 11, respectively). The mean percentages of sites with PD > or = 4 mm were significantly higher in the JIA group (3 +/- 4.7) than in the CTR group (0.4 +/- 1.7) (p = 0.012). The mean percentages of sites with proximal CAL > or = 2 mm were 0.7 (+/- 1.4) in the JIA group and 0.001 (+/- 0.2) in the CTR group (p = 0.022). CONCLUSION: Adolescents with JIA present more periodontal attachment loss than healthy controls, in spite of similar plaque and marginal bleeding levels.