Gingival crevicular fluid glycosaminoglycan levels in patients with chronic adult periodontitis

Abstract This study investigated levels of hyaluronan and chondroitin-4-sulphate in the crevicular fluid of patients with chronic adult periodontitis at diseased and healthy sites before and after treatment. The relationship between clinical diagnostic parameters and levels of glycosaminoglycans in gingival crevicular fluid were also analysed. Within each patient. 4 sites either mesial or distal and on single rooted teeth were classified as diseased or healthy using a modified gingival index, pocket depth and attachment loss. Crevicular fluid was collected from each site using glass micropipettes and analysed for glycosaminoglycan content by cellulose acetate electrophoresis. Significantly higher levels of chondroitin-4-sulphate were detected at diseased sites prior to treatment correlating with increased pocket depth or attachment levels. Following a period of treatment consisting of oral hygiene instruction and root planing, the patients were reassessed for their response to treatment by measuring the modified gingival index, pocket depth, attachment loss and levels of glycosaminoglycans. Analysis of glycosaminoglycan levels at diseased sites that demonstrated a poor response to treatment also demonstrated significantly higher levels of chondroitin-4-sulphate than those sites that responded well to treatment. Hyaluronan levels were less significantly associated with clinically succesful treatment. This study confirmed the use of the sulphated glycosaminoglycan chondroitin-4–sulphate as a potential diagnostic aid of periodontal tissue destruction; however, further longitudinal studies are required to assess their performance.     

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.     

Interleukin-1 beta levels in gingival crevicular fluid in type 2 diabetes mellitus and adult periodontitis.

Interleukin-1 beta (IL-1beta) is a potent bone-resorptive cytokine that also mediates soft-tissue destruction by stimulating prostaglandin production and inducing collagenase and other protease activity. The literature suggests that this substance may be an important mediator of attachment loss in human periodontitis, and indicates that IL-1beta may be useful for locating sites of periodontal disease activity. There is some evidence that IL-1beta is produced by cells of the periodontium, and that it can be detected in gingival crevicular fluid (GCF). Many factors are known to contribute to the destruction of periodontal tissue. One of the most important is immune deficiency in diabetes. The aim of this study was to measure and compare the concentration of IL-1beta in the GCF of patients with non-insulin-dependent diabetes mellitus (Type 2 DM), otherwise healthy adults with periodontitis, and individuals with no periodontal disease in order to assess whether diabetes alters IL-1beta levels. We also examined relationships between GCF levels and the clinical parameters of pocket depth, plaque index, and bleeding index in each group. Seventeen patients with Type 2 DM, 17 adult periodontitis patients (AP), and 17 healthy controls were selected. The levels of IL-1beta in the GCF were quantified by ELISA. The mean IL-1beta concentrations in the Type 2 DM, AP, and control groups were 200.1 +/- 65.34 pg/microl, 131.35 +/- 67.66 pg/microl, and 80.0 +/- 36.08 pg/microl, respectively. The levels in the diabetic patients were significantly higher than those in the AP and control subjects. There were no significant correlations between IL-1beta level and any of the clinical data parameters for each group. We believe that the macrophages may over produce IL-beta in Type 2 DM and increased IL-1beta levels in diabetic patients could be linked to altered immune function.     

Soluble interleukin-1 receptor type II levels in gingival crevicular fluid in aggressive and chronic periodontitis

Background: Interleukin (IL)-1 is closely related to the initiation and progression of periodontal disease. IL-1 levels in the gingival crevicular fluid (GCF) of subjects with periodontitis are higher than those in periodontally healthy controls, and the levels of IL-1 correlate with disease severity. However, soluble IL-1 receptor type II (sIL-1RII), which acts as a decoy receptor for IL-1s, has not been investigated in detail in periodontal disease. The purpose of this study was to measure sIL-1RII levels in the GCF of subjects with chronic or aggressive periodontitis; the correlation between the sIL-1RII levels in GCF and clinical parameters also was examined. Methods: IL-1beta and sIL-1RII were measured in 64 GCF samples collected from 47 subjects with chronic periodontitis (CP) and 17 subjects with aggressive periodontitis (AgP). The clinical characteristics of each site were recorded at the time of GCF sampling. IL-1beta and sIL-1RII were measured by specific non-cross-reactive enzyme-linked immunosorbent assay. Results: The disease severity was comparable in CP and AgP. IL-1beta was detected in 98% of CP GCF samples and 88% of AgP GCF samples. sIL-1RII was detected in 55% of CP GCF samples and 35% of AgP GCF samples. However, the concentrations of IL-beta and sIL-1RII detected in GCF from subjects with CP or AgP were similar. Conclusion: sIL-1RII was detected more often in CP GCF than in AgP GCF, and there was no correlation between GCF sIL-1RII concentration and clinical parameters.     

Gingival crevicular fluid and plasma oxidative stress markers and TGM-2 levels in chronic periodontitis

ObjectiveThis study was aimed to evaluate the gingival crevicular fluid (GCF) and plasma transglutaminase-2 (TGM-2), total antioxidant capacity (TAC), total oxidant status (TOS), ferric reducing antioxidant power (FRAP) and thiobarbituric acid reactive substances (TBARS) in patients with chronic periodontal disease.Materials and methodsTwenty patients with chronic periodontitis (CP), 20 patients with gingivitis and 20 healthy subjects were enrolled in the study. Clinical periodontal parameters including probing depth, clinical attachment level, plaque index and papillary bleeding index were recorded. GCF and plasma levels of TGM-2, TAC, TOS, TBARS and FRAP were analyzed.ResultsGCF TGM-2 was significantly lower in CP group than in gingivitis patients (P = 0.006). GCF FRAP in CP and gingivitis groups was significantly lower than in healthy subjects (P < 0.001). Plasma FRAP level was lower in gingivitis group when compared to healthy subjects (P = 0.003). There was no significant difference in GCF and plasma TAC, TOS, TBARS and plasma TGM-2 levels among the study groups (P > 0.05). GCF TGM-2 level was positively correlated with GCF TAC and negatively correlated with CAL.ConclusionsDecreased FRAP in GCF and plasma indicating lower antioxidant status of CP patients might suggest the role of oxidative stress in periodontitis. GCF TGM-2 data might suggest that TGM2 is associated with stabilization of the extracellular matrix and wound healing in periodontium rather than gingival inflammation.     

Gingival crevicular fluid leptin levels in periodontitis patients with long-term and heavy smoking

BACKGROUND: The aim of the present study was to evaluate gingival crevicular fluid (GCF) leptin levels and the influence of long-term and heavy smoking on GCF leptin levels in patients with chronic periodontitis. METHODS: In this study, 143 individuals were divided into three groups: non-smokers (NS), smokers (S), and control (C). Three subgroups of NS and S were grouped as follows: a) probing depth (PD) 5 mm. For each patient, PD, gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), and clinical attachment level (CAL) values were recorded. The GCF leptin levels obtained from sampling sites were determined by using enzyme-linked immunosorbent assay kits. RESULTS: The GCF leptin levels were found significantly lower in the a and b subgroups in the S group than those in the NS group (P <0.05). The inflammatory markers GI and GBTI showed significant correlations with leptin in NS (P <0.05). CONCLUSIONS: Our results suggest that higher leptin GCF levels in healthy sites in periodontitis patients may play a protective role in periodontal disease. Further studies are needed to determine the cellular origin of the leptin in the gingiva and the effect of plasma leptin levels on GCF leptin concentrations.     

Gingival crevicular fluid monocyte chemoattractant protein-1 and RANTES levels in patients with generalized aggressive periodontitis

BACKGROUND: Local and systemic inflammatory and immune mechanisms may be implicated in the pathogenesis of the aggressive forms of periodontal disease. Chemokines, monocyte chemoattractant protein-1 (MCP-1) and regulated on activation, normal T cells expressed and secreted RANTES (regulated on activation, normal T cells expressed and secreted), are involved in the activation and recruitment of inflammatory and immune cells to the infected sites and thereby mediating a variety of pathophysiological conditions. The aim of the present study was to examine the gingival crevicular fluid (GCF) levels of MCP-1 and RANTES in patients with generalized agressive periodontitis (G-AgP). METHODS: MCP-1 and RANTES levels were investigated in GCF samples of 10 patients with G-AgP and 10 periodontally healthy subjects. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing and plaque. In the G-AgP group, GCF samples were collected from the two approximal sites; from one single-rooted tooth and from one first molar tooth with > or =6 mm probing depth. In the healthy group, GCF samples were collected from one of the single-rooted teeth. GCF MCP-1 and RANTES levels were quantified by enzyme immunoassay. RESULTS: The G-AgP patients had significantly higher GCF MCP-1 and RANTES levels compared to the healthy group (p<0.05). GCF MCP-1 and RANTES levels were positively correlated with both probing depth and clinical attachment loss (p<0.05). There was no correlation between GCF MCP-1 and RANTES levels and the percentage of sites with bleeding (p>0.05). CONCLUSIONS: The results of the present study suggest that MCP-1 and RANTES could play key roles in both activation and recruitment of inflammatory and immune cells in periodontal environment of G-AgP patients. In conclusion, these CC chemokines may be considered in the biological mechanism underlying the pathogenesis and progression of G-AgP.     

慢性牙周炎伴2型糖尿病患者龈沟液中脂联素水平的检测及意义

目的：探究牙周炎伴2型糖尿病患者龈沟液中脂联素水平及意义。方法：纳入慢性牙周炎伴糖尿病患者（DM&CP）、慢性牙周炎患者（CP）、健康对照者（H）各20例,记录其临床指标（SBI、PLI、PD 和 AL）,并收集龈沟液（GCF）样本,用龈沟液测量仪 periotron8000对 GCF 进行定量,用脂联素 ELISA 试剂盒检测样本中脂联素含量,比较组间检测指标的差异以及临床指标与 GCF 中脂联素水平的相关性。结果：DM&CP 组 GCF 中脂联素水平显著低于其他2组（P ＜0．05）,CP 患者龈沟液脂联素水平与牙周健康组相比无统计学差异（P ＞0．05）。GCF 中脂联素水平与临床指标 PD 值、AL 值有负相关性（P ＜0．05）,与 SBI、PLI 无明显相关（P ＞0．05）。结论：龈沟液中脂联素水平降低可能与 DM&CP 发生发展有关。     

伴牙周炎糖尿病患者血清和龈沟液中C反应蛋白的检测及意义

目的:了解龈沟液和血清中C反应蛋白(C-reactive protein,CRP)水平与牙周炎症状况、血糖控制情况的关系.方法:检测伴慢性牙周炎2型糖尿病组、慢性牙周炎组、2型糖尿病组和健康人群组血清和龈沟液中CRP浓度、糖化血红蛋(glycosylated hemoglobin,HbAlc)水平,记录牙周探诊深度(probing depth,PD)和龈沟出血指数(sulcus bleeding index,SBI).采用SPSS10.0软件包进行独立样本t检验和Spearman相关分析.结果:伴慢性牙周炎2型糖尿病组、慢性牙周炎组、2型糖尿病组血清CRP均比正常对照组显著升高(P＜0.01),且伴慢性牙周炎2型糖尿病组血清CRP水平最高,显著高于慢性牙周炎组(P＜0.01)和2型糖尿病组(P＜0.05);4组的龈沟液CRP水平均远低于血清水平,且4组间无显著差异(P＞0.05);血清CRP与龈沟液CRP无相关性(P＞0.05);血清CRP与PD、SBI和HbAlc显著相关(P＜0.01).结论:CRP可能参与了牙周炎和2型糖尿病之间的互相影响;龈沟液CRP水平不能反映牙周病炎症程度和糖尿病病情.     

Gingival crevicular fluid levels of aspartate amino transferase, sulfide ions and N-benzoyl-DL-arginine-2-naphthylamide in diabetic patients with chronic periodontitis

BACKGROUND: The aim of this study is to analyze the correlations between plaque index (PlI), gingival index (GI), probable pocket depth (PPD), clinical attachment level (CAL), aspartate aminotransferase (AST), N-benzoyl-DL-arginine-2-naphthylamide (BANA) and sulfide ion activity (SIA) of diabetic patients with chronic periodontitis with regard to disease activity detected by AST levels. MATERIAL AND METHODS: A total of 95 sites from eight diabetic patients with chronic periodontitis and 74 sites from eight systemically healthy patients with chronic periodontitis were enrolled in the study. The patients had no history of periodontal treatment or any antibiotic therapy during the last 6 months and were nonsmokers. All the sites selected for the study had a CAL of at least 2 mm. Gingival crevicular fluid volumes (GCFV) were measured in all sites. RESULTS: According to the result of AST analysis, 45 sites were AST positive and 50 were AST negative in the diabetic group and 36 sites were AST positive and 38 were AST negative in the control group. There was a significant correlation between BANA hydrolysis and PPD in both diabetic and control groups, but no correlation between PPD and AST levels. A significant correlation was observed between AST-positive sites and GI, but not between GI and BANA hydrolysis. In both groups, the correlation between SIA and BANA hydrolysis was significant, but no correlation was revealed between SIA and AST levels in either diabetic or control groups. CONCLUSION: The GCF metabolites had significant correlations with periodontally diseased sites in patients with chronic periodontitis, whether diabetic or systemically healthy, and may help to confirm clinical findings.     

Gingival crevicular fluid osteocalcin in adult periodontitis

This study aimed to detect the levels of osteocalcin in gingival crevicular fluid (GCF) from healthy (< or =3 mm sulcus depth and non-bleeding) and diseased sites (> or =6 mm probing depth and bleeding) in subjects with adult periodontitis, in order to further investigate its potential as a possible marker of the disease process. Periodontal probing depths, attachment levels and gingival indices were recorded from one healthy and one diseased site in each of 20 subjects with adult periodontitis. Both GCF accumulated in the periodontal pocket or sulci and GCF flowing into the periodontal pocket or sulci over a three-minute interval were sampled. The amounts of osteocalcin in each GCF sample was determined using immunoassays. A mean of 2.34 ng/site (2.7 microg/ml) osteocalcin was found at diseased sites and a mean of 2.47 ng/site (5.47 microg/ml) was found at healthy sites for the accumulated GCF collection method. A mean of 0.17 ng/ site (2.17 microg/ml) osteocalcin was found at diseased sites and a mean of 0.14 ng/ site (1.85 microg/ml) at healthy sites for the flow method of GCF collection. There were no statistically significant differences between osteocalcin levels in diseased and healthy sites in subjects with adult periodontitis.     

Gingival crevicular fluid EMAP-II, MIP-1alpha and MIP-1beta levels of patients with periodontal disease

BACKGROUND: Periodontal diseases may differ, which could be attributed to the factors that might modify the host response to microbial pathogens. The aim of this study was to examine gingival crevicular fluid (GCF) levels of EMAP-II, MIP-1alpha and MIP-1beta in patients with different periodontal diseases (EMAP-II, endothelial-monocyte activating polypeptide; MIP-1alpha, macrophage inflammatory protein-1alpha; MIP-1beta, macrophage inflammatory protein-1beta). METHODS: Eighty-two subjects were included in this study. GCF samples were collected from 26 patients with generalized aggressive periodontitis (G-AgP), 26 patients with chronic periodontitis (CP), 15 with gingivitis and 15 periodontally healthy subjects. Clinical periodontal parameters were recorded. GCF EMAP-II, MIP-1alpha and MIP-1beta levels were quantified by enzyme immunoassay. RESULTS: GCF EMAP-II levels of G-AgP group were higher than those of gingivitis and healthy groups (p<0.008). G-AgP group showed a trend for higher GCF EMAP-II levels compared with CP group (p>0.008). G-AgP, CP, gingivitis and healthy groups had comparable GCF MIP-1alpha and MIP-1beta levels. CONCLUSIONS: Our results suggest that elevated GCF EMAP-II could contribute to the pathogenesis of G-AgP. Alternatively, EMAP-II reflects the extent of the inflammatory activity in the periodontal tissues. At this point, MIP-1alpha and MIP-1beta levels in GCF do not seem to play a discriminatory role in periodontitis. Our data document for the first time the essential role of EMAP-II in the pathogenesis of different periodontal diseases.