Gingival crevicular fluid transforming growth factor-beta1 in several forms of periodontal disease

BACKGROUND: Transforming growth factor-beta(1) (TGF-beta(1)) has significant effects on periodontal host response regulation. Limited knowledge on the role of TGF-beta(1) in various periodontal disease types and particularly in advanced periodontitis forms warranted the present study. The aim of the present study was to evaluate the gingival crevicular fluid (GCF) TGF-beta(1) levels in patients with different forms of periodontal disease. METHODS: GCF TGF-beta(1) levels were investigated in 32 chronic periodontitis (CP), 30 generalized aggressive periodontitis (G-AgP), 15 gingivitis patients and 16 periodontally healthy subjects. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, plaque and bleeding on probing. TGF-beta(1) levels were analyzed by enzyme-linked immunosorbent assay. The results were expressed in terms of total amount (pg) and concentration (pg/microl). RESULTS: G-AgP and CP groups had significantly elevated GCF TGF-beta(1) total amount compared to healthy group (p<0.008). Moreover, GCF TGF-beta(1) total amount of G-AgP group was significantly higher than that of gingivitis group (p<0.008). G-AgP and CP groups had similar GCF TGF-beta(1) total amount (p>0.008). Significant correlation was found between GCF TGF-beta(1) total amount and all clinical periodontal parameters (p<0.05). CONCLUSIONS: The results of the present study suggest contribution of TGF-beta(1) to the pathogenesis of advanced chronic and aggressive periodontitis. TGF-beta(1) may thus be one of the components modulating exaggerated host response together with other major mediators of inflammation.     

Gingival crevicular fluid laminin-5 gamma2-chain levels in periodontal disease

AIM: Our study aimed to examine the molecular forms and gingival crevicular fluid (GCF) levels of laminin-5 gamma2-chain in patients with different periodontal disease, and compare the effects of P.gingivalis trypsin-like proteinase on intact laminin-5 gamma2-chain species. METHODS: Eighteen patients with generalized aggressive periodontitis (G-AgP), 29 patients with chronic periodontitis (CP), 20 with gingivitis and 20 periodontally healthy subjects were included. Probing depth, clinical attachment loss, presence of bleeding on probing and plaque were recorded. Molecular forms and GCF laminin-5 gamma2-chain levels and the effects of P. gingivalis trypsin-like proteinase on intact laminin-5 gamma2-chain were analysed by computer-quantitated Western immunoblotting. RESULTS: Laminin-5 gamma2-chain 40 and 70 kDa fragments could be detected in all groups, in varying levels.The CP group had elevated GCF laminin-5 gamma2-chain fragment levels compared with the gingivitis and healthy groups (p<0.008).The G-AgP group had GCF laminin-5 gamma2-chain fragment levels similar to the gingivitis and healthy groups (p>0.008). GCF laminin-5 gamma2-chain fragments differed clearly from the multiple lower molecular size fragments of P.gingivalis trypsin-laminin-5 gamma2-chain proteinases. CONCLUSION: Increased GCF laminin-5 gamma2-chain fragments in periodontitis sites with deep periodontal pocket suggest that these cleaved 40 and 70 kDa fragments could reflect the extent of the inflammatory reaction in CP.     

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.     

广泛型侵袭性牙周炎患者龈沟液中白介素-17的检测

目的 比较广泛型侵袭性牙周炎患者与健康人龈沟液中白介素-17(IL-17)的表达水平及与临床指标的关系。方法 选择广泛型侵袭性牙周炎患者18例和健康人16例,共68颗牙,记录临床牙周检查指标,用滤纸条法收集龈沟液。采用抗体夹心ELISA法测定广泛型侵袭性牙周炎患者治疗前、治疗后3个月及健康对照者龈沟液中IL-17总量和浓度。结果 广泛型侵袭性牙周炎患牙治疗前龈沟液中IL-17的总量和浓度高于牙周健康牙,基础治疗3个月后广泛型侵袭性牙周炎患牙龈沟液中IL-17的总量和浓度较治疗前下降。广泛型侵袭性牙周炎患牙龈沟液中IL-17浓度与探诊深度、附着丧失和出血指数呈正相关关系,而IL-17总量仅与探诊深度呈正相关关系。结论 龈沟液中IL-17浓度可能与广泛型侵袭性牙周炎牙周破坏及炎症的严重程度相关。?     

牙周非手术治疗对重度慢性牙周炎患者龈沟液中C反应蛋白的影响

目的检测牙周基础治疗对慢性牙周炎患者龈沟液中C反应蛋白(CRP)的影响,为牙周病活动期诊断及判断牙周治疗的效果提供一定的客观依据。方法治疗前及治疗后1、3、6、12个月,用滤纸条收集30例重度慢性牙周炎患者的60个重度牙周炎牙位(探诊深度PD≥6 mm)和60个轻度牙周炎牙位(PD≤4 mm)的龈沟液并称重,用酶联免疫吸附测定法(ELISA)测定CRP的含量并记录牙周临床指标,15例牙周健康者的30个健康牙位作为对照。结果深牙周袋牙位的CRP在龈沟液中的浓度((968.06±360.54)pg/m L)显著高于浅牙周袋牙位((291.65±65.62)pg/m L),且疾病牙位的CRP浓度均显著高于健康牙位((33.47±24.53)pg/m L),龈沟液中CRP浓度与探诊深度(r=0.825,P<0.05)、附着丧失(r=0.833,P<0.05)、菌斑指数(r=0.741,P<0.05)呈正相关关系。同时,牙周基础治疗后沟液中CRP浓度明显降低,并且与口腔卫生情况有关。结论龈沟液中CRP浓度与牙周破坏程度有关,非手术治疗后龈沟液中CRP浓度下降。     

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.     

Characterization of cellular infiltrate, detection of chemokine receptor CCR5 and interleukin-8 and RANTES chemokines in adult periodontitis

Leukocyte migration is essential for immune surveillance of tissues by focusing immune cells to sites of antigenic challenge. The control of leukocyte migration depends on the combined actions of adhesion molecules and a vast array of chemokines and their receptors. The purpose of the present study was to investigate the involvement of Interleukin-8 (IL-8), RANTES, the associated infiltrating cells and expression of CCR5 chemokine receptors in periodontitis; furthermore, the effect of periodontal therapy on these parameters was evaluated. Patients included in the study had moderate to advanced periodontal disease with at least 5-6 teeth with probing depth > 6 mm, attachment loss > or =3 mm and extensive radiographic bone loss. The inflammatory infiltrate was analyzed by immunohistochemistry in gingival biopsies obtained from subjects at the beginning of the study and 2 months after periodontal treatment. Gingival crevicular fluid (GCF) was collected for 30 seconds using periopaper strips, and chemokines were quantified by ELISA. The cellular components of the inflammatory infiltrate included B (CD19) and T (CD3, CD4+ and CD8+) lymphocytes and monocytes/macrophages (CD11c). CCR5 chemokine receptor expressing cells were exclusively found in periodontitis gingiva. IL-8 and RANTES were detected in the periodontitis group, obtaining a total amount of 212.5 pg and 42.0 pg, respectively. However, IL-8 was also detectable in the GCF of the healthy group (total amount of 44.8 pg). Periodontal therapy reduced the cell number in the infiltrate and the levels of IL-8 and RANTES, suggesting a relationship between these chemokines and periodontal status. We propose that the presence of these chemokines and the expression of chemokine receptors may represent a marker of lymphocyte subsets with the ability to migrate to inflammatory sites.     

Chemokine RANTES in gingival crevicular fluid of adult patients with periodontitis

Background, aims: This study presents the first evidence on the presence of the chemokine RANTES in the gingival fluid crevicular (GCF) of patients with periodontitis. RANTES is a chemokine that selectively attracts and activates macrophages and lymphocytes. Leucocytes play a critical rôle in the host response to the subgingival microflora. Method: In this study, the presence de RANTES in GCF was determined in samples obtained from adult patients with periodontitis and from control subjects with clinically healthy gingiva. GCF was collected from different probing depths (<3 mm, 4–6 mm, >6 mm) (n=72); and active (n=12) and inactive sites (n=12). An active site was defined as attachment loss >2 mm, as determined by sequential probing and the tolerance method. GFC was collected for 30 s using Periopaper^® strips, and RANTES was quantified by ELISA. Results: The presence of RANTES was detected exclusively in the group of patients with periodontitis, presenting a total amount of 40.43±16 pg and a concentration 67.80±41 pg/μl. RANTES concentration was significantly higher in probing depth <3 mm than in probing depth >6 mm (87.24 versus 51.87, p=0.014). Total amount and concentration in the GCF samples from active sites were higher that in inactive sites (p>0.05). Conclusions: The finding that RANTES is found only in patients with periodontitis, may represent a general feature of chronic inflammatory in periodontal diseases. Finally, RANTES may be implicated in the biological mechanisms underlying the pathogenesis and progression of periodontal disease.     

Gingival crevicular fluid interleukin-36β (-1F8), interleukin-36γ (-1F9) and interleukin-33 (-1F11) levels in different periodontal disease

Background

Periodontal inflammation is driven by the coordinated action of a number of factors, including the IL-1 family. Our study aimed to examine the levels of interleukin (IL)-36β, IL-36γ and IL-33 levels in gingival crevicular fluid (GCF) from patients with different periodontal diseases.

Materials and methods

A total of 80 subjects, 20 patients with generalized aggressive periodontitis (G-AgP), 20 patients with chronic periodontitis (CP), 20 with gingivitis and 20 periodontally healthy subjects were included. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, papillary bleeding index and plaque index. GCF cytokine levels were analysed by ELISA.

Results

CP, gingivitis and healthy groups had similar GCF IL-36β total amount (p > 0.008). G-AgP group had elevated IL-36β total amount compared to CP group (p < 0.008). G-AgP group had similar GCF IL-36β total amount to gingivitis and healthy groups (p > 0.008). GCF IL-36γ and IL-33 total amounts of the study groups were similar (p > 0.05).

Conclusions

The present study demonstrated for the first time the presence of IL-36β, IL-36γ and IL-33 GCF levels with different periodontal diseases. High levels of IL-36-β in the AgP group in comparison to CP group might suggest that periodontitis in the aggressive form could be related to the increase in GCF IL-36β.     

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.     

The investigation of glutathione peroxidase, lactoferrin, myeloperoxidase and interleukin-1beta in gingival crevicular fluid: implications for oxidative stress in human periodontal diseases

BACKGROUND: Human periodontal diseases are inflammatory disorders that are the result of complex interactions between periodontopathogens and the host's immune response. Two important and interrelated factors are involved in the pathophysiological progression of periodontal diseases, i.e. the activation of immune system and the production of oxygen radicals and their related metabolites. Increased production of oxygen radicals may contribute to oxidative stress, which is reported to be involved in many diseases, including periodontal diseases. OBJECTIVES: The objective of this study was to investigate glutathione peroxidase, lactoferrin and myeloperoxidase, which play an essential role in free radical production and defenses, and the proinflammatory cytokine interleukin-1beta (IL-1beta), which is important in the regulation of immunological and inflammatory reactions in human periodontal diseases. METHODS: Gingival crevicular fluid (GCF) samples were collected from 27 subjects, 19 periodontitis patients and eight healthy controls, ranging in ages from 24 to 62 years. Clinical parameters were recorded. GCF glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta were analyzed by enzyme-linked immunosorbent assays (ELISA). RESULTS: The periodontitis sites exhibited significantly greater total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta than healthy sites. Total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta was positively correlated with plaque index, gingival index, probing depth and probing attachment level (p < 0.05). CONCLUSION: The imbalance between the levels of myeloperoxidase/IL-1beta and glutathione peroxidase/lactoferrin could result in tissue damage of reactive oxygen species (ROS) in periodontitis which is initiated and perpetuated by the chronic insults of periodontopathogens.     

Evaluation of t-PA, PAI-2, IL-1beta and PGE(2) in gingival crevicular fluid of rheumatoid arthritis patients with periodontal disease

AIMS: This study was undertaken to compare periodontal conditions, gingival crevicular fluid (GCF) levels of tissue-type plasminogen activator (t-PA), its inhibitor plasminogen activator inhibitor-2 (PAI-2), interleukin-1beta (IL-1beta), prostaglandin E(2) (PGE(2)) in rheumatoid arthritis (RA) patients and control groups. METHODS: Twenty-three RA patients, 17 systemically healthy patients with periodontal disease (PD), and 17 systemically and periodontally healthy subjects were recruited. GCF samples were obtained from two single-rooted teeth. Full-mouth clinical periodontal measurements were recorded at six sites/tooth. GCF samples were analysed using relevant ELISA kits. Data were tested statistically by appropriate tests. RESULTS: Total amounts of t-PA, PAI-2 and PGE(2) in GCF samples of the healthy control group were significantly lower than the other groups (p<0.05). The RA group exhibited a higher total amount of t-PA in GCF samples than the PD group (p<0.05). PAI-2, IL-1beta and PGE(2) total amounts were similar in RA and PD groups (p>0.05). CONCLUSION: The coexistence of RA and periodontitis does not seem to affect clinical periodontal findings or systemic markers of RA. Similar inflammatory mediator levels in RA and PD groups, despite the long-term usage of corticosteroids, non-steroidal anti-inflammatory drugs, suggest that RA patients may have a propensity to overproduce these inflammatory mediators.     

Gingival crevicular fluid levels of monocyte chemoattractant protein-1 in periodontal health and disease

Objectives

Monocyte chemoattractant protein-1 (MCP-1) stimulates the chemotaxis of monocytes and also several cellular events associated with chemotaxis thus causes recruitment of inflammatory cells. Its increased gingival crevicular fluid (GCF) levels in periodontal disease have been reported in previous studies. The present study has been carried out to assess the role of MCP-1 in periodontal disease progression and also to determine the effect of periodontal treatment on MCP-1 concentration in GCF.

Design

A total of 60 subjects were divided into three groups (n = 20) based on gingival index (GI), probing pocket depth (PPD) and clinical attachment loss (CAL): healthy (group I), gingivitis (group II) and chronic periodontitis (group III). A fourth group (group IV) consisted of 20 subjects from group III, 6-8 weeks after treatment (i.e. scaling and root planing). GCF samples collected from each patient were quantified for MCP-1 using ELISA.

Results

The mean MCP-1 concentration in GCF was found to be the highest in group III, i.e. 72.60 pg/μl. The mean MCP-1 concentration in group I was 19.70 pg/μl and in group IV was 8.50 pg/μl. The mean MCP-1 concentration (37.00 pg/μl) in group II was found to lie in between the concentrations obtained in groups I and III.

Conclusions

GCF MCP-1 levels increased progressively with the progression of disease and decreased after treatment. Levels of MCP-1 correlated positively with clinical parameters like GI, PPD and CAL thus it can be considered as an inflammatory biomarker in periodontal disease and also deserves further consideration as a therapeutic target.     

Variations in crevicular fluid elastase levels in periodontitis patients on long-term maintenance

Granulocyte elastase was determined in the gingival crevicular fluid (GCF) of 18 periodontitis patients. They initially had similar severity of disease but had responded differently to 5-yr maintenance, 13 responders and 5 non-responders. A total of 102 sites were investigated and categorized as: i) consistently healthy, ii) healthy after treatment, iii) gingivitis, and iiii) periodontitis, according to clinical criteria. GCF elastase activity was determined with a granulocyte-specific substrate. The sites from non-responders had consistently higher elastase levels than the corresponding category of sites from responders, despite similar gingival inflammation and periodontal destruction, with the exception of consistently healthy sites. Within the non-responders, the periodontitis sites had higher elastase levels than the gingivitis sites commensurate with probing depth, while no difference existed between gingivitis sites and sites healthy after treatment, despite a difference in probing depth. In contrast, in the responders similar elastase levels were found at the periodontitis sites and gingivitis sites despite difference in probing depth, while both diseased sites had higher elastase levels than the sites healthy after treatment, commensurate with probing depth. This study suggests that increased granulocyte-specific elastase levels in GCF may serve as a diagnostic marker for refractory periodontitis patients.     

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.     

Relationship between levels of aspartate aminotransferase in gingival crevicular fluid and conventional measures of periodontal status assessed using PocketWatch: a cross-sectional study

The aim of this cross-sectional study was to determine, using PocketWatch, the relationship between the level of aspartate aminotransferase (AST) in gingival crevicular fluid (GCF) and conventional measures of periodontal status, such as probing depth, attachment level, bleeding on probing and gingival index, in patients with untreated chronic periodontitis. A total of 15 patients with chronic periodontitis were enrolled. Their periodontal status and AST levels in their GCF were measured (n = 93) and statistically analyzed. There was a statistically significant difference in AST levels between diseased periodontal sites and healthy sites (p < 0.0001). The coefficients of correlation between AST levels and probing depth, attachment level and gingival index at all sites were 0.436, 0.266 and 0.468 (Spearman rank correlation). The correlation coefficients were too small to show a definite relationship between AST levels and individual measures of clinical periodontal status. However, AST levels may help to confirm clinical observations in patients with chronic periodontitis before therapy, since AST levels differentiate active and inactive periodontal diseased sites.     

Cigarette smoking, salivary/gingival crevicular fluid cotinine and periodontal status. A 10-year longitudinal study

BACKGROUND, AIMS: The primary purpose of this study was to determine the association of salivary and gingival crevicular fluid (GCF) cotinine levels with periodontal disease status in smokers and non-smokers. METHODS: 147 male smokers and 30 male non-smokers were included in the current longitudinal study. The 177 individuals were part of a group of 200 subjects (89%) seen 10 years previously for a baseline survey. Oral hygiene indices, probing depth and attachment loss were recorded. Salivary and GCF cotinine levels of 58 smokers were determined by means of ELISA. RESULTS: Results indicated that no significant difference was found in subjects who smoked, when compared to subjects who did not smoke with respect to plaque accumulation and calculus deposits. Smokers, however, had fewer gingival bleeding sites. Cigarette smoking was associated with a greater increase in probing depth and attachment loss, as well as greater tooth loss at an earlier age. There was greater tooth loss in smokers than non-smokers (p < 0.001). 11 smokers became edentulous, while only 1 non-smoker lost all his teeth within 10 years. The degree of periodontal tissue breakdown was different in each age group with greater periodontal deterioration as age increased. All smokers had detectable salivary and GCF cotinine. Mean GCF cotinine was about 4x higher than mean salivary cotinine levels. Individuals who smoked > or = 20 pack years when compared to <20 pack years, had significantly higher saliva and GCF cotinine levels (p < or = 0.05). CONCLUSION: Neither salivary cotinine nor GCF cotinine was significantly correlated with probing depth, attachment loss and tooth loss (p > 0.05).     

IL-6 levels in gingival crevicular fluid (GCF) from patients with non-insulin dependent diabetes mellitus (NIDDM), adult periodontitis and healthy subjects

Cytokines play an important role in the pathology associated with chronic inflammatory diseases. One of these cytokines, interleukin 6 (IL-6) is a major mediator of the host response to tissue injury, infection and bone resorption. In the present study, gingival crevicular fluid (GCF) level of IL-6 was determined in patients with non-insulin dependent diabetes mellitus (NIDDM) with periodontitis, adult periodontitis, and healthy controls by use of an enzyme linked immunosorbent assay (ELISA). Twenty-four NIDDM patients with periodontitis, twenty-four adult periodontitis and twenty-four healthy controls were selected for the study. GCF sampling was performed on the vestibular aspects of maxillary incisors and canine teeth. Plaque index (PI), gingival index (GI), gingival bleeding time index (GBTI), probing depth (PD) and probing attachment levels (PAL) were recorded from each sampling area and also the entire dentition. NIDDM and adult periodontitis patients had numerous sites with radiographic evidence of alveolar bone resorption, loss of attachment and pocket depth greater than 3 mm. The mean GCF IL-6 level was 2.43 +/- 0.97 ng/ml in NIDDM patients, 1.31 +/- 0.92 ng/ml in adult periodontitis and 0.62 +/- 0.58 ng/ml in healthy subjects, respectively (p < 0.05). GCF IL-6 levels were markedly higher in NIDDM and adult periodontitis groups compared to the healthy controls. No correlation was found between GCF IL-6 levels and all clinical parameters. These findings suggested that GCF IL-6 levels were significantly higher in the area of inflammation and periodontal destruction locally. The high IL-6 levels in NIDDM patients might be due to different microbial flora in periodontal pockets and altered immune system. Future studies are needed to evaluate the complex interaction among IL-6 GCF levels, host response and local microbial environment in the NIDDM patients.