Gingival crevicular fluid osteopontin levels in periodontal health and disease

BACKGROUND: Osteopontin (OPN), a glycosylated phosphoprotein, is a bone matrix component produced by osteoblasts, osteoclasts, and macrophages as a multifunctional cytokine. OPN anchors osteoclasts to the bone surface, and its absence leads to impaired bone resorption. The aim of the present study was to assess the relation between clinical parameters and concentrations of OPN within gingival crevicular fluid (GCF) from inflamed gingiva and periodontitis sites and, subsequently, after the treatment of periodontitis sites. METHODS: A total of 45 subjects were divided into the following three groups based on modified gingival index (MGI) and Ramfjord periodontal disease index (PDI) scores: healthy (group I), gingivitis (group II), and chronic periodontitis (group III). A fourth group consisted of 15 subjects from group III, 6 to 8 weeks after treatment (i.e., scaling and root planing [SRP]). GCF samples collected from each patient were quantified for OPN using the enzymatic immunometric assay. Further, the correlation between OPN levels in situ with clinical parameters was analyzed in all groups and before and after treatment in periodontitis patients. RESULTS: The highest mean OPN concentration in GCF (14.347 microg/ml) was observed in group III, and the lowest mean OPN concentration in GCF (2.522 microg/ml) was observed in group I. Its levels in group III decreased to 8.419 microg/ml after treatment (group IV). Further, GCF OPN levels in all the groups showed a statistically significant positive correlation with clinical attachment loss (P <0.05). CONCLUSIONS: OPN levels increase in GCF from healthy to periodontitis states, and periodontal treatment results in the reduction of OPN levels. The data indicate that OPN may play a key role in, and could be considered a biomarker of, periodontal disease progression.     

Gingival crevicular fluid levels of leukotriene B4 in periodontal health and disease

BACKGROUND: Leukotriene B(4) (LTB(4)) is a membrane-derived lipid mediator formed from arachidonic acid. LTB(4) is among the most potent stimulants of polymorphonuclear leukocytes (PMNs) and, thus, participates in tissue injury by recruiting PMNs in a pathophysiologic scenario of periodontal diseases. The aim of the present study was to assess the relationship between clinical parameters and concentrations of LTB(4) within gingival crevicular fluid (GCF) from inflamed gingiva and periodontitis sites before and after the treatment of periodontitis. METHODS: Sixty subjects were divided into three groups with 20 subjects in each group: healthy (group 1), gingivitis (group 2), and chronic periodontitis (group 3). Groups were based on periodontal disease index (PDI), clinical attachment loss (CAL), and radiographic evidence of bone loss. Group 4 consisted of the subjects in group 3 at 6 to 8 weeks after treatment, i.e., scaling and root planing (SRP). GCF samples collected from each patient were quantified for LTB(4) using an enzymatic immunometric assay. In addition, the correlation between in situ LTB(4) levels and clinical parameters was analyzed in each group. RESULTS: The highest mean LTB(4) concentration in GCF was observed in group 3 (185.2 pg/microl), and the lowest was observed in group 1 (39.6 pg/microl). Its level in group 3 decreased to 79.35 pg/microl after treatment (group 4). Further, GCF LTB(4) levels in all groups showed a statistically significant positive correlation with PDI and CAL (P <0.005). CONCLUSION: The substantial increase in GCF LTB(4) concentrations with the severity of periodontal disease and a concomitant decrease in its level following SRP in subjects with periodontitis suggest a possible role for LTB(4) in the progression of periodontal disease.     

Gingival crevicular fluid fibronectin degradation in periodontal health and disease

The molecular forms of fibronectin (FN) in gingival crevicular fluid of five subjects with at least two sites exhibiting clinical signs of inflammation and pockets of at least 4 mm (test group) and five subjects with clinically healthy periodontium (control group) were investigated. Samples were collected with standard filter paper strips. In the test group samples from both diseased and healthy sites were collected. After collection the test group received one episode of periodontal treatment (scaling and root planning). The sampling and clinical recording were repeated for the diseased sites after about 2 wk. The crevicular fluid FN was analyzed using sodium dodecyl sulphate gel electrophoresis followed by western blotting with polyclonal antibodies against FN. Both intact FN and FN fragments were found in all samples. A larger proportion of FN was in degraded form in the diseased sites than in the healthy or the treated sites. FN was also degraded into smaller peptide fragments in the diseased than in the treated sites. These results suggest that crevicular fluid FN is partially degraded both in periodontal health and disease and that the degree of degradation of FN increases with periodontal inflammation and decreases with periodontal treatment.     

Gingival crevicular fluid fibronectin degradation in periodontal health and disease

Abstract— The molecular forms of fibronectin (FN) in gingival crevicular fluid of five subjects with at least two sites exhibiting clinical signs of inflammation and pockets of at least 4 mm (test group) and five subjects with clinically healthy periodontium (control group) were investigated. Samples were collected with standard filter paper strips. In the test group samples from both diseased and healthy sites were collected. After collection the test group received one episode of periodontal treatment (scaling and root planing). The sampling and clinical recordings were repeated for the diseased sites after about 2 wk. The crevicular fluid FN was analyzed using sodium dodecyl sulphate gel electrophoresis followed by western blotting with polyclonal antibodies against FN. Both intact FN and FN fragments were found in all samples. A larger proportion of FN was in degraded form in the diseased sites than in the healthy or the treated sites. FN was also degraded into smaller peptide fragments in the diseased than in the treated sites. These results suggest that crevicular fluid FN is partially degraded both in periodontal health and disease and that the degree of degradation of FN increases with periodontal inflammation and decreases with periodontal treatment.     

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.     

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 levels of SLIT3 are increased in periodontal disease

This study aims to investigate the levels of SLIT3 in gingival crevicular fluid (GCF) of healthy and periodontal disease subjects, and their correlations to periodontal disease. A total of 45 periodontal patients and 45 periodontally healthy volunteers were enrolled. The clinical parameters, radiographic bone loss and the levels of SLIT3, receptor activator of NF‐κB ligand (RANKL) and osteoprotegerin (OPG) in GCF were measured. The prevalences of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia in subgingival plaque were also analyzed. The expression of SLIT3 and RANKL was detected in the periodontium of experimental periodontitis in rats and lipopolysaccharide (LPS)‐induced mouse macrophage. The total amounts and concentrations of SLIT3 and RANKL were significantly higher in periodontitis than those in healthy, while the level of OPG was significantly lower (p < .05). Significant positive correlations were observed between the level of GCF SLIT3 and clinical attachment level and radiographic bone loss (p < .05). There existed a significant positive correlation between SLIT3 and RANKL (p < .05). Increased expression of SLIT3 and RANKL was observed in the periodontium of periodontal rats. SLIT3 expression was induced by LPS stimulation in macrophages. These results suggest that SLIT3 may act as a diagnostic indicator of periodontal disease and should be further investigated.     

Gingival crevicular fluid matrix metalloproteinase-25 and -26 levels in periodontal disease

BACKGROUND: Tissue destruction associated with the progression of periodontal disease is caused by a cascade of host and microbial proteolytic enzymes. Host-derived matrix metalloproteinases (MMPs) play an important role in the degradation of the extracellular matrix. Leukolysin/membrane-type 6 (MT-6)/MMP-25, the latest member of the MT-MMP subgroup of the MMP family, is primarily expressed by neutrophils and involved in extracellular matrix turnover. Matrilysin-2/MMP-26 (endometase), a novel member of the matrilysin subgroup of the MMP family, can degrade the extracellular matrix, alpha1-antitrypsin, and activate pro-MMP-9. Our study aimed to examine the levels, molecular forms, and degrees of activation of MMP-25 and MMP-26 in gingival crevicular fluid (GCF) from patients with different periodontal diseases. METHODS: A total of 105 subjects, 35 with generalized aggressive periodontitis (GAgP), 29 with chronic periodontitis (CP), 20 with gingivitis, and 21 periodontally healthy subjects, were included in this study. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing, and plaque. GCF MMP-25 and MMP-26 levels were analyzed by computer-quantitated Western immunoblotting using specific antibodies. RESULTS: The 57-kDa soluble pro-MMP-25 and 45- to 47-kDa active form of MMP-25 were detected by Western immunoblots in CP and GAgP GCF, and lesser levels of these soluble MMP-25 immunoreactive bands were detected in gingivitis GCF. An enhanced and similar degree of MMP-25 activation was found in GAgP, CP, and gingivitis groups. There were no detectable MMP-25 immunoreactivities in the healthy subjects' GCF. GAgP and CP groups had elevated GCF MMP-26 levels and degrees of activation compared to the gingivitis and healthy groups (P <0.008). The gingivitis group had higher GCF MMP-26 levels and degree of activation compared to the healthy group (P <0.008). CONCLUSIONS: The present study demonstrated the presence of soluble or shed forms of MMP-25 and MMP-26 in GCF of patients with different periodontal diseases. Increased levels and activation of MMP-25 and MMP-26 in GCF are associated with an enhanced severity of periodontal inflammation, suggesting that these novel MMPs can participate in the progression of periodontal diseases. They may prove to be diagnostically useful and could be targets of medication in the future.     

Leptin levels in gingival crevicular fluid in periodontal health and disease

BACKGROUND AND OBJECTIVE: A high concentration of leptin is associated with healthy gingival tissue, and the concentration of leptin decreases as periodontal disease progresses. However, to date, the leptin concentration in gingival crevicular fluid has not been documented. Hence, the present study was carried out to explore the presence of leptin in gingival crevicular fluid in periodontal health and disease, and to probe further into its possible role in periodontal disease progression. MATERIAL AND METHODS: A total of 45 adult patients were selected, based on their body mass index, for the study. They were categorized into three groups of 15 patients each, based on their periodontal tissue status, as follows: group I (clinically healthy gingiva with no loss of attachment); group II (chronic gingivitis with no loss of attachment); and group III (chronic periodontitis). Gingival crevicular fluid samples of 1 microL were collected extracrevicularly using white color-coded 1-5 microL calibrated volumetric microcapillary pipettes from one site in each person, and samples were analyzed for leptin using a commercially available enzyme-linked immunosorbent assay kit. RESULTS: The concentration of leptin in gingival crevicular fluid of patients in group I (2292.69 pg/mL) was statistically higher (p < 0.05) than in those of groups II (1409.95 pg/mL) and III (1071.89 pg/mL). This suggests a negative correlation of gingival crevicular fluid leptin concentration with clinical attachment loss (p < 0.05). CONCLUSION: As periodontal tissue destruction increased, there was a substantial decrease in gingival crevicular fluid leptin concentration. This observation extends our knowledge of the protective role of leptin in periodontal health.     

Gingival crevicular fluid and plasma levels of neuropeptide Substance-P in periodontal health, disease and after nonsurgical therapy

Background and Objective: The level of Substance‐P in gingival crevicular fluid has been found to correlate with clinical measures of periodontal disease. The present study was designed to assess the relationship between clinical parameters and levels of Substance‐P in the gingival crevicular fluid from inflamed gingiva, periodontitis sites and after treatment of periodontitis sites, and to correlate them to the Substance‐P levels of plasma. Material and Methods: Thirty, age‐ and gender‐matched subjects were divided into three groups (healthy, gingivitis and chronic periodontitis) based on modified gingival index scores and clinical attachment loss. A fourth group consisted of 10 subjects from the periodontitis group, 6–8 wk after initial therapy. Plasma and gingival crevicular fluid samples were collected and quantified for Substance‐P using an enzyme immunoassay. Results: The mean concentration of Substance‐P, both in gingival crevicular fluid and plasma, was observed to be highest in the periodontitis group (45.13 pg/mL in gingival crevicular fluid and 67.8 pg/mL in plasma) and lowest in the healthy group (6.07 pg/mL in gingival crevicular fluid and below the detection level in plasma). The mean Substance‐P concentration in the gingivitis group (11.42 pg/mL in gingival crevicular fluid and 38.8 pg/mL in plasma) and in the after‐treatment group (7.58 pg/mL in gingival crevicular fluid and 39.7 pg/mL in plasma) lay between the highest and lowest values. In all groups the gingival crevicular fluid levels showed a statistically significant positive correlation with that of plasma and clinical attachment loss. Conclusion: Substance‐P levels were highest in the gingival crevicular fluid from sites with periodontal destruction; however, periodontal treatment resulted in the reduction of Substance‐P levels. Gingival crevicular fluid and plasma Substance‐P levels showed a positive correlation in all of the groups.     

Plasma and crevicular fluid osteopontin levels in periodontal health and disease

BACKGROUND AND OBJECTIVE: The level of osteopontin in gingival crevicular fluid has been found to correlate with clinical measures of periodontal disease. The present study was designed to assess the relationship between clinical parameters and osteopontin levels of the gingival crevicular fluid from inflamed gingivae, periodontitis sites and after treatment of periodontitis sites, and to correlate them to the osteopontin levels of the plasma. MATERIAL AND METHODS: Thirty, gender-matched subjects were divided into three groups--healthy, gingivitis and chronic periodontitis--based on modified gingival index scores and clinical attachment loss. The fourth group consisted of 10 subjects in the periodontitis group, 6-8 wk after initial therapy. Plasma and gingival crevicular fluid samples were collected and quantified for osteopontin using an enzyme immunoassay. RESULTS: The highest mean gingival crevicular fluid and plasma osteopontin concentrations were observed in the periodontitis group (1575.01 and 1273.21 ng/mL, respectively) and the lowest in the healthy group (1194.80 and 476.35 ng/mL, respectively). After treatment of the periodontitis group, the level of osteopontin decreased to 1416.15 in gingival crevicular fluid and to 1051.68 ng/mL in plasma. In all groups the gingival crevicular fluid osteopontin levels showed a statistically significant positive correlation with that of plasma and clinical attachment loss. CONCLUSION: Osteopontin levels were highest in the gingival crevicular fluid from sites with periodontal destruction; however, periodontal treatment resulted in the reduction of osteopontin levels. Gingival crevicular fluid and plasma osteopontin levels showed a positive correlation in all of the groups.     

Gingival crevicular fluid and serum leptin: their relationship to periodontal health and disease

BACKGROUND & AIMS: Leptin is a pleiotrophic hormone produced by adipose tissue and it plays an important role in protection of the host from inflammation and infection. The purpose of this study is to determine the presence of leptin in gingival crevicular fluid (GCF) and serum samples and to find out their association, if any. METHODS: Forty two subjects were selected based on their body mass index and were divided into three groups of 14 each; healthy (Group I), chronic gingivitis (Group II) and chronic periodontitis (Group III). GCF samples (by microcapillary pipettes) and serum samples (by venipuncture) were collected to estimate the levels of leptin using enzyme linked immunosorbent assay kit. RESULTS: The highest mean leptin concentration in GCF was obtained for Group I (2658 pg/ml) and the least for Group III (1312 pg/ml). In contrast, the lowest serum leptin concentration was obtained for the Group I (8783 pg/ml), and the highest for Group III (12082 pg/ml). This suggests a negative correlation of GCF leptin concentration and a positive correlation of serum leptin concentration as the clinical attachment level progresses (p<0.05). CONCLUSION: These results suggest that greater the periodontal destruction, lesser is the GCF leptin concentration and greater the serum leptin concentration.     

Gingival crevicular fluid and serum visfatin concentration: their relationship in periodontal health and disease

Background: Visfatin is a pleiotropic mediator that acts as growth factor, cytokine, and enzyme involved in energy including nicotinamide adenine dinucleotide metabolism and was recently demonstrated to exert several proinflammatory functions. The purpose of this study is to determine the presence of visfatin in gingival crevicular fluid (GCF) and serum samples and to find out their association, if any. Methods: At the beginning of the study, 40 individuals (20 males and 20 females; age range: 23 to 53 years) were selected and divided into three groups based on the gingival index, probing depths, clinical attachment levels, and radiologic parameters (bone loss). Group 1 (10 patients with healthy periodontium; age range: 25‐36 years), group 2 (15 patients with gingivitis; age range: 25‐36 years), and group 3 (15 patients with chronic periodontitis; age range: 23‐53 years) GCF (by microcapillary pipettes) and serum (by venipuncture) samples were collected to estimate levels of visfatin using an enzyme‐linked immunosorbent assay kit. Results: Mean visfatin concentrations increased in GCF and serum with the severity of disease from healthy to gingivitis to periodontitis groups and differed significantly (P <0.05). However, it was found that GCF values were higher than serum values. The highest to lowest visfatin concentrations were found in groups 3 through 1, respectively. Visfatin in GCF and serum correlated positively with periodontal parameters in the chronic periodontitis group. Conclusions: The results suggest that GCF and serum visfatin concentrations increase with the severity of periodontal disease. Hence, visfatin values were considered an inflammatory marker in periodontal disease in GCF and serum. Visfatin also deserves further consideration as a therapeutic target.     

Gingival crevicular fluid and plasma acute-phase cytokine levels in different periodontal diseases

Background: The aim of the present study is to investigate gingival crevicular fluid (GCF) and plasma acute-phase cytokines, interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-11 (IL-11), oncostatin M (OSM), and leukemia inhibitory factor (LIF) levels in patients with different periodontal diseases. Methods: Eighty individuals were included in this study; 20 with chronic periodontitis (CP), 20 with generalized aggressive periodontitis (GAgP), 20 with gingivitis, and 20 classified as healthy (H). Probing depth, clinical attachment level, plaque index, and papilla bleeding index were recorded. Plasma and GCF IL-1β, IL-6, IL-11, OSM, and LIF levels were analyzed by enzyme-linked immunosorbent assay. Results: CP and GAgP groups had significantly higher GCF IL-1β, IL-6, and IL-11 levels when compared with the H group (P <0.05). Conversely, GCF LIF levels of the CP and GAgP groups were lower than those of the H group (P <0.05). GCF OSM levels did not differ significantly among study groups. Plasma levels of all the cytokines studied were not significantly different among the study groups. Conclusions: Based on the present data, elevated IL-1β, IL-6, and IL-11 GCF levels, but not plasma levels, are suggested as reliable inflammatory biomarkers in periodontal diseases. Decreased LIF levels in diseased groups might reflect the possible beneficial effects of LIF in the modulation of inflammatory response in gingiva.     

Gingival crevicular fluid gelatinase and its relationship to periodontal disease in human subjects

Collagenolytic enzymes released by neutrophils are associated with the destruction of periodontium in periodontal diseases. Measurement of these enzymes in gingival crevicular fluid (GCF) could be used to test for periodontal diseases and thereby simplify diagnosis. To test this hypothesis, gelatinase (MMP-9) was analyzed in GCF samples with a simple assay system. GCF was collected by a mouthrinse method from 10 patients with gingivitis (G); 10 well-treated and maintained periodontitis patients (TP) without detectable loss of attachment; and 9 patients with recurrent loss of periodontal attachment (greater than 2 mm) and/or abscess formation (RP). Clinical measurements including tooth mobility (MOB) and gingival attachment level (GAL) were made monthly for a maximum of 10 months. Active and latent forms of gelatinase were measured by a functional assay using gelatin substrate-gel enzymography and the activities were quantified by laser densitometry. Reproducibility analysis demonstrated that the assay (inter-gel, inter-assay, inter-scan) and diurnal variations were small compared to biological variation. The presence of active gelatinase was detected in 97.8% of TP samples, 86.4% of RP samples, but in only 11.4% of G samples. In addition, the mean active gelatinase activity was found to be significantly higher (p less than 0.001) in the RP (71,006 U) than the TP (43,814 U) groups, both of which were higher (p less than 0.001) than the G group (2824 U). During periods of attachment loss, samples from the RP group exhibited a 2-fold increase of mean active gelatinase activity (129,414 U).(ABSTRACT TRUNCATED AT 250 WORDS)     

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 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.     

Gingival crevicular fluid levels of neopterin in healthy subjects and in patients with different periodontal diseases

BACKGROUND: Neopterin, a metabolite of guanosine, belongs to the class of chemical compounds known as pteridines and is an early and valuable marker of cellular immunity. Recently, it was shown to be associated with the initiation and progression of periodontal disease. The aim of the present study was to assess the relationship between clinical parameters and concentrations of neopterin within gingival crevicular fluid (GCF) from inflamed gingiva and periodontitis sites before and after the treatment of periodontitis. METHODS: Sixty age (35 to 65 years)- and gender-matched (30 males and 30 females) subjects were recruited and divided into the following four groups of 15 subjects each based on gingival index, Ramfjord periodontal disease index, clinical attachment loss (CAL), and radiographic parameters (bone loss): healthy (group 1), gingivitis (group 2), mild periodontitis (group 3), and moderate to severe periodontitis (group 4). A fifth group consisted of the 15 subjects from group 4, 6 to 8 weeks after treatment (scaling and root planing). GCF was collected from each patient, and the neopterin levels were determined by enzyme immunoassay. Results were analyzed statistically. RESULTS: The mean concentration of neopterin in GCF was the highest in group 4 (51 nmol/l) and the lowest in group 1 (1.36 nmol/l). The mean neopterin concentrations in group 2 (9.69 nmol/l) and group 3 (16.58 nmol/l) fell between the highest and lowest values. This suggested a positive correlation between CAL and GCF neopterin concentrations. Neopterin levels in group 4 decreased to 1.77 nmol/l after treatment (group 5). CONCLUSIONS: Neopterin increased in parallel with the severity of inflammatory disease. Its levels in GCF may be potentially useful as an indicator of periodontal inflammation and the host response.     

Gingival crevicular fluid matrix metalloproteinase-13 levels and molecular forms in various types of periodontal diseases

BACKGROUND: The purpose of this study was to evaluate the levels, molecular forms and activation degree of matrix metalloproteinase-13 (MMP-13) in the gingival crevicular fluid (GCF) of patients with periodontal diseases and to correlate these findings with periodontal clinical parameters. METHODS: Sixty one subjects participated in this study as healthy (n = 18), gingivitis (n = 17), aggressive periodontitis (AgP; n = 15) and chronic periodontitis (CP; n = 11) groups. Clinical measurements and GCF samples were obtained from each subject. The molecular forms of MMP-13 in GCF samples were analyzed by Western immunoblotting method. Differences among the groups were assessed using non-parametric statistical analysis. RESULTS: In the CP group, levels of 29-30 kDa fragment of MMP-13, total MMP-13, and activated form of MMP-13 were significantly higher than in the healthy, gingivitis and AgP groups. GCF levels of all molecular forms of MMP-13 in AgP group were similar to those of healthy and gingivitis groups. Total and activated MMP-13 levels were positively correlated with all clinical parameters. 29-30 kDa fragment levels of MMP-13 were also positively correlated with papillary bleeding index and plaque index. CONCLUSION: These results indicate that elevated GCF MMP-13 levels may play an important role in the pathogenesis of CP. These data demonstrate, for the first time, pathologically activated and elevated MMP-13 in GCF.