Soluble Triggering Receptor Expressed on Myeloid Cells 1 (sTREM‐1) in Gingival Crevicular Fluid: Association With Clinical and Microbiologic Parameters

Background: Soluble triggering receptor expressed on myeloid cells 1 (sTREM‐1) belongs to the immunoglobulin superfamily and is involved in amplification of the inflammatory response to bacterial infection. This cross‐sectional study aims to investigate the levels of sTREM‐1 in gingival crevicular fluid (GCF) of individuals without periodontitis and with chronic periodontitis (CP) or generalized aggressive periodontitis (GAgP) and their association with the levels of key periodontal pathogens in subgingival plaque. Methods: GCF and subgingival plaque samples were obtained from healthy sites of participants without periodontitis (n = 20) and periodontitis sites of patients with CP (n = 22) and GAgP (n = 20). sTREM‐1 levels in GCF were measured by enzyme‐linked immunosorbent assay. Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans levels in subgingival plaque were analyzed by quantitative real‐time polymerase chain reaction. Results: sTREM‐1 levels in GCF were higher in CP and GAgP than healthy sites by 3.6‐ and 4.4‐fold, respectively, with no significant differences between the two forms of periodontitis. Moreover, sTREM‐1 levels in GCF were positively correlated with site‐specific clinical periodontal parameters and levels of P. gingivalis, T. denticola, and T. forsythia, but not A. actinomycetemcomitans, in subgingival plaque. Conclusion: Increased GCF levels of sTREM‐1 at diseased sites and their positive correlation with clinical and microbiologic parameters strengthen the association of this inflammatory marker with periodontitis.     

Matrix Metalloproteinase (MMP)‐8 and Tissue Inhibitor of MMP‐1 (TIMP‐1) Gene Polymorphisms in Generalized Aggressive Periodontitis: Gingival Crevicular Fluid MMP‐8 and TIMP‐1 Levels and Outcome of Periodontal Therapy

Background: The aim of the present study is to investigate matrix metalloproteinase (MMP)‐8 and tissue inhibitor of MMP‐1 (TIMP‐1) gene polymorphisms in generalized aggressive periodontitis (GAgP) and to assess the effects of MMP‐8 and TIMP‐1 genotypes on the outcomes of non‐surgical periodontal therapy. Methods: Genomic DNA was obtained from peripheral blood of 100 patients with GAgP and 167 periodontally healthy controls. MMP‐8 +17 C/G, ?799 C/T, ?381 A/G and TIMP‐1 372 T/C, *429 T/G polymorphisms were determined by polymerase chain reaction‐restriction fragment length polymorphism. Patients with GAgP received non‐surgical periodontal therapy and were followed for 6 months. Clinical periodontal parameters and gingival crevicular fluid (GCF) samples were collected at baseline and at follow‐up visits. GCF biomarkers were analyzed by immunofluorescence assay and enzyme‐linked immunosorbent assay. Results: Distribution of the MMP‐8 ?799 C/T genotypes was significantly different between the GAgP and control groups (P <0.005). TIMP‐1 372 T/C and *429 T/G genotypes in males were also significantly different between study groups (P <0.004). GCF MMP‐8 levels decreased until 3 months after non‐surgical therapy compared with baseline in T and G alleles, as well as G and C allele carriers (P <0.0125), whereas no significant decreased was observed in non‐carriers (P >0.0125). Conclusion: On the basis of the present findings, it can be suggested that MMP‐8 ?799 C/T and TIMP‐1 372 T/C, *429 T/G gene polymorphisms in males may be associated with the susceptibility to GAgP in the Turkish population.     

The combination of amoxicillin and metronidazole improves clinical and microbiologic results of one-stage, full-mouth, ultrasonic debridement in aggressive periodontitis treatment

Background: The aim of the present study is to assess clinical, microbiologic, and immunologic benefits of amoxicillin/metronidazole (AM) when performing full‐mouth ultrasonic debridement (FMUD) in generalized aggressive periodontitis (GAgP) treatment. Methods: Twenty‐four GAgP patients were divided into two groups: the FMUD group (n = 12), which received FMUD plus placebo, and the FMUD+AM group (n = 12), which received FMUD and 375 mg amoxicillin plus 250 mg metronidazole for 7 days. The following clinical outcomes were tested: plaque and bleeding on probing indices, pocket probing depth (PD), relative gingival margin position (GMP), and relative clinical attachment level (CAL). Total amount of Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans (Aa), Tannerella forsythia (Tf), and gingival crevicular fluid (GCF) concentration of interleukin (IL)‐10 and IL‐1β were also determined. All clinical, microbiologic, and immunologic parameters were assessed at baseline and at 3 and 6 months post‐therapy. The ANOVA/Tukey test was used for statistical analysis (α = 5%). Results: Amoxicillin/metronidazole used as an adjunct to the FMUD protocol added clinical and microbiologic benefits to GAgP treatment (P <0.05). FMUD+AM groups presented an additional PD reduction in initially deep PDs at the 3‐month follow‐up (3.99 ± 1.16 mm and 3.09 ± 0.78 mm for FMUD+AM and FMUD, respectively; P <0.05), a lower number of residual pockets at the 3‐ and 6‐month follow‐ups, and a statistical reduction in amounts of Aa (P <0.05). Analysis of Tf and Pg amounts, as well as IL‐10 and IL‐1β GCF concentrations failed to demonstrate a difference between the groups (P >0.05). Conclusion: It may be concluded that amoxicillin/metronidazole improves clinical and microbiologic results of FMUD in GAgP treatment.     

Alcohol Consumption and Periodontitis: Quantification of Periodontal Pathogens and Cytokines

Background: There are few studies on periodontal status related to microbiologic and immunologic profiles among individuals not or occasionally using alcohol and those with alcohol dependence. The aim of this study is to determine the effect of alcohol consumption on the levels of subgingival periodontal pathogens and proinflammatory cytokines (interleukin [IL]‐1β and tumor necrosis factor [TNF]‐α) in the gingival fluid among individuals with and without periodontitis. Methods: This observational analytic study includes 88 volunteers allocated in four groups (n = 22): individuals with alcohol dependence and periodontitis (ADP), individuals with alcohol dependence and without periodontitis (ADNP), individuals not or occasionally using alcohol with periodontitis (NAP), and individuals not or occasionally using alcohol without periodontitis (NANP). Levels of Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Eikenella corrodens, and Fusobacterium nucleatum were determined by real‐time polymerase chain reaction on the basis of the subgingival biofilm, and IL‐1β and TNF‐α were quantified by enzyme‐linked immunosorbent assay in gingival fluid samples. Results: Individuals with alcohol dependence showed worse periodontal status and higher levels of P. intermedia, E. corrodens, F. nucleatum, and IL‐1β than non‐users. No significant correlations between TNF‐α and bacterial levels were observed. However, in the ADP group, higher levels of E. corrodens were correlated with higher levels of IL‐1β. Conclusion: A negative influence of alcohol consumption was observed on clinical and microbiologic periodontal parameters, as well as a slight influence on immunologic parameters, signaling the need for additional studies.     

Clinical and microbiologic evaluation, by real-time polymerase chain reaction, of non-surgical treatment of aggressive periodontitis associated with amoxicillin and metronidazole

Background: The aim of the present study is to evaluate the clinical and microbiologic changes resulting from non‐surgical periodontal treatment associated with amoxicillin and metronidazole in individuals with aggressive periodontitis. Methods: Fifteen individuals with aggressive periodontitis received non‐surgical periodontal treatment and 45 days after completion of treatment were treated with antibiotics. Clinical data and samples of subgingival plaque were collected at baseline, 45 days after the non‐surgical periodontal treatment, and 1 month after the use of antimicrobial agents. After 3 and 6 months, only clinical data were collected. The presence and quantification of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), Treponema denticola (Td), and Dialister pneumosintes were determined by real‐time polymerase chain reaction. Results: All clinical parameters, with the exception of clinical attachment level (CAL), had significantly (P <0.05) improved at the end of the third month after non‐surgical therapy associated with antibiotics. There was significant (P <0.05) reduction in the quantities of Td and Tf. After 1 month, there were significant (P <0.05) reductions in the frequencies of Pg and Tf. Conclusion: Non‐surgical mechanical treatment associated with the use of amoxicillin and metronidazole led to an improvement in all clinical parameters studied, except for CAL, and significantly reduced the amount of subgingival Tf and Td.     

Chemerin as a Novel Crevicular Fluid Marker of Patients With Periodontitis and Type 2 Diabetes Mellitus

Background: The objectives of the present study are to: 1) determine whether gingival crevicular fluid (GCF) chemerin is a novel predictive marker for patients with chronic periodontitis (CP) with and without type 2 diabetes mellitus (t2DM); 2) analyze the relationship between chemerin and interleukin (IL)‐6 in periodontally healthy individuals and in patients with CP and with and without t2DM; and 3) evaluate the effect of non‐surgical periodontal therapy on GCF chemerin levels. Methods: Eighty individuals were split into four groups: 20 who were systemically and periodontally healthy (CTRL), 20 with t2DM and periodontally healthy (DM‐CTRL), 20 systemically healthy with CP (CP), and 20 with CP and t2DM (DM‐CP). Individuals with periodontitis were treated with non‐surgical periodontal therapy. GCF sampling procedures and clinical periodontal measures were performed before and 6 weeks after treatment. Enzyme‐linked immunosorbent assay was used to measure chemerin and IL‐6 levels. Results: Greater values for GCF chemerin and IL‐6 levels were found in CP groups than in periodontally healthy groups, in DM‐CP than in CP, and in DM‐CTRL than in CTRL (P <0.008). GCF chemerin and IL‐6 levels decreased following therapy in CP groups (P <0.02). A comprehensive overview of all groups showed a statistically significant positive correlation of chemerin with IL‐6, glycated hemoglobin, sampled‐site clinical attachment level, and gingival index (P <0.05). Conclusions: In this study, periodontitis and t2DM induced aberrant secretion of chemerin, and non‐surgical periodontal therapy influenced the decrease of GCF chemerin levels in patients with CP with and without t2DM. Furthermore, it suggests GCF chemerin levels may be considered a potential proinflammatory marker for diabetes, periodontal disease, and treatment outcomes.     

Azithromycin as an Adjunctive Treatment of Generalized Severe Chronic Periodontitis: Clinical,Microbiologic, and Biochemical Parameters

Background: This study examines the efficacy of azithromycin in combination with non‐surgical periodontal therapy on clinical and microbiologic parameters and gingival crevicular fluid (GCF) matrix metalloproteinases‐8 (MMP‐8) levels over 6 months in patients with severe generalized chronic periodontitis (CP). Methods: Twenty‐eight of 36 patients with severe generalized CP were included in this randomized, double‐masked, placebo‐controlled, parallel‐arm study. They were randomly assigned to azithromycin or placebo groups (500 mg, once daily for 3 days). Probing depth (PD), clinical attachment level, dichotomous presence or absence of supragingival plaque accumulation, and bleeding on probing were recorded. GCF samples were obtained from one single‐rooted tooth with PD ≥ 6 mm, whereas microbiologic samples were collected from two single‐rooted teeth with PD ≥ 6 mm. Microbiologic parameters were analyzed by quantitative real‐time polymerase chain reaction for Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Fusobacterium nucleatum, Prevotella intermedia, and total bacteria. GCF MMP‐8 levels were determined by immunofluorescence assay. Results: Azithromycin and placebo groups demonstrated similar but significant improvements in all clinical parameters (P <0.05). A. actinomycetemcomitans, P. gingivalis, T. forsythia, P. intermedia, and total bacteria significantly decreased over the 6‐month period in both groups, whereas F. nucleatum was significantly reduced in all visits in the azithromycin group, with the levels also being lower compared with those of the placebo group (P <0.05). The azithromycin and placebo groups exhibited significant reduction in GCF MMP‐8 levels at the post‐treatment visit and at 2 weeks (P <0.05). Conclusion: On the basis of the present findings, it can be concluded that adjunctive azithromycin provides no additional benefit over non‐surgical periodontal treatment on parameters investigated in patients with severe generalized CP.     

Investigation of a Novel Predictive Biomarker Profile for the Outcome of Periodontal Treatment

Background: An ability to predict the response to conventional non‐surgical treatment of a periodontal site would be advantageous. However, biomarkers or tests devised to achieve this have lacked sensitivity. The aim of this study is to assess the ability of a novel combination of biomarkers to predict treatment outcome of patients with chronic periodontitis. Methods: Gingival crevicular fluid (GCF) and subgingival plaque were collected from 77 patients at three representative sites, one healthy (probing depth [PD] ≤3 mm) and two diseased (PD ≥6 mm), at baseline and at 3 and 6 months after treatment. Patients received standard non‐surgical periodontal treatment at each time point as appropriate. The outcome measure was improvement in probing depth of ≥2 mm. Concentrations of active enzymes (matrix metalloproteinase [MMP]‐8, elastase, and sialidase) in GCF and subgingival plaque levels of Porphyromonas gingivalis, Tannerella forsythia, and Fusobacterium nucleatum were analyzed for prediction of the outcome measure. Results: Using threshold values of MMP‐8 (94 ng/μL), elastase (33 ng/μL), sialidase (23 ng/μL), and levels of P. gingivalis (0.23%) and T. forsythia (0.35%), receiver operating characteristic curves analysis demonstrated that these biomarkers at baseline could differentiate healthy from diseased sites (sensitivity and specificity ≥77%). Furthermore, logistic regression showed that this combination of these biomarkers at baseline provided accurate predictions of treatment outcome (≥92%). Conclusion: The “fingerprint” of GCF enzymes and bacteria described here offers a way to predict the outcome of non‐surgical periodontal treatment on a site‐specific basis.     

Subgingival microbiota of periodontally untreated Mexican subjects with generalized aggressive periodontitis

BACKGROUND AND AIM: Specific microbial profiles that may distinguish between generalized aggressive-periodontitis (GAgP) and generalized chronic-periodontitis (GCP) have, to date, not been described. The purpose of the present study was to describe the subgingival microbial composition of Mexican subjects with GAgP and compare it with that of individuals with GCP and periodontal health (PH). MATERIAL AND METHODS: Seventy-seven subjects with GAgP (n=19), GCP (n=39) and PH (n=19) were selected. Clinical measurements included plaque accumulation, gingival erythema, bleeding on probing, suppuration, pocket depth and attachment level. Up to 28 subgingival plaque samples were obtained from each subject and analysed using the checkerboard DNA-DNA hybridization technique. RESULTS: GAgP and GCP subjects harboured significantly higher levels and/or proportion of Porphyromonas gingivalis, Tannerella forsythia (levels: p<0.001, proportion: p<0.01), Prevotella nigrescens (p<0.05 levels) and "red" complex species (p<0.001 proportion) than PH subjects. All GAgP subjects were carriers of P. gingivalis and P. nigrescens. No significant differences in any of the 40 microbial species tested were detected between GAgP and GCP subjects. CONCLUSIONS: Our results revealed that the microbial differences between GAgP and GCP subjects were only discrete and none of the bacterial species tested seemed to specifically differentiate the subgingival microbial profile of either periodontitis group.     

Effect of Non‐Surgical Periodontal Treatment on Visfatin Concentrations in Serum and Gingival Crevicular Fluid of Patients With Chronic Periodontitis and Type 2 Diabetes Mellitus

Background : This study aims to assess visfatin concentrations in serum and gingival crevicular fluid (GCF) and investigate this relationship in patients with type 2 diabetes mellitus (T2DM) and chronic periodontitis (CP) before and after non‐surgical periodontal treatment. Methods: Fifty‐four patients with T2DM and CP were recruited. The patients were randomly divided into two groups: treatment and control. Serum and GCF visfatin concentrations and glycated hemoglobin (HbA1c) levels were measured by enzyme‐linked immunosorbent assay at different time points (at baseline and 3 and 6 months after non‐surgical periodontal treatment). Results: Serum and GCF visfatin concentrations showed no significant differences between the groups at baseline (t test, P >0.05). A significant decline of visfatin in the treatment group was found in serum and GCF 3 months after non‐surgical periodontal treatment (t test, P <0.01). Baseline and 3‐month HbA1c levels were not significantly different, but at 6 months, a statistically significant difference was detected (t test, P >0.05). Conclusions: The data suggest that non‐surgical periodontal treatment is helpful for glucose control, an effect that may be associated with reduced visfatin in patients with T2DM and periodontitis. Furthermore, the data suggest that visfatin may be considered an inflammatory marker for periodontal diseases.     

Effect of Initial Periodontal Therapy on Oxidative Stress Markers in Gingival Crevicular Fluid,Saliva, and Serum in Smokers and Non‐Smokers With Chronic Periodontitis

Background: The aim of this case‐control study with an intervention arm is to determine the effect of initial periodontal treatment on oxidative stress biomarkers in smokers and non‐smokers with chronic periodontitis (CP). Methods: The study included 47 patients with CP (24 smokers [S+P+] and 23 non‐smokers [S?P+]) and 46 periodontally healthy individuals (23 smokers [S+P?] and 23 non‐smokers [S?P?]) for a total of 93 participants. Gingival crevicular fluid (GCF), serum, and saliva samples were obtained and clinical periodontal measurements were recorded at baseline and at the first and third months after periodontal therapy. 8‐hydroxydeoxyguanosine (OHdG) and 4‐hydroxynonenal (HNE) and enzyme activity of glutathione peroxidase (GSH‐Px) were analyzed with enzyme‐linked immunosorbent assay. Results: The level of 8‐OHdD in GCF was found to be significantly higher in both periodontitis groups compared with both periodontally healthy groups. 8‐OHdG and GSH‐Px in saliva in both periodontitis groups were significantly increased compared with the S?P? group. In the S+P+ group, 4‐HNE in GCF was found to be significantly higher than in periodontally healthy participants. After initial periodontal treatment, the levels of 8‐OHdG in GCF and saliva were significantly decreased in both periodontitis groups. Conclusion: Initial periodontal therapy may be helpful for diminishing oxidative stress in periodontitis.     

Association of Gingival Crevicular Fluid Cortisol/Dehydroepiandrosterone Levels With Periodontal Status

Background: The aim of the present study is to examine whether anxiety and depression scale scores change with regard to clinical periodontal status and to investigate the association between the levels of stress‐related hormones in gingival crevicular fluid (GCF) and extent/severity of periodontal disease. Methods: One hundred twenty participants who fulfilled the study inclusion criteria were chosen. Patients with chronic periodontitis (CP) and those with healthy periodontal tissues/mild gingivitis were included. The clinical examinations were performed on the day after the psychologic evaluations which included anxiety and depression measurements. GCF sampling was undertaken the following day. Commercially available enzyme‐linked immunosorbent assay kits were used to determine GCF cortisol and dehydroepiandrosterone (DHEA) levels. Study groups were assigned as follows: group 1, non‐periodontitis; group 2, localized CP; and group 3, generalized CP. Results: There were no significant differences with respect to age, sex, education, income level, occupation, or smoking history among the groups (P >0.05). There were no significant differences between the non‐periodontitis and CP groups for any of the psychosocial scales (P >0.05). Group 3 had significantly higher mean DHEA scores compared with group 1 (P <0.05); however, the median cortisol scores showed no statistically significant differences among the three groups (P >0.05). Conclusions: Anxiety/depression scores and GCF cortisol levels did not show any difference with regard to clinical periodontal status. However, a significant association was found between elevated levels of GCF DHEA and the severity of periodontitis.     

Does Obstructive Sleep Apnea Increase the Risk for Periodontal Disease? A Case‐Control Study

Background: A possible association between periodontitis and obstructive sleep apnea (OSA) has been suggested. The aim of this study is to compare periodontitis prevalence between controls and patients with OSA by assessing clinical periodontal parameters and gingival crevicular fluid (GCF) levels of interleukin (IL)‐1β, tumor necrosis factor (TNF)‐α, and high‐sensitive C‐reactive protein (hs‐CRP); serum hs‐CRP was also sampled. Methods: A case‐control study was performed that included 163 individuals: 83 individuals (18 females and 65 males) with OSA and 80 non‐OSA individuals (23 females and 57 males) as controls. The test group was classified according to OSA severity. Clinical periodontal measurements were recorded, and GCF samples were collected. GCF hs‐CRP, IL‐lβ, and TNF‐α levels were analyzed using an enzyme‐linked immunosorbent assay method. Serum hs‐CRP was measured by latex‐enhanced immunoturbidimetric assay. Results: Prevalence of periodontitis in the OSA group (96.4%) was significantly higher than in the control group (75% [P <0.001]). Severe periodontitis prevalence was higher in the OSA group than control group. All periodontal clinical parameters and GCF IL‐lβ concentrations were significantly higher in patients with OSA than in controls (P = 0.001). No significant differences were found between the mild OSA and moderate‐to‐severe OSA groups. Additionally, there was no significant difference in GCF TNF‐α and hs‐CRP levels between the groups (P >0.05). Serum hs‐CRP levels were significantly higher in patients with OSA. A significant correlation was found between GCF IL‐1β and all clinical parameters. Conclusions: Results demonstrated higher prevalence of periodontitis and higher levels of GCF IL‐1β and serum hs‐CRP in patients with OSA. However, there is still a need for randomized clinical trials testing oral care interventions.     

Clinical and Microbiologic Evaluation of Scaling and Root Planing per Quadrant and One‐Stage Full‐Mouth Disinfection Associated With Azithromycin or Chlorhexidine: A Clinical Randomized Controlled Trial

Background: Conflicting data about the protocol of choice for non‐surgical periodontal therapy with adjuvant use are still reported. This study aims to evaluate, through clinical and microbiologic parameters, the systemic use of azithromycin (AZ) and chlorhexidine (CHX) as adjuvants to non‐surgical periodontal treatment performed by one‐stage full‐mouth disinfection (FMD) within 24 hours or conventional quadrant scaling (QS) in four weekly sections. Methods: In this randomized controlled trial, 85 patients diagnosed with chronic periodontitis underwent different treatment protocols, in six groups: three FMD groups and three QS groups, each with no adjuvants, with CHX, and with AZ. Clinical periodontal parameters were recorded, and total and quantitative bacterial counts of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Streptococcus oralis were measured with real‐time polymerase chain reaction at baseline and 90 and 180 days after treatment. Results: In all groups, a significant reduction was observed in the percentage of periodontal diseased sites, gingival index, plaque index, and clinical attachment level gain at 90 days, demonstrating effectiveness of the treatment, independently of the adjuvant. The FMD with CHX group showed higher reduction in probing depth and percentage of periodontal diseases sites, as well as lower total bacterial count, than all the other groups at 180 days. Conclusions: The adjuvant use of AZ did not provide any significant benefit, independently of the treatment protocol. The adjuvant use of CHX showed a more expressive and significant improvement in clinical and microbiologic parameters, especially in the FMD protocol, followed by QS.     

Effects of non-surgical periodontal treatment on clinical response, serum inflammatory parameters, and metabolic control in patients with type 2 diabetes: a randomized study

Background: Scientific evidence on the effects of chronic periodontitis on diabetes mellitus remains inadequate and inconclusive. This intervention study is designed to evaluate the effects of periodontal treatment on clinical response, systemic inflammatory parameters, and metabolic control in patients with Type 2 diabetes. Methods: A total of 134 patients were randomly allocated into two treatment groups and one control group. Treatment group 1 underwent non‐surgical periodontal treatment at baseline and additional subgingival debridement at the 3‐month follow‐up. Patients in treatment group 2 received non‐surgical periodontal treatment and supragingival prophylaxis at the 3‐month follow‐up, and those in the control group received no intervention throughout the study. All participants were reexamined at 1.5, 3, and 6 months after initial treatment. At each visit, clinical periodontal examinations were conducted and blood samples were taken to evaluate high‐sensitivity C‐reactive protein (hsCRP), tumor necrosis factor‐α (TNF‐α), glycated hemoglobin (HbA1c), fasting plasma glucose (FPG), and lipid profiles. Results: Both treatment groups had a significantly lower hsCRP level after periodontal therapy (P <0.05). Although HbA1c declined significantly in treatment group 2 (P <0.05), the intergroup difference for HbA1c, FPG, TNF‐α, and lipid profiles was not statistically significant after therapy (P >0.05). Conclusions: Non‐surgical periodontal treatment can effectively improve periodontal and circulating inflammatory status. Despite a lack of strong evidence, trends in some results support improved glycemic control after periodontal treatment in patients with diabetes.     

8‐Hydroxy‐Deoxyguanosine Levels in Gingival Crevicular Fluid and Saliva in Patients With Chronic Periodontitis After Initial Periodontal Treatment

Background: This study evaluates the effects of initial periodontal treatment on the gingival crevicular fluid (GCF) and salivary levels of 8‐hydroxy‐deoxyguanosine (8‐OHdG) as a marker of oxidative deoxyribonucleic acid (DNA) damage in patients with chronic periodontitis (CP). Methods: At baseline, clinical parameters were determined and GCF and saliva samples were obtained from 24 patients with CP and 24 individuals with clinically healthy periodontium. GCF, saliva samples, and clinical periodontal measurements were repeated at day 10, 1 month, and 3 months following initial periodontal therapy in patients with CP. 8‐OHdG levels of GCF and saliva samples were investigated by using an enzyme‐linked immunosorbent assay. Results: Statistically significant higher 8‐OHdG levels of GCF and a significant decrease after initial periodontal therapy were determined in the CP group (P <0.001). A significant positive correlation was found between 8‐OHdG levels of GCF and clinical periodontal measurements (P <0.001). However, salivary levels of 8‐OHdG did not differ between groups or during initial periodontal therapy (P >0.05). Conclusions: This study reveals that DNA injury and oxidative stress increase in tissue cells and especially in periodontal pockets in patients with CP, and the periodontal treatment results in a significant decrease of 8‐OHdG levels in the GCF samples. To the best of our knowledge, this study evaluates for the first time, 8‐OHdG levels in GCF, which is shown to be more useful as a biomarker than saliva. 8‐OHdG was found to be important and may reveal the severity of periodontal disease and the effect of periodontal therapy.     

Effect of MMP-1 promoter polymorphisms on GCF MMP-1 levels and outcome of periodontal therapy in patients with severe chronic periodontitis

Aims: The aims of this study were to investigate (1) the matrix metalloproteinase‐1 (MMP‐1) promoter polymorphisms in severe chronic periodontitis (CP), (2) the relationship of periodontal therapy outcome with these genotypes, and (3) the gingival crevicular fluid (GCF) MMP‐1 levels–MMP‐1 genotype correlation. Material and Methods: Genomic DNA was obtained from the peripheral blood of 102 patients with severe CP and 98 periodontally healthy subjects. MMP‐1 ?519A/G and ?1607 1G/2G polymorphisms were determined by the polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) method. Fifty‐eight CP patients received non‐surgical periodontal therapy and were followed for 6 months. Clinical periodontal parameters and GCF samples were collected at baseline and at 6 months. GCF MMP‐1 levels were analysed by enzyme‐linked immunosorbent assay (ELISA). Results: The distribution of MMP‐1 genotypes did not significantly differ between the study groups. On the other hand, the ?1607 2G allele frequency of severe CP patients was higher than that of healthy subjects. MMP‐1 ?519G allele carriers had higher GCF MMP‐1 levels and percentage of sites with 4–6 mm clinical attachment level (CAL) compared with AA genotypes after non‐surgical periodontal therapy (p<0.05). Conclusions: These data suggest that the ?1607 2G polymorphic allele of the MMP‐1 gene could be associated with susceptibility to severe CP in the Turkish population. It seems that ?519AG and GG genotypes could play a role in the outcome of periodontal therapy.     

Clinical and Immunoinflammatory Evaluation of One‐Stage Full‐Mouth Ultrasonic Debridement as a Therapeutic Approach for Smokers With Generalized Aggressive Periodontitis: A Short‐Term Follow‐Up Study

Background: This study aims to evaluate the effect of one‐stage full‐mouth ultrasonic debridement (OSFMUD) on clinical and immunoinflammatory parameters in smokers with generalized aggressive periodontitis (GAgP). Methods: Fourteen smoking and 14 non‐smoking patients with GAgP were selected. After initial supragingival therapy, patients were treated by OSFMUD. Full‐mouth parameters evaluated were: 1) plaque index (PI); 2) bleeding scores (BS); 3) probing depth (PD); and 4) clinical attachment level (CAL). Clinical evaluation was performed, and gingival crevicular fluid (GCF) was collected for selected sites (ss) at baseline and 1, 3, and 6 months. GCF was analyzed via enzyme‐linked immunosorbent assay for: 1) receptor activator of nuclear factor‐κ B ligand (RANKL); 2) osteoprotegerin (OPG); 3) interleukin (IL)‐6; and 4) tumor necrosis factor (TNF)‐α, whereas secreted osteoclastogenic factor of activated T‐cells (SOFAT) was evaluated by Western blotting. Results: Significant reduction (P <0.05) was observed between baseline and 6 months for: 1) PI; 2) BS; and 3) PD, with no difference between smoking and non‐smoking patients (P >0.05). Regarding CAL, only non‐smoking patients showed a significant decrease (P <0.05). Significant reduction (P <0.05) was observed in both groups for: 1) PIss; 2) PDss; 3) bleeding on probing; and 4) relative CAL. Smoking and non‐smoking patients presented significantly decreased levels of IL‐6 and TNF‐α over time (P <0.05); however, no difference was observed between groups (P >0.05). RANKL was significantly different (P <0.05) only for non‐smokers at 6 months, whereas OPG was not significant (P >0.05). SOFAT expression was significantly lower (P <0.05) after OSFMUD for non‐smokers only. Conclusion: Considering the clinical and immunoinflammatory parameters evaluated in this short‐term follow‐up study, it can be concluded that OSFMUD can be used as an alternative treatment for smokers with GAgP.     

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

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

Gingival Crevicular Fluid Levels of Sclerostin,Osteoprotegerin, and Receptor Activator of Nuclear Factor‐κB Ligand in Periodontitis

Background: To investigate changes in the levels and relative ratios of sclerostin, osteoprotegerin (OPG), and receptor activator of nuclear factor‐κB ligand (RANKL) in the gingival crevicular fluid (GCF) of patients with periodontitis after non‐surgical periodontal treatment. Methods: Fifty‐four individuals (27 healthy controls and 27 patients with chronic periodontitis [CP]) were enrolled in the study. Periodontitis patients received non‐surgical periodontal therapy. GCF sampling and clinical periodontal parameters were assessed before and 6 weeks after therapy. Sclerostin, OPG, and RANKL levels were measured by enzyme‐linked immunosorbent assay, and their relative ratios were calculated. Results: Total amounts and concentrations of sclerostin were significantly higher in patients with CP than in healthy individuals (P <0.025) and decreased after treatment (P <0.05). The RANKL/OPG ratio was significantly lower in healthy individuals than in patients with periodontitis before and after treatment (P <0.025), but no significant difference was observed in patients with periodontitis after treatment (P >0.05). The sclerostin/OPG and sclerostin/RANKL ratios were significantly lower in healthy individuals than in patients with periodontitis before and after treatment (P <0.025) and decreased in patients with periodontitis after treatment (P <0.05). Conclusions: The GCF sclerostin level may be more reliable than the RANKL/OPG ratio as a diagnostic and prognostic marker of periodontal disease and treatment outcome. Regulation of sclerostin levels may aid the development of new therapeutic strategies for the treatment of periodontal disease.