Avani Rangaraju Pradeep

Background: Simvastatin (SMV) assists in bone regeneration and has an anti‐inflammatory effect when delivered or applied locally. The present clinical trial is designed to investigate the effectiveness of 1.2‐mg SMV as a local drug delivery system as an adjunct to scaling and root planing (SRP) for the treatment of Class II furcation defects.Methods: Seventy‐two patients with mandibular buccal Class II furcation defects were randomized and categorized into two treatment groups: SRP plus placebo (group 1) and SRP plus 1.2‐mg SMV (group 2). Clinical parameters were recorded at baseline before SRP and at 3 and 6 months; they included modified sulcus bleeding index (mSBI), probing depth (PD), and relative vertical (RVAL) and horizontal (RHAL) attachment levels. At baseline and after 6 months, radiologic assessment of bone defect fill was performed.Results: Both therapies resulted in significant improvements. The decrease in mSBI score at 6 months was greater in group 2 (2.02 ± 0.23) compared with group 1 (1.80 ± 0.22). The mean decrease in PD at 6 months was 1.30 ± 1.0 and 4.05 ± 1.31 mm in groups 1 and 2, respectively. A significantly greater gain in mean RVAL and RHAL was found in group 2 than in group 1 (P Conclusion: Locally delivered SMV provides a comfortable and flexible method to improve clinical parameters and also to enhance bone formation.

Background: Levels of visfatin in serum and gingival crevicular fluid (GCF) were explored in patients with periodontal health, periodontal disease with and without type 2 diabetes mellitus (t2 DM) and were found to be elevated with periodontal disease, and were correlated with periodontal clinical parameters. DM and chronic periodontitis (CP) are associated with each other. Adipokines, specifically visfatin, are secreted from adipocytes and are thought to cause insulin resistance. The purpose of this study is to determine the presence of visfatin in serum and GCF in t2 DM among individuals with CP and to find an association, if any.Methods: Thirty individuals (15 males and 15 females) were selected based on their clinical parameters into three groups: group 1 (10 healthy), group 2 (10 well‐controlled t2 DM among individuals with CP), and group 3 (10 individuals with CP and without diabetes). Serum and GCF samples were collected to estimate the levels of visfatin using enzyme linked immunosorbent assay.Results: The mean visfatin concentration increased in both serum and GCF in individuals with t2 DM with CP. Also, it was observed that visfatin in both serum and GCF correlated positively with all the periodontal parameters.Conclusions: All the samples in each group tested positive for visfatin assay. Serum and GCF visfatin concentration in both t2 DM with CP and individuals with CP and without diabetes correlated positively with all the clinical parameters. Additional large‐scale longitudinal studies should be performed to confirm positive correlations.

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 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.

Pentraxins are classical mediators of inflammation and markers of acute-phase reactions. Pentraxin-3 (PTX3) is believed to be a true independent indicator of disease activity. It has been associated with clinical outcomes in incident chronic kidney disease (CKD) and periodontal diseases. Periodontitis is lately being considered as a risk factor for CKD. However, no data are available on elevated PTX3 in patients with CKD associated with periodontitis.

Background: Pentraxins are classic mediators of inflammation and markers of acute‐phase reactions. Pentraxin‐3 (PTX3) is the first‐identified long pentraxin and is believed to be a true independent indicator of disease activity. Although a classic pentraxin, C‐reactive protein, and its association with various systemic diseases is well documented in the periodontal literature, there is no data on PTX3 to our knowledge.Methods: Forty participants (20 males and 20 females; age range: 23 to 50 years) were involved in the study. Participants were divided into three groups based on gingival index, probing depth, and clinical attachment level: the healthy group (group 1; n = 10), gingivitis group (group 2; n = 15), and periodontitis group (group 3; n = 15). Gingival crevicular fluid (GCF) and plasma samples collected from each subject were quantified for PTX3 levels using an enzyme‐linked immunosorbent assay.Results: In tandem with the disease progression from healthy to gingivitis to periodontitis, the mean PTX3 concentrations increased in GCF and plasma. However, GCF values were higher than plasma values. It was found that PTX3 concentration was highest in group 3 and lowest in group 1. PTX3 concentrations also correlated positively with periodontal parameters.Conclusions: GCF and plasma PTX3 concentrations correlated positively in all groups. However, within the limits of the present study, the differences in plasma PTX3 levels were not found to be statistically significant. Hence, GCF PTX3 values were considered a marker of inflammatory activity in periodontal disease. However, PTX3 deserves further consideration as a therapeutic target. Additional large‐scale studies should be carried out to confirm positive correlations.

Aim: Increased C-reactive protein levels have been found in all active inflammations, including periodontitis. This study aims to assess the C-reactive protein levels in periodontal disease progression. Methods: Forty-five patients were divided into the following three groups (n = 15) based on gingival index, probing pocket depth, and clinical attachment level: healthy (group I), gingivitis (group II), and chronic periodontitis (group III). Gingival crevicular fluid and serum samples were quantified for C-reactive protein using enzyme-linked immunosorbent assay. Results: The mean C-reactive protein concentration in gingival crevicular fluid and serum was found to be highest in group III (1233.33 ng/mL for gingival crevicular fluid, 5483.33 ng/mL for serum), and least in group I (60 ng/mL and 413 ng/mL for gingival crevicular fluid and serum, respectively) The mean C-reactive protein concentration in group II (453.33 ng/mL for gingival crevicular fluid and 3565.33 ng/mL for serum) was found to be intermediate. Conclusions: C-reactive protein levels in gingival crevicular fluid and serum increased proportionately with the severity of periodontal disease. They correlated positively with clinical parameters, including gingival index, probing pocket depth, and clinical attachment level. Thus, it can be considered as a periodontal inflammatory biomarker and deserves further consideration.

The purpose of this article is to report a case of pemphigus vulgaris associated with periodontitis (plaque-induced inflammation), and the role of a dermatologist and a periodontist in its management. This case reaffirms the fact that plaque control is the most important procedure in preventing periodontal infection in pemphigus vulgaris patients. These patients should be informed about the risk of periodontitis and encouraged to pursue long-term periodontal follow up to prevent their periodontal disease progression.

Chronic infections have been reported to be risk factors for coronary heart disease and ischemic stroke. However, the association of coronary heart disease and ischemic stroke with periodontal disease, which is also a chronic inflammatory disease, needs to be evaluated. The present case-control study was designed to determine if an association exists between periodontal disease and cerebrovascular accident in the Indian population. This case-control study consisted of 200 subjects (100 cases and 100 controls) who were 33-68 years of age. Cases were examined within 5 d after their first acute ischemic attack. Clinical parameters recorded included plaque index, gingival index, probing pocket depth and clinical attachment loss. The medical questionnaire collected information on family history of stroke, dietary history, history of smoking and history of alcohol consumption. Cases were additionally scrutinized for diabetes, hypertension and total serum cholesterol level. The education level of patients was also considered. The mean plaque index, gingival index, probing pocket depth and clinical attachment loss values of subjects with cerebrovascular accident were significantly higher when compared with those of the control group (p < 0.05). In fully adjusted logistic regression analysis, a probing pocket depth of > 4.5 mm was found to be the most significant factor for stroke (odds ratio = 8.5; confidence interval = 1.1-68.2) followed by hypertension (odds ratio = 7.6; confidence interval = 3.3-17.1) and smoking (odds ratio = 3.1; confidence interval = 1.3-7.4). The data from this study support the proposed link between periodontitis and cerebrovascular accident in the Indian population. However, further studies are necessary to verify and quantify the role of oral infections and genetic factors in the process of atherosclerosis.

Background: Interleukin (IL)‐18 is a proinflammatory cytokine of the IL‐1 superfamily and is unique, with the capacity to induce T‐helper (Th)1 or Th2 differentiation depending on the immunologic context. Monocyte chemoattractant protein (MCP)‐1 is a CC chemokine responsible for chemotaxis of monocytes. A previous study showed the induction of MCP‐1 by IL‐18 in mice macrophages. The present study was carried out to examine the gingival crevicular fluid (GCF) levels of IL‐18 and MCP‐1 in periodontal health and disease and to evaluate any correlation between IL‐18 and MCP‐1 GCF levels.Methods: Sixty subjects (30 males and 30 females; age range: 26 to 49 years) participated in the study. The subjects were initially divided into three groups, consisting of 20 subjects in each group, based on the gingival index, probing depth (PD), clinical attachment loss (AL), and radiologic parameters (bone loss): healthy (group 1), gingivitis (group 2), and periodontitis (group 3), whereas patients in group 3 after treatment constituted group 4. GCF samples were collected from all of the groups to estimate the levels of IL‐18 and MCP‐1 using enzyme‐linked immunosorbent assay.Results: The mean IL‐18 and MCP‐1 concentrations in GCF were highest in group 3 (330.61 pg/μl and 73.3 pg/μl, respectively). The results suggest that IL‐18 and MCP‐1 levels increased in GCF from periodontal health to disease and decreased after periodontal therapy. Levels of IL‐18 and MCP‐1 positively correlated with PD and clinical AL in group 3. In addition, IL‐18 and MCP‐1 levels significantly correlated with each other in groups 2, 3, and 4.Conclusions: GCF IL‐18 and MCP‐1 concentrations increased in periodontal disease compared to health and correlated positively with the severity of disease. Further, based on the positive correlation of IL‐18 and MCP‐1 found in this study, it can be proposed that IL‐18 may promote an inflammatory response by the induction of MCP‐1 production and the subsequent recruitment and activation of circulating leukocytes at the inflammatory site.