Intensive Periodontal Therapy Research Articles

Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets.

Background“Quantile-dependent expressivity” occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g., C-reactive protein, CRP) is high or low relative to its distribution. We have previously shown that the heritabilities (h2) of coffee and alcohol consumption, postprandial lipemia, lipoproteins, leptin, adiponectin, adiposity, and pulmonary function are quantile-specific. Whether CRP heritability is quantile-specific is currently unknown.MethodsSerum CRP concentrations from 2,036 sibships and 6,144 offspring-parent pairs were analyzed from the Framingham Heart Study. Quantile-specific heritability from full-sib (βFS, h2 ={(1 + 8rspouseβFS)0.5 − 1}/(2rspouse)) and offspring-parent regression slopes (βOP, h2 = 2βOP/(1 + rspouse)) were estimated robustly by quantile regression with nonparametric significance determined from 1,000 bootstrap samples.ResultsQuantile-specific h2 (±SE) increased with increasing percentiles of the offspring’s age- and sex-adjusted CRP distribution when estimated from βOP (Ptrend = 0.0004): 0.02 ± 0.01 at the 10th, 0.04 ± 0.01 at the 25th, 0.10 ± 0.02 at the 50th, 0.20 ± 0.05 at the 75th, and 0.33 ± 0.10 at the 90th percentile, and when estimated from βFS (Ptrend = 0.0008): 0.03±0.01 at the 10th, 0.06 ± 0.02 at the 25th, 0.14 ± 0.03 at the 50th, 0.24 ± 0.05 at the 75th, and 0.53 ± 0.21 at the 90th percentile.ConclusionHeritability of serum CRP concentration is quantile-specific, which may explain or contribute to the inflated CRP differences between CRP (rs1130864, rs1205, rs1800947, rs2794521, rs3091244), FGB (rs1800787), IL-6 (rs1800795, rs1800796), IL6R (rs8192284), TNF-α (rs1800629) and APOE genotypes following CABG surgery, stroke, TIA, curative esophagectomy, intensive periodontal therapy, or acute exercise; during acute coronary syndrome or Staphylococcus aureus bacteremia; or in patients with chronic rheumatoid arthritis, diabetes, peripheral arterial disease, ankylosing spondylitis, obesity or inflammatory bowel disease or who smoke.

Chronic Periodontitis and Hypertension:A Systematic Review

Aim: To conduct a systematic review evaluating associations between periodontal disease and hypertension. Method: A MEDLINE literature search of papers published between 2000 and March 2016 was conducted. Cross-sectional studies, prospective studies and nested case-control studies that studied the association between periodontitis and hypertension formed the mainstay of this literature review. This systematic review was conducted on the guidelines of the Cochrane Systematic Reviews and the conclusive evidence was based on the Canadian task force on preventive health care guidelines. Results: A total of 21 articles were searched for relevancy, determined by article title, abstract and full copy, resulting in a yield of 17 studies that met our inclusion criteria. 1) There is a fair evidence (II-2 Grade B recommendation) for an association between chronic periodontitis and blood pressure with OR of 2.93 (95% CI:1.25-6.84) but the association becomes stronger when restricted with those with hypertension or taking anti-hypertensive medications: OR = 4.20(95% CI:1.28-13.80). 2) A good evidence (I, Grade A recommendation) that intensive periodontal therapy decrease cardiovascular risk scores (Framingham) at 296 mm (1.53% F 1.20% (95% CI 1.05-2.24, P = .0290) and 2.00% F 1.42% (95% CI 0.98-4.09, P = .0568). Conclusions: With the available literature we conclude that, 1. There is a fair evidence for an association between chronic periodontitis and hypertension. 2. Intensive periodontal therapy reduces the systemic inflammatory markers and systolic blood pressure imminently at 6 months after the end of periodontal treatment.

Metabolic syndrome and periodontal disease: An overview for physicians.

The metabolic syndrome (MetS) (also known as insulin resistance syndrome, syndrome X) is a cluster of factors associated with increased risk of developing coronary heart disease or type 2 diabetes mellitus. Several studies in the past have reviewed an association between MetS and periodontitis. Periodontal disease is considered an infectious and chronic inflammatory disease, and it has been considered to be a potential risk in cardiovascular and respiratory diseases and diabetes, and has implications in adverse pregnancy outcomes, osteoporosis, and so on. These systemic disorders have been documented as capable of affecting the periodontium or treatment of periodontal disease. Oral inflammatory lesions have different basic mechanisms concerning the possible association with systemic diseases. They concern local spread, metastatic spread, or immunologic cross-reactivity. In many studies, sometimes contrasting, periodontal pathogens have been evaluated in atheromatous plaques isolated from patients with chronic periodontitis. Oral inflammatory lesions have been shown unequivocally to contribute to elevated systemic inflammatory responses. In some studies, intensive periodontal therapy showed a significant reduction in c-reactive protein levels, interleukin-6, and low-density lipoprotein cholesterol after 2 months. The aim of this article is to reflect the association between MetS and periodontitis and to suggest an understanding to promote interprofessional practice; with proper oral care and plaque control, we can reduce the severity of MetS.

Effect of Intensive Periodontal Therapy on Blood Pressure and Endothelial Microparticles in Patients With Prehypertension and Periodontitis: A Randomized Controlled Trial.

Although some studies show a positive association between periodontitis and blood pressure (BP) elevation, research on the effect of intensive periodontal treatment on decline in BP levels and endothelial microparticles (EMPs) without any antihypertensive management is lacking. Therefore, the present clinical trial explores whether intensive periodontal therapy would lower BP levels and EMPs of patients with prehypertension with periodontitis. From a total 107 patients, 95 underwent randomization (47 assigned to control-treatment [CT] group and 48 assigned to intensive-treatment [IT] group) and completed the trial. Patients received intervention for 4 consecutive weeks and were followed for 6 months. Levels of BP and EMPs were evaluated at baseline and 1, 3, and 6 months after intervention. Periodontal conditions were significantly improved (P <0.05) 6 months after intensive periodontal treatment. In parallel, the primary outcomes including systolic and diastolic BP and EMPs were markedly reduced in the IT group compared with the CT group (absolute difference: 12.57 and 9.65 mm Hg and 581.59/μL, respectively; 95% confidence intervals: 10.45 to 14.69, 7.06 to 12.24, and 348.12 to 815.06, respectively; P <0.05). Reduction in BP levels and EMPs was related to improvement in probing depth (r = 0.358, 0.363, and 0.676, respectively, by the Pearson product-moment correlation; P = 0.009, 0.008, and P <0.001, respectively). To the best knowledge of the authors, the present study demonstrates for the first time that intensive periodontal intervention without any antihypertensive medication therapy may be an effective means to lower levels of BP and EMPs in patients with prehypertension with periodontitis.

A Randomized Controlled Trial of Intensive Periodontal Therapy on Metabolic and Inflammatory Markers in Patients With ESRD: Results of an Exploratory Study

A Randomized Controlled Trial of Intensive Periodontal Therapy on Metabolic and Inflammatory Markers in Patients With ESRD: Results of an Exploratory Study

A Randomized Controlled Trial of Intensive Periodontal Therapy on Metabolic and Inflammatory Markers in Patients With ESRD: Results of an Exploratory Study

Periodontitis is a novel risk factor for inflammation and cardiovascular disease in the dialysis population. Limited information exists about the impact of periodontal therapy in patients receiving dialysis. Randomized controlled trial to assess feasibility and gather preliminary data. Dialysis patients with moderate/severe chronic periodontitis. Intensive treatment, consisting of scaling and root planing, extraction of hopeless teeth, and placement of local-delivery antibiotics, was performed at the baseline visit for treatment-group patients and after study completion for control-group patients. Outcomes were feasibility (screening, recruitment, enrollment, adverse events, and study withdrawal/completion), clinical periodontal parameters (probing depth, clinical attachment level, bleeding on probing, gingival index, and plaque index), and serum albumin and interleukin 6 levels at 3 and 6 months postintervention. 342 dialysis patients were approached for participation: 53 were randomly assigned, with 26 participants assigned to immediate treatment and 27 assigned to a control arm for treatment after 6 months. 51 patients completed baseline appointments; 46 were available for 3-month follow-up, 45 were available for 6-month follow-up examinations, and 43 completed all visits. At 3 months, there was a statistically significant improvement for the treatment group compared to the control group for 3 periodontal parameters: mean probing depth (P = 0.008), extent of probing depth ≥4 mm (P = 0.02), and extent of gingival index ≥1 (P = 0.01). However, by 6 months, the difference between groups was no longer present for any variable except probing depth ≥4 mm (P = 0.04). There was no significant difference between groups for serum albumin or high-sensitivity interleukin 6 level at any time when adjusted for body mass index, diabetic status, and plaque index. Small sample size and relatively healthy population, imbalance in diabetes. This small trial demonstrates successful cooperation between dentists and nephrologists and successful recruitment, treatment, and retention of dialysis patients with periodontitis. Larger studies with longer follow-up are needed to determine whether treatment can improve markers of inflammation and morbidity.

Short-term effects of intensive non-surgical periodontal therapy and low-dose doxycycline on serum levels of IL-6, TNF-α and lipid profile in advanced periodontitis

Adjunctive use of sub-antimicrobial dose doxycycline (SDD) is a mode of host modulation therapy for periodontitis. However, the potential of SDD for moderating serum inflammatory mediators has not been investigated extensively. This study evaluated the effects of intensive scaling and root planning (ITSRP) ± SDD on the serum levels of tumor necrosis factor-alpha (TNF-, interleukin-6 (IL-6) and lipid profile in advanced periodontitis. Forty systemically healthy patients were randomly assigned into two groups to take either a placebo or an SDD adjunctive to ITSRP in a double-blind controlled clinical trial. At baseline and after 4 weeks, we collected blood samples and recorded clinical indices. Statistically significant changes in TNF- and IL-6 serum levels did not occur in either group compared to baseline. A significant increase in high-density lipoprotein (HDL) cholesterol levels and a decrease in white blood cell counts were observed in the SDD group. Between groups, significantly greater improvements in pocket depth, clinical attachment level, mean number of pockets ≥ 7 mm and IL-6 alteration occurred in the SDD group. This study demonstrated the effectiveness of combining ITSRP with SDD in gaining periodontal attachment, IL-6 alteration and HDL cholesterol levels over ITSRP alone. Adjunctive use of SDD is likely to have a protective role against vascular events by mediating patient HDL levels. Further investigation among a high-risk population is recommended. Key words: Double-blind method, doxycycline, inflammatory mediators, cholesterol high-density lipoprotein (HDL), periodontitis, root planning, serum.

The effect of a periodontal intervention on cardiovascular risk markers in Indigenous Australians with periodontal disease: the PerioCardio study

BackgroundIndigenous Australians experience an overwhelming burden of chronic disease, including cardiovascular diseases. Periodontal disease (inflammation of the tissues surrounding teeth) is also widespread, and may contribute to the risk of cardiovascular diseases via pathogenic inflammatory pathways. This study will assess measures of vascular health and inflammation in Indigenous Australian adults with periodontal disease, and determine if intensive periodontal therapy improves these measures over a 12 month follow-up. The aims of the study are: (i) to determine whether there is a dose response relationship between extent and severity of periodontal disease and measures of vascular health and inflammation among Indigenous Australian adults with moderate to severe periodontal disease; and (ii) to determine the effects of periodontal treatment on changes in measures of vascular health and inflammation in a cohort of Indigenous Australians.Methods/DesignThis study will be a randomised, controlled trial, with predominantly blinded assessment of outcome measures and blinded statistical analysis. All participants will receive the periodontal intervention benefits (with the intervention delayed 12 months in participants who are randomised to the control arm). Participants will be Indigenous adults aged ≥25 years from urban centres within the Top End of the Northern Territory, Australia. Participants assessed to have moderate or severe periodontal disease will be randomised to the study's intervention or control arm. The intervention involves intensive removal of subgingival and supragingival calculus and plaque biofilm by scaling and root-planing. Study visits at baseline, 3 and 12 months, will incorporate questionnaires, non-fasting blood and urine samples, body measurements, blood pressure, periodontal assessment and non-invasive measures of vascular health (pulse wave velocity and carotid intima-media thickness). Primary outcome measures are pulse wave velocity and carotid intima-media thickness.DiscussionThe study will assess the periodontal-cardiovascular disease relationship among Indigenous Australian adults with periodontal disease, and the effectiveness of an intervention aimed at improving periodontal and cardiovascular health. Efforts to understand and improve Indigenous oral health and cardiovascular risk may serve as an important means of reducing the gap between Indigenous and non-Indigenous health in Australia.Trial RegistrationAustralia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12610000817044

Effects of periodontal therapy on glucose management in people with diabetes mellitus

AimThe primary aim of this study was to examine the effects of intensive periodontal therapy on HbA1c in a mixed diabetes mellitus (DM) (types 1 and 2) population with moderate periodontitis (PD). MethodsA total of 93 subjects with PD and DM, recruited from referrals to the Department of Endocrinology at the Perugia Hospital, were included in a follow-up cohort clinical study comprising two parallel periodontal therapy groups—one receiving intensive periodontal therapy (IPT, n=44) and the other serving as controls (CPT, n=49)—with an 8-month follow-up. Clinical periodontal examinations and blood samples were collected 4 and 8months after the completion of therapy. ResultsThe IPT group presented with greater reductions of all periodontal indices compared with the CPT group at both follow-ups (P<0.001). Whereas, after 4months, there were no major differences in HbA1c levels between groups, after 8months, the IPT group presented with a 0.57% (95% CI: 0.12 to 1.09) greater reduction in HbA1c than the CPT group (P=0.03). This reduction was independent of age, gender, smoking and body mass index. However, the difference in HbA1c was greater in individuals with type 2 DM (0.95% reduction, 95% CI: 0.32 to 1.58; P=0.004) compared with those with type 1 DM. ConclusionIPT resulted in greater improvement of gingival health in patients with DM. Improved oral health in those with type 2 DM may have an effect on medium-term glucose management and could possibly lead to long-term health benefits. (ISRCTN00559156).

Periodontitis and risk for atherosclerosis: an update on intervention trials

Periodontitis has been associated with an increased risk of cardiovascular events. The nature of the association is unclear because both periodontitis and cardiovascular disease (CVD) share a host of risk factors. Intervention trials are critical to explore the relationship. If the association were causal, successful periodontal therapy will lead to an attenuation of the effect - CVD. The paper reviewed the design and the results of intervention trials aimed at improving systemic inflammation, endothelial dysfunction, carotid atherosclerosis and cardiovascular events. Early systematic reviews and a definitive controlled clinical trial indicate that intensive periodontal therapy results in a decrease in systemic inflammation and an improvement of endothelial dysfunction in systemically healthy subjects. A pilot trial has indicated the feasibility to assess the impact of periodontal therapy on carotid atherosclerosis in a primary cardiac prevention design. Efforts to test causality in the relationship between periodontitis and CVD are ongoing. Evidence to date is consistent with the notion that severe generalized periodontitis causes systemic inflammation and endothelial dysfunction. Periodontitis has effects that go beyond the oral cavity and its treatment and prevention may contribute to the prevention of atherosclerosis.

Cardiovascular disease and periodontitis: an update on the associations and risk

Associations between periodontitis and cardiovascular diseases have been recognized. New literature since the last European Workshop on Periodontology has been reviewed. The lack of reliable epidemiological data on disease prevalence makes an assessment of the associations and risks between periodontitis and cardiovascular diseases difficult. Two recent meta-analysis reports have identified associations between periodontitis and cardiovascular diseases (odds ratios: 1.1-2.2). Different surrogate markers for both disease entities, including serum biomarkers, have been investigated. Brachial artery flow-mediated dilatation, and carotid intima media thickness have in some studies been linked to periodontitis. Studies are needed to confirm early results of improvements of such surrogate markers following periodontal therapy. While intensive periodontal therapy may enhance inflammatory responses and impair vascular functions, studies are needed to assess the outcome of periodontal therapies in subjects with confirmed cardiovascular conditions. Tooth eradication may also reduce the systemic inflammatory burden of individuals with severe periodontitis. The role of confounders remain unclear. Periodontitis may contribute to cardiovascular disease and stroke in susceptible subjects. Properly powered longitudinal case-control and intervention trials are needed to identify how periodontitis and periodontal interventions may have an impact on cardiovascular diseases.

Association of Serum Interleukin-6 Concentration with a Functional IL6 −6331T&amp;gt;C Polymorphism

Interleukin-6 (IL-6) concentrations vary substantially among individuals. This study aimed to identify novel genetic markers to explain these differences. We sequenced a region 6-kb upstream of the IL6 [interleukin 6 (interferon, beta 2)] transcription start site in a search for functional variants and detected 3 common variants: -6331T>C, -6101A>T, and -5617/-5616C/A>T/G. IL6 -6331T>C (C allele frequency, 0.20; 95% confidence interval, 0.16-0.24) showed strong negative linkage disequilibrium with -174G>C (D' = -0.97) and was studied further in 309 individuals who underwent coronary artery bypass grafting. Patients with the TT genotype had higher IL-6 concentrations 6 h after surgery than those with the CC genotype (mean, 199.4 ng/L vs 114.9 ng/L; P = 0.02). A similar association was seen in a cohort of 173 patients who underwent intensive periodontal therapy: Individuals with the CC genotype had significantly lower IL-6 concentrations 24 h after therapy than TT patients (mean, 0.78 ng/L vs 5.00 ng/L; P < 0.0001). A similar trend was observed in 203 healthy individuals from northern Europe (1.29 ng/L for the TT genotype vs 0.89 ng/L for the CC genotype; P = 0.07). Reporter assays that used a sequence flanking the -6331 single-nucleotide polymorphism spliced upstream to the IL-6 minimal promoter driving luciferase gene expression demonstrated a 1.3-fold increase in promoter activity (P < 0.01) for constructs containing -6331T. Electrophoretic mobility shift assays revealed enhanced binding of transcription factor Oct-1 to the T allele. IL6 -6331T is associated with increased IL-6 concentrations in an acute inflammatory state via a mechanism involving binding of the Oct-1 transcription factor. This finding may help resolve conflicting studies based on the IL6 -174G>C variant.

Severity of periodontal disease correlates to inflammatory systemic status and independently predicts the presence and angiographic extent of stable coronary artery disease

Periodontal disease (PD) has been recognized as a risk factor for systemic diseases, but its involvement in the pathogenesis of coronary artery disease (CAD) remains debated. We sought to evaluate the potential relations between severity of the PD, inflammatory response and angiographic lesions extent in patients with stable CAD. A total of 131 subjects referred to our centre for coronary angiography were evaluated for presence and extension of CAD, then divided into two groups, one with presence of lesions (cases, n = 85) and other one with absence of lesions (controls, n = 46). Mean periodontal pocket depth (PPkD), high sensitivity C reactive protein (hs-CRP), serum amyloid A protein (SAA) and fibrinogen levels were measured in all patients. Cases and controls did not differ according to their baseline characteristics and prevalence of traditional cardiovascular risk factors. PPkD was greater in patients with CAD than in controls (2.24 +/- 1.28 mm vs 1.50 +/- 0.93 mm, P < 0.001 by Student's t-test). Systemic inflammatory response was more pronounced in cases than in controls, with higher values of hs-CRP, SAA and fibrinogen. Furthermore, PPkD values correlated with hs-CRP (r = 0.80, P < 0.001), SAA (r = 0.71, P < 0.001), fibrinogen levels (r = 0.72, P < 0.001) and the American College of Cardiology/American Heart Association angiographic score (r = 0.68, P < 0.001) in cases. Multivariate analysis indicated a persistent independent correlation between PPkD and angiographic score after adjustment for inflammatory markers levels. In the present study, PD lesions predicted presence of CAD stenosis in patients with cardiovascular risk factors. PD severity was correlated to angiographic extent of coronary lesions, independent of systemic inflammatory status. Those results suggest that these patients might benefit from an intensive periodontal therapy to prevent CAD progression.

Influence of Periodontal Therapy on the Regulation of Soluble Cell Adhesion Molecule Expression in Aggressive Periodontitis Patients

Inflammatory periodontal disease is associated with an increased risk of cardiovascular disease. Circulating cell adhesion molecules (CAM) (intercellular adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1], and E-selectin) have been suggested as potential candidate markers of endothelial dysfunction, which contribute to the pathogenesis of cardiovascular diseases. The regulation of CAM in subjects with severe periodontitis and the influence of periodontal intervention on systemic CAM levels are not clear. The aim of this study was to determine whether intensive periodontal therapy reduces serum levels of CAM in patients with generalized aggressive periodontitis. Blood samples were collected at six treatment time points from 21 patients with previously untreated generalized aggressive periodontitis (mean age: 34.6 +/- 4.3 years). Patients received subgingival scaling and root planing and antibiotic therapy and were monitored over a 6-month recall period. Serum levels of soluble ICAM-1 (sICAM-1), VCAM-1 (sVCAM-1), and E-selectin (sE-selectin) were measured by enzyme-linked immunosorbent assay. sE-selectin plasma levels decreased significantly (P <0.01) during periodontal therapy. Mean plasma levels were 65.95 ng/ml before treatment and 44.71 ng/ml 6 months after antibiotic therapy. sICAM-1 and sVCAM-2 serum levels were unaffected by therapeutic intervention. Periodontal therapy reduces plasma sE-selectin levels. Whether this leads to a reduction in risk of future cardiovascular events in patients with aggressive periodontal disease warrants further studies.

Periodontal infections cause changes in traditional and novel cardiovascular risk factors: Results from a randomized controlled clinical trial

Chronic infections, such as periodontitis, are associated with increased risk of systemic diseases driven by a persistent low-grade systemic inflammation and metabolic changes. Severity of periodontitis has also been associated with increased systolic blood pressure (BP). However, the issue remains poorly investigated. We aimed to estimate the effect of periodontal therapy on traditional and novel cardiovascular risk factors in systemically healthy individuals who have periodontitis. We enrolled 40 otherwise healthy patients with severe chronic generalized periodontitis in a 6-month pilot intervention trial. Individuals were randomized either to a standard course of periodontal therapy (subgingival scaling and root planing) or an intensive one (including the adjunctive use of a locally delivered antimicrobial, IPT). Compared to control, IPT produced significant reductions in a cluster of inflammatory markers at 1 (P = .0406) and 2 (P = .0060) months together with an improvement in lipid markers at 2 (P = .0320) and 6 (P = .0432) months after therapy. Intensive periodontal therapy produced greater reductions in IL-6 at 1 (0.4 +/- 0.2 ng/L difference, 95% CI 0.03-0.9, P = .0284) and 2 months (0.3 +/- 0.2 ng/L difference, 95% CI 0.1-0.8, P = .0284), together with decreases in C-reactive protein (0.4 +/- 0.2 mg/L difference, 95% CI 0.01-0.8, P = .0438) and total cholesterol (0.3 +/- 0.1 mmol/L difference, 95% CI 0.04-0.6, P = .0254). Moreover, a 7 +/- 3-mm Hg decrease in systolic BP was observed at 2 months in the IPT group (95% CI 1-12, P = .0211), and this difference was greater in current smokers (14 +/- 5 mm Hg 95% CI 3-25, P = 0.0124). Intensive periodontal therapy subjects exhibited a 1.53% +/- 1.20% (95% CI 1.05-2.24, P = .0290) and 2.00% +/- 1.42% (95% CI 0.98-4.09, P = .0568) decreases in cardiovascular risk scores (Framingham) at 2 and 6 months, respectively, when compared to those in the standard group. Our findings suggest that intensive periodontal treatment reduces systemic inflammatory markers and systolic BP, and improves lipid profiles with subsequent changes in cardiovascular risk when compared to standard therapy.

Periodontal therapy: a novel acute inflammatory model

We designed a clinical trial at the Eastman Dental Hospital with the objective of developing a novel in vivo inflammatory model. We recruited 55 subjects suffering from severe periodontitis. Participants received intensive periodontal therapy. Blood samples were collected at baseline and 1 and 7 and 30 days after treatment and processed for a series of biomarkers (TNF-alpha, IL-6, CRP and Fibrinogen) by high-sensitivity assays and differential blood counts (standard laboratory procedures). TNF-alpha levels were significantly raised only after 1 day of therapy (P<0.01) whereas IL-6 (P<0.01), CRP (P<0.001) and Fibrinogen (P<0.001) concentrations peaked 24 hrs after and returned to baseline values within one month following therapy. Mild neutrophilia, monocytosis and lymphopenia were also observed. Intensive periodontal therapy induces a one week moderate inflammatory response and therefore it is proposed as a novel therapeutic and reliable non drug-induced in vivo model of acute inflammation.

Short-term Effects of Intensive Periodontal Therapy on Serum Inflammatory Markers and Cholesterol

Severe periodontitis has been associated with increased systemic inflammation. In a three-arm preliminary randomized trial, we investigated the impact of standard (SPT) and intensive periodontal therapy (IPT) on serum inflammatory markers and cholesterol levels. Medical and periodontal parameters, C-reactive protein (CRP), interleukin-6 (IL-6), total cholesterol, and LDL cholesterol were evaluated in 65 systemically healthy subjects suffering from severe generalized periodontitis. Two months after treatment, both SPT and IPT resulted in significant reductions in serum CRP compared with the untreated control (0.5 +/- 0.2 mg/L for SPT, P = 0.030 and 0.8 +/- 0.2 mg/L for IPT, P = 0.001). Similar results were observed for IL-6. Changes in inflammation were independent of age, gender, body mass index, and ethnicity, but a significant interaction between cigarette smoking and treatment regimen was found. The IPT group also showed a decrease in total and LDL cholesterol after 2 months. Analysis of these data indicates that periodontitis causes moderate systemic inflammation in systemically healthy subjects.