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Objective: To investigate the role of smoking as a confounding factor in the association between periodontal pocketing and blood pressure. Materials and methods: After restriction to 45–64-year-old subjects without hypertension, diabetes, rheumatic diseases, obesity and with no history of cardiovascular diseases or ongoing lipid-lowering medications, the study population consisted of 307 subjects of the Health 2000 Survey in Finland. Systolic and diastolic blood pressure and pulse pressure (mmHg) were used as outcome variables. Periodontal condition was measured by the number of teeth with ≥4 mm periodontal pockets. β-estimates and 95% confidence intervals (CI) were obtained from linear regression models. Analyses were made in the whole study population and stratified according to smoking habits/history. Results: The number of teeth with ≥4 mm periodontal pockets associated statistically significantly with systolic blood pressure and pulse pressure in the whole study population. Among never-smokers or daily smokers, there were no consistent nor statistically significant associations between the number of teeth with ≥4 mm periodontal pockets and systolic/diastolic blood pressure or pulse pressure. Conclusions: Smoking appeared to confound the association between periodontal condition and blood pressure. Thorough control for the effect of smoking was not obtained using multivariate models.

Background: Periodontitis has been associated with inflammatory processes in arterial walls such as impairment in endothelial function and thickening of intima media. As inflammation plays a role also in arterial stiffening, an association between periodontal inflammation and arterial stiffness can be expected. So far, conflicting results of the association between periodontal disease and arterial stiffness have been reported. Many of the earlier studies were conducted in specific populations and heterogeneous measures of both arterial stiffness and periodontal status were used. In this population-based study we aimed to investigate whether periodontal pocketing and gingival bleeding are associated with ultrasound-based measures of arterial stiffness. Methods: In this cross-sectional study, two sets of data based on the national Health 2000 Survey in Finland were formed. Data set I comprised never-smoking 45–64-year-old dentate (≥ 10 natural teeth), non-diabetic, non-rheumatic, non-obese (BMI ≤ 30 kg/m²), non-hypertensive subjects with no coronary artery disease or ongoing lipid-lowering medications (n = 157). Data set II was formed of an unrestricted 45–74-year-old dentate population (n = 536). Four arterial stiffness measures (carotid artery compliance, Peterson’s elastic modulus, Young’s elastic modulus and beta stiffness index) based on an ultrasound examination of the common carotid artery were used. Periodontal parameters included the number of teeth with ≥ 4 mm deep periodontal pockets and the number of sextants with gingival bleeding. β-estimates, confidence intervals, and p-values were obtained from linear regression models. Results: In Data set I, the adjusted β-estimates for the association between the number of teeth with ≥ 4 mm deep periodontal pockets and Peterson’s elastic modulus and Young’s elastic modulus were 15.80 (p = 0.12) and 61.02 (p = 0.22), respectively. The respective β-estimates were 31.06 (p = 0.17) and 121.16 (p = 0.28) for the association between the number of bleeding sextants and these two stiffness measures. The results in Data set II were in line with the results in Data set I, with the exception that the adjusted β-estimates for the associations between Peterson’s elastic modulus and Young’s elastic modulus and periodontal parameters were closer to null. Conclusions: This population-based study did not provide evidence of an association between periodontal condition and arterial stiffness.

Aim: To investigate whether obesity, central obesity, and weight gain are associated with periodontal pocketing. Materials and methods: A never-smoking sub-population (n = 725) of the Northern Finland Birth Cohort 1966 was categorized based on body mass index (BMI; participants with normal weight, overweight, and obesity) and waist circumference (WC; participants without central obesity and with central obesity) at ages 31 and 46. The categories were combined to define whether the participants stayed in the respective BMI and WC categories or moved on to a higher category during follow-up. A periodontal examination was done at age 46. Results: WC was more consistently associated with periodontal pocketing than BMI. The relative risks for the number of sites with periodontal pocket depth (PPD) ≥4 mm and bleeding PPD ≥4 mm in participants with central obesity both at age 31 and at age 46 were 1.7 (95% confidence interval [CI] 1.4–2.0) and 2.1 (95% CI 1.6–2.6). The corresponding values for participants who had no central obesity at age 31 but had central obesity at age 46 were 1.6 (95% CI 1.4–1.8) and 1.9 (95% CI 1.6–2.3). Conclusion: Of all the studied measures, central obesity appeared to be most strongly associated with the inflammatory condition of the periodontium.

Aim: To study whether periodontal condition is associated with the development of type 2 diabetes mellitus (T2DM). Materials and Methods: A population‐based follow‐up study was conducted among persons born in 1935 and living in the city of Oulu, Finland (n = 395). The baseline examinations were done during 1990–1992, and the follow‐up examinations were done during 2007–2008. The data were gathered by questionnaires, laboratory tests and clinical measurements. Poisson regression models were used in the data analyses. Results: The adjusted rate ratios (RR) with 95% confidence intervals (95% CI) for the incident T2DM among subjects with 4–5 mm deep periodontal pockets (n = 98), among subjects with 6 mm deep or deeper periodontal pockets (n = 91), and among edentulous subjects (n = 118) were 1.32 (95% CI: 0.69–2.53), 1.56 (95% CI: 0.84–2.92) and 1.00 (95% CI: 0.53–1.89), respectively, compared to dentate subjects without deepened (4 mm deep or deeper) periodontal pockets (n = 88). The adjusted RR per site (the number of sites with deepened periodontal pockets as a continuous variable) was 1.02 (95% CI: 1.00–1.04). Conclusions: Poor periodontal condition may be a predictor of the development of T2DM. However, the causality between periodontal condition and the development of T2DM remains uncertain.

The aim of this study was to investigate the nature of the association between obesity and periodontal infection and the association of statin medication with periodontal infection. This study was based on the nationally representative Health 2000 Survey, conducted by the National Institute for Health and Welfare (former National Public Health Institute of Finland) in 2000–2001. Article I included 396 dentate, non-diabetic subjects, aged 30–59 years, who had never smoked and who participated in the Follow-up Study on Finnish Adults’ Oral Health about four years later. Article II included 2,784 dentate, non-diabetic subjects, aged 30–49 years. Article III included 425 dentate, non-diabetic, non-rheumatic subjects, aged 45–64 years, who had never smoked and who participated in the in-depth examinations of the Health 2000 Survey. Article IV included 1,297 dentate, non-diabetic subjects, aged 30–49 years, who had never smoked. Article V included 2,032 dentate, non-diabetic, non-rheumatic subjects, aged 40–69 years, who did not smoke. The data used in this study were collected via home-visit interviews, self-administered questionnaires, clinical health examinations and laboratory measurements. In this general population of Finnish adults, high BMI was found to be associated with the incidence of new teeth with pathologically deepened periodontal pockets during four-year follow-up. On the other hand, the presence of teeth with deepened periodontal pockets was found to be associated with obesity in an exposure-response manner. Serum IL-6 levels were found to be associated with the number of teeth with deepened periodontal pockets, but no consistent association was found between serum TNF-α, triglyceride, HDL-C or LDL-C levels and periodontal infection. Statin medication was found to be inversely associated with the number of teeth with deepened periodontal pockets among subjects with visible signs of gingival inflammation, whereas among subjects with no signs of inflammation, statin medication was associated with an increased likelihood of having periodontal infection. The results of this study support the view that obesity could be causally related to the development of periodontal infection, but does not provide evidence that high body weight could be considered a major risk factor. The present study also suggests that a bi-directional association between obesity and periodontal infection is possible. The present study suggests that elevated serum IL-6 could mediate the association of obesity with periodontal infection. The results of this study also suggest that statins could be beneficial as a part of periodontal treatment. Tiivistelmä Tämän tutkimuksen tarkoituksena oli selvittää lihavuuden ja parodontaali-infektion välisen yhteyden luonnetta sekä statiinien käytön yhteyttä parodontaali-infektioon. Tutkimus perustui kansalliseen Terveys 2000 -tutkimukseen, jonka toteutti Terveyden ja hyvinvoinnin laitos (entinen Kansanterveyslaitos) vuosina 2000 ja 2001. Artikkeli I perustui 396 hampaalliseen henkilöön, jotka olivat ei-diabeetikkoja, 30–59-vuotiaita, eivät koskaan olleet tupakoineet sekä olivat osallistuneet suunterveyden seurantatutkimukseen neljä vuotta myöhemmin. Artikkeli II perustui 2784 hampaalliseen henkilöön, jotka olivat ei-diabeetikkoja, 30–49-vuotiaita eivätkä olleet koskaan tupakoineet. Artikkeli III perustui 425 hampaalliseen henkilöön, joilla ei ollut diabetesta tai reumaa, olivat 45–64-vuotiaita, eivät koskaan olleet tupakoineet ja olivat osallistuneet Terveys 2000 -tutkimuksen täydentäviin tutkimuksiin. Artikkeli IV perustui 1297 hampaalliseen henkilöön, jotka olivat ei-diabeetikkoja, 30–49-vuotiaita eivätkä olleet koskaan tupakoineet. Artikkeli V perustui 2032 hampaalliseen henkilöön, jotka olivat ei-diabeetikkoja, ei-reumaatikkoja, 40–69-vuotiaita, jotka olivat hampaallisia eivätkä tupakoineet. Tutkimuksen aineisto kerättiin kotihaastattelusta, kyselyistä, kliinisestä tutkimuksesta sekä laboratoriomittauksista. Korkean painoindeksin todettiin olevan yhteydessä uusien ientaskuhampaiden ilmaantumiseen seurannan aikana. Toisaalta ientaskuhampaiden esiintymisen todettiin olevan yhteydessä lihavuuteen altistus-vastesuhteen mukaisesti. Seerumin IL-6 pitoisuuden todettiin olevan yhteydessä ientaskuhampaiden lukumäärään, mutta seerumin TNF-α-, triglyseridi-, LDL-kolesteroli- tai HDL-kolesterolipitoisuudella ei todettu yhteyttä ientaskuhampaiden lukumäärään. Statiinien käytön todettiin olevan käänteisesti yhteydessä ientaskuhampaiden lukumäärään henkilöillä, joilla oli näkyviä merkkejä ikenen inflammaatiosta. Henkilöillä, joilla ei ollut näkyviä merkkejä inflammaatiosta, statiinien käyttö oli yhteydessä suurentuneeseen todennäköisyyteen ientaskuhampaiden esiintymiseen. Tämän tutkimuksen tulokset tukevat käsitystä, että lihavuus voi olla kausaalisesti yhteydessä parodontaali-infektion kehittymiseen, mutta ei puolla käsitystä, että sitä voitaisiin pitää merkittävänä riskitekijänä. On myös mahdollista, että lihavuuden ja parodontaali-infektion välillä on kaksisuuntainen yhteys. Tämän tutkimuksen tulosten mukaan on mahdollista, että kohonnut seerumin IL-6 pitoisuus voi välittää lihavuuden yhteyden parodontaali-infektioon. Tutkimuksen tulosten mukaan on myös mahdollista, että statiineista voi olla hyötyä osana parodontaalihoitoa.