Construction of a Biological Age Score to Predict Tooth Loss over 10 Years.

The aim of the present study was to construct a biological age score reflecting one's physiologic capability and aging condition with respect to tooth loss over 10 y. From the follow-up to the population-based Study of Health in Pomerania (i.e., SHIP-2), 2,049 participants were studied for their baseline biomarker measures 10 y before (i.e., in SHIP-0). Metabolic and periodontal data were regressed onto chronological age to construct a score designated as "biological age." For either sex separately, the impact of this individualized score was used to predict tooth loss in the follow-up cohort in comparison with each participant's chronological age. Outcome data after 10 y with respect to tooth loss, periodontitis, obesity, and inflammation were shown to be better for biologically younger subjects than as expected by their chronological age, whereas for the older subjects, data were worse. Especially for tooth loss, a striking increase was observed in subjects whose biological age at baseline appeared to be higher than their chronological age. Biological age produced significantly better tooth loss predictions than chronological age (P < 0.001). Areas under receiver operating characteristic curves for tooth loss of ≥3 teeth in men during follow-up were 0.811 and 0.745 for biological and chronological age, respectively. For women, these figures were 0.788 and 0.724. For total tooth loss, areas under the curve were 0.890 and 0.749 in men and 0.872 and 0.752 in women. Biological age combines various measures into a single score and allows identifying individuals at increased risk of tooth loss.

Does periodontitis affect diabetes incidence and haemoglobin A1c change? An 11-year follow-up study.

AIM: As periodontitis may contribute to the pathogenesis of diabetes, the effects of periodontitis on diabetes incidence and HbA1c change was quantified in a prospective cohort. METHODS: Data from an 11-year follow-up of the Study of Health in Pomerania were analyzed to evaluate the effects of periodontitis on incident diabetes and long-term HbA1c changes in 2047 subjects aged 20-81years. Diabetes was based on self-reported physician diagnoses, antidiabetic medication use, or HbA1c≥6.5% or non-fasting blood glucose levels ≥11.1mmol/L. To assess periodontal status, periodontal pockets were probed, and their depth and clinical attachment levels measured. For both measures, means and percentages of sites≥3mm were calculated. In addition, all probing depths≥4mm were summed (cumulative probing depth). Modified Poisson and multivariable linear models were applied, adjusted for age, gender, highest level of general education, marital status, waist circumference, physical activity, smoking status and follow-up time. RESULTS: Over a mean follow-up period of 11.1years, 207 subjects developed diabetes. Baseline mean clinical attachment levels (CAL) and probing depths (PPD) were not significantly associated with either diabetes incidence [mean CALs, fourth quartile, incidence rate ratio=0.819, 95% confidence interval (CI): 0.489-1.370; P=0.446] or long-term changes in HbA1c (mean CAL, fourth quartile, ß=-0.086, 95% CI: -0.187, -0.016; P=0.098). Sensitivity analyses using alternative exposure definitions confirmed these results. CONCLUSION: Contrary to the currently available literature, no convincing evidence was found of any potential association between periodontitis and diabetes incidence or HbA1c change.

Exome Variant Analysis of Chronic Periodontitis in 2 Large Cohort Studies.

Periodontitis is characterized by inflammation of the gingival tissue. The main risk factors are socioeconomic factors, sex, age, smoking, and diabetes, but periodontal disease has also a genetic background. Previous genome-wide association studies failed to reveal genome-wide significant associations of single common single-nucleotide polymorphisms with chronic periodontitis. Using the Illumina ExomeChip data of 6,576 participants of the German population-based cohort studies Study of Health in Pomerania (SHIP) and SHIP-Trend, the authors performed single variant and also gene-based association studies of rare and common exonic variations on different periodontal case definitions. Although our study comprised the largest sample size to date to assess genetic predisposition for chronic periodontitis, the authors found no significant association. This study emphasizes that for chronic periodontitis, large sample sizes will be necessary to find genetic associations, even when examining rare genetic variants.

Association of Periodontal Destruction and Diabetes with Mortality.

Current evidence indicates the effects of periodontitis on diabetes as well as mortality, for which diabetes itself represents a risk factor. However, the possible interaction of these 2 chronic conditions regarding mortality has not yet been investigated. Therefore, the purpose of this study was to evaluate whether periodontal destruction interacts with diabetes on all-cause and cardiovascular disease (CVD) mortality or if diabetes serves as a mediator in this association. The study sample comprised 3,327 participants aged 20 to 81 y from the Study of Health in Pomerania. Periodontal destruction was assessed via clinical attachment level (CAL) and the number of missing teeth. Information on mortality (date and ICD-10 code) was ascertained from death certificates. Directed acyclic graphs were used to identify potential confounders, and Cox proportional hazard models were applied. In 36,701 person-years of follow-up, 263 study participants deceased, 89 due to CVD. Fully adjusted main effect models resulted in hazard ratios of 1.01 (95% confidence interval [95% CI]: 1.002 to 1.01) for extent of CAL ≥3 mm, 1.10 (95% CI: 1.03 to 1.18) for mean CAL, and 1.03 (95% CI: 1.01 to 1.04) for the number of missing teeth regarding all-cause mortality. Analogous results were obtained for CVD mortality, with hazard ratios of 1.01 (95% CI: 0.99 to 1.02), 1.10 (95% CI: 0.98 to 1.23), and 1.02 (95% CI: 0.99 to 1.05) for extent of CAL, mean CAL, and the number of missing teeth, respectively. Findings did not indicate additive interaction of periodontal destruction and diabetes regarding all-cause and CVD mortality. Similarly, no substantial evidence was found to demonstrate the presence of multiplicative interaction or mediation. Besides adjustment for baseline covariates, time-varying covariates were also considered and led to comparable results. In summary, despite their reciprocal relationship, periodontal destruction and diabetes may be independent risk factors for all-cause and CVD mortality.

Reduced Bone Stiffness in Women Is Associated with Clinical Attachment and Tooth Loss: The Study of Health in Pomerania.

The authors evaluated the association of reduced bone stiffness of the calcaneus with clinical attachment loss (CAL) and tooth loss. The authors analyzed data from 4,678 subjects (2,384 women), aged 20 to 88 y, from the second follow-up of the population-based Study of Health in Pomerania (SHIP-2) and the baseline examination of the SHIP-Trend cohort. Bone stiffness, characterized by the stiffness index (SI) and the osteoporotic fracture risk (OFR), was assessed by quantitative ultrasound of the heel. SI and OFR were significantly associated with the mean CAL in women. While 1) the SI showed a significant association with the mean CAL and 2) the OFR with the median number of teeth in just the postmenopausal women, the OFR showed a significant association with mean CAL for both pre- and postmenopausal women. In postmenopausal women, a 10-unit increase in the SI was associated with a decrease in the mean CAL of 0.05 mm (95% confidence interval [CI]: -0.10 to 0.00; P = 0.046). Moreover, the adjusted median number of teeth was 21.4 (95% CI: 20.9 to 21.9) among the postmenopausal women with a low OFR, while it was 19.1 (95% CI: 17.8 to 20.3; P = 0.001) among the postmenopausal women with a high OFR. For the premenopausal women with a low OFR, the mean CAL was 1.60 mm (95% CI: 1.53 to 1.66), while for the premenopausal women with a high OFR, it was 2.24 mm (95% CI: 1.78 to 2.69; P = 0.006). Reduced bone stiffness was associated with clinical attachment and tooth loss in women but not in men.

Magnesium/Calcium Ratio in Serum Predicts Periodontitis and Tooth Loss in a 5-Year Follow-up.

In the cross-sectional Study of Health in Pomerania (SHIP-0), subjects with an adequate magnesium supply had a lower risk of periodontal disease and more teeth than those with low magnesium levels. The authors analyzed 5-y follow-up data (SHIP-1) to determine whether the baseline magnesium levels had a long-term effect on attachment level and number of teeth lost. Of the participants examined dentally in the baseline study, 3,300 (75%) were examined for progression or recession of periodontal attachment level after 5 y. For 2,432 subjects, the authors related the outcome variables of periodontal attachment level and tooth loss to baseline characteristics, especially serum magnesium and calcium concentrations, as well as systemic markers of inflammation. The progression of periodontitis was associated with the magnesium/calcium (Mg/Ca) ratio at baseline in a dose-dependent manner. Progression of mean attachment loss was prevented in the upper quartile of the Mg/Ca ratio ( P < 0.001) with antagonistic effects of magnesium and calcium irrespective of inflammatory state. With respect to tooth loss, Mg/Ca exerted dimorphic effects. In inflammatory states as indicated by high C-reactive protein (>3 mg/L), tooth loss was prevented in subjects with high Mg/Ca ratio (incidence rate ratio = 0.60, 95% confidence interval: 0.45 to 0.80, P = 0.001), but the contrary was observed in subjects with low C-reactive protein levels (incidence rate ratio = 1.14, 95% confidence interval: 0.97 to 1.34, NS). Similar results were observed with stratifying the regression on tooth loss by interleukin 6 or fibrinogen threshold. An adequate magnesium serum level and Mg/Ca balance may prevent progression of attachment level and tooth loss, especially in inflammatory states. Knowledge Transfer Statement: The results of this study present evidence that an adequate magnesium supply may be important in the prevention of periodontal diseases and future tooth loss. A diet high in magnesium could improve periodontal health, notwithstanding its beneficial effects on systemic disease. In populations with a high prevalence of hypomagnesemia, additional intake of supplements is advisable.

Prospective Study of Serum 25-hydroxy Vitamin D and Tooth Loss.

Vitamin D deficiency and oral diseases (periodontitis, caries, and tooth loss) are highly prevalent in Germany. Previous studies suggested that vitamin D might be a modifiable and protective factor for periodontitis, caries, and tooth loss. However, prospective studies investigating such associations are limited. We explored the association between the concentration of serum 25-hydroxy vitamin D (25OHD) and incidence of tooth loss, progression of clinical attachment loss (CAL) ≥ 3 mm, and progression of restorative and caries status in a population-based longitudinal study. We analyzed data from 1,904 participants from the Study of Health in Pomerania with a five-year follow-up. Generalized estimating equation models were applied to evaluate tooth-specific associations between serum 25OHD and incidence of tooth loss, progression of CAL ≥ 3 mm, and progression of restorative and caries status. Age, sex, education, smoking status, alcohol drinking, waist circumference, dental visit frequency, reasons of dental visit, vitamin D or calcium supplements, and season of blood draw were considered as confounders. Serum 25OHD was inversely associated with incidence of tooth loss. A significant dose-response relationship (p = .0022) was observed across the quintiles of serum 25OHD. After adjusting for multiple confounders, each 10-µg/L increase of serum 25OHD was associated with a 13% decreased risk of tooth loss (risk ratio: 0.87; 95% confidence interval: 0.79, 0.96). The association was attenuated for changes of CAL ≥ 3 mm when adjusting for multiple confounders. No significant association was found between serum 25OHD and caries progression. Vitamin D might be a protective factor for tooth loss. The effect might partially be mediated by its effect on periodontitis.

Sex Differences of Tooth Loss and Obesity on Systemic Markers of Inflammation.

Sex-specific differences in the incidence of periodontitis and tooth loss may be related to different phenotypes of obesity and their associations with low-grade inflammation. The aim of this study was to evaluate associations of adiposity and low-grade inflammation with tooth loss in men and women. Follow-up data of 2,714 participants from the cohort of Study of Health in Pomerania were analyzed for anthropometric measures, periodontitis, tooth loss, C-reactive protein (CRP), and interleukin 6. Regression analyses were used to estimate the effect of obesity on tooth loss within sex strata. During the follow-up period, men lost more teeth in relation to their obesity status than did women. In contrast, there was a steeper increase in CRP levels across obesity levels in women as compared to men. Incidence rate ratio (IRR) of tooth loss associated with elevated CRP, however, was higher in men (IRR = 1.50; 95% confidence interval [CI]: 1.27, 1.77) than women (IRR = 1.18; 95% CI: 1.02, 1.37). Negative binomial regression with number of lost teeth as outcome revealed dose-response dependencies on body mass index and waist-to-hip ratio. Adjusted for covariates, the IRR of tooth loss associated with the third tertile of waist-to-hip ratio was 1.37 (95% CI: 1.04, 1.80) and 1.53 (95% CI: 1.14, 2.05) in men and women, respectively. Tooth loss related to CRP cutoff of 2 mg/L was significant in men (IRR = 1.33; 95% CI: 1.07, 1.66; p = .006) but not in women (IRR = 0.92; 95% CI: 0.73, 1.17; p = .689). This study suggests that both adiposity and subclinical inflammation affect tooth loss, with distinct differences between men and women. Obesity as a risk factor of tooth loss is particularly related to CRP in men but not in women.

Magnesium deficiency is associated with periodontal disease.

In the multifactorial pathogenesis of periodontitis, there are still unknown factors influencing the outcome of the disease. An association between magnesium and periodontitis has been suggested by preliminary studies. However, relevant clinical data are lacking. We investigated the association between magnesium status and periodontal health in a population-based analysis. We conducted a cross-sectional epidemiological investigation involving 4290 subjects aged 20-80 yrs. We recorded periodontal risk factors and determined concentrations of serum magnesium and calcium, relating them to periodontal parameters. In a matched-pair study, 60 subjects using oral magnesium-containing drugs and 120 without were compared. In subjects aged 40 yrs and older, increased serum Mg/Ca was significantly associated with reduced probing depth (p<0.001), less attachment loss (p=0.006), and a higher number of remaining teeth (p=0.005). Subjects taking Mg drugs showed less attachment loss (p<0.01) and more remaining teeth than did their matched counterparts. These results suggest that nutritional magnesium supplementation may improve periodontal health.

Risk determinants of periodontal disease--an analysis of the Study of Health in Pomerania (SHIP 0).

BACKGROUND: In this study, risk determinants were determined for periodontal disease in the representative population sample (n=3146) of the Study of Health in Pomerania. METHODS: After examining the net random sample (response 69%) and exclusion of edentulous cases and those with missing values, 2595 subjects remained. Using a multivariate, fully adjusted logistic regression, different definitions of "periodontally diseased/healthy" were examined as the dependent variable (extent of attachment loss (AL> or =4 mm, combined AL and tooth loss). The independent variables used were sociodemographic factors (age, gender, income, education), medical factors (systemic diseases, drugs), behavioral factors (regular dental checkup, smoking), and oral factors (presence of supragingival calculus and plaque). RESULTS: The following risk determinants were found for AL: male gender, presence of supragingival plaque and calculus, smoking, low educational level. For the combination of AL and tooth loss, risk determinants were female gender, supragingival plaque, smoking, and low educational level. Consumption of antiallergic medications and regular dental checkups proved to be protective. Smoking was the most influential risk determinant. These parameters explained approximately 43-55% of the variation. CONCLUSION: These results concur with those of the literature. In order to explain disease status further, host-response and microbiological factors must also be examined.

Dental nomograms for benchmarking based on the study of health in Pomerania data set.

AIM: Benchmarking is a means of setting goals or targets. On an oral health level, it denotes retaining more teeth and/or improving the quality of life. The goal of this pilot investigation was to assess whether the data generated by a population-based study (SHIP 0) can be used as a benchmark data set to characterize different practice profiles. MATERIAL AND METHODS: The data collected in the population-based study SHIP (n=4310) in eastern Germany were used to generate nomograms of tooth loss, attachment loss, and probing depth. The nomograms included twelve 5-year age strata (20-79 years) presented as quartiles, and additional percentiles of the dental parameters for each age group. Cross-sectional data from a conventional dental office (n=186) and from a periodontology unit (n=130, Greifswald) in the study region as well as longitudinal data set of a another periodontology unit (n=135, Kiel) were utilized in order to verify whether the given practice profile was accurately reflected by the nomogram. RESULTS: In terms of tooth loss, the data from the conventional dental office agree with the median from the nomogram. For attachment loss and probing depth, some age groups yielded slight but not uniform deviations from the median. Cross-sectional data from the periodontology unit Greifswald showed attachment loss higher than the median in younger but not in older age groups. The probing depth was uniformly less than the median and tended toward the 25th percentile with increasing age. The longitudinal data of the Unit of Periodontology in Kiel showed a pronounced trend towards higher percentiles of residual teeth, meaning that the patients retained more teeth. CONCLUSION: The profile of the Pomeranian dental office does not deviate noticeably from the population-based nomograms. The higher attachment loss of the Unit of Periodontology in Greifswald in younger age strata clearly reflects their selection because of periodontal disease; the combination of higher attachment loss and decreased probing depth may reflect the success of the treatment. The tendency of attachment loss towards the median with increasing age may indicate that the Unit of Periodontology in Greifswald does not fulfill its function as a special care unit in the older subjects. The longitudinal data set of the Unit of Periodontology in Kiel impressively reflects the potential of population-based data sets as a means for benchmarking. Thus, nomograms can help to determine the practice profile, potentially yielding benefits for the dentist, health insurance company, or--as in the case of the special care unit--public health research.

Dose-effect relation of smoking and the interleukin-1 gene polymorphism in periodontal disease.

BACKGROUND: Periodontitis is a bacterial inflammatory disease leading to attachment loss with the consequence of tooth loss. There exists a multifactorial risk pattern including bacterial challenge, smoking, age, gender, diabetes, and socioeconomic and genetic factors. Smoking has the highest impact on the course of the disease modulated by all the other factors. Here, we report the relationship between smoking and the genetic polymorphism of interleukin-1 (IL-1). METHODS: In a randomly selected population-based study, we genotyped 1,085 test persons for the IL-1 genotype, examined their periodontal status, and assessed their smoking behavior including present and past quality and quantity of smoking. RESULTS: There was a significant dose-effect relationship between the exposure to tobacco smoke and the extent of periodontal disease assessed as attachment loss and tooth loss. Moreover, there was a gene-environmental interaction. Subjects bearing at least one copy of the variant allele 2 at positions IL-1A -889 and IL-1B +3954 (genotype positive) had an enhanced smoking-associated periodontitis risk as compared to their IL-1 genotype-negative counterparts. With genotype-negative non-smokers as a reference, logistic regression resulted in odds ratios of 0.98 (95% confidence interval: 0.83 to 1.14), 2.37 (1.96 to 2.87), and 4.50 (2.30 to 8.82) for genotype-positive non-smokers, genotype-negative smokers, and genotype-positive smokers, respectively. CONCLUSIONS: There is a gene-environmental interaction between smoking and the IL-1 genetic polymorphism. Smokers bearing the genotype-positive IL-1 allele combination have an increased risk of periodontitis. The IL-1 genotype has no influence in non-smokers.

The FcgammaRIIa polymorphism in children with atopic diseases.

BACKGROUND: Fcgamma receptor II (FcgammaRIIa) is the most widely distributed of the classes of FcR and is expressed in polymorphic forms on most types of hematopoietic cells. Recent data suggest that this polymorphism may be relevant to FcgammaRIIa function. This might be linked to variability in immune response and therefore related to the pathogenesis of atopic diseases. The aim of the study was to evaluate the FcgammaRIIa polymorphism in children with atopic diseases. METHODS: In the study were included 140 atopic children, 77 with food allergy and 126 healthy subjects as the control group. The FcgammaRIIa polymorphism was determined using the polymerase chain reaction method. RESULTS: The distribution of FcgammaRIIa genotypes in atopic children did not differ from that of healthy controls. Moreover, there was no association between the FcgammaRIIa genotypes and atopic diseases. CONCLUSION: It seems that the FcgammaRIIa polymorphism does not represent an important genetic risk factor for atopic diseases susceptibility.

The interleukin-1 polymorphism, smoking, and the risk of periodontal disease in the population-based SHIP study.

Several studies have shown a role for interleukin-1 gene cluster polymorphisms in the risk assessment for periodontal diseases. In the Study of Health in Pomerania (SHIP), 3148 subjects were randomly selected from the population and assessed for a broad range of diseases and environmental/behavioral risk factors. From the complete study group in the age 40 to 60 years, N = 1085 subjects were genotyped for the interleukin-1 genotype composite polymorphism in relation to periodontal parameters. The study objective was to elucidate the gene-environment interaction between the risk factors smoking and IL-1 polymorphism. An increased risk of periodontal disease was found for IL-1 genotype-positive smokers: odds ratio adjusted for age, sex, education, and plaque OR = 2.50 (95% C.I. 1.21 to 5.13; p = 0.013). This was not the case with subjects who never smoked: OR = 1.09 (0.73-1.62; p = 0.676). These results support the hypothesis of gene-environmental interaction in periodontitis.

Impact of genetic polymorphisms on the smoking-related risk of periodontal disease: the population-based study SHIP.

Periodontitis is a bacterial inflammatory disease leading to attachment loss with the consequence of tooth loss. There exists a multifactorial risk pattern including bacterial challenge, smoking, age, sex, diabetes, socio-economic and genetic factors. Smoking has the highest impact on the course of the disease modulated by all the other factors. Here, we report the relationship between smoking and the polymorphisms of genetic polymorphisms inflicted in the pathogenesis.In a randomly selected population-based study, 1083 subjects were typed for the polymorphisms of the IL-1 genotype, Fcgamma RIIIb receptor gene, myeloperoxidase and N-acetyltransferase (NAT2) and related to their periodontal state. Smoking behavior was assessed including present and past quality and quantity of smoking.There is a significant dose-effect relationship between the exposure to tobacco smoke and the extent of periodontal disease assessed as attachment loss and tooth loss. Moreover, there are gene-environmental interactions as subjects bearing variant genotypes show an enhanced smoking-associated risk of the disease modulated by these genotypes. In non-smokers, the impact of these genetic polymorphisms is mostly negligible.This study provides support for the hypothesis that subjects bearing genetic variants of polymorphically expressed phenotypes are at an increased risk of periodontitis when smoking. Mostly, this may be accomplished via the influence of smoking-related impairment on defense mechanisms rather than on the pathogenic pathways.

Expression of N-acetyltransferases in periodontal granulation tissue.

Smoking is a major risk of periodontal diseases. At the site of first contact, the gingiva is exposed to aromatic amines and polycyclic hydrocarbons. These are metabolized by the N-acetyltransferases (NAT), leading to local detoxification and/or activation reactions contributing to the risk of periodontal destruction in smokers. The purpose of this study was to detect the expression of N-acetyltransferase isoenzymes NAT1 and NAT2 in periodontal granulation tissue. In 24 specimens obtained from periodontitis patients or control subjects, mRNA encoding for NAT1 and NAT2 was detected by RT-PCR, and proteins were identified by immunohistochemistry. In periodontal granulation tissues, immunoreactivity for NAT1 and NAT2 was detected in infiltrating leukocytes and fibroblasts. In normal gingiva, both enzymes were found in epithelial cells, whereas NAT1 was also detected in endothelial cells. The results suggest that these enzymes may play a role in the defense against xenobiotics and the accelerated progression of periodontal disease in smokers.

Gender and smoking-related risk reduction of periodontal disease with variant myeloperoxidase alleles.

Myeloperoxidase (MPO) is an oxidative enzyme expressed in polymorphonuclear leukocytes. It is involved in the defence against periodontal bacteria, and is also able to mediate inflammatory tissue destruction in periodontal disease. A G/A polymorphism in the promoter region of the MPO gene at position -463 has been assumed to exert profound effects on the expression of the enzyme. It is the aim of this study to evaluate whether this polymorphism may influence the risk of periodontal diseases. A total of 3148 subjects were randomly selected from the general population in the SHIP study (Study of Health in Pomerania). Periodontal status, health-related and socio-economic items were assessed. All subjects aged 40-60 years (n = 1103) were included in this study, and 1083 genotyped for the MPO -463 G/A polymorphism by PCR and RFLP methods. The genotype frequencies determined were homozygous wild type G/G 65.9% (95% CI 63.5-68.6), heterozygous A/G 31.4% (28.8-34.4), and homozygous variant A/A 2.7% (2.0-3.8). Only female subjects have a significantly reduced risk of severe periodontal disease when bearing the variant genotypes A/G or A/A. In female subjects the reduction in periodontal risk was significant for non-smokers (OR = 0.48; 95% CI 0.23-0.96); the smoke-related increase in risk was also reduced (OR = 0.50; 95% CI 0.22-1.10). When adjusted for age, smoking, and education the odds ratios were calculated as 0.52 (P = 0.01) and 0.97 (P = 0.90) for female and male subjects, respectively. The results of this study confirm the assumption that the MPO -463A allele variants are protective in the pathogenesis of periodontal diseases. This holds true only with women but not with men. The results are discussed with respect to the known influences of sexual hormones on MPO activity.

Smoking and polymorphisms of the interleukin-1 gene cluster (IL-1alpha, IL-1beta, and IL-1RN) in patients with periodontal disease.

BACKGROUND: Polymorphisms within the interleukin-1 cluster are known to be associated with adult periodontal disease. However, interactions of genetic with other risk factors, especially smoking, remain questionable. The aim of this cross-sectional study was to evaluate the genetic influence on periodontal variables in relation to environmental factors. METHODS: One-hundred fifty-four (154) Caucasian subjects were clinically and radiographically assessed for their periodontal status, their smoking history recorded, and their allelic pattern of IL-1alpha, IL-1beta, and IL-1RN polymorphisms determined by genotyping. RESULTS: In assessing periodontitis with mean probing depth, mean attachment loss, or mean bone loss, no differences were found in allele frequencies or combined allotypes between subjects with mild or moderate versus those with severe signs of periodontitis. However, the extent of attachment loss defined as percentage of sites >4 mm was significantly associated with the composite genotype of IL-1alpha/1beta in smokers (odds ratio [OR] = 4.00; 95% confidence interval [CI] 1.03 to 16.70; P= 0.02). No differences were found in genotype negative subjects irrespective of their smoking status. They had nearly identical attachment loss as genotype positive non-smokers. Similar non-significant results were found with respect to extent of bone loss. An increased risk of more extended attachment loss was observed also in individuals carrying mutations of the combined genotype IL-1alpha/IL-1RN, again showing enhanced risk only in genotype-positive and smoking subjects. CONCLUSIONS: The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive.

Anticardiolipin antibodies in ectopic pregnancies.

BACKGROUND: Anticardiolipin auto-antibodies are known to be inflicted in recurrent pregnancy losses and other adverse outcomes of pregnancy. However, their role in extrauterine pregnancies is unknown. OBJECTIVE: To clarify the association between anticardiolipin antibodies and extrauterine pregnancies. PATIENTS AND METHODS: About 30 patients with ectopic pregnancies confirmed histologically and 40 control subjects with intrauterine pregnancies were studied. Mean duration of pregnancy was 38 and 39 days, respectively. Serum levels of IgG, IgA, and IgM antibodies against cardiolipin were measured. In addition, measurements of human chorionic gonadotropin (beta hCG) and progesterone were made. RESULTS: Mean levels of IgA and IgM but not IgG antibodies were significantly higher in patients with ectopic pregnancies than in normal pregnant women. Distribution frequency histograms revealed that a subgroup of ectopic pregnancies exhibit antibody titers corresponding to that of intrauterine pregnancies, and others showing elevated levels. Markedly elevated antibody levels were observed in patients having low levels of beta hCG and/or progesterone. CONCLUSION: In view of the inflammatory events associated with some cases of ectopic pregnancies, elevated levels of anticardiolipin auto-antibodies may give clues to pathogenesis. Determination of IgM antibodies may help discriminate ectopic pregnancies with auto-immune pathogenesis from those caused by other factors.

Polymorphisms of Fc gamma-receptors RIIa, RIIIa, and RIIIb in patients with adult periodontal diseases.

Polymorphisms influencing the binding affinity between the Fcgamma receptors and IgG of different subclasses are thought to be of importance in the individual susceptibility to infections with Gram-negative bacteria contributing to periodontal disease. One hundred and fifty-four Caucasian subjects were clinically and radiographically examined for their periodontal status and genotyped for their allelic pattern of FcgammaRIIa, FcgammaRIIIa, and FcgammaIIIb polymorphism. In assessing periodontitis according to mean probing depth and attachment loss, no differences were found in allele frequencies or combined allotypes between the subjects with mild or moderate and those with severe signs of periodontitis. However, the extent and severity of bone loss were significantly associated with the genotype of the receptor FcgammaRIIIa. An increased risk of severe bone destruction was observed in individuals carrying the FcgammaRIIIa-VV genotype (OR = 5.3; 95% CI 1.4-26.2). FcgammaRIIIb is in linkage disequilibrium with FcgammaRIIIa. Hence it is also related to periodontal disease. There is no indication of an association between the polymorphism of FcgammaRIIa and periodontitis. The results are evidence that the FcgammaRIIIa genotype coding for the high affinity receptor imposes an additional risk of bone loss as does the FcgammaRIIIb genotype coding for the low affinity receptor.