Biomedical subjects

P Meisel

Publications and source records attributed to P Meisel.

At least 19 recordsLinked to original sources

PubMed2005

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.

Adult↗

PubMed2005

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.

Adult↗

PubMed2004

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.

Adolescent↗

PubMed2004

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.

Adult↗

PubMed2004

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.

Adult↗

PubMed2003

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.

Adult↗

PubMed2002

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.

Adult↗

PubMed2002

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.

Acetyltransferases↗

PubMed2002

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.

Adult↗

PubMed2001

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.

Adult↗

PubMed2001

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.

Adult↗

PubMed2001

Prediction of metabolic activity from genotype: the gene-dose effect of N-acetyltransferase.

Metabolic activity of the polymorphic N-acetyltransferase (NAT2) is determined by the mutation pattern of the NAT2 gene. This results in interindividual differences in the metabolic capacity (the phenotype), with continuous distribution of the activities rather than qualitative distinction between rapid and slow acetylators. To determine whether the phenotype might be predicted solely from the mutation pattern of NAT2, quantitative relationships were calculated between mutation patterns of the NAT2 gene and the phenotype of NAT2 assessed either in vitro or in vivo. Healthy volunteers were examined for the velocity at which they metabolized sulfamethazine, and human liver cytosols were measured for NAT2 enzymatic activity, obtaining in vivo and in vitro metabolic phenotype, respectively. Typing of the NAT2 gene was performed by polymerase chain reaction, restriction fragment length analysis, or allele-specific polymerase chain reaction. Multiple linear regression analysis provided quantitative relationships between allelic pattern and the NAT2 activities measured in vivo and in vitro. Estimates showed the influence of particular allelic configurations on enzyme activity in vitro and the extent of acetylation of the probe drug in vivo, resulting in a strict gene-dose effect. Comparison of in vitro results with in vivo phenotyping figures showed a high degree of correspondence, indicating that the one is the reflection of the other.

Adult↗

PubMed2000

Polymorphism of the N-acetyltransferase (NAT2), smoking and the potential risk of periodontal disease.

Periodontal disease is a common multifactorial process that leads to bone destruction and tooth loss. Interactions of environmental and genetic factors determine the extent and severity of periodontal disease. Smoking is one of the risk factors for periodontal disease, and the risk may be influenced by the polymorphism of N-acetyltransferase (NAT2) via metabolism of smoke-derived xenobiotics. We therefore hypothesized that a NAT2 genotype would be a risk factor for periodontal disease. A total of 154 Caucasian subjects were assigned to one of two groups (1) no or mild and (2) severe periodontal disease based on radiographic (bone destruction) and clinical criteria (probing depth, attachment loss) and the number of teeth. In all subjects genotyping for mutations on NAT2 was performed by means of PCR and RFLP analysis. In the less-affected group genotyping showed a fraction of predicted slow and rapid acetylators (53.6% and 46.4%, respectively) corresponding to the normal distribution in Caucasians. Severely affected patients were predominantly slow acetylators, the odds ratios being between 2.38 and 5.02 for the NAT2-related risk depending on the outcome parameters chosen. Adjustment for age had no influence on these findings. Our data indicate that the slow acetylator phenotype is associated with a higher risk of periodontitis, especially with respect to the severity of the disease. Possible implications with respect to the risk associated with smoking are discussed.

Acetylation↗

PubMed2000

Disposition of propafenone in a poor metabolizer of CYP2D6 with Gilbert's syndrome.

Gilbert's syndrome, a genetic deficiency in bilirubin UDP-glucuronosyltransferase (UGT1A1), may dispose to increased toxicity of propafenone in poor metabolizers (PMs) of cytochrome P4502D6 because glucuronidation of propafenone is the major metabolic pathway for drug elimination in PMs. A patient with Gilbert's syndrome who is also PM participated in an interaction study with propafenone and rifampicin along with five otherwise healthy PMs. Using stable isotope techniques, the pharmacokinetics of single doses of 140 mg propafenone i.v. (unlabelled) and 300 mg propafenone p.o. (labelled) were compared between the index patient and the five healthy controls. Propafenone did not accumulate in the plasma of the index patient either before or during induction: AUC(0-infinity) of propafenone in the index patient was within the 95% confidence interval of controls; AUC(0-infinity) of propafenone glucuronide and amount of urinary excretion of propafenone glucuronide in the patient were within or even greater than the 95% confidence intervals of controls. Therefore, individuals with Gilbert's syndrome who also have a PM phenotype appear to be at no higher risk for toxicity of propafenone than otherwise healthy PMs. An indirect conclusion from these in vivo data might be that propafenone is not a substrate of the UGT1A1 isoform.

Adult↗

PubMed1997

Relationship between human genotype and phenotype of N-acetyltransferase (NAT2) as estimated by discriminant analysis and multiple linear regression: 1. Genotype and N-acetylation in vivo.

Twenty-six healthy Caucasian subjects were evaluated for polymorphic N-acetyltransferase (NAT2) metabolic activity in vivo by sulfamethazine phenotyping and for their respective NAT2 genotype. Application of discriminant analysis allowed the separation of the rapid and slow acetylators solely on the base of their respective mutation pattern with identical results as achieved by the classical method of discrimination according to the phenotyping results. Multiple linear regression analysis was used to obtain a quantitative relationship between allelic pattern and the phenotypic outcome. It is shown that the computation methods produce relationships enabling the influence of particular mutations and/or allelic configurations on the metabolic activity in vivo to be estimated. This may be important in cases of discordant or overlapping phenotype and genotype results as well as in investigating the NAT2 polymorphism as a risk factor for cancer and other disease in epidemiological studies.

Acetylation↗

PubMed1997

In-vitro binding of propiverine hydrochloride and some of its metabolites to serum albumin in man.

The distribution and pharmacological action of propiverine, a bladder spasmolytic agent, are affected by the extent of plasma-protein binding. Because attempts to assess the albumin-binding of propiverine have produced conflicting results, the binding parameters of the drug and some of its metabolites to serum albumin in man have been re-evaluated. In man propiverine is bound to serum albumin at a single site with high affinity (KA1 = 1.45 x 10(4) L mol-1) and at least two sites with low affinity (KA2 = 2.5 x 10(2) L mol-1). The metabolites of propiverine, namely M2 (dealkylated propiverine), M5 (the N-oxide of propiverine) and M6 (the N-oxide of M2), are less firmly bound to serum albumin; this is considered to be non-specific binding. Binding experiments with human serum revealed that there are additional binding proteins. At therapeutic plasma levels the extent of binding was calculated to be 90, 15, 60, and 20% for propiverine and the metabolites M2, M5, and M6, respectively. The strong binding of propiverine to serum proteins controls its availability to the liver. Because the metabolites are not tightly bound to serum proteins, after metabolism of propiverine its metabolites are easily eliminated.

Benzilates↗

PubMed1993

[Do drugs in pregnancy modify neonatal jaundice?].

An increased incidence of neonatal jaundice has been observed in babies born to mothers who were treated with different drugs before or during delivery. In this review literature data on such drugs are collected which are under suspicion to produce increased levels of bilirubin in the newborn infant. Despite numerous attempts to show significant effects of these drugs on neonatal hyperbilirubinaemia most of them give contradictory results. Nevertheless, agents that stimulate uterine motility (oxytocin) as well as drugs that inhibit uterine motility (ritodrine) may have an icterogenic effect. Possible mechanisms of their actions are described. Thus, even if there is some association between drugs given prenatally and jaundice developing postnatally, no practical consequences arise except in such cases where additional risk factors may increase the danger of bilirubin encephalopathies in jaundiced infants.

Anesthesia, Epidural↗

PubMed1991

N-acetylation and debrisoquine hydroxylation polymorphisms in patients with Gilbert's syndrome.

1. N-acetylation and debrisoquine hydroxylation phenotypes were determined in 54 patients with Gilbert's syndrome and in 247 (sulphamethazine) and 76 (debrisoquine) non-related healthy volunteers. 2. Forty (74.1%) of the patients and 135 (54.7%) of the healthy volunteers were slow acetylators (chi 2 = 6.87). In the patients, the cumulative urinary excretion of sulphamethazine up to 6 h (Ae(0,6)) was significantly lower. No differences in the frequency of debrisoquine poor metabolizers were observed: Gilbert's syndrome 5/54 (9.3%), healthy volunteers 5/76 (6.6%). The metabolic ratios were similar in both groups as well as the urinary recoveries of debrisoquine and its 4-hydroxy metabolite. 3. Gilbert's syndrome seems to be related in some way to N-acetylation but not to the debrisoquine hydroxylation polymorphism.

Acetylation↗