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Biomedical subjects

Matthias Folwaczny

Publications and source records attributed to Matthias Folwaczny.

At least 19 recordsLinked to original sources

Role of the NFKB1 -94ins/delATTG promoter polymorphism in IBD and potential interactions with polymorphisms in the CARD15/NOD2, IKBL, and IL-1RN genes.

BACKGROUND: Recently, an association of the NFKB1 polymorphism -94ins/delATTG with ulcerative colitis (UC) has been reported. This 4-bp insertion/deletion polymorphism is localized in the promoter region of the NFKB1 gene and appears to be functionally relevant. The aim of the present study was to confirm the association of the -94ins/delATTG (W/D) NFKB1 promoter polymorphism with UC in a population of German origin and to test for a potential association with Crohn's disease (CD). Furthermore, potential interactions of the -94ins/delATTG polymorphism with the IKBL and the IL-1RN genes should be determined. MATERIALS AND METHODS: The study population comprised 630 patients with CD, 365 patients with UC, and 974 healthy controls. Genotyping was performed using polymerase chain reaction and restriction fragment length polymorphism analysis. For statistical evaluation, the chi-square test and the Fisher exact test were used. RESULTS: No significant association of the W/D NFKB1 polymorphism with CD or UC was detected. In addition, no significant interactions between the -94ins/delATTG NFKB1 polymorphism and polymorphisms within the IKBL and the IL-1RN genes, respectively, were found in CD or UC. Also, no significant interactions of the NFKB1 polymorphism with mutations of the CARD15/NOD2 gene and with clinical phenotypes were detected in CD. Moreover, no associations of the NFKB1 polymorphism were found in UC depending on disease localization. CONCLUSIONS: The present study could not confirm the reported association of the -94ins/delATTG NFKB1 polymorphism with UC and also found no evidence for a role of this polymorphism in CD. The results do not give evidence for a role of this NFKB1 polymorphism in the pathogenesis of UC and CD.

Adaptor Proteins, Signal Transducing↗

Cell death effects of resin-based dental material compounds and mercurials in human gingival fibroblasts.

In order to test the hypothesis that released dental restorative materials can reach toxic levels in human oral tissues, the cytotoxicities of the resin-based dental (co)monomers hydroxyethylmethacrylate (HEMA), triethyleneglycoldimethacrylate (TEGDMA), urethanedimethacrylate (UDMA), and bisglycidylmethacrylate (BisGMA) compared with methyl mercury chloride (MeHgCl) and the amalgam component mercuric chloride (HgCl2) were investigated on human gingival fibroblasts (HGF) using two different test systems: (1) the modified XTT-test and (2) the modified H 33342 staining assay. The HGF were exposed to various concentrations of the test-substances in all test systems for 24 h. All tested (co)monomers and mercury compounds significantly (P<0.05) decreased the formazan formation in the XTT-test. EC50 values in the XTT assay were obtained as half-maximum-effect concentrations from fitted curves. Following EC50 values were found (mean [mmol/l]; s.e.m. in parentheses; n=12; * significantly different to HEMA): HEMA 11.530 (0.600); TEGDMA* 3.460 (0.200); UDMA* 0.106 (0.005); BisGMA* 0.087 (0.001); HgCl2* 0.013 (0.001); MeHgCl* 0.005 (0.001). Following relative toxicities were found: HEMA 1; TEGDMA 3; UDMA 109; BisGMA 133; HgCl2 887; MeHgCl 2306. A significant (P<0.05) increase of the toxicity of (co)monomers and mercurials was found in the XTT-test in the following order: HEMA < TEGDMA < UDMA < BisGMA < HgCl2 < MeHgCl. TEGDMA and MeHgCl induced mainly apoptotic cell death. HEMA, UDMA, BisGMA, and HgCl2 induced mainly necrotic cell death. The results of this study indicate that resin composite components have a lower toxicity than mercury from amalgam in HGF. HEMA, BisGMA, UDMA, and HgCl2 induced mainly necrosis, but it is rather unlikely that eluted substances (solely) can reach concentrations, which might induce necrotic cell death in the human physiological situation, indicating that other (additional) factors may be involved in the induction of tissue (pulp) inflammation effects after dental restauration.

Apoptosis↗

Cytotoxic and genotoxic effects of resin monomers in human salivary gland tissue and lymphocytes as assessed by the single cell microgel electrophoresis (Comet) assay.

Malignant tumors of the three major pairs and the numerous minor salivary glands in humans are rare, and little is known about their various etiologies. Considering the fact that resin monomers from dental restorative materials are released into the saliva and diffuse into the tooth pulp or gingiva, mucosa, and salivary glands, this may potentially contribute to tumorigenesis. Resin monomers may also be reabsorbed and reach the circulating blood as well. Whereas the cytotoxic potential of some components has been clearly documented, data on genotoxicity in human target cells require further investigation. In the present study, genotoxic and cytotoxic effects of three common methacrylates are investigated in human samples of salivary glands and peripheral lymphocytes. The Comet assay was used to quantify DNA single strand breaks, alkali labile and incomplete excision repair sites in salivary gland probes and lymphocytes of 10 volunteers. The xenobiotics investigated were triethyleneglycoldimethacrylate (TEGDMA), urethanedimethacrylate (UDMA), and 2-hydroxyethylmethacrylate (HEMA), with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and dimethyl sulfoxide (DMSO) as controls. DNA migration was analyzed using the tail moment according to Olive (OTM). Cytotoxicity was monitored using trypan blue staining. With TEGDMA concentrations at 10(-5)m (10(-3)m), UDMA at 10(-7)m (10(-7)m), and HEMA at 10(-3)m (10(-5)m) significant enhancements of DNA migration were achieved in tissue cells (lymphocytes) as compared to the negative controls. At higher concentrations of up to 2.5x10(-2)m, induced DNA migration was expressed by OTM at 10.7 for TEGDMA in tissue cells (8.7 in lymphocytes), 10.5 for UDMA (6.4), and 9.7 for HEMA (6.1). The viability of the cell systems was not affected as concerns the threshold level for the assay of 75% viable cells except for the highest concentration tested for TEGDMA and UDMA in tissue cells. At higher concentration levels, all tested substances induced significant enhancement of DNA migration in the Comet assay as a possible sign for genotoxic effects in human salivary glands and lymphocytes. These data add to the results of prior studies in human peripheral lymphocytes and give evidence of a possible risk factor for tumor initiation in human salivary glands.

Aged↗

Association of polymorphisms in the interleukin-18 gene in patients with Crohn's disease depending on the CARD15/NOD2 genotype.

UNLABELLED: An increased expression of interleukin-18 (IL-18), a proinflammatory cytokine inducing interferon-gamma, has been found in Crohn's disease (CD). In the IL-18 gene, several partly functional relevant polymorphisms are known. This study sought to investigate associations of IL-18 polymorphisms in inflammatory bowel disease and CD according to CARD15/NOD2 mutation status and clinical phenotypes. METHODS: The IL-18 polymorphisms -607, -137, and the third position of codon 35 (c35/3) were genotyped in 210 patients with CD, 140 patients with ulcerative colitis, and 265 healthy controls using polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: Frequencies of alleles and genotypes of the 3 polymorphisms and of the respective haplotypes and diplotypes displayed no significant differences between the whole groups of patients with CD and ulcerative colitis, respectively, compared with the controls. After stratification of patients with CD for CARD15/NOD2 status, significant associations of genotypes -137 CC (P = 0.018) and c35/3 CC (P = 0.010) and of the diplotype 2-2 (P = 0.018) were found in cases carrying CARD15/NOD2 mutations. Associations of genotypes -137 GG (P = 0.015) and c35/3 AA (P = 0.030) with colonic disease only in cases positive for CARD15/NOD2 mutations and of the genotype -607 AA (P = 0.007) with fistulas in cases negative for CARD15/NOD2 mutations were observed. CONCLUSIONS: In this study, significant differences of several genotypes and diplotypes within the IL-18 gene in CD depending on CARD15/NOD2 status have been found. In context with an increased expression of IL-18 in CD, it remains to be shown whether the expression of IL-18 is influenced by CARD15/NOD2 mutation status.

Adult↗

Polymorphisms of the interleukin-18 gene in periodontitis patients.

BACKGROUND: Interleukin (IL)-18 regulates the expression of the proinflammatory cytokine interferon (IFN)-gamma. The present study sought to test the putative involvement of six different IL-18 gene polymorphisms in pre-disposition to destructive periodontal disease. METHODS: A total of 123 patients with periodontitis and 121 healthy controls were genotyped for six IL-18 polymorphisms at position -656, -607, -137, +113, +127 and codon 35/3. Genotyping has been performed by PCR and restriction fragment length polymorphism analysis. The frequencies of alleles and genotypes as well of haplotypes within both study groups were compared using the Pearson Chi-square test at a level of significance of 5% (p<0.05). RESULTS: Coseggregation was found to be 100% for the two polymorphisms at position -656 and -607 as well as for the polymorphisms at position -137, +113, and +127. The distribution of genotypes for the IL-18 gene polymorphism at position -656/-607 (p=0.854), at position -137/+113/+127 (p=0.320), and at codon 35/3 (p=0.481) was not significantly different among periodontitis patients if compared with healthy control subjects. The distribution of haplotype combinations for the -607 and -137 polymorphism also showed not significant difference between the both study groups (p=0.545). CONCLUSION: Herein the six different IL-18 gene polymorphisms were not associated with destructive periodontal disease.

Adult↗

Ablation of temporomandibular joint structures of a pig with a fibre-guided 308 nm excimer laser light--an in vitro investigation.

PURPOSE: The present in vitro investigation was carried out to assess the efficacy of treatment with 308 nm excimer laser radiation applied to the structures of the temporomandibular joint of a pig. Laser parameters suitable to ensure adequate clinical efficiency with only minor thermal damage to the surrounding tissues were to be determined. MATERIAL AND METHODS: Tissue structures of the temporomandibular joint (cortical and cancellous bone, cartilage, disc and muscle) were extracted from freshly killed pigs and served as specimens. The specimens were embedded in polymethylmethacrylate. The laser light was applied after horizontal sectioning and measurement of thickness. The number of impulses that were necessary to perforate the specimen was counted and the rate of ablation determined. In addition, the irradiated surface was investigated histologically and the degree of tissue alteration was evaluated. RESULTS: The lowest energy threshold for ablation was found at an energy density of 0.8 J/cm2. Depending on the type of tissue, the maximum rate of ablation was evaluated as 1.7-6.3 microm/pulse. The depth of the thermal alteration to the surrounding tissue was about 30-70 microm. CONCLUSION: The guidable 308 nm excimer laser light offers a combination of precise tissue ablation with only minimal thermal damage to the surrounding tissue.

Animals↗

Genotoxicity and cytotoxicity of dental materials in human lymphocytes as assessed by the single cell microgel electrophoresis (comet) assay.

OBJECTIVES: Resin monomers may be released from restorative dental materials and can diffuse into the tooth pulp or the gingiva, and can reach the saliva and the circulating blood. Whereas the cytotoxic potential of some components has been clearly documented, possible genotoxicity in human target cells demands further investigation. METHODS: The Comet assay was used to quantify DNA single strand breaks, alkali labile and incomplete excision repair sites in lymphocytes of 10 volunteers. The xenobiotics investigated were 2-hydroxyethylmethacrylate (HEMA), triethyleneglycoldimethacrylate (TEGDMA), urethane dimethacrylate (UDMA), and bisphenol A-glycidyl methacrylate (Bis-GMA) with N-methyl-N'-nitro-N-nitrosoguanidine and dimethyl sulfoxide as controls. DNA migration was quantified using the tail moment according to Olive (OTM) and DNA migration was considered to be elevated at OTM levels above 2. Cytotoxicity was monitored using trypan blue. RESULTS: In the negative controls, OTM ranged between 1.0 and 1.2. With HEMA concentrations above 10(-6)M, TEGDMA 10(-3)M, Bis-GMA 10(-4)M, and UDMA above 10(-6)M relevant enhancements of DNA migration (OTM>2) were achieved. At higher concentrations of up to 2.5x10(-2) induced DNA migration was expressed by OTM of 3.3 for HEMA, 4.5 for TEGDMA, 7.4 for Bis-GMA, and 2.8 for UDMA. Relevant cytotoxic effects were also seen but vitality levels were at a critical range of 71% for Bis-GMA and 73% for TEGDMA, only. SIGNIFICANCE: In higher concentration levels, all tested substances induced significant but minor enhancement of DNA migration in the Comet assay as a possible sign for limited genotoxic effects. However, with the highest levels of DNA migration being combined with elevated cytotoxic effects, a low in vivo genotoxic strain appears to be posed by the resin components.

Adult↗

Lack of association between the TNF alpha G -308 A promoter polymorphism and periodontal disease.

BACKGROUND: Immunorelevant gene polymorphisms might influence the susceptibility for periodontal disease. The present study assessed the frequency of a promoter polymorphism (-308G-to-A) of the tumour necrosis factor (TNF)alpha gene in patients with periodontitis and controls. METHODS: Eighty-one patients with generalized chronic periodontitis and 80 healthy controls were genotyped for the -308 polymorphism of the TNF alpha gene by PCR amplification and subsequent restriction fragment length polymorphism analysis. The diagnosis of chronic periodontitis was made for each subject on basis of standardized clinical and radiographic criteria. RESULTS: In patients with peridontitis and controls, the frequency of the TNF alpha-308 A allele was comparable (19.1% [31/162] versus 13.8% [22/160]; p=0.193). CONCLUSION: The present study revealed no association between the -308 TNF alpha gene polymorphism and periodontal disease.

Adenine↗

The CD14 -159C-to-T promoter polymorphism in periodontal disease.

BACKGROUND: A single-nucleotide promoter polymorphism in the CD14 gene was associated with various inflammatory conditions. The present study sought to determine the frequency of the CD14 -159C-to-T polymorphism among subjects with periodontitis and healthy control individuals. METHODS: A total of 70 patients with periodontal disease and 75 healthy controls were genotyped for the CD14 -159C-to-T polymorphism. Genotyping was performed by polymerase chain reaction and restriction fragment length polymorphism analysis. The allele frequencies and distribution of genotypes within both study groups were compared using Fisher's exact test at a level of significance of 5% (p<0.05). RESULTS: Overall, the frequency for the CD14 -159T allele in patients with periodontitis was 39.3% (55/140) and 48.0% (72/150) for the controls (p=0.135). The CD14 -159C allele was significantly more prevalent (p=0.013) among females with periodontitis (33.3%; 24/72) as compared with healthy control subjects (55.6%; 30/54). In contrast, the distribution of the CD14 -159C-to-T polymorphism showed no significant difference among males with and without periodontitis (p=0.816). CONCLUSION: Herein, the C -159T promoter polymorphism of the CD14 gene was associated in female but not in male patients with periodontal disease.

Adult↗

The 3020insC mutation of the NOD2/CARD15 gene in patients with periodontal disease.

The 3020insC mutation of the NOD2/CARD15 gene leads to impaired activation of nuclear factor-kappa B (NF-kappaB) in vitro. As the destruction of periodontal tissue is mediated via activation of NF-kappaB, with subsequent transcription of proinflammatory cytokines, the c-insertion mutation of the NOD2/CARD15 gene might contribute to the proposed genetic background of periodontitis. The present study analysed the frequency of this mutation in 80 patients with chronic periodontal disease and 122 healthy controls. The 3020insC mutation was identified by employing the polymerase chain reaction followed by restriction fragment length polymorphism analysis. The prevalence of the 3020insC mutation of the NOD2/CARD15 protein in patients with periodontitis was 1.9% (three of 160) and that for the control group was 2.0% (five of 244) (P = 0.942). Hence, unlike in Crohn's disease, the 3020insC mutation of the NOD2/CARD15 gene does not seem to influence the pathophysiology of periodontitis.

Adult↗

The effectiveness of InGaAsP diode laser radiation to detect subgingival calculus as compared to an explorer.

BACKGROUND: The aim of the present study was to compare the ability of the diode laser to detect residual calculus with that of an explorer. METHODS: The root surface of 40 extracted human teeth, each partially covered with subgingival calculus, was instrumented with curets under simulated clinical conditions in a manikin. The samples were randomly assigned to two study groups. In group A, the root surface was treated with an explorer until it appeared free of mineralized deposits upon examination. The samples in group B were instrumented until the relative intensity of fluorescence as induced with diode laser radiation was below a threshold value of 5. The root surface of each sample was then examined for residual calculus using standardized digital images. The statistical analysis was performed with a non-paired t test at a level of significance of 5% (P < 0.05). RESULTS: The root surface of single-rooted teeth showed residual calculus on 0.19 +/- 0.37 x 10(7) microm2 in the laser group and on 0.11 +/- 0.26 x 10(7) microm2 in the explorer group (P = 0.19). For multirooted teeth, the mean calculus-covered area was 0.50 +/- 0.48 x 10(7) microm2 for the teeth evaluated with an explorer and 0.27 +/- 0.43 x 10(7) microm2 for the diode laser group (P = 0.02). CONCLUSION: The present findings indicate that the detection of subgingival calculus is significantly improved using 655 nm diode laser radiation compared to an explorer for molars but not for single-rooted teeth.

Arsenic↗

Influence of parameters on root surface roughness following treatment with a magnetostrictive ultrasonic scaler: an in vitro study.

BACKGROUND: This in vitro study aimed to evaluate the influence of different parameters, i.e., lateral force, instrument power setting, and the shape of the working tip, on the roughness of root surfaces following treatment with a magnetostrictive ultrasonic scaling device. METHODS: The study sample comprised a total of 102 extracted human molars, premolars, canines, and incisors. The samples were randomly divided into 10 equal units of 10 each for treatment with the ultrasonic device at a lateral force of 0.5 N and 2.0 N, a low and high instrument power setting, and with a straight and angulated shaped working tip. Twenty samples were treated manually using curets at a lateral force of 0.5 N and 2.0 N. Two samples were left untreated as controls. The mean (Ra) and maximum (Rmax) surface roughness of each sample was recorded. The statistical analysis was performed using analysis of variance (three-way ANOVA) at a level of significance of 5% (P < 0.05). RESULTS: The mean surface roughness (+/-SD) using different parameters ranged from 0.6 +/- 0.1 microm to 1.8 +/- 0.3 microm. The maximum surface roughness (+/-SD) was between 4.8 +/- 1.3 microm and 17.2 +/- 4.3 microm. The mean surface roughness (+/-SD) for samples treated with curets at a lateral force of 0.5 N was 0.5 +/- 0.0 microm and 0.4 +/- 0.1 microm at 2.0 N. The maximum surface roughness (+/-SD) was 3.7 +/- 0.8 microm at 0.5 N and 3.9 +/- 1.4 microm at 2.0 N. CONCLUSIONS: The findings of the present study indicate that the shape of the working tip and the lateral force significantly influence the mean and maximum surface roughness of root surfaces treated with a magnetostrictive ultrasonic scaling device. At any specific parameter, the surface roughness was significantly higher for the ultrasonic scaling device as compared to the hand curet.

Analysis of Variance↗

Stabilization effects of CAD/CAM ceramic restorations in extended MOD cavities.

PURPOSE: Using extended, standardized MOD preparations, it was the aim of this in vitro study to examine the performance of CAD/CAM ceramic inlays in comparison to composite inlays after mechanical and thermal fatigue loading in terms of marginal quality and stabilization of the remaining tooth structure. MATERIALS AND METHODS: Standardized cavities with different wall thicknesses were prepared in 90 extracted premolars; 10 additional premolars remained untreated. Composite inlays (Tetric) and CAD/CAM restorations (Cerec II; Vita Mark II) were adhesively placed in the cavities. After loading in a chewing simulator, quantitative and qualitative marginal gap examinations were conducted and fracture resistance determined. RESULTS: The results show that ceramic inlays provide significantly greater stabilization and better marginal quality than do composite inlays. CONCLUSION: Chairside-fabricated ceramic inlays inserted using adhesive technology are able to stabilize weakened cusps. In the case of very thin remaining walls (about 1.3 mm), however, the marginal quality and the cusp-stabilizing effect are also reduced.

Bicuspid↗

Prevalence of the chemokine receptor CCR5-Delta32 gene mutation in periodontal disease.

A 32-base-pair deletion in the CCR5 gene was previously shown to influence the susceptibility for several infectious diseases. The present study compared the frequency of the CCR5-Delta32 mutation among subjects with periodontal disease and healthy control individuals. The prevalence of the CCR5-Delta32 mutation was determined in 81 patients with generalized periodontitis and 121 healthy controls. Standardized clinical and radiographic criteria were used for the diagnosis of periodontitis for each subject. The CCR5-Delta32 mutation was identified by PCR amplification and subsequent agarose gel electrophoresis. Genotype and allele frequencies among both study groups were compared using Fisher's exact test at a level of significance of 5% (P<0.05). The frequency of the CCR5-Delta32 allele was 9.9% (16/162) for periodontitis patients and 10.7% (26/216) for the healthy controls. The allele frequencies between periodontitis patients and the control group for the CCR5-Delta32 mutation were not significantly different (P=0.801). The present study revealed no association between the CCR5-Delta32 mutation and susceptibility to periodontal disease.

Adolescent↗