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ABSTRACT: OBJECTIVES: This in vitro study was established to examine whether visfatin thought to be a link between periodontitis and obesity is produced by periodontal ligament (PDL) cells and, if so, whether its synthesis is modulated by microbial and/or biomechanical signals. MATERIALS AND METHODS: PDL cells seeded on BioFlex® plates were exposed to the oral pathogen Fusobacterium nucleatum ATCC 25586 and/or subjected to biomechanical strain for up to 3 days. Gene expression of visfatin and toll-like receptors (TLR) 2 and 4 was analyzed by RT-PCR, visfatin protein synthesis by ELISA and immunocytochemistry, and NFκB nuclear translocation by immunofluorescence. RESULTS: F. nucleatum upregulated the visfatin expression in a dose- and time-dependent fashion. Preincubation with neutralizing antibodies against TLR2 and TLR4 caused a significant inhibition of the F. nucleatum-upregulated visfatin expression at 1 day. F. nucleatum stimulated the NFκB nuclear translocation. Biomechanical loading reduced the stimulatory effects of F. nucleatum on visfatin expression at 1 and 3 days and also abrogated the F. nucleatum-induced NFκB nuclear translocation at 60 min. Biomechanical loading inhibited significantly the expression of TLR2 and TLR4 at 3 days. The regulatory effects of F. nucleatum and/or biomechanical loading on visfatin expression were also observed at protein level. CONCLUSIONS: PDL cells produce visfatin, and this production is enhanced by F. nucleatum. Biomechanical loading seems to be protective against the effects of F. nucleatum on visfatin expression. CLINICAL RELEVANCE: Visfatin produced by periodontal tissues could play a major role in the pathogenesis of periodontitis and the interactions with obesity and other systemic diseases.
Clinical Oral Investigations 02/2013; · 2.36 Impact Factor
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Arne S Schaefer,
Gregor Bochenek,
Thomas Manke,
Michael Nothnagel,
Christian Graetz,
Anneke Thien,
Yvonne Jockel-Schneider,
Inga Harks,
Ingmar Staufenbiel,
Cisca Wijmenga, [......],
Joerg Meyle,
Peter Eickholz,
Leonardo Trombelli,
Chiara Scapoli,
Rahime Nohutcu,
Corinna Bruckmann,
Christof Doerfer, Søren Jepsen,
Bruno G Loos,
Stefan Schreiber
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ABSTRACT: AIM: Many studies investigated the role of genetic variants in periodontitis, but few were established as risk factors. We aimed to validate the associations of recent candidate genes in aggressive periodontitis (AgP). MATERIAL AND METHODS: We analysed 23 genes in 600 German AgP patients and 1441 controls on the Illumina custom genotyping array Immunochip. We tested a suggestive association in a Dutch and German/Austrian AgP case-control sample, and a German chronic periodontitis (CP) case-control sample using Sequenom iPlex assays. We additionally tested the common known risk variant rs1333048 of the gene ANRIL for its association in a Turkish and Italian population. RESULTS: None of the analysed genes gave statistical evidence for association. Upon covariate adjustment for smoking and gender, in the pooled German-Austrian AgP sample, IL10 SNP rs6667202 was associated with p = 0.016, OR = 0.77 (95% CI = 0.6-0.95), and in the Dutch AgP sample, adjacent IL10 SNP rs61815643 was associated with p = 0.0009, OR = 2.31 (95% CI = 1.4-3.8). At rs61815643, binding of the transcription factor PPARG was predicted. ANRIL rs1333048 was associated in the Turkish sample (pallelic = 0.026, OR = 1.67 [95% CI = 1.11-2.60]). CONCLUSIONS: Previous candidate genes carry no susceptibility factors for AgP. Association of IL-10 rs61815643 with AgP is suggested. ANRIL is associated with periodontitis across different populations.
Journal Of Clinical Periodontology 02/2013; · 3.00 Impact Factor
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ABSTRACT: Human beta-defensins (hBDs) and the C-C chemokine ligand 20 (CCL20) produced by gingival epithelial cells (GECs) and fibroblasts (HGFs) are antimicrobial peptides (AMPs) that play an important role in innate immunity. The aim of this study was to determine the differential immune response of GECs and HGFs to the oral commensal Streptococcus gordonii (SG) and the pathogen Porphyromonas gingivalis (PG).
In addition to the analysis of gingival biopsies, primary GECs and HGFs were exposed to SG and/or PG, and expression of various AMPs and pro-inflammatory mediators was studied by real-time PCR and ELISA.
Gene expression of AMPs was detected in gingival connective tissue. Both SG and PG induced the mRNA-expression of hBD-2 and hBD-3 in GECs as well as HGFs after 24 h (p < 0.05). In HGFs, the commensal bacterium SG stimulated the mRNAs of hBD-3 and CCL20 after 24 h (p < 0.05), while not in GECs. In GECs, the inductive effect of PG on the mRNA-expression of hBD-2 was amplified when cells were first exposed to commensal SG (for 1 h) prior to stimulation with PG (SG-PG; p < 0.05).
Our data indicate that cell-bacteria interactions and/or bacteria-bacteria cross-talk may have an impact on AMP-regulation in gingiva.
Journal Of Clinical Periodontology 07/2012; 39(10):913-22. · 3.00 Impact Factor
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ABSTRACT: Aim:
Orthodontic malpractice as well as hyperocclusal forces can
aggravate periodontitis-induced destruction of tooth-supporting
tissues, but the underlying mechanisms for the co-destructive
effect of biomechanical loading are yet to be elucidated. This
in-vitro study was performed to investigate whether biomechanical
forces modulate the response of periodontal ligament (PDL)
cells to inflammation.
Materials and Methods:
PDL cells (from six donors) grown on
BioFlex® plates were treated with interleukin (IL) 1, which is
increased at inflamed periodontal sites, and/or subjected to cyclic
tensile strain (CTS) of low (3%) and high (20%) magnitudes
for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β,
IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1
(COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by
real-time PCR and ELISA. The wound fill rate was examined in an
in-vitro wound healing assay. For statistical analyses, Student’s
t-test and ANOVA were applied (p<0.05).
Results:
In general, the IL1β-induced expression of proinflammatory
mediators was significantly enhanced by CTS on day 1 and
significantly downregulated on day 6. CTS of high magnitude
significantly inhibited the IGF1 synthesis but significantly upregulated
VEGF under normal and inflammatory conditions. In
general, CTS also downregulated the IL1β-induced COL1, ALP,
and RUNX2 expression. From day 5 on, the lowest wound fill rate
was observed in cells which were simultaneously exposed to inflammatory
and biomechanical signals.
Conclusion:
These findings suggest that orthodontic and occlusal
loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix
and osteogenic proteins but not via augmentation of periodontal
inflammation.
Hintergrund und Ziel:
Unsachgemäß durchgeführte kieferorthopädische
Zahnbewegungen wie auch okklusale Überbelastungen
können eine parodontitisinduzierte Destruktion des Parodontiums
verstärken. Die zugrunde liegenden Mechanismen für den destruktionsverstärkenden
Effekt der biomechanischen Belastung sind
jedoch noch ungeklärt. In dieser In-vitro-Studie sollte untersucht
werden, ob biomechanische Kräfte die Reaktion von parodontalen
Ligament-(PDL-)Zellen auf Entzündungsreize modulieren.
Material und Methodik:
Auf BioFlex®-Platten kultivierte PDL-Zellen
von sechs Patienten wurden mit Interleukin (IL) 1β, das an
entzündeten parodontalen Stellen erhöht ist, inkubiert und/oder
einer zyklischen Zugbelastung (CTS) niedriger (3%) und hoher
(20%) Stärke für 1 und 6 Tage ausgesetzt. Die Synthese von proinflammatorischen
Mediatoren (IL1β, IL8, COX2), Wachstumsfaktoren
(IGF1, VEGF, TGFβ1), Kollagen Typ 1 (COL1) und osteogenen
Proteinen (ALP, RUNX2) wurde mittels Real-Time-PCR und ELISA
analysiert. Die Rate der Wundauffüllung wurde mit einem In-vitro-Wundheilungsassay untersucht. Für die statistische Auswertung
kamen der Student’s t-Test und ANOVA zur Anwendung (p<0,05).
Ergebnisse:
Im Allgemeinen wurde die IL1β-induzierte Expression
der proinflammatorischen Mediatoren durch CTS am Tag 1 signifikant
verstärkt und am Tag 6 signifikant gehemmt. CTS hoher Stärke
reduzierte signifikant die IGF1-Synthese, führte aber zu einer signifikanten
Steigerung von VEGF unter normalen und entzündlichen
Bedingungen. CTS hemmte im Allgemeinen auch die IL1β-induzierte Expression von COL1, ALP und RUNX2. Ab dem fünften
Tag wurde die geringste Wundheilungsrate in den Kulturen beobachtet,
die gleichzeitig entzündlichen und biomechanischen Signalen
ausgesetzt waren.
Schlussfolgerung:
Diese Ergebnisse legen nahe, dass kieferorthopädische
und okklusale Kräfte zur parodontalen Destruktion durch
Herunterregulation extrazellulärer Matrixproteine und osteogener
Differenzierungsmarker, jedoch nicht durch Verstärkung der parodontalen
Entzündung bei Parodontitispatienten beitragen
könnten.
Key Words:
Orthodontic load-Biomechanical forces-Inflammation-Periodontitis-Periodontium-PDL cells-Cytokines
Schlüsselwörter:
Kieferorthopädische Belastung-Biomechanische Kräfte-Entzündung-Parodontitis-Parodont-PDL-Zellen-Zytokine
Journal of Orofacial Orthopedics / Fortschritte der Kieferorthopädie 04/2012; 71(6):390-402. · 0.86 Impact Factor
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Gesa M Richter,
Christian Graetz,
Pia Pohler,
Michael Nothnagel,
Henrik Dommisch,
Marja L Laine,
Mathias Folwaczny,
Barbara Noack,
Peter Eickholz,
Birte Groessner-Schreiber, Søren Jepsen,
Bruno G Loos,
Stefan Schreiber,
Arne S Schaefer
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ABSTRACT: Involvement of TLR2 in the pathophysiology of periodontitis has widely been discussed, but hitherto, no validated genetic associations were reported. Previous association studies lacked sufficient statistical power and adequate haplotype information to draw unambiguous conclusions. The aim of this study was to comprehensively investigate TLR2 linkage disequilibrium (LD) regions for their potential associations with periodontitis in two large analysis populations of aggressive (AgP) and chronic periodontitis (CP) of North West European descent.
The study population comprised 598 AgP patients, 914 CP patients and 1804 healthy controls. Analysis of TLR2 LD regions was performed with haplotype tagging SNPs (tagSNPs) using SNPlex and TaqMan genotyping assays. Genotypic, dominant, multiplicative, and recessive genetic models were tested. The genotypes were adjusted for the covariates smoking, diabetes, and gender. Resequencing was performed by Sanger technology.
Upon covariate adjustment and correction for multiple testing, no tagSNPs showed significant associations with AgP or CP. Targeted resequencing of exon 3 in 47 AgP cases identified carriership of two common and three rare variants.
Common LD regions of TLR2 do not show genetic associations with periodontitis in the North West European population. Resequencing of exon 3 could not identify disease-associated rare variants in TLR2.
Journal Of Clinical Periodontology 01/2012; 39(4):315-22. · 3.00 Impact Factor
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ABSTRACT: Periodontitis is an inflammatory disease caused by pathogenic microorganisms, such as Porphyromonas gingivalis, and characterized by the destruction of the periodontium. Obese individuals have an increased risk for periodontitis and show decreased serum levels of adiponectin. This in-vitro study was established to examine whether adiponectin modulates critical effects of lipopolysaccharide (LPS) from P. gingivalis on oral epithelial cells (OECs).
The presence of adiponectin and its receptors in human gingival tissue samples and OECs was analyzed by immunohistochemistry and PCR. Furthermore, OECs were treated with LPS and/or adiponectin for up to 72 h, and the gene expression and protein synthesis of pro- and anti-inflammatory mediators, matrix metalloproteinases (MMPs) and growth factors were analyzed by real-time PCR and ELISA. Additionally, cell proliferation, differentiation and in-vitro wound healing were studied. The nuclear translocation of NFκB was investigated by immunofluorescence. Gingival tissue sections showed a strong synthesis of adiponectin and its receptors in the epithelial layer. In cell cultures, LPS induced a significant up-regulation of interleukin (IL) 1β, IL6, IL8, MMP1 and MMP3. Adiponectin abrogated significantly the stimulatory effects of LPS on these molecules. Similarly, adiponectin inhibited significantly the LPS-induced decrease in cell viability and increase in cell proliferation and differentiation. Adiponectin led to a time-dependent induction of the anti-inflammatory mediators IL10 and heme oxygenase 1, and blocked the LPS-stimulated NFκB nuclear translocation.
Adiponectin may counteract critical actions of P. gingivalis on oral epithelial cells. Low levels of adiponectin, as observed in obese individuals, may increase the risk for periodontal inflammation and destruction.
PLoS ONE 01/2012; 7(2):e30716. · 4.09 Impact Factor
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ABSTRACT: Bacterial pathogens are frequently detected in atheromatous lesions, however, their contribution to atherosclerosis remains unknown. The present study was aimed to explore the effect of the P. gingivalis cysteine protease gingipain towards the proinflammatory response of human aortic endothelial cells (HAECs).
HAECs were exposed to gingipains (Rgps) extracted from the oral pathogen P. gingivalis. In addition, HAECs were co-stimulated with the TLR ligands P. gingivalis LPS, E. coli LPS or heat-killed P. gingivalis (HKPG) in combination with gingipain-active or gingipain-inactive extracts. After stimulation, IL-8 mRNA expression and protein synthesis were analysed by RT-PCR and ELISA. Means and standard errors were computed following by statistical testing (P ≤ 0.05).
In HAECs, Rgps significantly increased the IL-8 mRNA (5.8 ± 1.1-fold) and protein expression (523.0 ± 57.5 pg/ml) compared to untreated controls. Co-stimulation experiments showed a significant synergistic effect for the IL-8 mRNA expression and protein synthesis when HAECs were exposed to a combination of the purified TLR ligands (P. gingivalis or E. coli LPS) or HKPG and gingipain-active extracts.
These results demonstrated the synergistic effects of TLR ligands and P. gingvalis cysteine proteases for the proinflammatory responses in artery vascular endothelial cells and highlight a mechanism by which bacteria may contribute to the development of atherosclerosis.
Archives of oral biology 07/2011; 56(12):1583-91. · 1.65 Impact Factor
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ABSTRACT: Although enamel matrix derivative (EMD) has been shown to promote periodontal regeneration, it is unknown whether the actions of EMD are modulated by occlusal loading. This in vitro study was performed to investigate whether biomechanical forces regulate the response of periodontal ligament (PDL) cells to EMD.
Human PDL cells were treated with EMD in the presence and absence of cyclic tensile strain (CTS) of various magnitudes for ≤ 14 days. Synthesis of transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF), growth factor receptors, collagen, and runt-related transcription factor 2- (RUNX2), cell numbers and adhesion, wound fill rate, and calcium accumulation were analyzed by real-time polymerase chain reaction, enzyme-linked immunosorbent assay, a wound healing assay, and alizarine red S staining.
Wound fill rate, cell numbers and adhesion, and expression of TGF-β1, VEGF, collagen, and RUNX2 were significantly increased by EMD. In the presence of CTS, the EMD-induced effects were significantly reduced. The inhibition of the EMD-upregulated VEGF expression by CTS was blocked by a specific inhibitor of nuclear factor-kappa B signaling. Moreover, CTS downregulated receptors for growth factors involved in the actions of EMD. CTS also antagonized significantly the EMD-induced calcium deposition.
These in vitro findings suggest that the beneficial actions of EMD on PDL cell functions critical for periodontal regeneration are jeopardized by biomechanical loading. Clinical studies should clarify whether protection of teeth against occlusal forces in the early healing stage may positively affect the outcome of regenerative therapy with EMD.
Journal of Periodontology 03/2011; 82(12):1725-34. · 2.60 Impact Factor
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ABSTRACT: The concept of platform switching has been introduced to implant therapy, however long-term data are sparse. The aim of this study was to biochemically investigate the inflammatory response mediated by MMP-8 to platform switching after 3 years of loading, in order to understand the long-term effect of implant/abutment mismatching on peri-implant health.
A total of 70 implants had been inserted in the posterior maxilla in 26 patients and were randomly assigned to one of the four treatment regimens (implant diameter 3.8 [control group], 4.3 [Test group 1, T(1)], 4.8 [Test group 2, T(2)] and 5.5 mm [Test group 3, T(3)]). All implants were restored using a 3.8 mm abutment. In the test groups, this restoration resulted in a mismatching of 0.25-0.85 mm of implant-abutment diameters.
Thirty-six months after prosthetic rehabilitation, peri-implant sulcular fluid samples were taken from two aspects of all implants and from periodontally healthy adjacent teeth. Samples were processed in a conventional ELISA using monoclonal antibodies recognizing the active entity of MMP-8. In the test groups, MMP-8 mean values were 2.76 ng for T(1) (SD: 2.91), 3.30 ng for T(2) (SD: 1.94) and 3.18 ng for T(3) (SD: 2.46). For the control group, MMP-8 mean value was 3.6 ng (SD: 2.23), whereas 3.38 ng (SD: 2.2) was recorded at the adjacent teeth. There were no statistically significant differences in MMP-8 values between the groups (P=0.113, Kruskal-Wallis). Conclusions: The presence of an implant/abutment mismatching specific for this prosthetic concept is compatible with long-term peri-implant health as demonstrated by analysis of a sensitive biomarker of the peri-implant inflammatory response.
Clinical Oral Implants Research 03/2011; 23(5):556-9. · 2.51 Impact Factor
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Periodontology 2000 02/2011; 55(1):167-88. · 3.96 Impact Factor
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Journal Of Clinical Periodontology 02/2011; 38(2):103-7. · 3.00 Impact Factor
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ABSTRACT: The concept of platform switching has been introduced to implant dentistry based on observations of reduced peri-implant bone loss. However, randomized clinical trials are still lacking. This study aimed to test the hypothesis that platform switching has a positive impact on crestal bone-level changes.
Two implants with diameters of 4 mm were inserted epicrestally into one side of the posterior mandibles of 25 subjects. After 3 months of submerged healing, the reentry surgery was performed. On the randomly placed test implant, an abutment 3.3 mm in diameter was mounted, resulting in a horizontal circular step of 0.35 mm (platform switching). The control implant was straight, with an abutment 4 mm in diameter. Single-tooth crowns were cemented provisionally. All patients were monitored at short intervals over the course of 1 year. Standardized radiographs and microbiological samples from the implants' inner spaces were obtained at baseline (implant surgery), and after 3, 4, and 12 months.
After 1 year, the mean radiographic vertical bone loss at the test implants was 0.53±0.35 mm and at the control implants, it was 0.58±0.55 mm. The mean intraindividual difference was 0.05±0.56 mm, which is significantly <0.35 mm (P=0.0093, post hoc power 79.9%). The crestal bone-level changes depended on time (P<0.001), but not on platform switching (P=0.4). The implants' internal spaces were contaminated by bacteria, with no significant differences in the total counts between the test and the control at any time point (P=0.98).
The present randomized clinical trial could not confirm the hypothesis of a reduced peri-implant bone loss at implants restored according to the concept of platform switching.
Clinical Oral Implants Research 02/2011; 22(10):1185-92. · 2.51 Impact Factor
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ABSTRACT: This in vitro study was established to investigate whether the regenerative capacity of periodontal ligament (PDL) cells in the presence of enamel matrix derivative (EMD) is modulated by inflammation.
PDL cells were grown in the presence or absence of EMD under normal and inflammatory conditions for up to 14 days. In order to mimic an inflammatory environment, cells were incubated with interleukin (IL)-1β. Cells were also exposed to transforming growth factor (TGF)-β1 and insulin-like growth factor (IGF)-1 under both conditions. For analysis of wound healing, an in vitro wound fill assay was used. The synthesis of growth factors, markers of proliferation, and osteogenic differentiation, as well as collagen was studied by real-time polymerase chain reaction, enzyme-linked immunoassay, and immunoblotting. Mineralization was assessed by alizarine red S and von Kossa staining.
EMD stimulated significantly the in vitro wound fill rate, cell proliferation and adhesion, synthesis of growth factors, and collagen, as well as mineralization. In the presence of IL-1β, these EMD effects were significantly reduced. IL-1β also inhibited significantly the wound fill rate induced by TGF-β1 and IGF-1.
Critical PDL cell functions that are associated with periodontal regeneration are reduced in an inflammatory environment.
Journal Of Clinical Periodontology 01/2011; 38(5):479-90. · 3.00 Impact Factor
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ABSTRACT: Enamel matrix derivative (EMD) used to promote periodontal regeneration has been shown to exert anti-inflammatory effects. This in vitro study was performed to investigate if the anti-inflammatory actions of EMD are modulated by the local cellular environment, such as inflammation or occlusal, i.e., biomechanical, loading. Human periodontal ligament cells were seeded on BioFlex plates and incubated with EMD under normal, inflammatory, and biomechanical loading conditions for 1 and 6 days. In order to mimic inflammatory and biomechanical loading conditions in vitro, cells were stimulated with interleukin (IL)-1β and exposed to dynamic tensile strain, respectively. The gene expression of IL-1β, IL-1 receptor antagonist (IL-1RN), IL-6, IL-8, IL-10, and cyclooxygenase (COX)-2 was analyzed by real-time RT-PCR and the IL-6 protein synthesis by enzyme-linked immunoassay. For statistical analysis, Student's t test, ANOVA, and post-hoc comparison tests were applied (p < 0.05). EMD downregulated significantly the expression of IL-1β and COX-2 at 1 day and of IL-6, IL-8, and COX-2 at 6 days in normal condition. In an inflammatory environment, the anti-inflammatory actions of EMD were significantly enhanced at 6 days. In the presence of low biomechanical loading, EMD caused a downregulation of IL-1β and IL-8, whereas high biomechanical loading significantly abrogated the anti-inflammatory effects of EMD at both days. Neither IL-1RN nor IL-10 was upregulated by EMD. These data suggest that high occlusal forces may abrogate anti-inflammatory effects of EMD and should, therefore, be avoided immediately after the application of EMD to achieve best healing results.
Clinical Oral Investigations 01/2011; 16(1):275-83. · 2.36 Impact Factor
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ABSTRACT: The temporal pattern of bone-level alterations in conventionally restored implants is dependent upon healing mode (open or submerged). This study examined the influence of healing on marginal bone levels at implants with a medium-rough surface including the implant collar and a clearance-fit implant-abutment connection restored according to a platform-switching concept.
Two implants were placed in the posterior mandible of 21 test subjects, randomly assigned to open (OH) or submerged (SH) healing. Standardized radiographs were obtained after implant surgery, before re-entry, after crown mounting, 1 and 2 years after implant surgery, and evaluated for implant-bone-level alterations (ΔIBL). Bacterial samples of the implants' inner cavities were analysed by cultivation. Statistics: Brunner-Langer Model, equivalence testings by Wilcoxon's (equivalence range ±0.4mm).
After 2 years, ΔIBL were -0.47±0.46mm (OH) and -0.54±0.38mm (SH). At the 1-year follow-up, all implants were contaminated with bacteria. ΔIBL (p<0.001) and the amount of bacterial contamination (p<0.001) significantly depended on time, but not on healing mode. ΔIBL of OH and SH were equivalent at all time points (all p0.044).
Platform-switched implants showed very limited peri-implant bone-level alterations. The healing-mode neither affected the total amount nor the temporal patterns of ΔIBL. Thus, the results for the tested implants with a non-rigid implant-abutment connection were similar to results reported previously for implants with a rigid implant-abutment connection.
Journal Of Clinical Periodontology 01/2011; 38(4):374-84. · 3.00 Impact Factor
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ABSTRACT: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation.
PDL cells (from six donors) grown on BioFlex(®) plates were treated with interleukin (IL) 1β, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student's t-test and ANOVA were applied (p<0.05).
In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals.
These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation.
Fortschritte der Kieferorthopädie 11/2010; 71(6):390-402. · 0.89 Impact Factor
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Arne S Schaefer,
Gesa M Richter,
Henrik Dommisch,
Markus Reinartz,
Michael Nothnagel,
Barbara Noack,
Marja L Laine,
Mathias Folwaczny,
Birte Groessner-Schreiber,
Bruno G Loos, Søren Jepsen,
Stefan Schreiber
[show abstract]
[hide abstract]
ABSTRACT: Epidemiological studies have indicated a relationship between coronary heart disease (CHD) and periodontitis. Recently, CDKN2BAS was reported as a shared genetic risk factor of CHD and aggressive periodontitis (AgP), but the causative variant has remained unknown. To identify and validate risk variants in different European populations, we first explored 150 kb of the genetic region of CDKN2BAS including the adjacent genes CDKN2A and CDKN2B, covering 51 tagging single nucleotide polymorphisms (tagSNPs) in AgP and chronic periodontitis (CP) in individuals of Dutch origin (n=313). In a second step, we tested the significant SNP associations in an independent AgP and CP population of German origin (n=1264). For the tagSNPs rs1360590, rs3217992, and rs518394, we could validate the associations with AgP before and after adjustment for the covariates smoking, gender and diabetes, with SNP rs3217992 being the most significant (OR 1.48, 95% CI 1.19 to 1.85; p=0.0004). We further showed in vivo gene expression of CDKN2BAS, CDKN2A, CDKN2B, and CDK4 in healthy and inflamed gingival epithelium (GE) and connective tissue (CT), and detected a significantly higher expression of CDKN2BAS in healthy CT compared to GE (p=0.004). After 24 h of stimulation with Porphyromonas gingivalis in Streptococcus gordonii pre-treated gingival fibroblast (HGF) and cultured gingival epithelial cells (GECs), we observed a 25-fold and fourfold increase of CDKN2BAS gene expression in HGFs (p=0.003) and GECs (p=0.004), respectively. Considering the global importance of CDKN2BAS in the disease risk of CHD, this observation supports the theory of inflammatory components in the disease physiology of CHD.
Journal of Medical Genetics 10/2010; 48(1):38-47. · 6.36 Impact Factor
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ABSTRACT: To assess the subjective intensities of pain during supportive periodontal treatment using a sonic scaler or an Er:YAG laser.
Forty patients with two residual periodontal pockets following conventional periodontal therapy were treated using a sonic scaler and an Er:YAG laser in a split-mouth design. A visual analogue scale was used for pain assessment directly after each treatment procedure. Additionally, pain was recorded during the treatment of 11 patients at intervals of 0.5 s using an inter-modal intensity comparison.
Pain assessment during treatment showed that laser treatment (median pain score: 0.71 U, maximum: 9.94 U, minimum: 0 U) caused less pain than the sonic device (median pain score: 2.17 U, maximum: 11.26 U, minimum: 0 U) (p<0.05) with no difference in the treatment time (p>0.05). These results could be confirmed by the visual analogue scale: pain scores assessed after laser treatment (median: 1 U, maximum: 7 U, minimum: 0 U) were lower than those after sonic instrumentation (median: 3.5 U, maximum: 7.5 U, minimum: 0 U) (p<0.05).
Using an Er:YAG laser during supportive periodontal treatment, painful sensations can be reduced compared with sonic scaler instrumentation.
Journal Of Clinical Periodontology 04/2010; 37(4):340-5. · 3.00 Impact Factor
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ABSTRACT: This in vitro study assessed the visualization quality of the periodontal ligament space in cone-beam computerized tomography (CBCT) compared with intraoral radiographs (CR).
A phantom mimicking variable periodontal ligament spaces (0-0.42 mm) was radiographed using CBCT and CR. Fifteen datasets of each modality were randomly mixed and presented twice to 19 experienced examiners and once to 19 inexperienced examiners.
Zero-millimeter gaps were recognized in 84.4% of CBCT and in 81.6% of CR images. On CBCT scans, gaps of 0.19 mm were identified with an accuracy of 93%-100% compared with 70.2%-81.7% using CR. Experienced examiners recognized gaps of >or=0.19 mm on CBCT repeatedly with nearly 100% accuracy.
Compared with CR, CBCT provides better visualization of simulated periodontal ligament space in this phantom.
Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics 02/2010; 109(2):e95-101. · 1.50 Impact Factor
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ABSTRACT: This randomized-controlled trial aimed to evaluate marginal bone level alterations at implants restored according to the platform-switching concept, using different implant/abutment mismatching.
Eighty implants were divided according to the platform diameter in four groups: 3.8 mm (control), 4.3 mm (test group(1)), 4.8 mm (test group(2)) and 5.5 mm (test group(3)), and randomly placed in the posterior maxilla of 31 patients. After 3 months, implants were connected to a 3.8-mm-diameter abutment and final restorations were performed. Radiographic bone height was measured by two independent examiners at the time of implant placement (baseline), and after 9, 15, 21 and 33 months.
After 21 months, all 80 implants were clinically osseointegrated in the 31 patients treated. A total of 69 implants were available for analysis, as 11 implants had to be excluded from the study due to early unintentional cover screw exposure. Radiographic evaluation showed a mean bone loss of 0.99 mm (SD = 0.42 mm) for test group(1), 0.82 mm (SD = 0.36 mm) for test group(2) and 0.56 mm (SD = 0.31 mm) for test group(3). These values were statistically significantly lower (P<0.005) compared with control (1.49 mm, SD = 0.54 mm). After 33 months, five patients were lost to follow-up. Evaluation of the remaining 60 implants showed no difference compared with 21 months data except for test group(2) (0.87 mm) and test group(3) (0.64 mm). There was an inverse correlation between the extent of mismatching and the amount of bone loss.
This study suggested that marginal bone level alterations could be related to the extent of implant/abutment mismatching. Marginal bone levels were better maintained at implants restored according to the platform-switching concept.
Clinical Oral Implants Research 01/2010; 21(1):115-21. · 2.51 Impact Factor
