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| 2. |
- Andersson, Bengt-Åke, et al.
(författare)
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Cigarette smoking affects microRNAs and inflammatory biomarkers in healthy individuals and an association to single nucleotide polymorphisms is indicated
- 2019
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Ingår i: Biomarkers. - : Taylor & Francis. - 1354-750X .- 1366-5804. ; 24:2, s. 180-185
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Cigarette smoke induces inflammation and remodels immune response. Genetic and epigenetic alterations might be involved in the pathogenesis of smoking related diseases. In this study, we investigated the effect of smoking on systemic inflammation biomarkers and epigenetic changes at microRNA (miRNA) expression level. We also examined if the levels of inflammatory biomarkers were associated with selected single nucleotide polymorphisms (SNPs).METHOD: From 39 smokers and 101 non-smokers, levels of total white blood cells (WBCs) and its subpopulations, plasma cytokines/chemokines/proteins and miRNAs were analysed. For three biomarkers, C-reactive protein (CRP), MCP-1 and IFN-γ that were affected by smoking, the influence of SNPs was analyzed.RESULT: Elevated levels of total WBCs, neutrophils, monocytes, lymphocytes, CRP, MCP-1, IFN-γ and lower levels of miR-21 were detected in smokers. The elevated levels of IFN-γ in smokers was only statistically significantly associated with rs2069705 AG/GG SNP-genotype.CONCLUSIONS: A lower level of oncomir miRNA-21 and a higher level of immune modelling cytokine IFN-γ detected in smokers could be a protective immune response to cigarette smoke. The higher level of IFN-γ in smokers with a specific SNP genotype also suggests that a genetic interaction with smoking might predict the pathobiology of smoking related disease.
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| 3. |
- Ekström, Jörgen, 1944, et al.
(författare)
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Neural- and Hormonal-induced Protein Synthesis and Mitotic Activity in the Rat Parotid Gland and the Dependence on NO-generation
- 2007
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Ingår i: Journal of Oral Biosciences. - : Elsevier. - 1349-0079 .- 1880-3865. ; 49:1, s. 31-38
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Tidskriftsartikel (refereegranskat)abstract
- Nitric oxide (NO) is a likely parasympathetic nonadrenergic, noncholinergic transmitter in parotid glands, since parasympathetic nerves contain NO-synthase. Parasympathetic stimulation (30 min, atropine + phentolamine + propranolol) increased the protein synthesis ([3H] leucine uptake) by 142% (10 Hz) and 200% (40 Hz). Surprisingly, neither the neuronal type NO-synthase inhibitor N-PLA, nor the unspecific inhibitor L-NAME reduced the response. Moreover, the parasympathetic nonadrenergic, noncholinergic (40 Hz, 30 min)-evoked increase (65%) in mitotic activity ([3H] thymidine uptake) was unaffected by the NO-synthase inhibitors. Sympathetic nerves lack NO-synthase, yet inhibition of NO-generation reduced the β-adrenoceptor mediated response to sympathetic stimulation. Whereas the protein synthesis increased by 192% to stimulation (50 Hz, 1s every tenth s for 30 min) under just α-adrenoceptor blockade, the response was more than halved in the presence of N-PLA to 86%) or L-NAME to 91%). Furthermore, the β-adrenoceptor mediated increase in mitotic activity 122%) to sympathetic stimulation 20 Hz, 4 min every fifth min for 30 min), under α-adrenoceptor blockade, was reduced to 49% N-PLA) and 47% (L-NAME). Pentagastrin (20 µg/kg, I. V. infused for one h) increased the protein synthesis by 17%. N-PLA prevented this increase but did not affect the basal protein, while cholecystokinin receptor blockers reduced both the basal protein synthesis (by 20%), and the pentagastrin-induced increase. Thus, implying that strong rather than weak stimuli of the cholecystokinin receptors activate neuronal type NO-synthase. Despite being of the neuronal type, the NO-synthase generating NO in response to stimulation of β-adrenoceptors or cholecystokinin receptors was probably of parenchymal origin.
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| 4. |
- Ekström, Jörgen, 1944, et al.
(författare)
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Nitric oxide-dependent mitotic activity in salivary glands of the rat upon sympathetic stimulation.
- 2004
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Ingår i: Arch Oral Biol. ; 49:11, s. 889-94
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Tidskriftsartikel (refereegranskat)abstract
- Incorporation of [3H]thymidine into trichloroacetic acid (TCA)-insoluble material of the parotid and submandibular glands was used as an index of mitotic activity following unilateral electrical stimulation of the sympathetic innervation (20 Hz, 4 min every fifth minute over 34 min). Stimulation under beta-adrenoceptor blockade (propranolol 2 mg/kg, intravenous) alone or combined with alpha-adrenoceptor blockade (phentolamine 2 mg/kg, intravenous) did not increase the rate of [3H]thymidine incorporation into the two types of glands. However, under alpha-adrenoceptor blockade the [3H]thymidine incorporation increased into the parotid glands, by 122% (compared to the glands on the contralateral side), but not into the submandibular glands. In the presence of the neuronal type NO-synthase (nNOS) blocker N-PLA (30 mg/kg, intravenous) or the unselective NO-synthase blocker L-NAME (30 mg/kg, intravenous), this increase was reduced to 49 and 47%, respectively. Thus, the major part of the sympathetically nerve-evoked beta-adrenoceptor-mediated mitotic response was found to depend on the activity of neuronal type NO-synthase to generate NO. Since the sympathetic nerve fibres of the parotid gland lack NO-synthase, the neuronal type NO-synthase subjected to the inhibitors is likely to be of parenchymal origin.
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| 5. |
- Ekström, Jörgen, et al.
(författare)
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Nitric oxide-dependent mitotic activity in salivary glands of the rat upon sympathetic stimulation
- 2004
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Ingår i: Archives of Oral Biology. - : Elsevier. - 0003-9969 .- 1879-1506. ; 49:11, s. 889-894
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Tidskriftsartikel (refereegranskat)abstract
- Incorporation of [3H]thymidine into trichloroacetic acid (TCA)-insoluble material of the parotid and submandibular glands was used as an index of mitotic activity following unilateral electrical stimulation of the sympathetic innervation (20 Hz, 4 min every fifth minute over 34 min). Stimulation under β-adrenoceptor blockade (propranolol 2 mg/kg, intravenous) alone or combined with α-adrenoceptor blockade (phentolamine 2 mg/kg, intravenous) did not increase the rate of [3H]thymidine incorporation into the two types of glands. However, under α-adrenoceptor blockade the [3H]thymidine incorporation increased into the parotid glands, by 122% (compared to the glands on the contralateral side), but not into the submandibular glands. In the presence of the neuronal type NO-synthase (nNOS) blocker N-PLA (30 mg/kg, intravenous) or the unselective NO-synthase blocker L-NAME (30 mg/kg, intravenous), this increase was reduced to 49 and 47%, respectively. Thus, the major part of the sympathetically nerve-evoked β-adrenoceptor-mediated mitotic response was found to depend on the activity of neuronal type NO-synthase to generate NO. Since the sympathetic nerve fibres of the parotid gland lack NO-synthase, the neuronal type NO-synthase subjected to the inhibitors is likely to be of parenchymal origin. © 2004 Elsevier Ltd. All rights reserved.
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| 6. |
- Kvarnvik, Christine, et al.
(författare)
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Clinical and radiographic periodontal status in hypertensive patients with or without obstructive sleep apnea 10 years after diagnosis and CPAP initiation
- 2024
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Ingår i: Clinical and Experimental Dental Research. - : John Wiley & Sons. - 2057-4347. ; 10:2
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Through inflammation and hyposalivation, obstructive sleep apnea (OSA) is suggested to affect periodontal status over time. Our aim was to compare the clinical and radiographic periodontal status of hypertensive patients with or without long-term presence of OSA, treated or untreated with continuous positive airway pressure treatment (CPAP).MATERIALS AND METHODS: In 2007-2009, a screening for OSA was conducted among 394 hypertensive primary care patients. Polygraphy was used to create three groups: no OSA, non-CPAP, or adherent CPAP based on the apnea hypopnea index (AHI). After 10 years, a cross-sectional sleep and periodontal examination including a clinical and radiographic examination, a questionnaire, and a matrix metalloproteinase-8 (MMP-8) chair-side test was conducted. Based on levels of alveolar bone, bleeding on probing (BoP), and probing pocket depth (PPD), patients were categorized into four periodontal stages: periodontal health/gingivitis and three periodontal disease stages. Periodontal status and periodontal stages were compared between the OSA (n = 49), non-CPAP (n = 38), or adherent CPAP (n = 34) groups.RESULTS: The 121 patients (53% women) had a median age of 71 years. No differences were seen between the OSA groups regarding median number of teeth (p = .061), teeth/implants, (p = .107), plaque index (p = .245), BoP (p = .848), PPD ≥ 4 mm (p = .561), PPD ≥ 6 mm (p = .630), presence of MMP-8 (p = .693) except for bone loss (p = .011). Among patients with stage periodontal health/gingivitis a significant difference was seen, as 70% of those were categorized as no OSA, 20% as non-CPAP, and 10% as adherent CPAP (p = .029). Differences were not seen in periodontal disease stages.CONCLUSIONS: Hypertensive patients with obstructive sleep apnea (OSA) did not have an adverse clinical periodontal status compared to patients without OSA. However, when combining radiographic and clinical status into periodontal stages, patients without OSA more frequently exhibited periodontal health or gingivitis compared to patients without OSA, regardless of CPAP treatment.
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| 7. |
- Lewin, N. L., et al.
(författare)
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Influence of single nucleotide polymorphisms among cigarette smoking and non-smoking patients with coronary artery disease, urinary bladder cancer and lung cancer
- 2021
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 16
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Tidskriftsartikel (refereegranskat)abstract
- Introduction Cigarette smoke is suggested to be a risk factor for coronary artery disease (CAD), urinary bladder cancer (UBCa) or lung cancer (LCa). However, not all heavy smokers develop these diseases and elevated cancer risk among first-degree relatives suggests an important role of genetic factor. Methods Three hundred and ten healthy blood donors (controls), 98 CAD, 74 UBCa and 38 LCa patients were included in this pilot study. The influence of 92 single nucleotide polymorphisms (SNPs) and impact of cigarette smoking were analysed. Results Out of 92 SNPs tested, differences in distribution of 14 SNPs were detected between controls and patient groups. Only CTLA4 rs3087243 showed difference in both CAD and UBCa patient group compared to control group. Stratified by smoking status, the impact of smoking was associated to frequencies of 8, 3 and 4 SNPs in CAD, UBCa, LCa patients, respectively. None of these 92 SNPs showed a statistically significant difference to more than one type of disease among smoking patients. In non-smoking patients, 7, 3 and 6 SNPs were associated to CAD, UBCa, LCa, respectively. Out of these 92 SNPs, CTLA4 rs3087243 was associated to both non-smoking CAD and UBCa. The XRCC1 rs25487 was associated to both non-smoking UBCa and LCa. Conclusion SNPs might be important risk factors for CAD, UBCa and LCa. Distribution of the SNPs was specific for each patient group, not a random event. Impact of cigarette smoking on the disease was associated to the specific SNP sequences. Thus, smoking individuals with SNPs associated to risk of these serious diseases is an important target group for smoking cessation programs.
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| 8. |
- Omar, Omar, et al.
(författare)
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Cellular and molecular reactions to dental implants
- 2020
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Ingår i: Dental Implants and Bone Grafts. - Duxford : Elsevier. - 9780081024782 - 9780081024799 ; , s. 183-205
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Bokkapitel (refereegranskat)abstract
- This chapter provides an overview of the cellular interactions and the genetic regulations at the bone-implant interface, based on experimental in vivo studies and the available studies in humans. The first part discusses the current knowledge on the cellular and molecular events governing the initial cell recruitment, early inflammation, and the transition from inflammation to bone formation and remodeling during the phases of osseointegration. The modulation of these events, by different implant surfaces, and their relationship with the structural and functional development of the interface, are emphasized. A subsequent section is focused on selected key biological factors, potentially involved in the osteogenic differentiation of mesenchymal stem cells or in coupling of bone formation and remodeling at the interface. Further, possible phenotypic polarizations of macrophages at the interface, in vivo, is discussed. Finally, some insights on possible dysregulations of the molecular activities at the interface, under selected bone-compromising conditions, are provided.
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| 9. |
- Risolo, M., et al.
(författare)
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The effect of reconstructive techniques as treatment modality for peri-implant osseous defects - a systematic review and meta-analysis
- 2023
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Ingår i: Acta Odontologica Scandinavica. - : Taylor & Francis. - 0001-6357 .- 1502-3850. ; 81:7, s. 569-77
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Forskningsöversikt (refereegranskat)abstract
- ObjectivesThe aim of this systematic review is to compare conventional peri-implant flap surgery and reconstructive surgical techniques regarding evidence of remission from peri-implantitis.Material and methodsSearches were made among randomized controlled trials evaluating clinical aspects and the changes in marginal bone level before and after surgical treatment of peri-implantitis, with and without bone substitute.ResultsNine published articles and 442 patients were eligible for inclusion in the study. Reconstructive techniques exhibited a greater extent of defect fill than conventional surgical techniques alone. No significant differences could be found for clinical measures of peri-implant disease (bleeding on probing and reduction of probing depth) from baseline to the 12-month follow-up.ConclusionsWith regards to the clinical measures of disease, our review shows that there are no differences between open flap debridement and regenerative surgery. From an esthetic standpoint, it may however be that regenerative measures may lead to improvement but further publications with this focus will be necessary to verify this.
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| 10. |
- Sayardoust, Shariel, et al.
(författare)
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Clinical, radiological, and gene expression analyses in smokers and non-smokers, Part 2 : RCT on the late healing phase of osseointegration
- 2017
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Ingår i: Clinical Implant Dentistry and Related Research. - : John Wiley & Sons. - 1523-0899 .- 1708-8208. ; 19:5, s. 901-915
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Tidskriftsartikel (refereegranskat)abstract
- Background: The mechanisms behind the impact of smoking on osseointegration are not fully understood.Purpose: To investigate the initial clinical and molecular course of osseointegration of different implants in smokers and non-smokers in a randomized controlled trial (RCT).Materials and Methods: Smoking (n = 16) and non-smoking (n = 16) patients received 3 implant types: machined, oxidized, and laser-modified surfaces. Baseline bone biopsies were retrieved from the implant sites. After 60 and 90 days, the pain score, implant stability quotient (ISQ), and peri-implant crevicular fluid (PICF) gene expression were analyzed. Furthermore, radiological and clinical assessments were made at 90 days.Results: At 90 days, no pain was reported, irrespective of smoking habit. A higher ISQ was found in smokers compared with non-smokers. Marginal bone loss (MBL) was greater in smokers than in non-smokers. The comparison of implant surfaces revealed greater MBL exclusively at the machined implants in smokers. At 90 days in smokers, the PICF around machined implants revealed a higher expression of the proinflammatory cytokine, interleukin-6 (IL-6), and a lower expression of the osteogenic gene, osteocalcin (OC), compared with the PICF around modified implants. Furthermore, OC expression was lower at machined implants in smokers compared with machined implants in non-smokers. After adjustment for age and implant location (maxilla/mandible), multivariate regression revealed the following predictors of MBL: smoking, bleeding on probing at 90 days, hypoxia-inducible factor 1 alpha (HIF-1α) expression at baseline and IL-6 expression in PICF at 90 days.Conclusions: During the early phase of osseointegration, non-smokers and smokers present a similar, high implant survival. In contrast, smokers present a greater MBL, particularly at machined implants. HIF-1α baseline expression in the recipient bone and IL-6 expression in PICF cells are important molecular determinants for MBL after 90 days. It is concluded that smoking has an early effect on osseointegration, which is dependent on the implant surface properties and the local host response.
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