1. |
- Almqvist, Sofia, 1980, et al.
(author)
-
Amelogenins modulate cytokine expression in LPS-challenged cultured human macrophages.
- 2012
-
In: Cytokine. - : Elsevier BV. - 1096-0023 .- 1043-4666. ; 58:2, s. 274-9
-
Journal article (peer-reviewed)abstract
- Amelogenins are enamel matrix proteins with a proven ability to restore tissues in patients with advanced periodontitis and chronic skin wounds. To explore the mechanisms of action of amelogenins in wound inflammation, the in vitro effect on the expression of selected cell mediators involved in inflammation and tissue repair from human monocyte-derived macrophages was studied. Macrophages were treated with amelogenins in serum-enriched medium with simultaneous lipopolysaccharide (LPS) stimulation, for 6, 24 and 72 h, and the conditioned culture medium was analysed for 28 different cytokines. Amelogenin treatment directed the LPS-induced release of both pro- and anti-inflammatory cytokines towards an alternatively activated macrophage phenotype. This change in activation was also demonstrated by the amelogenin-induced secretion of alternative macrophage activation-associated CC chemokine-1 (AMAC-1, also known as CCL18; p<0.001), a well-documented marker of alternative activation. Amelogenins were also shown significantly to increase the macrophage expression of vascular endothelial growth factor and, to a lesser but significant extent, insulin-like growth factor-1 after 24h of culture. The results of the present in vitro study show that monocyte-derived macrophages stimulated by inflammatory agonist LPS respond to the treatment with amelogenins by reducing the pro-inflammatory activity and increasing the expression of tissue repair mediators.
|
|
2. |
|
|
3. |
- Anders, Halldin, et al.
(author)
-
Improved osseointegration and interlocking capacity with dual acid treated implants: a rabbit study.
- 2016
-
In: Clinical Oral Implants Research. - : Wiley. - 0905-7161 .- 1600-0501. ; 27, s. 22-30
-
Journal article (peer-reviewed)abstract
- Aim To investigate how osseointegration is affected by different nano- and microstructures. The hypothesis was that the surface structure created by dual acid treatment (AT-1), applied on a reduced topography, might achieve equivalent biomechanical performance as a rougher surface treated with hydrofluoric acid (HF). Materials and methods In a preclinical rabbit study, three groups (I, II, and III) comprised of test and control implants were inserted in 30 rabbits. The microstructures of the test implants were either produced by blasting with coarse (I) or fine (II) titanium particles or remained turned (III). All test implants were thereafter treated with AT-1 resulting in three different test surfaces. The microstructure of the control implants was produced by blasting with coarse titanium particles thereafter treated with HF. The surface topography was characterized by interferometry. Biomechanical (removal torque) and histomorphometric (bone–implant contact; bone area) performances were measured after 4 or 12 weeks of healing. Results Removal torque measurement demonstrated that test implants in group I had an enhanced biomechanical performance compared to that of the control despite similar surface roughness value (Sa). At 4 weeks of healing, group II test implants showed equivalent biomechanical performance to that of the control, despite a decreased Sa value. Group III test implants showed decreased biomechanical performance to that of the control. Conclusions: The results of the present study suggest that nano- and microstructure alteration by AT-1 on a blasted implant might enhance the initial biomechanical performance, while for longer healing time, the surface interlocking capacity seems to be more important.
|
|
4. |
- Eriksson, Anders, 1957, et al.
(author)
-
Elevation of cytokines in peritoneal fluid and blood in patients with liver cirrhosis
- 2004
-
In: Hepato-Gastroenterology. - 0172-6390. ; 51:56, s. 505-9
-
Journal article (peer-reviewed)abstract
- BACKGROUND/AIMS: Liver cirrhosis, described as the endstage of a necroinflammatory process, is often accompanied by ascites formation. The rationale for this study was the hypothesis that patients with liver cirrhosis have a low-grade chronic inflammatory response, which leads to an increased amount of proinflammatory cytokines accumulated in ascites. Twenty-five patients with liver cirrhosis complicated by ascites and twelve healthy volunteers were prospectively included in the study. METHODOLOGY: Ascites and blood samples from the patients were obtained for analysis of inflammatory cytokines using enzyme-linked immunosorbent assay methodology. Blood samples were taken from the healthy volunteers to obtain reference values. RESULTS: Plasma and ascites concentrations of interleukin-1alpha, interleukin-6, and tumor necrosis factor-alpha were significantly elevated in the patients compared with plasma levels in the group of healthy controls. Significant elevation of interleukin-10 concentrations was found in ascites but not in plasma in the patients. There was no significant difference in interleukin-10 levels between patient and control plasma. CONCLUSIONS: The findings suggest that elevated cytokine concentrations in ascites and serum could perpetuate an inflammatory reaction that may be a source of preservation of an ongoing systemic inflammatory reaction. This may contribute to the maintenance, and even progress, of the liver dysfunction, leading to exaggerated ascites development.
|
|
5. |
- Esposito, Marco, 1965, et al.
(author)
-
Immunohistochemistry of soft tissues surrounding late failures of Brånemark implants.
- 1997
-
In: Clinical oral implants research. - 0905-7161. ; 8:5, s. 352-66
-
Journal article (peer-reviewed)abstract
- The objective of the present investigation was to characterize the cellular composition of the soft tissues surrounding consecutively retrieved late failures of Brånemark implants. Criteria for implant failure were signs of loss of osseointegration (radiographic peri-fixtural radiolucency and mobility). The clinical history of the implants did not include adverse symptoms. At the time of retrieval, percussion-induced pain was experienced at 4/8 implants, but no macroscopical signs of inflammation or infection or infection was observed. Immunohistochemistry was applied on 6 marginal peri-implant specimens and on specimens of deeper tissues associated with the previously load-bearing implant surface from 8 failed implants, whereas 6 clinically healthy mucosal specimens and 4 hyperplastic biopsies from stable implants served as controls. The immunohistochemical evaluation showed that the soft tissues surrounding failed implants contained a large number of macrophages (CD68), HLA-DR positive cells, lymphocytes and plasma cells preferentially accumulated towards the removed implant surface. PMNs were a rare finding. Downgrowth of epithelium, in some cases encapsulating the whole fixture, was observed in sections where an intact implant/soft tissue interface was preserved. Healthy control mucosal specimens always contained labelled cells, albeit in a low amount, whereas hyperplastic control samples displayed an intense inflammatory and immunological response with numerous positive cells and PMNs scattered throughout the biopsy. In conclusion, failed implants were characterized by a chronic inflammatory response of the surrounding tissues with macrophages as the predominant labelled cell type, while hyperplastic tissues around stable implants were distinguished by an acute inflammatory process. These findings suggest that an on-going infection is unlikely to be the etiological factor for the late failures of dental implants examined in this study.
|
|
6. |
|
|
7. |
|
|
8. |
- Gretzer, Christina, 1954
(author)
-
Macrophage-material surface interactions
- 2000
-
Doctoral thesis (other academic/artistic)abstract
- Material surface-stimulated activation of the macrophage and the release of mediators has been suggested to be an important factor for inflammation and tissue regeneration around biomedical implants. Macrophage interactions with particles released from implants as well as macophage-bacteria interactions are also involved in implant loosening processes. The development of relevant in vitro models, which would allow a selective manipulation of biologic and implant components in a less complex environment, is therefore important. The aim of this thesis was to develop experimental model systems and to use these to increase the knowledge of macrophage interactions at an implant surface. An in vitro model of human monocyte-surface interactions was established with a single cell population. The influence of polystyrene (PS), thin metal (TiO2) coating, PS particles of 1 and 3 µm Ø, lipopolysaccharide (LPS) and protein pre-coating on macrophage activation was studied. The phenotype of macrophages was analysed by monoclonal antibodies (CD14, 27E10 and RM3/1). Cytokine (IL-1a, TNF-a and IL-10) and hydrogen peroxide (H2O2) secretion was evaluated. Annexin-V, propidium iodide (PI) and lactate dehydrogenase (LDH), was used to differ between apoptosis and cell death. A co-culture model with monocytes and thyrocytes was established and used to analyse material surface-cell-cell interactions. An animal experimental model with s.c. implant in the dorsum of rats was developed for studies on inflammatory cell recruitment, distribution and activity around and adherent to implants in vivo. Light microscopy (LM) and transmission electron microscopy (TEM) were used for the analysis of cell morphology on the implant surfaces in vitro and in vivo. Secretion of IL-1a was dependent on the type and concentration of exogenous stimuli, culture time and protein pre-adsorption. Although, the mere interaction between the surface and cells caused an IL-1a secretion, no major differences were observed between cells on PS and Ti-sputtered PS. Adherent macrophages changed their phenotype depending on culture time and the type of added stimuli. After 24 h, macrophage oxidative metabolism was downregulated and could not be further stimulated by LPS and particles. LPS upregulated CD14 and stimulated an increased release of IL-1a, TNF-a and IL-10. Fibrinogen was found to exert a modulatory effect on several events, including an increased monocyte adhesion and reduced apoptosis. Fibrinogen also caused a reduction of IL-10 secretion, irrespective of stimuli. The epithelial barrier of cultured thyrocytes was impaired in co-culture with monocytes secreting IL-1a stimulated by particles or LPS without cell-cell contact. A neutralizing antibody markedly reduced the effect of IL-1a, suggesting IL-1a as a potent factor in this model system of cell-cell communication. The macrophage was the predominant cell type between day 3-28 in exudate around PS and Ti in vivo. A spontaneous secretion of H2O2 by adherent macrophages was demonstrated. The oxidative metabolism of the implant-adherent macrophages was downregulated after 7 days post-implantation. In summary, the developed in vitro and in vivo models allow detailed studies on the influence of synthetic material and biologic components on macrophage behaviour at implant surfaces.
|
|
9. |
|
|
10. |
- Göransson, Anna, 1970, et al.
(author)
-
Inflammatory response to oxidised surface with Mg 2+ -ions incorporated in vitro
- 2004
-
In: 7th World Biomaterials Congress, Sidney, 17 -21 May 2004.
-
Conference paper (peer-reviewed)abstract
- Introduction Oxide films that grow spontaneously on titanium surfaces in contact with air may explain the bio-passivity of the material. Various procedures have been carried out to modify the properties of titanium oxide films to further improve the biocompatibility. Anodic oxidation is one technique to increase the thickness of the oxide layer that demonstrates significant stronger bone response in vivo. The concomitant increase in surface roughness and size and presence of pores of the thicker oxide layer seems to work as a potential contributor to the results (1). Attempts to implant ion in the oxide layers to overcome the drawbacks of calcium phosphate coatings (hydroxylapatite) such as i.e. delaminating and biodegradation during function seem promising (2). However the reasons why a thicker oxide layer with and without incorporated ions is favourable compared to conventionally turned and blasted surfaces are not fully understood. The aim of this study was to compare the early inflammatory response to the turned, blasted and electrochemically oxidised surface with Mg 2+ ions incorporated. Materials and Methods A total of 108 pure titanium discs were prepared with a turned surface. Thirty-six were kept as turned controls while 36 were blasted with 75 μm Al2O3 particles and 36 underwent electrochemically oxidation and Mg 2+ ion incorporation. MicroXam™, (Phase-Shift, Tucson, Arizona, USA) was used to for topographical characterisation. The disks were incubated with human mononuclear cells isolated from buffy coats of healthy blood donors (C-lab, Blood Supply Unit Sahlgrenska University hospital, Sweden) and cultured at a concentration of 106 cells/ml in 24 well cell culture plates. Half of the discs with the different treated surfaces were immediately treated with LPS while half were left without any stimuli. The incubation times were 24 and 72h. After each incubation period the incubation medium was collected and centrifuged. The supernatant was analysed with respect to cell viability and cytokine levels. Cell viability was estimated by analysing the content of lactatdehydrogenas (LDH)(Sahlgrenska University hospital, C-lab) and a commercially available ELISA assay (Biotrak system™, Amersham Bioscience, UK) was used to quantify TNF-α and IL -10 levels. The cells adherent to the material was stained with 2,6- diamidino-2-phenyindole (DAPI) (Sigma, USA) to evaluate the total cell number. In order to characterize differentiation of the adherent cells expression of 27E10 and RM3/1 (Biogenisis, UK) was used. The marker 27E10 and RM3/1 define acute and chronic inflammatory phenotypes respectively. Differentiated cells were evaluated as the percentage of positively stained cells from the total cell numbers. Results Surface evaluation revealed similar roughness for the turned control and the anodised surface with Mg 2+ ions incorporated while the blasted surface demonstrated a rougher surface profile (fig 1, 2). Fig 1 Fig 2 Sa-average height deviation (ym) SURFACE CTR Blasted Anodised+Mg Mean SA 1,2 1,0 ,8 ,6 ,4 ,2 0,0 Sdr-developed surface area (%) SURFACE CTR Blasted Anodised+Mg Mean SDR 40 30 20 10 0 LDH values were generally low for all surfaces (within the range of 0.8-1.6 μkat/l) but were slightly increased after LPS stimulation and after 72h. TNF-α was transient higher day one and after LPS stimulation especially on the turned control surface (fig 3, 4) Fig 3 Fig 4 TNF-a 24h (pg/ml) SURFACE CTR Blasted Anodised+Mg Mean C 3000 2000 1000 0 LPS LPSLPS+ TNF-a 72h (pg/ml) SURFACE CTR Blasted Anodised+Mg Mean C 400 300 200 100 0 LPS LPSLPS+ IL-10 levels were generally low irrespective of time. Increased IL-10 amounts after LPS stimulation and after 24 h were observed for all surfaces. The total cell numbers decreased on all surfaces from 24h to 72h but there were no major difference between stimulated and un-stimulated wells. Acute monocytic phenotype 27E10 marker dominated on all surfaces while the expression of the chronic RM3/1 marker was almost absent on all surfaces both at 24 and 72h. Conclusion The present study indicates a surface topography- and chemistry related difference in the acute inflammatory response with a stronger acute inflammatory response to the turned control compared to the blasted and anodised surface with Mg 2+ ions incorporated. References 1.Göransson, A, Jansson, E, Tengvall, P, Wennerberg, A. Bone formation after 4 weeks …topography : an in vivo study. Biomaterials 2002; 24: 197-205 2.Sul YT. PhD Thesis 2002, Göteborg University, Sweden
|
|