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- Pelegrine, A. A., et al.
(författare)
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Can bone marrow aspirate concentrate change the mineralization pattern of the anterior maxilla treated with xenografts? A preliminary study
- 2016
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Ingår i: Contemporary Clinical Dentistry. - : Medknow. - 0976-237X. ; 7:1, s. 21-26
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To evaluate bony reconstruction of the atrophic anterior maxilla using particulate grafts with or without autologous bone marrow aspirate concentrate (BMAC). Materials and Methods: Eight patients with atrophy of the anterior maxilla due to teeth loss were selected and split into groups according to the type of material used: Control Group (CG) (n = 4) - particulate xenograft only and Test Group (TG) (n = 4) -a combination of particulate xenograft and BMAC. Both groups received a collagen membrane to cover the xenograft. After 4 months, during implant placement, a sample of bone was removed from the graft area using a 2 mm diameter trephine bur. The specimens were fixed and preserved for histomorphometric evaluation, which included the following parameters: Mineralized tissue (MT) and non-MT (NMT). Cone beam computed tomography was performed at 3 time intervals to measure bone thickness: (1) Before grafting, (2) 4 months and (3) 8 months postgrafting, using localized bone gain (mm) as the outcome variable. Results: Tomographic analysis revealed bone gain in CG of 3.78 +/- 1.35 mm and 4.34 +/- 1.58 mm at 4 and 8 months, respectively. TG showed an increase of 3.79 +/- 0.52 mm and 4.09 +/- 1.33 mm after 4 and 8 months, respectively. Histomorphometric analysis revealed that, for CG, MT- and NMT-related values were 52.3% +/- 16.78% and 47.70% +/- 5.55%, respectively, whereas for TG, they were 65.04% +/- 20.98% and 34.96 +/- 10.38, respectively. Conclusion: Although radiographic bone gain appeared similar between the groups, the use of BMAC obtained via the BMAC (R) method revealed an increased mineralization trend in the anterior maxilla. It must be highlighted, however, that this is a preliminary study with a relatively small sample population and further studies with larger sample sizes are needed to verify these results.
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- Pircher, J, et al.
(författare)
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Cathelicidins prime platelets to mediate arterial thrombosis and tissue inflammation
- 2018
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 9:1, s. 1523-
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Tidskriftsartikel (refereegranskat)abstract
- Leukocyte-released antimicrobial peptides contribute to pathogen elimination and activation of the immune system. Their role in thrombosis is incompletely understood. Here we show that the cathelicidin LL-37 is abundant in thrombi from patients with acute myocardial infarction. Its mouse homologue, CRAMP, is present in mouse arterial thrombi following vascular injury, and derives mainly from circulating neutrophils. Absence of hematopoietic CRAMP in bone marrow chimeric mice reduces platelet recruitment and thrombus formation. Both LL-37 and CRAMP induce platelet activation in vitro by involving glycoprotein VI receptor with downstream signaling through protein tyrosine kinases Src/Syk and phospholipase C. In addition to acute thrombosis, LL-37/CRAMP-dependent platelet activation fosters platelet–neutrophil interactions in other inflammatory conditions by modulating the recruitment and extravasation of neutrophils into tissues. Absence of CRAMP abrogates acid-induced lung injury, a mouse pneumonia model that is dependent on platelet–neutrophil interactions. We suggest that LL-37/CRAMP represents an important mediator of platelet activation and thrombo-inflammation.
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- Pruenster, Monika, et al.
(författare)
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Extracellular MRP8/14 is a regulator of β2 integrin-dependent neutrophil slow rolling and adhesion.
- 2015
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 6
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Tidskriftsartikel (refereegranskat)abstract
- Myeloid-related proteins (MRPs) 8 and 14 are cytosolic proteins secreted from myeloid cells as proinflammatory mediators. Currently, the functional role of circulating extracellular MRP8/14 is unclear. Our present study identifies extracellular MRP8/14 as an autocrine player in the leukocyte adhesion cascade. We show that E-selectin-PSGL-1 interaction during neutrophil rolling triggers Mrp8/14 secretion. Released MRP8/14 in turn activates a TLR4-mediated, Rap1-GTPase-dependent pathway of rapid β2 integrin activation in neutrophils. This extracellular activation loop reduces leukocyte rolling velocity and stimulates adhesion. Thus, we identify Mrp8/14 and TLR4 as important modulators of the leukocyte recruitment cascade during inflammation in vivo.
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