Influence of concentration and preparation of platelet rich fibrin on human bone marrow mononuclear cells <i>(in vitro)</i>

Verboket, René D.; Herrera-Vizcaíno, Carlos; Thorwart, Kirsten; Booms, Patrick; Bellen, Marlene; Al‐Maawi, Sarah; Sader, Robert; Marzi, Ingo; Henrich, Dirk; Ghanaati, Shahram

doi:10.1080/09537104.2018.1530346

Cited by 13 publications

(10 citation statements)

References 47 publications

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“…This growth factor, for example, pushes proliferation of osteogenic cells in vitro [81]. In addition, endothelial cells followed a similar pattern of displaying an increase in migration upon exposure to PRF [40]. Although the activation of platelets might account for these observations [11], the precise mechanism remains to be elucidated.…”

Section: Discussionmentioning

confidence: 98%

“…Conversely, one study showed an inhibitory effect of PRF on alkaline phosphatase activity [52]. In two other reports, PRF failed to change alkaline phosphatase activity and did not change alkaline phosphatase expression in rat calvaria osteoblasts [28] and bone marrow cells [40], respectively. Taken together, all but three studies reported an increase of alkaline phosphatase in response to PRF exposure.…”

Section: Alkaline Phosphatase and Alizarin Red Stainingmentioning

confidence: 94%

“…With respect to changes in the expression of extracellular matrix protein, PRF increased collagen type 1 in mesenchymal cells of the bone [45], skin [65], and gingiva [38,73]. Likewise, PRF increased the expression of osteopontin, MMP2, and MMP9 in human bone marrow cells [40]. Conversely, PRF reduced the expression of bone sialoprotein and osteocalcin along with a transient downregulation of collagen type 1 in periodontal ligament cells [52].…”

Section: Growth Factors and Extracellular Matrixmentioning

confidence: 99%

“…In contrast, PRF failed to induce proliferation of L929 fibroblasts [53] and human mesenchymal stem cells on collagen scaffolds [17]. In general, PRF maintained cell viability [33, 63-66, ] without inducing apoptosis [40]. Overall, there is a general consensus that PRF has a potent mitogenic activity.…”

Section: Selection Of Studiesmentioning

confidence: 99%

“…PRF caused a moderate expression of various growth factors in mesenchymal and endothelial cells such as TGFβ [38,46,52,56,65,36], PDGF [23,38,40,46,52,56,65,36], and VEGF [23,37,58]. Dental pulp cells treated with PRF increased expression of dentin sialoprotein and dentin matrix protein 1 [29,34,49].…”

Section: Growth Factors and Extracellular Matrixmentioning

confidence: 99%

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Effect of platelet-rich fibrin on cell proliferation, migration, differentiation, inflammation, and osteoclastogenesis: a systematic review of in vitro studies

et al. 2019

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Objective To systematically assess the effects of platelet-rich fibrin (PRF) on in vitro cellular behavior. Methods A systematic electronic search using MEDLINE database was performed. In vitro studies using PRF were considered and articles published up to June 31, 2018 were screened. Eligible studies were selected based on the use of human PRF. Results In total, 1746 titles were identified with the search terms, from these 37 met the inclusion criteria and were chosen for data extraction. In addition, 16 new studies, mainly published in 2019, were also included in the analysis resulting in 53 studies. No meta-analysis could be performed due to the heterogeneity of study designs. Included studies show that PRF enhances proliferation, migration, adhesion, and osteogenic differentiation on a variety of cell types along with cell signaling activation. Furthermore, PRF reduces inflammation, suppresses osteoclastogenesis, and increases the expression of various growth factors in mesenchymal cells. Summary and conclusions Despite some notable differences of the studies, the overall findings suggest a positive effect of PRF on cell proliferation, migration, adhesion, differentiation, and inflammation pointing towards a therapeutic potential in regenerative dentistry. Clinical relevance PRF serves as a reservoir of bioactive molecules to support wound healing and bone regeneration. Although the cellular mechanisms by which PRF supports the clinical outcomes remain unclear, in vitro research provides possible explanations. This systematic review aims to provide an update of the existing research on how PRF affects basic physiological processes in vitro. The overall findings suggest that PRF induces cell proliferation, migration, adhesion, and differentiation along with possessing anti-inflammatory properties further supporting its therapeutic potential in wound healing and bone regeneration.

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Section: Discussionmentioning

confidence: 98%

Section: Alkaline Phosphatase and Alizarin Red Stainingmentioning

confidence: 94%

Section: Growth Factors and Extracellular Matrixmentioning

confidence: 99%

Section: Selection Of Studiesmentioning

confidence: 99%

Section: Growth Factors and Extracellular Matrixmentioning

confidence: 99%

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Effect of platelet-rich fibrin on cell proliferation, migration, differentiation, inflammation, and osteoclastogenesis: a systematic review of in vitro studies

et al. 2019

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Determination of the effective dose of bone marrow mononuclear cell therapy for bone healing in vivo

Janko

Pöllinger

Schaible

et al. 2020

Eur J Trauma Emerg Surg

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Introduction Cell-based therapy by bone marrow mononuclear cells (BMC) in a large-sized bone defect has already shown improved vascularization and new bone formation. First clinical trials are already being conducted. BMC were isolated from bone marrow aspirate and given back to patients in combination with a scaffold within some hours. However, the optimal concentration of BMC has not yet been determined for bone healing. With this study, we want to determine the optimal dosage of the BMC in the bone defect to support bone healing. Material and methods Scaffolds with increasing BMC concentrations were inserted into a 5 mm femoral defect, cell concentrations of 2 × 10 6 BMC/mL, 1 × 10 7 BMC/mL and 2 × 10 7 BMC/mL were used. Based on the initial cell number used to colonize the scaffolds, the groups are designated 1 × 10 6 , 5 × 10 6 and 1 × 10 7 group. Bone healing was assessed biomechanically, radiologically (µCT), and histologically after 8 weeks healing time. Results Improved bone healing parameters were noted in the 1 × 10 6 and 5 × 10 6 BMC groups. A significantly higher BMD was observed in the 1 × 10 6 BMC group compared to the other groups. Histologically, a significantly increased bone growth in the defect area was observed in group 5 × 10 6 BMC. This finding could be supported radiologically. Conclusion It was shown that the effective dose of BMC for bone defect healing ranges from 2 × 10 6 BMC/mL to 1 × 10 7 BMC/mL. This concentration range seems to be the therapeutic window for BMC-supported therapy of large bone defects. However, further studies are necessary to clarify the exact BMC-dose dependent mechanisms of bone defect healing and to determine the therapeutically effective range more precisely.

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Modification of collagen-based sponges can induce an upshift of the early inflammatory response and a chronic inflammatory reaction led by M1 macrophages: an in vivo study

et al. 2020

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Background The present study evaluated the cellular tissue reaction of two equine-derived collagen hemostatic sponges (E-CHS), which differed in thickness after pressing, over 30 days in vivo. The inflammatory response during physiological wound healing in sham-operated animals was used as control group. Material and methods First, the E-CHS was pressed by applying constant pressure (6.47 ± 0.85 N) for 2 min using a sterile stainless-steel cylinder until the material was uniformly flattened. Consequently, the original (E-CHS), the pressed (P-E-CHS), as well as the control group (CG; sham operation) were studied independently. The 3 groups were evaluated in vivo after subcutaneous implantation in Wistar rats during 3, 15, and 30 days. Histochemical and immunohistochemical methods provided observations of biomaterial degradation rate, cellular inflammatory response, and vascularization pattern. A derivative of human blood known as platelet-rich fibrin (PRF) was used as an ex vivo model to simulate the initial biomaterial-cell interaction. Segments of E-CHS and P-E-CHS were cultivated for 3 and 6 days with PRF, and the release of pro-inflammatory proteins was measured using ELISA. PRF cultivated alone was used as a control group. Results At day 3, the CG induced a statistically significant higher presence of monocytes/macrophages (CD68+), pro-inflammatory macrophages (M1; CCR7+), and pro-wound healing macrophages (M2; CD206+) compared to E-CHS and P-E-CHS. At the same time point, P-E-CHS induced a statistically significant higher presence of CD68+ cells compared to E-CHS. After 15 days, E-CHS was invaded by cells and vessels and showed a faster disintegration rate compared to P-E-CHS. On the contrary, cells and vessels were located only in the outer region of P-E-CHS and the biomaterial did not lose its structure and accordingly did not undergo disintegration. The experimental groups induced similar inflammatory reaction primarily with positive pro-inflammatory CD68+/CCR7+ macrophages and a low presence of multinucleated giant cells (MNGCs). At this time point, significantly lower CD68+/CCR7+ macrophages and no MNGCs were detected within the CG when compared to the experimental groups (P < 0.05). After 30 days, E-CHS and P-E-CHS were fully degraded. All groups showed similar inflammatory reaction shifted to a higher presence CD206+ macrophages. A low number of CCR7+ MNGCs were still observable in the implantation bed of both experimental groups. In the ex vivo model, the cells and fibrin from PRF penetrated E-CHS. However, in the case of P-E-CHS, the cells and fibrin stayed on the surface and did not penetrate towards materials central regions. The cultivation of P-E-CHS with PRF induced a statically significant higher release of pro-inflammatory proteins compared to the CG and E-CHS after 3 days. Conclusion Altering the original presentation of a hemostatic sponge biomaterial by pressing modified the initial biomaterial-cell interaction, delayed the early biomaterial’s degradation rate, and altered the vascularization pattern. A pressed biomaterial seems to induce a higher inflammatory reaction at early time points. However, altering the biomaterial did not modify the polarization pattern of macrophages compared to physiologic wound healing. The ex vivo model using PRF was shown to be an effective model to simulate the initial biomaterial-cell interaction in vivo. Clinical relevance A pressed hemostatic sponge could be applied for guided tissue regeneration and guided bone regeneration. In that sense, within the limitations of this study, the results show that the same biomaterial may have two specific clinical indications.

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Influence of concentration and preparation of platelet rich fibrin on human bone marrow mononuclear cells (in vitro)

Cited by 13 publications

References 47 publications

Effect of platelet-rich fibrin on cell proliferation, migration, differentiation, inflammation, and osteoclastogenesis: a systematic review of in vitro studies

Effect of platelet-rich fibrin on cell proliferation, migration, differentiation, inflammation, and osteoclastogenesis: a systematic review of in vitro studies

Determination of the effective dose of bone marrow mononuclear cell therapy for bone healing in vivo

Modification of collagen-based sponges can induce an upshift of the early inflammatory response and a chronic inflammatory reaction led by M1 macrophages: an in vivo study

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