Tensile strength assay comparing the resistance between two different autologous platelet concentrates (leucocyte-platelet rich fibrin versus advanced-platelet rich fibrin): a pilot study

Background: Since the leucocyte-platelet rich fibrin (L-PRF) was published in 2001, many studies have been developed, analyzing its properties, and also verifying new possibilities to improve it. Thereby, it emerges the advanced-platelet rich fibrin (A-PRF) with a protocol that optimizes the properties obtained by the L-PRF. Nonetheless, there is a gap in the literature to landmark the evolutive process concerning the mechanical properties in specific the resistance to tensile strength which consequently may influence the time for membrane degradation. Thus, this study had the goal to compare the resistance to the traction of membranes produced with the original L-PRF and A-PRF protocols, being the first to this direct comparison. Findings: The harvest of blood from a healthy single person, with no history of anticoagulant usage. We performed the protocols described in the literature, within a total of 13 membranes produced for each protocol (n = 26). Afterward, the membranes were prepared and submitted to a traction test assessing the maximal and the average traction achieved for each membrane. The data were analyzed statistically using the unpaired t test. Regarding average traction, A-PRF obtained a value of 0.0288 N mm−2 and L-PRF 0.0192 N mm−2 (p < 0.05 using unpaired t test). For maximal traction, A-PRF obtained 0.0752 N mm−2 and L-PRF 0.0425 N mm−2 (p < 0.05 using unpaired t test). Conclusion: With this study, it was possible to conclude that indeed A-PRF has a significative higher maximal traction score and higher average traction compared to L-PRF, indicating that it had a higher resistance when two opposing forces are applied.info:eu-repo/semantics/publishedVersio

Transglutaminase-2 Regulation by Arecoline in Gingival Fibroblasts

Transglutaminase-2 (TGM-2) stabilizes extracellular matrix (ECM) proteins by cross-linking and has been implicated in several fibrotic disorders. Arecoline present in betel quid has been proposed as one of the causative factors for oral submucous fibrosis (OSMF). Hence, we hypothesize that arecoline may regulate TGM-2 and may have a role in the pathogenesis of OSMF. The expression of TGM-2 was studied in OSMF tissues by real-time RT-PCR analysis, and significant overexpression was observed in most OSMF tissues (P = 0.0112) compared with normal tissues. Arecoline induced TGM-2 mRNA and protein expression as well as TGM-2 activity in human gingival fibroblast cells. The addition of methocramine hemihydrate (M-2 muscarinic acetylcholine receptor selective antagonist) or 8'-bromo-cAMP abolished arecoline-mediated TGM-2 induction, suggesting a role for M-2 muscarinic acid receptor and a repressor role for cAMP. Our study provides evidence for TGM-2 overexpression in OSMF and its regulation by arecoline in oral fibroblasts