Impact of L-PRF on pain and healing outcomes in lower third molar surgery: a randomized split-mouth trial.

This study explored the effects of L-PRF on pain, soft tissue healing, periodontal condition, and post-extraction bone repair of mandibular third molars (3Ms). A randomized, prospective, triple-blind, split-mouth clinical trial was conducted with 34 volunteers. Eligible patients were randomly allocated into two treatments: G1 (without L-PRF), G2 (alveoli filled with L-PRF), in which the removal of bilateral 3Ms was performed at the same surgical time. Outcomes were assessed according to a visual analogue scale (pain), soft tissue scoring system (wound healing), periodontal probing of mandibular second molar. Bone repair was determined by volumetric analysis (ITK-SNAP software) and fractal analysis (ImageJ software). An intention-to-treat approach to Statistical analysis was used. L-PRF reduced pain in the 7-day postoperative follow-up (p = 0.019) and not only improved soft tissue healing after 1 month of follow-up (p = 0.021), but also probing depth (distal face) in 3 months postoperatively (p = 0.011). Significant alveolar reduction occurred in 3 months after surgery in both treatments (p < 0.05), however, this was more significant in G1 (p = 0.016). The fractal dimension showed no statistical differences. L-PRF improved postoperative clinical parameters of pain, soft tissue healing, and periodontal condition, suggesting that it has a beneficial effect on preserving the alveolar ridge and accelerating the initial repair process.

Impact of L-PRF on pain and healing outcomes in lower third molar surgery: a randomized split-mouth trial

Abstract This study explored the effects of L-PRF on pain, soft tissue healing, periodontal condition, and post-extraction bone repair of mandibular third molars (3Ms). A randomized, prospective, triple-blind, split-mouth clinical trial was conducted with 34 volunteers. Eligible patients were randomly allocated into two treatments: G1 (without L-PRF), G2 (alveoli filled with L-PRF), in which the removal of bilateral 3Ms was performed at the same surgical time. Outcomes were assessed according to a visual analogue scale (pain), soft tissue scoring system (wound healing), periodontal probing of mandibular second molar. Bone repair was determined by volumetric analysis (ITK-SNAP software) and fractal analysis (ImageJ software). An intention-to-treat approach to Statistical analysis was used. L-PRF reduced pain in the 7-day postoperative follow-up (p = 0.019) and not only improved soft tissue healing after 1 month of follow-up (p = 0.021), but also probing depth (distal face) in 3 months postoperatively (p = 0.011). Significant alveolar reduction occurred in 3 months after surgery in both treatments (p < 0.05), however, this was more significant in G1 (p = 0.016). The fractal dimension showed no statistical differences. L-PRF improved postoperative clinical parameters of pain, soft tissue healing, and periodontal condition, suggesting that it has a beneficial effect on preserving the alveolar ridge and accelerating the initial repair process.

Effect of Mesenchymal Stem Cells Overexpressing BMP-9 Primed with Hypoxia on BMP Targets, Osteoblast Differentiation and Bone Repair.

Bone formation is driven by many signaling molecules including bone morphogenetic protein 9 (BMP-9) and hypoxia-inducible factor 1-alpha (HIF-1α). We demonstrated that cell therapy using mesenchymal stem cells (MSCs) overexpressing BMP-9 (MSCs+BMP-9) enhances bone formation in calvarial defects. Here, the effect of hypoxia on BMP components and targets of MSCs+BMP-9 and of these hypoxia-primed cells on osteoblast differentiation and bone repair was evaluated. Hypoxia was induced with cobalt chloride (CoCl2) in MSCs+BMP-9, and the expression of BMP components and targets was evaluated. The paracrine effects of hypoxia-primed MSCs+BMP-9 on cell viability and migration and osteoblast differentiation were evaluated using conditioned medium. The bone formation induced by hypoxia-primed MSCs+BMP-9 directly injected into rat calvarial defects was also evaluated. The results demonstrated that hypoxia regulated BMP components and targets without affecting BMP-9 amount and that the conditioned medium generated under hypoxia favored cell migration and osteoblast differentiation. Hypoxia-primed MSCs+BMP-9 did not increase bone repair compared with control MSCs+BMP-9. Thus, despite the lack of effect of hypoxia on bone formation, the enhancement of cell migration and osteoblast differentiation opens windows for further investigations on approaches to modulate the BMP-9-HIF-1α circuit in the context of cell-based therapies to induce bone regeneration.