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Review
. 2025 Feb;97(1):74-94.
doi: 10.1111/prd.12570. Epub 2024 Jun 24.

How to explain the beneficial effects of leukocyte- and platelet-rich fibrin

Juan Blanco  1 , Angel García  2 , Lidia Hermida-Nogueira  2 , Ana B Castro  3
Affiliations
Review

How to explain the beneficial effects of leukocyte- and platelet-rich fibrin

Juan Blanco et al. Periodontol 2000. 2025 Feb.

Abstract

The survival of an organism relies on its ability to repair the damage caused by trauma, toxic agents, and inflammation. This process involving cell proliferation and differentiation is driven by several growth factors and is critically dependent on the organization of the extracellular matrix. Since autologous platelet concentrates (APCs) are fibrin matrices in which cells, growth factors, and cytokines are trapped and delivered over time, they are able to influence that response at different levels. The present review thoroughly describes the molecular components present in one of these APCs, leukocyte- and platelet-rich fibrin (L-PRF), and summarizes the level of evidence regarding the influence of L-PRF on anti-inflammatory reactions, analgesia, hemostasis, antimicrobial capacity, and its biological mechanisms on bone/soft tissue regeneration.

Keywords: analgesic; antibacterial; antimicrobial; bone healing; bone regeneration; hemostatic; leukocyte‐ and platelet‐rich fibrin; pain; soft tissue regeneration; wound healing.

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Conflict of interest statement

All (co)‐authors declare that they have no conflict of interest. The Department of Oral Health Sciences, Unit of Periodontology at KU Leuven owns research chairs from several implant companies: Dentsply Sirona, Straumann, and Henry Schein.

Figures

FIGURE 1
FIGURE 1
Schematic illustration of the effects of leukocyte and platelet rich fibrin.
FIGURE 2
FIGURE 2
Schematic diagram of the three pairs of polypeptide chains (Aα, Bβ, and ϒ) of fibrinogen. Indicated in the figure the location for carbohydrate attachment (CHO), thrombin (T) and plasmin cleavage (P). Aα, Bβ and γ chains form the D‐domain and these are joined by α‐helical ropes to the central E‐domain to give the characteristic fibrinogen structure.
FIGURE 3
FIGURE 3
Diagram illustrates the process of fibrin assembly and crosslinking. Fibrils exhibit branching and engage in lateral associations to create broader fibrils and fibers. Factor XIII or its activated form, XIIIa, facilitates the formation of ε‐(γ‐glutamyl) lysine isopeptide bonds, leading to the swift development of γ‐dimers. The formation of γ‐trimers and γ‐tetramers occurs more gradually through interfibril γ‐chain crosslinking, enhancing the clot's resistance to fibrinolysis.
FIGURE 4
FIGURE 4
Schematic illustration of the shift from M1 to M2 promoted by the leukocyte and platelet rich fibrin membrane and the effects of the cytokines secreted on osteogenesis.
See this image and copyright information in PMC

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