Background and objective: Leucocyte- and platelet-rich fibrin (L-PRF) has been developed to stimulate wound healing response. However, it is currently unknown whether smoking affects the biological responses elicited by L-PRF on Periodontal ligament derived mesenchymal stromal cells (PDL-MSC). This study analyzes the kinetics of biomolecule release from L-PRF derived from smokers and nonsmokers and their effect on periodontal ligament cell proliferation and migration as essential biological activities during wound healing. Methods: Biomolecules present in L-PRF exudates and conditioned media (LPRF-CM) collected from smokers and nonsmokers were analyzed by Luminex arrays. PDL-MSC obtained from one nonsmoker were treated with L-PRF exudates or LPRF-CM derived from both smokers and nonsmokers. The parameters evaluated included cell proliferation, determined by Ki67 immunostaining and migration assessed using transwell assays. Also, cells were treated with nicotine in the presence of Fetal bovine serum (FBS) 10% or LPRF-CM. Results: A similar biomolecular profile was detected in L-PRF exudates and LPRF-CM from smokers and nonsmokers, stimulating (PDL-MSC) proliferation and migration to a comparable degree. Nicotine reduced cell proliferation and migration of periodontal cells; however, this effect was recovered in the presence of LPRF-CM. Conclusion: L-PRF derived from smokers could be an autologous source of biomolecules to stimulate cell biological activities involved in wound healing in smokers who have difficulties in ceasing this habit. Clinical trials are required to evaluate the impact of L-PRF on healing responses in smokers.
|Journal||Journal of Oral Pathology and Medicine|
|State||Accepted/In press - 2022|
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- cell migration
- cell proliferation
- platelet-rich fibrin
- wound healing