Abstract
Leucocyte- and platelet rich fibrin (L-PRF) is an autologous biomaterial used in regenerative procedures. It has an antimicrobial activity against P. gingivalis although the mechanism is not fully understood. It was hypothesized that L-PRF exudate releases hydrogen peroxide and antimicrobial peptides that inhibit P. gingivalis growth. Agar plate and planktonic culture experiments showed that the antimicrobial effect of L-PRF exudate against P. gingivalis was supressed by peroxidase or pepsin exposure. In developing multi-species biofilms, the antimicrobial effect of L-PRF exudate was blocked only by peroxidase, increasing P. gingivalis growth with 1.3 log genome equivalents. However, no effect was shown on other bacteria. Pre-formed multi-species biofilm trials showed no antimicrobial effect of L-PRF exudate against P. gingivalis or other species. Our findings showed that L-PRF exudate may release peroxide and peptides, which may be responsible for its antimicrobial effect against P. gingivalis. In addition, L-PRF exudate had an antimicrobial effect against P. gingivalis in an in vitro developing multi-species biofilm.
Highlights
Microorganisms associated with both caries and periodontal diseases are metabolically highly specialized and organized in multi-species microbial biofilms
Leucocyte- and platelet rich fibrin (L-PRF) exudate exposed to trypsin and L-PRF exudate diluted in phosphate-buffered saline (PBS) always resulted in an inhibition of P. gingivalis, on both blood agar and modified Brain Heart Infusion (BHI) agar plates (Table 1)
L-PRF exudate exposed to horseradish peroxidase (HRP) or pepsin never showed an inhibition of P. gingivalis
Summary
Microorganisms associated with both caries and periodontal diseases are metabolically highly specialized and organized in multi-species microbial biofilms. Some highly specialized members of those communities can play an important role in provoking a dysbiosis and deregulation of the host immune response driven by several specific factors such as environmental stressors, inflammation and positive feedback loops. This may result in the destruction of periodontal tissues in susceptible individuals (Sanz et al, 2017). The intra-oral presence of this microorganism has been identified as a risk factor for pulmonary infections, preterm delivery and low birth weight (Scannapieco, 2006; Offenbacher et al, 2006) Their presence in atherosclerotic plaques was shown to increase the risk of myocardial infarction, and it was isolated from dentoalveolar abscesses (Dymock et al, 1996; Sanz et al, 2020)
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