Objective: This study evaluated the impact of photobiomodulation (PBM) on the healing of the donor palatal area following free gingival graft (FGG) harvesting by examining changes in transforming growth factor (TGF)-β1, platelet-derived growth factor (PDGF)-BB, and interleukin (IL)-8 levels in palatal wound fluid (PWF). Material and methods: Thirty patients were selected and randomly assigned to receive PBM (laser group) or PBM sham (sham group) in the palatine area after FGG harvesting. A neodymium-doped yttrium aluminum garnet (Nd:YAG) laser (1064 nm) was applied to the test sites immediately after surgery and every 24 h thereafter for 4 days. PWF was collected on Days 7 and 12, and PWF TGF-β1, PDGF-BB, and IL-8 levels were analyzed by enzyme-linked immunosorbent assays (ELISA). Results: PWF TGF-β1, PDGF-BB, and IL-8 levels were significantly lower on Day 12 than on Day 7 for both groups. PWF TGF-β1, PDGF-BB, and IL-8 levels of the laser group were significantly higher than those of sham group on Day 7 (p < 0.05). PWF TGF-β1 levels were also significantly higher in laser group than in the sham group on Day 12; however, differences in PDGF-BB and IL-8 levels between groups on Day 12 were statistically nonsignificant. Conclusions: Observed increases in PWF TGF-β1, PDGF-BB, and IL-8 levels suggest that PBM may accelerate wound healing by stimulating production of selected mediators.
Chemerin is a chemoattractant protein that directs inflammatory cells that express its receptor chemokine receptor-like 1 (ChemR23) towards sites of inflammation. C-C chemokine receptor-like 2 (CCRL2), is the other receptor of chemerin, improves the interaction between chemerin and ChemR23. The aim of this study was to evaluate the expression of chemerin and its receptors in gingival tissues with healthy and periodontitis. Tissue biopsy samples were obtained from 20 patients with chronic periodontitis and from the gingiva of 20 healthy individuals undergoing a crown lengthening process. Quantitative real-time PCR (qPCR) was used to examine the mRNA expression of chemerin, ChemR23 and CCRL2. Additionally, protein expression was measured by immunohistochemistry. Both qPCR and immunohistochemistry results revealed that the expression of chemerin and ChemR23 was significantly higher in tissues with periodontitis than in healthy tissues (P = 0.001 and, P = 0.015, respectively). There were no significant differences between healthy tissues and those with periodontitis in terms of mRNA expression of CCRL2, whereas a more intense staining was observed in tissues with periodontitis. The mRNA expression levels of chemerin showed a positive correlation with plaque index, gingival index, probing pocket depth and clinical attachment level (r = 0.448, r = 0.460, r = 0.439 and, r = 0.459, respectively, P< 0.01). To the best of our knowledge, this study is the first to examine the expression of chemerin, ChemR23 and CCRL2 in gingival tissues. Our study suggests that chemerin may play a role in the pathogenesis of periodontitis by causing chemoattraction of immune cells that direct ChemR23 receptors to the site of inflammation.
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