The effect of titanium-platelet rich fibrin on periodontal intrabony defects: A randomized controlled split-mouth clinical study.

This study aimed to determine the contribution of titanium prepared platelet-rich fibrin (T-PRF) with open flap debridement (OFD) on clinical, biochemical and radiographic measurements of periodontal regeneration. Twenty periodontitis patients with bilateral intrabony defects and stage III grade A periodontitis were included in the study. A total of 40 defects were randomly selected for OFD alone (control group, n = 20) or combined OFD+ T-PRF (test group, n = 20). Clinical and radiographic parameters (at baseline and nine months after surgery), and growth factor levels in gingival crevicular fluid (at baseline and at two, four, six, and twelve weeks after surgical treatment) were also evaluated. Considering the clinical parameters, alterations in probing pocket depth, gingival marginal level and clinical endpoint in the test regions treated with T-PRF significantly improved (P<0.05). Fibroblast growth factor-2 and platelet-derived growth factor-BB levels between the two groups in the second and fourth weeks were also significantly different (P<0.05). Furthermore, the receptor activator of nuclear factor κB ligand/osteoprotegerin ratio between the groups was significantly different in the second, fourth, sixth, and twelfth weeks (P<0.05). The bone-filling rate was also significantly greater in the test group than in the control group (P <0.001). Compared with OFD alone, combining T-PRF with the procedure was more successful with regards to clinical, radiographic, and biochemical measurements of periodontal regeneration.

CTRP4 ameliorates inflammation, thereby attenuating the interaction between HUVECs and THP-1 monocytes through SIRT6/Nrf2 signaling.

CTRP4, identified as an adipokine, has demonstrated notable anti-inflammatory and anti-obesity effects in various disease models. Consequently, our research sought to explore the impact of CTRP4 on inflammation and the interaction between endothelial cells and monocytes in hyperlipidemic conditions. Using Western blotting, we assessed the expression levels of various proteins in HUVECs and THP-1 monocytes. Our study findings indicate that treatment with CTRP4 effectively mitigated the attachment of THP-1 monocytes to HUVECs. Furthermore, it reduced the expression of adhesion molecules and inflammation indicators in experimental cells exposed to hyperlipidemic conditions. Notably, CTRP4 treatment led to an increase in SIRT6 expression and the nuclear translocation of Nrf2. Interestingly, when SIRT6 or Nrf2 was silenced using siRNA, the positive effects of CTRP4 in HUVECs and THP-1 cells were nullified. Our results suggest that CTRP4 exhibits anti-inflammatory properties, thereby improving the interaction between endothelial cells and monocytes through the SIRT6/Nrf2-dependent pathway. This study provides insights into CTRP4 as a potential therapeutic target for mitigating obesity-related atherosclerosis.