Clinical application of a positioning annular gingival cutter in minimally invasive stage II implant surgery.

BACKGROUND: Dental implant restoration is an effective therapy for missing teeth and is widely used in clinical practice to provide more treatment options for patients. OBJECTIVE: To explore the application of a positioning annular gingival cutter in minimally invasive stage II implant surgery and to evaluate its clinical effects. METHOD: Stage II implant surgery using a positioning annular gingival cutter was performed on 15 selected patients at 15 implant sites with sufficient keratinized gingival width in the posterior region. The patient underwent crown restoration 2 weeks after surgery and returned for follow-up 3 months later. The surgical effects were recorded for each patient, including the duration of surgery, postoperative pain and swelling, keratinized gingiva width, probing depth (PD) measurements, and the percentage of bleeding on probing (BOP) before surgery, during crown restoration, and 3 months after crown restoration. The data were subjected to a paired sample t-test using Statistical Product and Service Solutions (SPSS) 25.0. RESULTS: The duration of stage II implant surgery using a positioning annular gingival cutter was 9.23 ± 1.63 min, and the duration of postoperative pain and swelling was 0.73 ± 0.35 and 0.81 ± 0.35 d, respectively. The keratinized gingiva width was 2.93 ± 0.41 mm before surgery and 2.91 ± 0.46 mm after crown restoration, demonstrating no significant reduction (P> 0.05). The keratinized gingiva width remained stable 3 months after crown restoration, with an average of 2.85 ± 0.49 mm, without significant reduction (P> 0.05). No obvious inflammation is observed. PD was 2.60 ± 0.52 mm and BOP was 10%. CONCLUSION: The use of a positioning annular gingival cutter in stage II implant surgery achieves a positive and stable clinical effect within a short time.

Inhibitory effect of ghrelin on nicotine-induced VCAM-1 expression in human umbilical vein endothelial cells.

Endothelial dysfunction is thought to be a major cause of vascular injury in smokers. Ghrelin is a recently discovered peptide that plays a modulatory role in atherosclerosis. However, it is unknown how ghrelin regulates nicotine-induced vascular cell adhesion molecule-1 (VCAM-1) expression. We examined nicotine-induced VCAM-1 expression in human umbilical vein endothelial cells pretreated with ghrelin and detected the activity of protein kinase C (PKC), p38 mitogen-activated protein kinase (p38 MAPK), and nuclear factor (NF)-kappaB. Our study showed that ghrelin inhibited nicotine-induced VCAM-1 expression in human umbilical vein endothelial cells in a concentration-dependent and time-dependent way. We also found that ghrelin inhibited nicotine-induced PKC, p38 MAPK, and NF-kappaB activation. The results suggest that ghrelin inhibits nicotine-induced VCAM-1 expression, and PKC, p38 MAPK, and NF-kappaB play active roles in that process. Exogenous ghrelin may provide a possible approach for preventing or reversing atherosclerosis in smokers.

[Upregulated PGC-NRF-mtTFA expressions contributed to the development of atherosclerosis in rabbits fed with a high fat diet].

OBJECTIVE: To investigate the relationship between PPAR coactivator 1 (PGC-1), nuclear respiratory factor (NRF), mitochondrial transcription factor A (mtTFA) expressions of vascular smooth muscle cells (VSMC) and development of atherosclerosis in a rabbit model. METHODS: Atherosclerotic model was established by feeding the rabbits with high-fat diet for 4, 8 and 12 weeks (n = 10 each). Another 8 rabbits fed with normal diet served as normal controls. Intima-media ratio, mRNA and protein expressions of PGC-1, NRF, mtTFA and SMemb, a marker for synthetic VSMC, were detected on aorta specimens. RESULTS: With the blood lipid increased, the intima-media ratio rose from (0.031 +/- 0.010) microm up to (0.814 +/- 0.258) microm during 12 weeks. Increasing SMemb means that synthetic VSMC grew more and more. The expressions of PGC-1 became significant after 4 weeks (P < 0.01), while that of NRF-1 and mtTFA rose significantly after 8 weeks (P < 0.01). CONCLUSIONS: The PGC-NRF-mtTFA pathway might play a critical role in VSMC proliferation and development of atherosclerosis.