Hyperbaric oxygen therapy restores wound healing in irradiated gingiva to a similar level to that in healthy gingiva.

OBJECTIVE: This study aimed to investigate the involvement of mitochondrial biogenesis, and determine the extent of fibroblast proliferation and cellular apoptosis, in the gingiva of patients who had undergone head and neck radiation, after receiving hyperbaric oxygen therapy (HBOT), in comparison with normal gingiva. METHOD: A total of 16 patients who had undergone head and neck radiation with HBOT and six healthy subjects were included in the study. After the completion of radiation therapy, patients received HBOT at 2 ATA for 90 minutes per session, and for 20 sessions per patient. Samples of gingival tissues were then taken. The levels of: transforming growth factor beta (TGF-ß); phospho-nuclear factor kappa-light-chain-enhancer of activated B cells (p-NFÏ°B); nuclear factor kappa-light-chain-enhancer of activated B cells (NFÏ°B); proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α); phospho-dynamin-related protein 1 at ser616 (p-Drp1ser616); dynamin-related protein 1 (Drp1); Bcl-2-associated X-protein (Bax); and B-cell lymphoma 2 (Bcl-2) were determined using a Western blot. Independent t-test and Chi-squared tests were used in the study. RESULTS: There were no differences in the levels of TGF-ß, p-NFÏ°B, NFÏ°B, p-Drp1ser616, Drp1, Bax and Bcl-2 between the two groups. However, the level of PGC-1α was greater in irradiated gingival tissues with HBOT than in the healthy gingiva. CONCLUSION: Radiation-induced impaired wound healing can be improved by HBOT as indicated by levels of apoptosis, mitochondrial dynamics, cell proliferation and inflammation in irradiated gingiva with HBOT to a similar level to normal healthy gingiva. These findings may occur through an increase in mitochondrial biogenesis following HBOT.

The differences in mitochondrial function, mitochondrial dynamics, and cell death between odontogenic cysts/tumors and normal dental follicles.

We aimed to compare mitochondrial function, mitochondrial dynamics, apoptosis, and necroptosis between odontogenic cysts/tumors, including radicular cysts, dentigerous cysts, ameloblastoma, vs. dental follicles as control. We demonstrated that mitochondrial dysregulation and imbalanced mitochondrial dynamics were observed in ameloblastoma. Apoptosis was increased in dentigerous cysts, and ameloblastoma, while necroptosis was suppressed in ameloblastoma. Necroptosis in radicular cysts was higher than that of control, suggesting that the inflammation-associated cell death occurred in radicular cysts. Our findings suggest ameloblastoma exhibited mitochondrial dysfunction, decreased mitochondrial fusion, and potential apoptosis. Therefore, alleviating mitochondrial dysregulation and apoptosis may be novel-targeted therapy for odontogenic cysts and tumors.

The Effect of Warfarin on the Fibrin Architecture of Platelet-Rich Fibrin.

AIM: The aim of the study was to compare the macroscopic and microscopic factors, using scanning electron microscopy (SEM), of platelet-rich fibrin (PRF) between patients taking warfarin and healthy volunteers. MATERIALS AND METHODS: Twenty participants were selected (55 years old or older). Ten patients undertaking warfarin therapy with an International Normalized Ratio (INR) range from 2.50 to 4.00 acted as an experimental group and 10 healthy volunteers acted as a control group. Twenty-five-milliliter blood samples were collected from the 20 patients for PRF production and laboratory screening (INR and hematocrit). Then, PRF clots were compressed to a 1-millimeter membrane. All PRF sample macroscopic features (color, length, and width) were recorded and prepared for SEM evaluation. Images were obtained with SEM with 8000 times magnification. The percentage of the fibrin density was measured using ImageJ software (NIH, Bethesda, MD). Descriptive analysis was used to describe the macroscopic features. An independent t test and 1-way analysis of variance were used to compare both groups and each segment of PRF. RESULTS: All macroscopic features were totally identical. The fibrin density average from the upper to lower end was 89.09% ±â€Š1.99%, 88.11% ±â€Š3.25%, and 88.61% ±â€Š2.65% (control group) and 88.62% ±â€Š1.53%, 88.62% ±â€Š1.20%, and 89.54% ±â€Š2.17% (experimental group), respectively. There were no significant differences in the macroscopic features between the 2 groups and no differences in the microscopic features between the 2 groups and within each group. CONCLUSIONS: Warfarin did not have an effect on PRF when the macroscopic and microscopic features were compared between healthy volunteers and warfarin therapy volunteers.