Changes in alveolar bone width around maxillary implants, as determined through cone beam computed tomography based on bony landmarks: A preliminary study.

PURPOSE: This study aimed to investigate changes in alveolar bone width around dental implants and identify the anterior nasal spine (ANS), posterior nasal spine (PNS), and floor of the nasal cavity that can be used as reference landmarks for standardizing the orientation of different cone-beam computed tomography (CBCT) scans. MATERIALS AND METHODS: We enrolled two groups that comprised 30 implants. Two CBCT scans from the same patient after implant surgery in the first group were obtained to determine differences in the relative distance and angle between the ANS and apex of the dental implant. Then we compared the second group of patients' presurgical and postsurgical CBCT images to evaluate changes in alveolar bone width after dental implant surgery by the aforementioned bony landmarks. RESULTS: In the first group, no statistically significant differences were detected in the mean distance between the ANS, PNS and implant tip in different directions. In the second group, bone width increased at 1 mm (p = 0.020) and decreased at 4 mm (p < 0.001) and 7 mm (p < 0.001) below the alveolar bone crest after implant surgery. CONCLUSIONS: Within the limitations of the present study, the ANS, PNS, and floor of the nasal cavity can be useful in standardizing the orientation of CBCT scans and alveolar bone remodeling after implant surgery varied depending on the height and direction from the alveolar bone crest based on the three landmarks.

Surfactin induces ER stress-mediated apoptosis via IRE1-ASK1-JNK signaling in human osteosarcoma.

Osteosarcoma, one of primary bone tumor in children and young adults, has poor prognosis and drug resistances to chemotherapy. In order to reinforce the conventional therapies and antagonize the osteosarcoma in patients, a novel strategy is required for developing a new treatment. In this study, surfactin, a natural product from Bacillus subtilis, showed the efficiency of cell death in osteosarcoma, but not in normal cells. Surfactin triggers ER stress mechanism by promoting the aberrant Ca2+ release from ER lumen and ER-signaling to mitochondrial dysfunction following caspases activation mediating cell apoptosis. Surfactin-induced ER stress not only upregulated of glucose-regulated protein 78/94 and IRE1-ASK1-JNK pathway but also leading to calpains and Bcl-2 proteins family involving the release of cytochrome c. The releases into cytosol trigger the cleavage of caspase-9 and caspase-3 to induce cell apoptosis. In this study, surfactin demonstrated the potential functions to trigger the ER stress, ER stress-associated IRE1-ASK1-JNK signaling pathway, mitochondrial dysfunction, and caspase activations leading to programmed cell apoptosis. Importantly, implicating the signaling pathway that regulates the connection between ER stress and mitochondrial dysfunction causing apoptosis associated with surfactin. These results indicated a potential application of surfactin strengthen current conventional therapies.

Using Cone-Beam Computed Tomography to Assess Changes in Alveolar Bone Width around Dental Implants at Native and Reconstructed Bone Sites: A Retrospective Cohort Study.

The aim of this study was to use a cone-beam computed tomography (CBCT) to assess changes in alveolar bone width around dental implants at native and reconstructed bone sites before and after implant surgery. A total of 99 implant sites from 54 patients with at least two CBCT scans before and after implant surgery during 2010-2019 were assessed in this study. Demographic data, dental treatments and CBCT scans were collected. Horizontal alveolar bone widths around implants at three levels (subcrestal width 1 mm (CW1), subcrestal width 4 mm (CW4), and subcrestal width 7 mm (CW7)) were measured. A p-value of < 0.05 indicated statistically significant differences. The initial bone widths (mean ± standard deviation (SD)) at CW1, CW4, and CW7 were 6.98 ± 2.24, 9.97 ± 2.64, and 11.33 ± 3.00 mm, respectively, and the postsurgery widths were 6.83 ± 2.02, 9.58 ± 2.55, and 11.19 ± 2.90 mm, respectively. The change in bone width was 0.15 ± 1.74 mm at CW1, 0.39 ± 1.12 mm at CW4 (p = 0.0008), and 0.14 ± 1.05 mm at CW7. A statistically significant change in bone width was observed at only the CW4 level. Compared with those at the native bone sites, the changes in bone width around implants at reconstructed sites did not differ significantly. A significant alveolar bone width resorption was found only at the middle third on CBCT scans. No significant changes in bone width around implants were detected between native and reconstructed bone sites.