Maresin1 (MaR1) is an endogenous pro-resolving lipid mediator produced from polyunsaturated fatty acids and is believed to have antioxidant and anti-inflammatory properties. The objective of this study was to estimate MaR1′s impact on type 2 diabetic osteoporosis (T2DOP) and its pharmacological mode of action. An in vitro high-glucose model of the osteoblast cell line MC3T3-E1 was constructed and stimulated with MaR1. Type 2 diabetic rats were used to establish in vivo models of calvarial defects and were treated in situ with MaR1. The results revealed that, aside from preventing mortality and promoting the osteogenic capacity of MC3T3-E1 cells, MaR1 increased nuclear factor erythroid-2 related factor 2 (NRF2) signaling as well as the activity of glutathione peroxidase 4 (GPX4) and cystine-glutamate antiporter (SLC7A11) and caused the restraint of ferroptosis under hyperglycemic stimulation. However, the therapeutic impact of MaR1 was significantly diminished due to NRF2-siRNA interference and the ferroptosis activator Erastin. Meanwhile, these results were validated through in vivo experiments. These findings imply that MaR1 activated the NRF2 pathway in vivo and in vitro to alleviate high-glucose-induced ferroptosis greatly. More crucially, MaR1 might effectively reduce the risk of T2DOP.
Soft tissue seal around implant prostheses is considered the primary barrier against adverse external stimuli and is a critical factor in maintaining dental implants’ stability. Soft tissue seal is formed mainly by the adhesion of epithelial tissue and fibrous connective tissue to the transmembrane portion of the implant. Type 2 diabetes mellitus (T2DM) is one of the risk factors for peri-implant inflammation, and peri-implant disease may be triggered by dysfunction of the soft tissue barrier around dental implants. This is increasingly considered a promising target for disease treatment and management. However, many studies have demonstrated that pathogenic bacterial infestation, gingival immune inflammation, overactive matrix metalloproteinases (MMPs), impaired wound healing processes and excessive oxidative stress may trigger poor peri-implant soft tissue sealing, which may be more severe in the T2DM state. This article reviews the structure of peri-implant soft tissue seal, peri-implant disease and treatment, and moderating mechanisms of impaired soft tissue seal around implants due to T2DM to inform the development of treatment strategies for dental implants in patients with dental defects.
Mitochondria-associated membranes (MAMs), physical connection sites between the endoplasmic reticulum (ER) and the outer mitochondrial membrane (OMM), are involved in numerous cellular processes, such as calcium ion transport, lipid metabolism, autophagy, ER stress, mitochondria morphology, and apoptosis. Autophagy is a highly conserved intracellular process in which cellular contents are delivered by double-membrane vesicles, called autophagosomes, to the lysosomes for destruction and recycling. Autophagy, typically triggered by stress, eliminates damaged or redundant protein molecules and organelles to maintain regular cellular activity. Dysfunction of MAMs or autophagy is intimately associated with various diseases, including aging, cardiovascular, infections, cancer, multiple toxic agents, and some genetic disorders. Increasing evidence has shown that MAMs play a significant role in autophagy development and maturation. In our study, we concentrated on two opposing functions of MAMs in autophagy: facilitating the formation of autophagosomes and inhibiting autophagy. We recognized the link between MAMs and autophagy in the occurrence and progression of the diseases and therefore collated and summarized the existing intrinsic molecular mechanisms. Furthermore, we draw attention to several crucial data and open issues in the area that may be helpful for further study.
Background Osteogenesis of lateral window sinus elevation surgery is the key to placement of the subsequent implant, excessive collapse of the sub-antral space may adversely affect long-term stability of implants. At present, few studies focus on the influence of the contact area of the sub-antral space on osteogenesis. This study evaluated whether the change in the contact area of the sub-antral space with maxillary sinus bone and the Schneiderian membrane can affect osteogenesis. Methods Cone beam computed tomography (CBCT) images were collected of patients requiring maxillary sinus floor elevation (residual bone height < 6 mm) for standard-length implant placement before surgery, after surgery, and at 6-month follow-up visits. The postoperative sub-antral space volume (V1) and surface area (S1), and the remaining volume after six months of healing (V2) were measured. Then, the contact area of sub-antral space with maxillary sinus bone (Sbc) and the Schneiderian membrane (Smc), the absorbed volume during healing (Va), and the percentage of remaining volume (V2%) and absorbed volume (Va%) were calculated. The correlation between anatomical parameters was analyzed using multiple linear regression. Results A total of 62 maxillary sinuses from 56 patients were augmented, of which 57 were considered for the final analysis (5 withdrew due to perforation). Multiple linear regression results demonstrated that Sbc was significantly positively correlated with Va (β coefficient = 0.141, p < 0.01) without correlation between Smc and Va (β coefficient=-0.046, p = 0.470). There was a positive correlation between Sbc and V2% (β coefficient = 2.269, p <0.05). Conclusions This study confirmed that the size of the Sbc in lateral window sinus elevation surgery affected osteogenesis after six months of healing. Clinicians should assess the sinus contour type preoperatively, then consider whether it is necessary to expand the range of the Schneiderian membrane elevation to avoid excessive collapse of the sub-antral space. Trial registration Chinese Clinical Trial Registry(ChiCTR), ChiCTR2200057924. Registered 22 March 2022 - Retrospectively registered.
Background Osteogenesis of lateral window sinus elevation surgery is the key to placement of the subsequent implant, excessive collapse of the sub-antral space may adversely affect long-term stability of implants. At present, few studies focus on the influence of the contact area of the sub-antral space on osteogenesis. This study evaluated whether the change in the contact area of the sub-antral space with maxillary sinus bone and the Schneiderian membrane can affect osteogenesis. Methods Cone beam computed tomography (CBCT) images were collected of patients requiring maxillary sinus floor elevation (residual bone height < 6 mm) for standard-length implant placement before surgery, after surgery, and at 6-month follow-up visits. The postoperative sub-antral space volume (V1) and surface area (S1), and the remaining volume after six months of healing (V2) were measured. Then, the contact area of sub-antral space with maxillary sinus bone (Sbc) and the Schneiderian membrane (Smc), the absorbed volume during healing (Va), and the percentage of remaining volume (V2%) and absorbed volume (Va%) were calculated. The correlation between anatomical parameters was analyzed using multiple linear regression. Results A total of 62 maxillary sinuses from 56 patients were augmented, of which 57 were considered for the final analysis (5 withdrew due to perforation). Multiple linear regression results demonstrated that Sbc was significantly positively correlated with Va (β coefficient = 0.141, p < 0.01) without correlation between Smc and Va (β coefficient = − 0.046, p = 0.470). There was a positive correlation between Sbc and V2% (β coefficient = 2.269, p < 0.05). Conclusions This study confirmed that the size of the Sbc in lateral window sinus elevation surgery affected osteogenesis after six months of healing. Clinicians should assess the sinus contour type preoperatively, then consider whether it is necessary to expand the range of the Schneiderian membrane elevation to avoid excessive collapse of the sub-antral space. Trial registration: Chinese Clinical Trial Registry (ChiCTR), ChiCTR2200057924. Registered 22 March 2022–Retrospectively registered.
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