Charcoal

To determine the impact on the mechanical properties and surface features of ceramic-coated nickel-titanium (CC-Ni-Ti) archwires when subjected to charcoal, probiotic, and chlorhexidine mouthwashes in in vitro conditions.

Eighty samples of 25 mm were cut from the posterior end of preformed maxillary 0.016'' CC-Ni-Ti super elastic archwires (Koden Company, USA) and distributed into four equal groups. Each group of wires was immersed in artificial saliva (Wet Mouth Mouthwash, ICPA Health Products Ltd., India) (control), charcoal mouthwash (Hello activated charcoal extra freshening mouthwash, Hello Products LLC, USA), probiotic mouthwash (Perfora, Probiotic Rinse, India), and 0.2% chlorhexidine gluconate mouthwash (Sensorange, Orange Biotech, Pvt., Ltd., India) (experimental groups) for 90 min at 37 °C. All samples were taken out of their respective solutions and washed with distilled water prior to testing. A three-point bending test was performed on 15 samples from each group using a universal testing device. During the loading and unloading of the archwires, the yield strength (YS), flexural modulus of elasticity (E), and spring back ratio (YS/E) were calculated. The remaining five wires from each group were observed under the scanning electron microscope (SEM) for surface topography evaluation.

The mean differences of loading YS, E, and YS/E between chlorhexidine and charcoal are 302.91 MPa, 4.28 GPa, and 0.0004, whereas unloading values are 172.32 MPa, 4.16 GPa, and 0.0003, respectively, with a statistical significance of <0.001 in terms of YS and E. The mean differences of loading YS, E, and YS/E between charcoal and probiotic are 305.36 MPa, 4.54 GPa, and 0.0005, whereas unloading values are 173.77 MPa, 3.66 GPa, and 0.0003, respectively, with a statistical significance of <0.001 in terms of YS and E. The mean differences of loading YS, E, and YS/E between chlorhexidine and probiotic are 2.45 MPa, 0.26 GPa, and 0.00007, whereas unloading values are 1.44 MPa, 0.49 GPa, and 0.0000533, respectively, with no statistical significance of >0.001 in terms of YS, E, and YS/E. Surface topography alteration was clearly appreciated in the charcoal and probiotic mouthwash groups compared to charcoal mouthwash.

Loading and unloading of 0.016" ceramic-coated nickel-titanium archwires showed an increase in mechanical properties except for the spring back ratio on exposure to chlorhexidine, probiotic, and charcoal mouthwashes. Chlorhexidine and probiotic mouthwashes had a higher yield strength and flexural modulus of elasticity in comparison with charcoal mouthwash and artificial saliva on 0.016" ceramic-coated nickel-titanium archwires. More corrosive changes were seen on 0.016" ceramic-coated nickel-titanium archwires when immersed in chlorhexidine, followed by probiotic and charcoal mouthwashes.

Targeting of the apelin–apelin receptor (Apj) system may serve as a useful therapeutic intervention for the management of chronic kidney disease (CKD)‐induced skeletal muscle atrophy. We investigated the roles and efficacy of the apelin–Apj system in CKD‐induced skeletal muscle atrophy.

The 5/6‐nephrectomized mice were used as CKD models. AST‐120, a charcoal adsorbent of uraemic toxins (8 w/w% in diet), or apelin (1 μmol/kg) was administered to CKD mice to investigate the mechanism and therapeutic potential of apelin on CKD‐induced skeletal muscle atrophy. The effect of indoxyl sulfate, a uraemic toxin, or apelin on skeletal muscle atrophy was evaluated using mouse myoblast cells (C2C12 cells) in vitro.

Skeletal muscle atrophy developed over time following nephrectomy at 12 weeks, as confirmed by a significant increase of atrogin‐1 and myostatin mRNA expression in the gastrocnemius (GA) muscle and a decrease of lower limb skeletal muscle weight (P < 0.05, 0.01 and 0.05, respectively). Apelin expression in GA muscle was significantly decreased (P < 0.05) and elabela, another Apj endogenous ligand, tended to show a non‐significant decrease at 12 weeks after nephrectomy. Administration of AST‐120 inhibited the decline of muscle weight and increase of atrogin‐1 and myostatin expression. Apelin and elabela expression was slightly improved by AST‐120 administration but Apj expression was not, suggesting the involvement of uraemic toxins in endogenous Apj ligand expression. The administration of apelin at 1.0 μmol/kg for 4 weeks to CKD mice suppressed the increase of atrogin‐1 and myostatin, increased apelin and Apj mRNA expression at 30 min after apelin administration and significantly ameliorated weight loss and a decrease of the cross‐sectional area of hindlimb skeletal muscle.

This study demonstrated for the first time the association of the Apj endogenous ligand–uraemic toxin axis with skeletal muscle atrophy in CKD and the utility of therapeutic targeting of the apelin–Apj system.