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Lithium nitrate is an attractive lithium additive in the construction of high‐performance lithium metal anodes with a Li3N‐rich solid electrolyte interphase (SEI) layer. However, the eight‐electron transfer process induces high energy barriers between LiNO3 and Li3N. Herein, the inner Helmholtz plane is tuned on a Li deposition host to attain sluggish/rapid LiNO3 decomposition kinetics, resulting in different intermediate content distributions of Li species in the SEI. Notably, lithium oxynitride (LiNO) is identified as the decomposition intermediate, and experimental and simulation results confirm its role in obstructing LiNO3 decomposition. Moreover, the results reveal that the dipole–dipole interaction between LiNO and the polar V≡N bond can change the ionic/covalent character of the N═O bonds, considerably facilitating the energy transfer process of the N═O cleavage, and promoting a LiNO3 reduction to achieve a Li3N‐rich SEI. Consequently, when the electrolyte contains 0.37 m LiNO3, dendrite, and dead Li formation are suppressed effectively with the VN system, and an average Coulombic efficiency of 99.7% over 1000 cycles (1 mA cm−2, 1 mAh cm−2) can be attained. These results can promote the nitride oxidation break process and pave the way for fabricating high‐performance Li3N‐rich lithium metal batteries. [ABSTRACT FROM AUTHOR]

Periodontitis is a chronic infectious disease caused by bacterial irritation. As an essential component of the host immunity, macrophages are highly plastic and play a crucial role in inflammatory response. An appropriate and timely transition from proinflammatory (M1) to anti‐inflammatory (M2) macrophages is indispensable for treating periodontitis. As M2 macrophage‐derived exosomes (M2‐exos) can actively target inflammatory sites and modulate immune microenvironments, M2‐exos can effectively treat periodontitis. Excessive endoplasmic reticulum stress (ER stress) and unfolded protein response (UPR) are highly destructive pathological characteristics during inflammatory periodontal bone loss. Although melatonin has antioxidant and anti‐inflammatory effects, studies focusing on melatonin ER stress modulation remain limited. This study fabricates engineered M2‐exos loading with melatonin (Mel@M2‐exos) for treating periodontitis. As a result, M2‐exos drive an appropriate and timely macrophage reprogramming from M1 to M2 type, which resolves chronic inflammation and accelerated periodontal healing. Melatonin released from Mel@M2‐exos rescues the osteogenic and cementogenic differentiation capacity in inflammatory human periodontal ligament cells (hPDLCs) by reducing excessive ER stress and UPR. Injectable gelatin methacryloyl (GelMA) hydrogels with sustained‐release Mel@M2‐exos accelerate periodontal bone regeneration in rats with ligation‐induced periodontitis. Taken together, melatonin engineering M2 macrophage‐derived exosomes are promising candidates for inflammatory periodontal tissue regeneration. [ABSTRACT FROM AUTHOR]