In addition, NLRP3-mediated induction of IL-1β has been associated with osteoclast formation and neutrophil chemotaxis, processes that enhance alveolar bone resorption and impair endothelial function through a C-reactive protein (CRP)-dependent pathway, ultimately leading to an increased risk of endothelial dysfunction [34,35]. Here, NLRP3 is linked to endothelial dysfunction.