While further experimentation is required to definitively conclude that ASC and alterations in NF-kB activity are essential mechanistic elements in NLRP3-mediated apoptosis in bacterially challenged osteoblasts, these studies indicate that this NLR represents an important component underlying the direct initiation of apoptosis in this bone-forming cell type following challenge with intracellular bacterial pathogens and could, therefore, be a major contributory factor to bone loss at sites of infection. Here, NLRP3 is linked to infection.