Patients with leukocyte adhesion deficiency type I (LAD-I) — which results from mutation of the CD18 subunit of β2 integrins — have recurrent microbial infections and periodontal bone loss. A new study shows that bone loss in patients and in mouse models is not due to defective neutrophil extravasation and impaired surveillance of periodontal infection, but is caused by the excessive production of interleukin-17 (IL-17). These data support the 'neutrostat' model of neutrophil homeostasis, whereby the phagocytosis of apoptotic neutrophils in tissue sites suppresses the production of IL-23 and hence IL-17, which leads to the downregulation of granulopoiesis; this feedback regulation is disrupted in patients with LAD-I. This is the first study to link neutrostat disruption to IL-17-driven pathology, and has implications for therapeutic targeting of the IL-23−IL-17 axis in patients with LAD-I.