Abstract
In leukocyte adhesion deficiency type I, neutrophils fail to adhere to blood vessel walls and thus cannot transmigrate to peripheral tissues. Leukocyte adhesion deficiency type I patients invariably experience an aggressive form of generalized periodontitis, which has been historically attributed to defective neutrophil surveillance of the periodontal infection. This time-honored notion has now been challenged by a recent study, which showed that the underlying etiology involves a dysregulated host response that leads to overexpression of the proinflammatory and bone-resorptive cytokine IL-17.