Inflammation is a central component of the immune response. In its acute form it aids the transition from disease to health via the activation of numerous immune cells, enabling them to reach the site of infection/injury and orchestrate themselves to combat pathogens, facilitating resolution and repair to restore the host to health. However, chronic inflammation is deleterious to the host and differs from the “classical” acute inflammatory process in that the inflammation is not necessarily so readily obvious and is not self-limiting; rather, the immune system is in a constant state of low-grade activation and when challenged by pathogenic or sterile injury the response is heightened, resulting in prolonged tissue damage and a failure of efficient resolution mechanisms. Neutrophils are important mediators of acquired innate immune responses but may also contribute to the pathogenesis of chronic inflammatory diseases. Neutrophils are heavily involved in antimicrobial defence; their primary role is the localisation and elimination of pathogenic microorganisms. This, combined with their relatively short lifespan, has resulted in a traditional view of them as limited “kamikaze” cells. However, as detailed here, neutrophils have been shown to act with complexity and sophistication, orchestrating the immune/inflammatory response but also inadvertently contributing to tissue damage in different disease states. This thesis includes the study of neutrophil function in acute inflammatory episodes such as gingivitis and more chronic long-term health conditions such as obesity, chronic periodontitis and Papillon-Lefèvre Syndrome. The findings outlined here support the role of neutrophils as important contributors to both acute and chronic disease, showing these cells to be far more sophisticated than previously regarded.