**9. Neutrophil persistence and chronic inflammation**

Neutrophils are recruited to infection and inflammation sites by different chemoattractants such as interleukin 8 (IL‐8), complement fragment C5a, or chemokine CXCL5. They migrate through the junctional epithelium and finally arrive in the gingival sulcus and in gingival cre‐ vicular fluid. Neutrophils in saliva retain their phagocytic function, and their ability to gener‐ ate ROS [71, 72]. NETs containing trapped bacteria have been described within the gingival sulcus, in purulent periodontal pockets, and on the surface of gingival epithelial cells. On con‐ dition that neutrophils and NETs do not occur excessively and are rapidly cleared, relatively little damage to the adjacent tissues is induced. Nevertheless, it has been widely reported that neutrophils can be responsible for both host defense and host tissue damage. Release of pro‐ teolytic and collagenolytic enzymes as well as ROS within host tissues, often lead to extracel‐ lular matrix degradation and persistent inflammation, are the main causes of tissue damage. Normally, connective tissue is degraded to allow fast transmigration of neutrophils and other cells involved in wound healing but during periodontitis it produces a chronic inflammatory disease. Hence, inflammation overweighs resolution, and host tissue destruction becomes progressive, eventually resulting in pathological osteolysis and tooth loss [58].
