Resolution of Inflammation - Neutrophil action

Paraphased from Article: Van-Dyke TE & Serhan CN 2003 Resolution of inflammation: A New Padagrim for the Pathogenisis of Periodontal Diseases J Dent Res 82(2) 82-90

It is understood that Neutrophils are a part of the first line of defence and protect the host from infection by phagocytosis.

Evidence now suggests that periodontitis is the result of hyperfunctional neutrophil action, these cells release toxins from the cell in large amounts (which are responisible for tissue destruction) due to excess activity. Neutrophils are not deficient or hypofunctional in periodontitis.

Inflammation, a multicellular response (similar to atherosclerosis and thrombosis) is controlled by cell to cell interactions. The cell to cell interactions that occur during the inflammatory process can provoke “transcellular biosynthetic routes” that lead to either the anti-inflammatory or proinflammatory process. In regular functioning neutrophils the anti-inflammatory process produces breaking signals (lipoxins and others unknown) which stop the inflammatory process and restore haemostasis. However, the exaggerated signals produced by hyperfunctional neutrophils (such as leukotrines and prostaglandins) advances the inflammatory process thus leading to a chronic lesion.

Further to this, Lang et al states “the development of periodontitis only occurs in areas of long standing gingivitis”