What a week! We think we are getting there, we are arranging a meeting with Vicki Farmer to discuss the cellular biology, once we apply this info further, we will meet with a periodontist. IT NEEDS TO BE REFERENCED - don't worry

Inflammation denotes the body’s response to cellular injury by a variety of harmful stimuli including trauma, tissue necrosis and infection. The purpose of inflammation is to confine and neutralize the damaging agent, initiate repair of the tissues and restore them to original function. Acute and chronic inflammation are terms used to divide the phases of inflammation, however, they are not independent of each other and occur on a continuum.

Acute inflammation refers to the initial, non specific response triggered in the surrounding tissues of the harmful stimuli. Chemical mediator’s prostaglandins, leukotriene B4, serotonin, histamine and heparin are released causing vascular dilation, vascular permeability and neutrophil activation and migration. Neutrophils phagocytose bacteria and tissue debris; opsonisation (whereby complement and immunoglobulin alter the microorganism) enhances the efficacy of phagocytosis. Soft tissue destruction occurs due to the necessary release of collagenase. (Refer to Figure1). Clinically acute inflammation is observed as the cardinal signs- calor, dolor, rubor, tumour and impaired function (Bhatavadekar & Williams 2009; Lang et al 2009; Ohlrich et al 2009; Paquette & Williams 2000: Wolf & Hassel 2006) Depending on the severity, acute inflammation can occur within minutes, and usually lasts only for days. Acute inflammation can resolve or heal by repair; however, it may also progress to chronic inflammation, commonly acute and chronic inflammation responses coexist. Failure to restore the tissues to health can be a result of a dysregulated inflammatory response.

Concepts of inflammation have evolved and our understanding of the inflammatory response has become more sophisticated. Traditionally it was understood that resolution of inflammation was a passive process whereby a gradual “burning out” of neutrophil migration occurred; therapeutics for non responders to conventional therapy were therefore targeted at inhibiting the inflammatory response. New evidence postulates resolution is an active process determined in the acute phase of inflammation (REF REF REF).

According to this emerging evidence, after entering the tissues, PMN’s promote the switch from pro-inflammatory mediators; prostaglandins and leukotrines to anti-inflammatory mediators; lipoxins (and others unknown). Anti-inflammatory mediators initiate the terminal sequence or “breaking signals” for neutrophil recruitment, thus ceasing activation and migration and allowing apoptosis. However, for tissue resolution to occur, the toxins released must be removed. It is now understood that pro – resolution molecules promote macrophage clearance of apoptotic cells at the inflamed sites, and stimulation of anti-microbial activities of mucosal epithelial cells, promoting healing of the lesion. Lipoxins, derived from arachidonic acid, and Resolvin E1, Resolvin D1 and Protectin D1, derived from Omega- 3 fatty acids, constitute the known endogenous pro-resolution anti-inflammatory molecules. Inadequate resolution of acute inflammation and failure for the host to restore tissue homeostasis results in neutrophil-mediated tissue destruction (Van Dyke), not the initial inflammation itself.

Literature suggests inflammatory diseases of the body, inclusive of periodontal diseases, are a result of hyperfunctional neutrophils which release elevated levels of prostaglandins and leukotrines at the injured site which is thought to amplify inflammation. Haemostasis cannot be achieved as there is an imbalance in the levels of pro-inflammatory and anti-inflammatory mediators, thus leading to a chronic inflammatory lesion. It follows that if “the development of periodontitis only occurs in areas of long standing gingivitis” (Lang et al) failure to resolve inflammation inevitability becomes a risk factor for periodontal disease.