Our initial literature review

Here is a copy of our initial literature review... we have definately come along way since this!

Introduction
Chronic periodontitis is global pandemic, exhibiting a complex disease pathogenesis which remains incompletely understood (Alpdogan & Van Dyke 2005; Bhatavadekar & Williams 2009; Paquette & Williams 2000; Van-Dyke 2008; Van-Dyke & Serhan 2003). An increased understanding of cell biology and a better interpretation of the behaviour of periodontal tissues has demanded a greater understanding of disease pathogenesis by dental hygienists (Wolf & Hassel 2006). Furthermore, a dental hygienist currently assumes more responsibility of his/her patients, as the interrelationships between oral and general health are become evident.
Traditional treatment strategies (calculus removal) complement the understanding that primary mediators of periodontal destruction are plaque bacteria (Paquette & Williams 2000, Wolf & Hassel 2006). However, whilst gram negative microorganisms remain the primary etiologic determinant of the disease, emerging evidence places stronger emphasis on the host inflammatory response in the pathogenesis of periodontal destruction, thus highlighting one’s inflammatory response as a risk factor for periodontal disease (Paquette & Williams 2000; Alpdogan & Van Dyke 2005; Bhatavadekar & Williams 2009). Furthermore, literature now suggests new treatment strategies should incorporate modulation of the host inflammatory response to achieve complete healing of the condition (Alpdogan & Van Dyke 2005; Bhatavadekar & Williams 2009; Paquette & Williams 2000; Van-Dyke 2008; Van-Dyke & Serhan 2003; Wolf & Hassel 2006) This paper will present a learning contract for an Oral Health Elective responsive to the dental hygienists responsibility in emerging therapeutic developments regarding pro-resolution, anti-inflammatory agents.

Background

Bachelor of Oral Health students currently recognise periodontitis as inflammation and loss of periodontal attachment; however, a lack in the depth of understanding of the inflammatory response is apparent. Literature and teaching staff alike, acknowledge the many inconsistencies of periodontal disease, which challenges students to evaluate the information provided. Thus, a literature review has been performed to gain a higher level of knowledge. A broad search of the PubMed database was conducted from 1990 – 2010, using “periodontitis AND inflammation*[tiab]” and “periodontitis AND new treatment*[tiab]”. Relevant and recent papers published in English were reviewed, with the understanding that further searches will be conducted during the course of the Oral Health Elective.

Literature Review
It has been well recognised throughout literature, that predominance of gram negative flora and its by-products in the periodontium triggers a reactive inflammatory response in the host, classically described in terms of 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). The cause-and-effect of specific periodontopathogens, however, remains unclear. It is suggested that failure of the host to resolve persistent acute inflammation essentially leads to chronic inflammation. Chronic inflammation is characterized by a shift in the type of cells which are present at the site of inflammation; macrophages are the dominate cells in these injured tissue (Bhatavadekar & Williams 2009, Ling et al 2009; Schwab et al 2007; Van Dyke 2008; Wolf & Hassel 2006). Whilst, macrophages are defensive against periodontopathogens, the toxins released during this defense mechanism are injurious to the host. Thus, tissue destruction occurs during periodontal disease due to the host response rather than the initial inflammation. (Bhatavadekar & Williams 2009, Ling et al 2009; Schwab et al 2007; Van Dyke 2008; Wolf & Hassel 2006). This potentially exhibits a genetic, negative phenotype and predisposition. It logically follows that modulation of host response through blocking the inflammatory cascade may prevent disease progression, particularly for high-risk individuals non-responsive to conventional treatment, thus the notion of anti-inflammatory therapy (Van Dyke 2007).

Undesirable effects, including an unfavourable removal of protective benefits of inflammation and concomitant increase in infections questions the feasibility of such an approach (Bhatavadekar & Williams 2009, Serhan et al 2007). However, an increased understanding of resolution pathways has led to interest in proresolving lipid mediators which contribute to homeostasis (Van Dyke 2008). It is now evident that resolution of inflammation is an active, rather than passive process, whereby activation of proresolving molecules, including Resolvin E1 and Protectin D1 is required to eliminate inflammatory leukocytes and therefore prevent pathology (Bhatavadekar & Williams 2009; Schwab et al 2007; Serhan et al 2007; Van Dyke 2008). Van Dyke (2008) speculates that by introducing pharmacologic proresolving agents, resolution of inflammation would cause elimination of pathogenic bacteria in turn. This concept of control of inflammation confers new implications for pharmacological approaches for disease management; by targeting proresolution rather than inflammation alone; benefits of the inflammation may be harnessed in conjunction with a timely return to homeostasis (Bhatavadekar & Williams 2009; Van Dyke 2008). Although more research is required, animal models have shown effective resolution and healing obtained from Lipoxins and Resolvin E1 (Hasturk et al 2007; Romano 2006).

Whilst the suggested novel approaches of therapeutic modulation of host response of periodontal disease appear promising, their correct indications for use are unclear due a current lack of evidence (Bhatavadekar & Williams 2009). Thus, greater importance must be placed on a student’s understanding of the complete periodontal disease process, so that if/or when therapeutics are initiated into periodontal treatment they can be administered effectively.

ADD INS (just now thought of):
-Hygienists: epidemiological perspective, increase removal of calculus has not decreased prevalence of severe periodontitis (REFERENCE). – role of education as an adjunct to therapy must not be undermined.
-education in clinical setting is not effective- anticipatory guidance.
-upstream health promotion, common risk factor approach required.