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«EVALUATION OF ORAL NEUTROPHIL LEVELS AS A QUANTITATIVE MEASURE OF PERIODONTAL INFLAMMATORY LOAD IN PATIENTS WITH SPECIAL NEEDS By Anita Moosani BSc, ...»

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A Focus on Systemic Inflammation C reactive protein (CRP) and fibrinogen can be used as markers to evaluate the inflammatory status of an individual, and could be useful predictors of future cardiovascular events in various populations (Danesh et al., 2000). An association between periodontitis and increased CRP levels was first demonstrated in 1997 (Ebersole, Machen, Steffen & Willmann, 1997). More recent reports suggest that non-surgical periodontal treatment such as scaling and root planing can reduce CRP levels significantly (D‟Aiuto, Ready, & Tonetti, 2004; Lopez et al., 2011; Siribamrungwong & Puangpanngam, 2012). Notably, patients who brush their teeth infrequently (i.e. those with poor oral hygiene), had increased concentrations of CRP and fibrinogen when compared to those with good oral hygiene levels (de Oliveira, Watt, & Hamer, 2010). Furthermore, periodontal disease has been associated with moderate systemic inflammatory responses (D‟Aiuto, Ready, & Tonetti, 2004), as shown by elevated levels of CRP and other inflammatory biomarkers (Loos, Craandijk, Hoek, Wertheim-van Dillen, & van der Velden, 2000). Thus, a higher individual inflammatory load may result in increased cardiovascular risk based on serum CRP and fibrinogen concentrations due to the systemic inflammatory response consequent to low grade chronic periodontal infections (D‟Aiuto, Ready, & Tonetti, 2004). Hence, in addition to the putative problems caused by bacteremia, these findings are noteworthy as periodontal disease is a condition that presents with modifiable risk factors (inflammation and infection), which can be prevented and treated with predictable treatments that have minimal risk, as will be discussed later.

Oral Inflammation and Respiratory Tract Infections The evidence demonstrating an association between aspiration of pathogenic oral microorganisms and chronic lung infections is increasing (Scannapieco, Papandonatos, & Dunford, 1998; Scannapieco, 1999; Azarpazhooh & Leake, 2006; Paju & Scannapieco, 2007;

Raghavendran, Mylotte, & Scannapieco, 2007). In addition to direct microbial induction of aspirational respiratory infections, there is also evidence that host-derived mediators such as inflammatory cytokines, which are found in high levels in the saliva of patients with periodontal disease, could induce lung inflammation when aspirated and can lead to conditions such as pneumonia and chronic obstructive pulmonary disease (Scannapieco, 1999). Aspiration of bacteria from the oral cavity is a common route of infection for bacterial pneumonia, with dental plaque being a source of potential infectious agents and periodontal pockets acting as reservoirs (Azarpazhooh & Leake, 2006; Paju et al., 2009).

Scannapeico (1999) noted four possible mechanisms whereby oral bacteria may exert their pathogenic role. First, pulmonary pathogens may colonize dental plaque which is then aspirated. Second, bacterial enzymes associated with the pathogenesis of periodontal disease may assist respiratory pathogens in adhering to the airway. Third, hydrolytic enzymes in periodontitis may destroy the protective salivary pellicle on pathogenic bacteria, thus reducing bacterial clearance from mucosal surfaces via host protective mechanisms. Fourth, the cytokines released by inflammed periodontal tissues and peripheral cells may cause increased adherence receptors to be expressed on the mucosal surface and allow for respiratory pathogen colonization. Other proposed mechanisms for pulmonary infection are inhalation of air-borne bacteria or bacterial translocation by bacteremias (Paju & Scannapieco, 2007). Poor oral hygiene has been associated with a significant increase in likelihood of chronic respiratory disease and aspiration pneumonia in susceptible individuals, such as patients in intensive care units and notably for the purposes of this investigation, in patients with special needs (Scannapieco, 2005b; Sigal & Sigal, 2006). This is something that should be highly modifiable and in fact in 2006, Azarpazhooh and Leake reported that there is fair evidence demonstrating an association between oral status and pneumonia, and good evidence that improving oral hygiene and frequent professional oral health practices decreases the occurrence or progression of respiratory diseases. However, there might not be a simple approach to this issue insofar as patients with special needs are concerned.

The Special Needs Population at Increased Risk for Disease The literature shows that patients with special needs have more plaque and lower levels of oral hygiene than the general population (Anders & Davis, 2010). Patients with special needs often present with poor oral hygiene or are unable to maintain oral hygiene due to motor skill impairment, lack of self-help skills and understanding of complex tasks, poor cooperation, manual dexterity and coordination, or ineffective technique (Lindemann, Zaschel-Grob, Opp, Lewis, & Lewis, 2001). The importance of maintaining a level of optimal oral health in patients with special needs is clarified when recognizing the decreased ability of the body to defend itself in those with reduced salivary flow, diminished cough reflex, swallowing disorders, inability to perform or maintain good oral hygiene, or other physical disabilities (Thornton, al-Zahid, Campbell, Marchetti, & Bradley, 1989; Teng et al., 2002; Scannapieco, 2005; Paju & Scannapieco, 2007). Poor oral hygiene can be even worse in situations where the oral musculature is impaired so that natural cleansing of the oral cavity is limited (Shaw, Shaw, & Foster, 1989). In addition, patients who are not able to cooperate for dental treatment have been shown to lose more teeth secondary to periodontal disease or caries than patients who are cooperative (Gabre, Martinsson, & Gahnberg, 1999).





In most cases, the provision of oral hygiene is dependent on the caregiver. Therefore, the caregiver must be knowledgeable and proficient with regard to the delivery of oral care for their charges, and must also have an understanding of the importance to the patient of having a clean mouth (Cumella, Ransford, Lyons, & Burnham, 2000; Christensen, 2005).

Unfortunately, most caregivers do not receive formal training in oral hygiene regimes (Cumella, Ransford, Lyons, & Burnham, 2000), and thus the patients under their care do not have optimal oral hygiene or oral health in many cases.

In the face of poor oral hygiene, development of an anaerobic environment below the gingival margin ensues leading to the formation of subgingival plaque (i.e. a pathogenic biofilm). Consequently, at this point, professional dental care is required for complete removal of plaque. Although all forms of gingival inflammation do not necessarily develop into inflammatory periodontal disease, the development of this type of inflammation is still considered as one of the prerequisites for this tissue-destructive condition to develop (Boehm & Scannapieco, 2007). The potential role of bacteria contained within the oral biofilms as contributors to respiratory infections has already been discussed but it bears repeating that by improving oral hygiene and establishing a level of optimal oral health, this could also lead to improved periodontal health (Teng et al., 2002; Binkley, Haugh, Kitchens, Wallace, & Sessler, 2009), and perhaps an improvement in the overall morbidity and mortality rates seen in this population of patients (Sigal & Sigal, 2006). If this was the only problem to consider it would still represent a formidable concern. However, as will be discussed in more detail below, other issues that interfere with the establishment of optimal oral health include a general inability to establish diagnoses of oral disease and in concert, difficulties and in some cases inability to treat oral disease once identified in the special needs population (unless the patient can be placed under a general anaesthetic).

Treatment of Periodontal Diseases The primary goal of any therapeutic intervention in inflammatory disease is to restore the tissue to a state of homeostasis. Treatment for periodontal diseases aims to change or eliminate the causative organisms to decrease or eliminate inflammation, establish periodontal health, arrest disease progression, and prevent recurrence (Kim & Amar, 2006;

Van Dyke, 2007). It follows that regular disruption of the biofilm via regular oral hygiene practices allows for maintenance of a biofilm that is compatible with periodontal health, and personal and professional care is integral to preventing re-initiation of inflammation (Sanz & van Winkelhoff, 2011). Treatment objectives are complicated where an acute inflammatory response has progressed to chronic inflammation, as evidenced by tissue damage of the cellular matrix, scarring, fibrosis, or features of inadequate healing. Thus, timely clinical diagnosis and appropriate treatment intervention and host response (healing) is required to prevent the progression of disease from acute to chronic disease, for it to be more likely to achieve homeostasis (Van Dyke, 2007).

The foundation of treatment for periodontitis initially involves non-surgical debridement, referred to as scaling and root planing. This can be performed with manual instruments or electronic devices and the goal is to remove dental plaque and calculus, thereby reducing, eliminating, or at least controlling the pathogenic oral biofilm. When combined with regular personal oral hygiene, tissue inflammation is reduced and clinical attachment can be improved (Cobb, 1996; Drisko, 2001; Cobb, 2002; Suvan, 2005). A recent study has shown that non-surgical periodontal therapy also improves oral health-related quality of life (Wong, Ng, Corbet, & Keung Leung, 2012). If unsuccessful, non-surgical periodontal therapy may be supplemented with anti-bacterial treatment, or if that is not successful access surgery may be required (Kim & Amar, 2006). The patient‟s response to treatment is monitored at follow-up examinations at regular intervals, depending on the extent of disease and ability to maintain oral hygiene (Cohen, 2003; Pihlstrom, Michalowicz, & Johnson, 2005). Treatment is individualized at these appointments and typically consists of debridement, oral hygiene instructions, and continuation of attempts to control or eliminate risk factors for disease (Lamster, 1996; Renvert & Persson, 2004).

The anti-microbial approach to periodontal therapy is aimed at reducing the inflammatory load at the tooth and gingival interface. As previously noted, a consistent oral hygiene regimen consisting of tooth brushing and flossing to disrupt the oral biofilm is the mainstay in periodontal treatment. Despite attempts to manage the oral biofilm with such mechanical measures by the dentist and patient, clinical progression and signs of disease activity may persist, and therefore supplementation with chemotherapeutic agents is often considered to aid in the achievement of periodontal health. Chemotherapeutic agents include antiseptics that are applied topically, but do not contain antibiotics or disinfectants, and therefore do not provide a risk for bacterial resistance. Oral rinses such as chlorhexidine gluconate (Peridex™), irrigants such as hydrogen peroxide, and triclosan-containing toothpastes are examples of agents that are included in this category. Host modulation therapy is a newer approach to managing disease by inhibiting mediators of host tissue destruction such as MMPs, cytokines, and prostanoids. These agents include topical and systemic non-steroidal anti-inflammatory drugs, subantimicrobial-dose doxycycline, and systemic bisphosphonates (Ryan, 2005). The application of non-surgical therapy in the management of periodontal disease relies on proper case selection and compliance, including frequent re-evaluation and monitoring in order to achieve long term success (Drisko, 2001).

Conventional Methods for Diagnosis of Periodontal Diseases The Periodontal Probe The periodontal probe is the standard tool of measure used to distinguish between gingivitis and periodontitis (Ranney, 1993), and is based on readings of periodontal probing depths and clinical attachment loss (Armitage, 1999). However, problems with the conventional periodontal probe in its application to the clinical setting have been noted, even for patients who are not in the special needs category. For example, penetration of the probe is influenced by inflammation of the tissues, so that the probe tip can extend beyond the apical termination of the junctional epithelium during measurements compared to the healthy state (Anderson, Caffesse, Nasjleti, & Smith, 1991). Reproducing measurements using the periodontal probe is also challenging due to difficulties in replicating position, angulation, and insertion force (Khan & Cabanilla, 2009). Probing also has a notable measurement error of ± 1 mm. Objectively, this associates a significant measuring error to a pocket depth measurement, where a 5 mm probing depth would be associated with a 40% (2/5 mm) error.

The clinical implications of this are important to consider when assessing the diagnostic value of the periodontal probe and whether measurements using this instrument can be used reliably to determine whether the periodontal lesion in periodontitis is active or not. If the associated errors are not considered during interpretation, a patient could be identified incorrectly as being healthy or diseased due to measuring error, which could result in inappropriate treatment recommendations (Apsey, Kaciroti, & Loesche, 2006). Because the probing error is so large, it might be possible to consider probing depth measurements as being non-parametric, indicating that mean probing values should also probably be avoided in preference to frequency distributions. Finally, the periodontal probe demonstrates disease after active disease is already present and has caused damage to the periodontium (Lamster, Celenti, Jans, Fine, & Grbic, 1993), and cannot be used to prognosticate additional tissue destruction or, as alluded to above, to differentiate between an „active‟ periodontal lesion and a quiescent (i.e. non-progressing) lesion.



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