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Periodontal Disease: An Inflammatory Syndrome Periodontal diseases are manifestations of an inflammatory process. Inflammation is defined as, “a complex reaction to injurious agents such as microbes and damaged, usually necrotic, cells that consist of vascular responses, migration and activation of leukocytes, and systemic reactions” (Kumar, Abbas, & Fausto, 2005). Thus, the process of inflammation leads to dysregulation of the health-associated homeostatic relationships between tissue destruction and repair. Inflammation begins as an acute reaction of rapid onset and of relatively short duration, and is characterized by fluid exudate and leukocyte emigration into the periodontal pocket surrounding the affected tooth or teeth, consisting mostly of PMNs. In contrast, chronic inflammation occurs over a longer period of time and is mediated by cells such as lymphocytes and macrophages, as well as pathophysiological responses such as blood vessel proliferation and fibrosis of the surrounding tissues. Inflammation ceases when the invading agents and host mediators are removed (Kantarci & Van Dyke, 2005).

Pathogenesis of Periodontal Diseases The tissue destruction that is noted in periodontal disease is currently thought to occur as a result of an interaction between the pathogenic bacteria residing in the periodontal pocket and the host inflammatory response (Deas, Mackey, & McDonnell, 2003). Constituents of the microbial biofilm stimulate increased inflammatory infiltrate to the gingival crevice.

This infiltrate includes many serum components including markers of inflammation as well as particular cell types such as neutrophils, macrophages, and lymphocytes (Kim & Amar, 2006). Non-microbial components of the gingival crevicular fluid that are being affected by inflammation may contain microbe-derived factors including lipopolysaccharides. These agents can also activate the host immune response so that various pro- and anti-inflammatory cytokines are produced. The pro-inflammatory cytokines include tumor necrosis factor alpha (TNFa), prostaglandins (especially prostaglandin E2), as well as various hydrolytic enzymes, some of which are MMPs. In addition, T lymphocytes can be stimulated to release cytokines and lymphotoxin. These substances possess intense pro-inflammatory and catabolic activities, causing periodontal tissue breakdown, typically mediated by the MMPs noted above. It is thought that the presence of these inflammatory molecules and cells marks the transition from gingivitis to periodontitis, and PMNs are thought to be especially important in the latter (Page, 1998; Nussbaum & Shapira, 2011). Basically, the severity and extent of this destruction depends on dynamic interactions between the host inflammatory response and the destructive pathobiological responses around the affected teeth (Lee, Aitken, Sodek, & McCulloch, 1995; Kim & Amar, 2006; Jin, 2011).

Inflammatory Load: A Novel Term in Dentistry We propose that the inflammatory infiltrate as described above, which consists mostly of PMNs (Van Dyke & Hoop, 1990), and leads to the inflammatory cascade, may be described as the “inflammatory load” of an individual. The “inflammatory load” has been described in the medical literature (O‟Donovan et al., 2011; Bassiouni, Naidoo, & Wormald, 2012), as a measure of inflammatory markers in blood or other tissues (Jin et al., 2010). In the realm of dentistry and specifically in this study, this term would reflect the inflammatory burden of the individual in the presence of oral disease, which is modifiable by removing the stimulating factors with treatment (e.g. pathogenic bacteria within the oral biofilm), as will be discussed later.

The Role of Neutrophils in the Host’s Immune Response Neutrophils are a major cellular element of innate immunity (Lavelle, 1992; Hart, Shapira, & Van Dyke, 1994), are the predominant leukocytes in the blood (Miyasaki, 1991), and are vital in the host‟s immune response to virulent bacteria (Van Dyke & Hoop, 1990). With regard to differentiation and development of PMNs, their precursors are found in the bone marrow as stem cells. The process by which leukocytes are produced is called leuokpoiesis.

Cytokines such as interleukins and colony-stimulating factors regulate this process, and allow stem cells to develop into a myeloid stem cell or lymphoid stem cell. The myeloid pathway gives rise to the neutrophils, as well as monocytes, basophils, and eosinophils. Notably, the myeloid stem cell passes through five precursor stages in the process of differentiation and maturation into a PMN: myeloblast, promyelocyte, neutrophil myelocyte, neutrophilic metamyelocyte, and then neutrophilic band cell. The lymphoid pathway results in T- and Blymphocytes. After the stem cells differentiate and mature into PMNs, they are released into the bloodstream. Neutrophil development takes about 2 weeks, and approximately one hundred billion are produced daily (Deas, Mackey, & McDonnell, 2003). Neutrophils then migrate and adhere to the endothelium of blood vessels before passing into the connective tissues as extravascular cells (Van Dyke & Hoop, 1990). Under normal conditions of health, 90% of the body‟s PMNs reside in the bone marrow. Many of the daily produced neutrophils will undergo apoptosis prior to leaving the bone marrow. For neutrophils that are released, the half-life ranges from 6 to 9 hours (in circulation), to 1 to 4 days (in tissue; Trowbridge & Emling, 1997; Deas, Mackey, & McDonnell, 2003). Typically, after initiation of bacterial colonization (and invasion in some cases), PMNs will migrate to the site of infection.

Neutrophils pass from the connective tissue to the gingival sulcus via the intercellular spaces of the junctional epithelium (Attstrom, 1970; Schroeder, 1973). It is here that cells enter the oral cavity, continue to function without impairment, and can be collected for analyses (Klinkhamer, 1968).

Neutrophils are attracted to the site of infection in response to chemotactic molecules activated by invading microbes, such as complement proteins. The bacteria are then identified and engulfed by the PMN into a phagosome. The cell membrane of the phagosome fuses with the membranes of cytoplasmic granules, resulting in the release of granule contents (called “degranulation”), into the phagosome as well as the extracellular environment in order to kill the invading microbes. It is important to note at this point that the PMN cytoplasm contains several types of granules or specialized lysosomes that are classified as primary, secondary, and tertiary granules. The primary granules contain acid hydrolases, neutral proteases, cationic proteins, myeloperoxidase, and lysozymes. The secondary granules contain lysozymes, lactoferrin, and collagenase. Finally, the tertiary granules contain cytochrome b and alkaline phosphatase (Van Dyke & Hoop, 1990). These factors play an important role in bacterial killing but can also be used as markers of PMN activity, quantity, and inflammation (Cao & Smith, 1989).

The Role of Neutrophils in Periodontal Disease Neutrophils play a major role in the host response to invading periodontal pathogens (Hart, Shapira, & Van Dyke, 1994). The gingival sulcus is the major site of entry of leukocytes into the oral cavity (Sharry & Krasse, 1960). In fact, about 90% of leukocytes isolated from gingival crevicular fluid are PMNs (Woolweaver, Koch, Crawford, & Lundblad, 1972). The PMN is able to detect infection, migrate to the site of disease, destroy pathogens, and influence bacterial growth and colonization in periodontal tissues (Deas, Mackey, & McDonnell, 2003). Neutrophils have been found in the gingival crevice of clinically healthy gingival tissues (Attstrom, 1970; Raeste, Tapanila, & Tupakka, 1977), and have been shown to increase in quantity with gingival inflammation (Attstrom, 1970; Schroeder, 1973), and when comparing dentate to edentulous patients (Calonius, 1958). The number of granulocytes in saliva have also been shown to increase prior to the appearance of clinical gingivitis (Friedman & Klinkhamer, 1971), and line the junctional epithelium to wall off the periodontal tissues from the bacterial biofilm, before the involvement of chronic inflammatory cells (Miyasaki, 1991). An increased quantity of PMNs has also been noted to occur in the sulci of chronically inflamed gingiva (Attstrom, 1970). The protection conferred by the host response effectively defends against the bacterial insults that constantly threaten the health status of the periodontium in the majority of the population (Deas, Mackey, & McDonnell, 2003; Schenkein, 2006).

The Neutrophil’s Protective and Destructive Mechanisms Although the PMN is a protective cell, it can by way of its inherent activity, also contribute to destruction of the local tissues that it has infiltrated to defend against bacterial invasion.

The PMN employs two systems for bacterial killing, which are distinguished by their dependence on oxygen. The oxygen-independent system or “degranulation”, was described earlier, and releases enzymes through degranulation of primary and secondary granules in the cell cytoplasm. The oxygen-dependent pathway is further divided into two types. The myeloperoxidase-independent pathway results in free radical generation where nicotinamide adenine dinucleotide phosphate oxidase (NADPH) is bound to the cell membrane, and catalyzes the reduction of oxygen to superoxide anion, which is converted to hydrogen peroxide and hydroxyl radical. These free radical metabolites are only toxic to pathogens at high concentrations. The myeloperoxidase-dependent pathway involves the reaction between hydrogen peroxide and halide to form hypochlorous acid, chlorine, and the hypochlorite ion, which is highly toxic to bacteria, fungi, viruses, and mycoplasma, due to its intense oxidative capacity (Van Dyke & Hoop, 1990; Lamster, 1992; Trowbridge & Emling, 1997; Deas, Mackey, & McDonnell, 2003).

However as alluded to above, the protection provided by the PMN is not without consequence. As noted previously, the PMN plays a major role in the host response, and normally plays a protective role, defending against bacterial insults that threaten gingival health (Deas, Mackey, & McDonnell, 2003). Yet, these killing mechanisms have the potential to damage extracellular tissues via the release of granular constituents such as collagenases and MPOs, and reactive oxygen species (Van Dyke & Hoop, 1990; Lamster, 1992; Deas, Mackey, & McDonnell, 2003). In addition, ineffective or excessive response by the host can lead to tissue damage – an outcome that is influenced by individual factors (Miyasaki, 1991; Hart, Shapira, & Van Dyke, 1994; Van Dyke & Serhan, 2003). The destruction incurred may be dependent on the amount of time that the PMN is allowed to be present in the tissues. Persistently present PMNs, as in the case of gingivitis, where bacteria are consistently present can lead to tissue damage (Nussbaum & Shapira, 2011). Cell death through apoptosis as opposed to necrosis is critical in order to preserve tissue function and integrity. Apoptotic cells help to resolve inflammation by sending signals to macrophages, which engulf the PMNs and secrete anti-inflammatory cytokines, such as transforming growth factor beta (Fadok & Henson, 1998). If apoptosis is reduced, as is thought to occur in periodontal disease, then the macrophages that help to regulate the inflammatory response will also decrease, and the PMNs that are present will continue to release their destructive contents (Nussbaum & Shapira, 2011). Thus, in addition to killing bacteria, these cells continue to release products that can cause direct damage to extracellular matrices as well as other host cells.

A Focus on Bacteremias Periodontal infections are characterized by recurrent bacteremias, as evidenced by the identification of oral pathogens systemically (Offenbacher & Beck, 2005). The chronic and recurrent nature of periodontal disease allows for repeated hematogenous dissemination of periodontal microorganisms and exposure of the vasculature to oral microbes (Beck & Offenbacher, 2002). The microflora that reside in the oral biofilm are able to endure the hostile oral environment which is constantly under attack by host defenses such as serum antibody, complement, leukocytes, and salivary proteins. In the presence of inflammation, these organisms are able to thrive, invade host tissues, release factors such as lipopolysaccharides, and enter the systemic circulation (Offenbacher, Elter, Lin, & Beck, 2005). This can trigger the production of several systemic pro-inflammatory cytokines and mediators of tissue destruction such as C-reactive protein, TNFa, prostaglandin E2, and other cytokines (Kuo, Polson, & Kang, 2008). Patients with poor oral hygiene are at greater risk for the development of bacteremia, which increases with the severity of gingival inflammation (Silver, Martin, & McBride, 1977; de Oliveira, Watt, & Hamer, 2010). As will be discussed in more detail below, this is especially important in patients with special needs.

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