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Response to deep caries


After carious lesions with its bacterial before penetrated the main dentin and progressed in reparative dentin and/or pulp tissue appropriate, mass mobilization inflammatory defense will take place (43, 64) (Fig. 2.22). The most conspicuous feature is the aggregation of neutrophils. Often local abscess grows (Fig. 2.23). Clinically, during the excavation of caries, a drop of pus sometimes it may seem at the exposure site.

Although short-lived in acute inflammatory lesion, neutrophils release of tissue-destructive elements, including oxygen radicals, lysosomal enzymes and excessive amounts of nitrogen oxide. These substances contribute to the degradation of the tissues of the tooth pulp (see advanced concept 2.5). There will also be renewed and intense immunologic activity, expressed by the accumulation of immune system cells (35). Together, this means that the microbial load on the pulp has increased dramatically and the vital functions of pulp at this stage clearly under threat.

(Fig. 2.24). However, despite the massive bacterial attack and intense inflammatory reaction, the pulp can save vital functions over a long period of time, while the end result is likely to be pulpal necrosis.

Advanced concepts of 2.5 nitric oxide in the pulpal response to the carious exposition

In the acute tooth pulp of inflammatory foci of nitric oxide (NO) increases significantly (44). Endotoxins of Gram-negative bacteria and cytokines, such as interleukin-1 and tumor necrosis factor and interferon-gamma, are typical pathogens quick launch production NO production of enzymes. This occurs both in immune cells in the vascular endothelium in areas near and around the inflammatory site (51). NOT regarded as a Central component of the innate immunity, aimed at eliminating the invading microorganisms. Therefore, cannot increase blood flow and relax the draining of the blood vessels, thereby supporting the corresponding withdrawal and pressure control (7). Moreover, cannot have antibacterial activity and has a braking effect on the neutrophilic infiltration in the acute phase of inflammation (42). In fact, the final destruction of microorganisms phagocytosed by macrophages caused NO (28). These immune cells produce large amounts NOT. Thus, it cannot help in changing the acute tooth pulp inflammatory response (36).

The massive and prolonged LACK of education can have devastating consequences. It can react with oxygen free radicals, formed during the inflammatory process, to form a stable product, peroxynitrite. Peroxynitrite is a strong oxidizing agent that causes tissue damage (2). Thus, although it does NOT support defense in response moderate inflammation of tissues, severe reactions, such as the one on caries exposition of pulp, it can be highly toxic and contribute to the disintegration of the tissues. ..

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