The immune inflammatory response in periodontitis is complex and involves both innate and acquired immunity. Possible clinical outcomes will be discussed in relation to the inflammatory–immunologic changes throughout the disease process. Clinical features of the periodontal diseases are beyond the scope of this work but are within the context of the pathogenic mechanisms. This review will address the pathways of inflammation in periodontal diseases by focusing on immunologic mechanisms to elucidate sites of regulation. Regulation of immune–inflammatory mechanisms governs patient susceptibility and is modified by environmental factors ( 219, 220, 241). There is evidence that specific microbes are associated with the progressive forms of the disease however, the presence of these microorganisms in individuals with no evidence of disease progression suggests that the disease is the net effect of the immune response and the inflammatory processes, not the mere presence of the bacteria. However, identification of the true ‘pathogens’ in periodontitis has been elusive. The pathogenesis of periodontal diseases is mediated by the inflammatory response to bacteria in the dental biofilm ( Fig. Knowledge of how immune mechanisms and inflammatory responses are regulated is critical for understanding the pathogenesis of complex diseases, such as periodontitis. As microorganisms evolve more rapidly than their mammalian hosts, immune mechanisms that determine the ecological balance of commensal organisms also need to change to preserve homeostasis ( 65). Unlike many infectious diseases, periodontal diseases appear to be infections mediated by the overgrowth of commensal organisms, rather than by the acquisition of an exogenous pathogen. The ecological interactions between the host and microbes determine the severity of the disease. The human oral cavity harbors a substantial and continuously evolving load of microbial species. The etiology of periodontal diseases is bacteria. Thus, innate (inflammatory) immunity and acquired immunity must be coordinated to return the injured tissue to homeostasis ( 85). Immune mechanisms play further roles in the resolution of inflammation and in the healing process, including the repair and the regeneration of lost or damaged tissues. When inflammation becomes chronic, the adaptive immune response is activated with involvement of the cellular and non-cellular mechanisms of acquired immunity. If the insult or injury is not resolved, the response becomes chronic, which can be considered as nonphysiologic or pathologic. In the acute phase of inflammation, the response is rapid and of short duration. Inflammation is the physiological response to a variety of injuries or insults, including heat, chemical agents or bacterial infection.
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