Objective. Pentraxin 3 (PTX3), newly discovered inflammation marker, is a member of acute-phase proteins. The hypothesis, synthesis of gingival tissue and serum PTX-3 increases in the experimental periodontitis model (with 10-day and 40-day periods), was tested by detecting gingival tissue and serum PTX-3 levels in rats with experimental periodontitis. Methods. Thirty rats were randomly divided into three groups of ten animals each: ligature-induced experimental periodontitis groups (with 10-day (Group1) and 40-day periods (Group2)) and healthy group (Group3). At the end of experimental period, rats were sacrificed, and radiological and histomorphometric analyses were performed on the mandibles. PTX3 levels were measured in gingival tissue and serum samples using ELISA. Plasma fibrinogen levels were measured according to the nephelometric method. Results. Significant alveolar bone resorption and periodontal inflammation were evident in periodontitis groups. Levels of PTX3 in gingival tissue were statistically higher in Group 1 than those in groups 2 and 3 ( ). No significant difference was found in serum PTX3 levels between experimental periodontitis and control groups ( ). Plasma fibrinogen levels were significantly increased in the experimental periodontitis groups ( ). Conclusion. PTX3 seems to be associated with tissue destruction in earlier periods of inflammatory periodontal disease, contrary to the fibrinogen findings. 1. Introduction Periodontal disease is a multifactorial infectious disease; although the main cause of periodontal disease is the presence of periodontal microorganisms, subsequent progression and disease severity are considered to be determined by the host immune response [1–4]. Mediators produced as a part of host response that contribute to tissue destruction include acute-phase proteins, cytokines, and prostaglandins [5–8]. The acute-phase response is a nonspecific process that may occur in the initial host response to injuries, infections, ischaemic necrosis, or malignancy [9]. It is initiated by the activation of local macrophages and other cells (including fibroblasts and endothelial cells) and has a variety of functions including proinflammatory properties, activation of complement factors, neutralization of invasive pathogens, and stimulation of repair and regeneration of tissues [9, 10]. Data show that acute-phase proteins, plasma proteins, not only appear in acute inflammation, but also in longstanding, chronic conditions [10]. Acute-phase proteins are generally increased following a microbial infection [11]. It is,
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