Abstract
The aim of this study was to evaluate the effect of acute sepsis in the periodontal ligament, alveolar and furcation bone in absence of periodontitis induction through histological and immunohistochemical analyses. A septic rat model was established by cecal ligation and puncture (CLP). Twelve rats were randomly divided into CLP (n=6) and Sham (n=6) groups. The animals were euthanized at 24 h and hemimandibles were submitted to histomorfometric (bone matrix, collagenous fibers, fibroblasts, osteocytes, inflammatory cells, and blood vessels) and immunohistochemical (BMP-2/4, RANKL and osteocalcin) evaluation in alveolar bone, furcation bone and periodontal ligament. Our results demonstrated that histomorphometric parameters were similar in alveolar bone, furcation bone and periodontal ligament of Sham and CLP rats. Regarding to immunohistochemical analyses, the number of BMP-2/4 and RANKL immunolabeled cells was also similar in both groups. Furthermore, it was detected a reduction in the osteocalcin immunolabeled cells in periodontal ligaments of CLP compared to Sham rats (p=0.0014). In conclusion, the acute sepsis induction resulted in reduced number of osteocalcin labelled cells in periodontal ligament region. Moreover, no significant histological differences were observed in the periodontium of rats under acute sepsis. Considering the role of osteocalcin in bone remodeling, the study contributes to revealing the importance of careful periodontal evaluation in the presence of sepsis.
Highlights
Sepsis is a dysregulated pathophysiologic immune response to infection resulting in severe organ dysfunction
Osteocalcin immunolabeled cells in the alveolar bone and the furcation area were similar in Sham and cecal ligation and puncture (CLP) rats
Osteocalcin immunolabeled cells in periodontal ligament region was reduced (p=0,0014) in CLP compared to Sham rats (Fig. 6C)
Summary
Sepsis is a dysregulated pathophysiologic immune response to infection resulting in severe organ dysfunction. The World Health Organization indicated sepsis as a global health priority. The septic inflammatory response in the body is complicated by secondary end organ damage. Sepsis is fundamentally an inflammatory disease mediated by the host immune response. In this context, this condition result in dysregulated hyperinflammation that can lead to the many symptoms including disseminated intravascular coagulation and subsequent multi-organ dysfunction syndrome, inflammation-coagulation due to aberrant platelet activation, peripheral vasodilation leading to low blood pressure ensuing hypoperfusion of the kidney and kidney failure [4]. Altered levels of inflammatory mediators may be observed in septic patients [5]. Higher levels of proinflammatory mediators were shown in patients who died than in survivors, suggesting an association of high levels of these mediators and sepsis outcome [6]
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