Endotoxin tolerance drives neutrophil to infectious site.

The objective of this randomized animal study and laboratory investigation was to investigate whether lipopolysaccharide tolerance redirects neutrophil migration between organs. Male BALB/c mice received subcutaneous injections of lipopolysaccharide (1 mg/kg) for 5 days, followed by cecal ligation and puncture (CLP). Cytokines and adhesion molecules were measured after tolerance and CLP challenge. Increased numbers of neutrophils were observed in the peritoneal cavity of tolerant mice, which was associated with increased levels of adhesion molecules and chemokines. In contrast, nontolerant mice accumulated higher numbers of neutrophils in the lungs compared with those in the peritoneal cavity. Neutrophil function accessed by hydrogen peroxide production from neutrophils recovered from peritoneal cavity showed that tolerance increased the capacity to produce hydrogen peroxide. Mortality was reduced in tolerant animals. This study demonstrated that tolerance reduces leukocyte accumulation in the lung after CLP by redirecting neutrophils to the site of infection.

Gene expression reprogramming protects macrophage from septic-induced cell death.

Sepsis induces a systemic inflammatory response leading to tissue damage and cell death. LPS tolerance affects inflammatory response. To comprehend potential new mechanisms of immune regulation in endotoxemia, we examined macrophage mRNA expression by macroarray affected by LPS tolerance. LPS tolerance was induced with subcutaneous administration of 1 mg/kg/day of LPS over 5 days. Macrophages were isolated from the spleen and the expression of 1200 genes was quantitatively analyzed by the macroarray technique. The tolerant group displayed relevant changes in the expression of 84 mRNA when compared to naïve mice. A functional group of genes related to cell death regulation was identified. PARP-1, caspase 3, FASL and TRAIL genes were confirmed by RT-PCR to present lower expression in tolerant mice. In addition, reduced expression of the pro-inflammatory genes TNF-α and IFN-γ in the tolerant group was demonstrated. Following this, animals were challenged with polymicrobial sepsis. Flow cytometry analysis showed reduced necrosis and apoptosis in macrophages from the tolerant group compared to the naïve group. Finally, a survival study showed a significant reduction in mortality in the tolerant group. Thus, in the current study we provide evidence for the selective reprogramming of the gene expression of cell death pathways during LPS tolerance and link these changes to protection from cell death and enhanced survival rates.

Uso do plasma rico em plaquetas para reparação em defeitos ósseos do esqueleto maxilo-facial / Use of platelet-rich plasma in healing maxillofacial skeleton bone defects

A proposta deste trabalho foi rever e analisar a literatura sobre a utilização do uso do plasma rico em plaquetas (PRP), na reparação de defeitos ósseos do esqueleto maxilo-facial. O plasma rico em plaquetas PRP é um concentrado autógeno, facilmente obtido do sangue. Seu mecanismo de ação está baseado na ativação de fatores de crescimento, que são liberados no local pela degranulação plaquetária, portanto, estes fatores de crescimento se desenvolvem de maneira ordenada na proliferação e diferenciação celular, sendo capazes de ativar e acelerar a reparação óssea. O PRP está descrito na literatura como um avanço na estimulação e aceleração do osso e na reparação tecidual em geral; sua eficácia é amplamente comprovada por estudos de diversos autores, que apresentam vantagens expressivas, como o aumento do trabeculado ósseo, redução no tempo para a neoformação óssea principalmente quando estão associados a enxertos, podendo ser eles tanto autógenos, como alógenos ou xenógenos; melhorando assim a velocidade de maturação do enxerto e evidenciando sua relação com o aumento na quantidade e na densidade óssea. Esse sucesso obtido da associação do PRP com o enxerto autógeno possibilita a utilização do mesmo para cirurgias de reconstrução oral e defeitos ósseos maxilo-faciais em geral

Imaging modality correlations of an odontogenic keratocyst in the nevoid basal cell carcinoma syndrome: a family case report.

Multiple maxillary and mandibular cysts are principle features of nevoid basal cell carcinoma syndrome (NBCCS; Gorlin-Goltz syndrome). We present a family case report of NBCCS with odontogenic keratocyst where the findings on plain films, CT, clinical, and histopathologic examinations are compared and analyzed. The systemic manifestations included frontal bossing, odontogenic keratocyst, ectopic calcification in 1 patient, and bifid rib in 1 patient. CT examination displayed aspects of bone morphology not visible on the plain films. Odontogenic keratocyst diagnosis was confirmed by histopathological examination. The features identified by these combined clinical, imaging, and histologic findings are helpful in identifying an NBCCS patient, distinguishing keratocyst from others cysts or neoplasic lesions, and can therefore influence surgical management. NBCCS is a rare autosomal dominant cancer predisposition syndrome, which is important to recognize when a patient has multiple odontogenic keratocysts, because lifelong monitoring is essential for patient management.