Chronic conditions policies: oral health,a felt absence

The global health scenario shows an epidemic of non‐communicable diseases that lead to long‐term chronic conditions, some of which are incurable. Many infectious diseases, owing to their development and length, also generate chronic conditions. Similarly, non‐morbid states, such as pregnancy, and some life cycles such as adolescence and ageing, follow the same logic. Among all these chronic conditions there is a significant interrelationship with oral health, both in parallel events and common risk factors. This article presents cross‐sectional qualitative research into World Health Organisation recommended health policies to address chronic conditions. Several documents published by the organisation were analysed to verify the presence of references to oral health in relation to chronic conditions, particularly cardiovascular diseases and diabetes as these most frequently have oral manifestations. The analysis showed no significant references to oral health or its indicators within the published texts. The study recognises the value of the work developed by the World Health Organisation, as well as its worldwide leadership role in the development of health policies for chronic conditions. This article proposes a coalition of dentistry organisations that could, in a more forceful and collective way, advocate for a greater presence of oral health in drafting policies addressing chronic conditions.     

Interferon‐γ, Interleukins‐6 and ‐4, and Factor XIII‐A as Indirect Markers of the Classical and Alternative Macrophage Activation Pathways in Chronic Periodontitis

Background: Macrophages account for 5% to 30% of the inflammatory infiltrate in periodontitis and are activated by the classic and alternative pathways. These pathways are identified by indirect markers, among which interferon (IFN)‐γ and interleukin‐6 (IL)‐6 of the classic pathway and IL‐4 of the alternative pathway have been studied widely. Recently, factor XIII‐A (FXIII‐A) was reported to be a good marker of alternative pathway activation. The aim of this study is to determine the macrophage activation pathways involved in chronic periodontitis (CP) by the detection of the indirect markers IFN‐γ, IL‐6, FXIII‐A, and IL‐4. Methods: Biopsies were taken from patients with CP (n = 10) and healthy individuals (n = 10) for analysis of IFN‐γ, IL‐6, IL‐4, and FXIII‐A by Western blot (WB), immunohistochemistry (IHC), and enzyme‐linked immunosorbent assay (ELISA). The same biopsies of healthy and diseased gingival tissue were used, and the expressions of these markers were compared between healthy individuals and those with CP. Results: The presence of macrophages was detected by CD68+ immunohistochemistry and their IFN‐γ, IL‐6, IL‐4, and FXIII‐A markers by WB, IHC, and ELISA in all samples of healthy and diseased tissue. IL‐6, IL‐4, and FXIII‐A were significantly higher in patients with CP, whereas FXIII‐A was higher in healthy individuals. Conclusion: The presence of IFN‐γ, IL‐6, IL‐4, and FXIII‐A in healthy individuals and in patients with CP suggests that macrophages may be activated by both classic and alternative pathways in health and in periodontal disease.     

Simvastatin decreases nitric oxide overproduction and reverts the impaired vascular responsiveness induced by endotoxic shock in rats

Lipopolysaccharides (LPS) can be used to induce experimental endotoxic shock, which is characterized by a significant decrease in mean arterial pressure (MAP) and a decreased vasoconstrictor response that have been attributed to excessive nitric oxide production. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), in addition to lowering serum cholesterol levels, exert many pleiotropic effects, including anti-inflammatory action. In the present study, we investigated the effect of simvastatin, an HMG-CoA reductase inhibitor, on the production of nitric oxide and the cardiovascular response to LPS. Male Wistar rats were pretreated with different doses of simvastatin (10, 20, 40, and 80 mg/kg, i.p.) or saline 20 min before i.v. injection of LPS (1.5 mg/kg) or saline (control). MAP was continuously recorded and nitrate plasma concentration was determined during the 6-h experimental session at 1-h intervals. The pressor response to phenylephrine (1 microg/kg) was evaluated before and 6 h after LPS administration. In the LPS-treated group, there was a time-dependent increase in nitrate plasma concentration (P<0.001), and this response was decreased in simvastatin pretreated rats (P<0.001). We also observed that LPS decreased the pressor response to phenylephrine (P<0.001), an effect that was reverted by simvastatin pretreatment (P<0.05). However, simvastatin did not modify the decrease of MAP induced by LPS. We concluded that simvastatin decreases nitrate plasma concentration in response to LPS and recovers vascular responsiveness during an experimental endotoxic shock. These data suggest the potential use of HMG-CoA reductase inhibitors as a coadjuvant in the treatment of septic shock.