Objectives: To examine possible changes in the levels of salivary antioxidants, C-reactive protein (CRP), cortisol, pH, proteins, and blood in patients treated with fixed orthodontic appliances. Materials and Methods: Salivary samples from 21 orthodontic patients who met specific inclusion criteria were collected before the beginning of orthodontic treatment (T0; baseline), 1 hour after bonding (T1), and 4–6 weeks after bonding (T2). Oxidant-scavenging ability (OSA) was quantified using a luminol-dependent chemiluminescence assay. Cortisol and CRP levels were measured using immunoassay kits. pH levels and presence of proteins and blood in the samples were quantified using strip-based tests. Results: A significant decrease in salivary pH was observed after bonding (P ¼ .013). An increase in oxidant-scavenging abilities during orthodontic treatment was detected, but the change was not statistically significant. Cortisol and CRP levels slightly increased after bonding, but the difference was small without statistical significance. Changes in the presence of proteins and blood were also insignificant. Conclusions: Exposure to fixed orthodontic appliances did not show a significant effect on salivary parameters related to inflammation or stress, with the exception of a significant but transient pH decrease after bonding. (Angle Orthod. 2018;88:806–811.)

Candida albicans (C. albicans) is the most prevalent opportunistic human pathogenic fungus and can cause mucosal membrane infections and invade the blood. In the oral cavity, it can ferment dietary sugars, produce organic acids and therefore has a role in caries development. In this study, we examined whether the polyphenol rich extractions Polyphenon from green tea (PPFGT) and Padma Hepaten (PH) can inhibit the caries-inducing properties of C. albicans. Biofilms of C. albicans were grown in the presence of PPFGT and PH. Formation of biofilms was tested spectrophotometrically after crystal violet staining. Exopolysaccharides (EPS) secretion was quantified using confocal scanning laser microscopy (CSLM). Treated C. albicans morphology was demonstrated using scanning electron microscopy (SEM). Expression of virulence-related genes was tested using qRT-PCR. Development of biofilm was also tested on an orthodontic surface (Essix) to assess biofilm inhibition ability on such appliances. Both PPFGT and PH dose-dependently inhibited biofilm formation, with no inhibition on planktonic growth. The strongest inhibition was obtained using the combination of the substances. Crystal violet staining showed a significant reduction of 45% in biofilm formation using a concentration of 2.5mg/ml PPFGT and 0.16mg/ml PH. A concentration of 1.25 mg/ml PPFGT and 0.16 mg/ml PH inhibited candidal growth by 88% and EPS secretion by 74% according to CSLM. A reduction in biofilm formation and in the transition from yeast to hyphal morphotype was observed using SEM. A strong reduction was found in the expression of hwp1, eap1, and als3 virulence associated genes. These results demonstrate the inhibitory effect of natural PPFGT polyphenolic extraction on C. albicans biofilm formation and EPS secretion, alone and together with PH. In an era of increased drug resistance, the use of phytomedicine to constrain biofilm development, without killing host cells, may pave the way to a novel therapeutic concept, especially in children as orthodontic patients.

 Sepsis and septic shock are probably the least understood human disorders which worldwide take the lives of millions of patients. Sepsis may be defined as a multifactorial synergistic phenomenon where no unique damage-associated molecular patterns –alarming is identified which if successfully neutralized, might mitigate and protects against death in sepsis. 

Microorganisms which invade the blood stream may activate neutrophils to adhere to endothelial cells and to form oxidant – dependent nets rich in highly toxic nuclear histones claimed to be the main cause of death in sepsis due to the dysregulation of endothelial functions. However, the histone saga was recently critically debated since high levels circulating histones are also found in many clinical disorders unrelated to sepsis, therefore, histones may not be considered as a unique damage-associated molecular patterns- alarming but as additional markers of severe cell damage. 

We hereby argue that the main cause of tissue damage in sepsis may be an end result of a synergism between the numerous neutrophils pro inflammatory agents and the multiplicity of similar pro inflammatory agents generated by hemolytic steptoccocci and by additional pathogenic microorganism which recruit large numbers PMNs to the inflammatory sites. It is recommended that in sepsis caused by hemolytic streptococci and by additional toxigenic bacteria, a use of cocktails of antagonists might be more beneficial therapeutic strategies and this in view of the total failure to treat sepsis only by administrations of single antagonists. Also, targeting PMNs by immunological strategies should be sought for, to mitigate synergies between leukocytes and microbial cells.

The role of bacteriolysis in the pathophysiology of microbial infections dates back to 1893 when

Buchner and Pfeiffer reported for the first time the lysis of bacteria by immune serum and related

this phenomenon to the immune response. Later on, basic anti-microbial peptides and certain

beta-lactam antibiotics have been shown not only to kill microorganisms but also to induce bacteriolysis

and the release of cell-wall components.

In 2009, a novel paradigm was offered suggesting that the main cause of death in sepsis is due

to the exclusive release from activated human phagocytic neutrophils (PMNs) traps adhering

upon endothelial cells of highly toxic nuclear histone. Since activated PMNs also release a plethora

of pro-inflammatory agonists, it stands to reason that these may act in synergy with histone

to damage cells. Since certain beta lactam antibiotics may induce bacteriolysis, it is questioned

whether these may aggravate sepsis patient's condition. Enigmatically, since the term bacteriolysis

and its possible involvement in sepsis is hardly ever mentioned in the extensive clinical

articles and reviews dealing with critical care, we hereby aim to refresh the concept of bacteriolysis

and its possible role in the pathogenesis of post infectious sequelae.