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Oral Biofilms and Their Implication in Oral Diseases
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Georgios N. Belibasakis, Nagihan Bostanci
The demineralisation of the enamel and dentin occurring in dental caries is a consequence of a local drop in pH, caused by bacteria of the biofilm. Evidently, supragingival biofilms are directly exposed to the openness of the oral cavity and the affluent sugar availability in our nutrition. Given the appropriate fermentable carbohydrates, overgrowth and maturation of a supragingival biofilm will result in the domination of aerobic, or aerotolarant, and saccharolytic lactic acid–producing bacteria. As such, acidogenic and aciduric members of the mutans streptococci and lactobacilli are most well adapted to grow under these conditions, and their presence correlates well with caries. These bacteria adhere by means of cell surface adhesins to the receptors which are present on the saliva-coated tooth [6]. They degrade the carbohydrates derived from foods and form organic acids such as lactic, formic, acetic and/or succinic acid. Subsequently, the supragingival plaque pH falls to around 4 in several minutes. In particular, Streptococcus mutans is the dominating cariogenic species, followed by Streptococcus sobrinus and various members of the Lactobacillus spp. [7]. On the other hand, an inverse relationship between dental caries and other members of the Streptococcus spp. has also been reported, in particular Streptococcus sanguinis. S. sanguinis is capable of oxidising thiocyanate (SCN-) in saliva to hypothiocyanite (OSCN-), thereby repressing the glycolytic activity of mutans [8]. A number of Actinomyces spp. have been associated with the root cementum caries. This is a form of the disease that occurs in periodontitis-affected teeth, in which the root surface is exposed due to gingival recession. It is also proposed that the hard-tissue specificity (e.g. enamel, dentin or cementum) may influence the establishment of a caries-specific biofilm microflora [9,10].
Dysbiosis in Takayasu arteritis complicated with infectious endocarditis following tocilizumab administration
Published in Scandinavian Journal of Rheumatology, 2023
T Shirai, H Sato, T Ishii, H Fujii
The first patient was a 43-year-old female. Four years previously, aortic valve replacement (AVR) was performed for severe AR, which was histologically compatible with TAK. She was treated with prednisolone (PSL) and methotrexate (MTX), and relapse was observed 2 years before, when the PSL dose was 10 mg/day. Hence, 162 mg/week of subcutaneous TCZ was initiated, and PSL was tapered to 6 mg/day. She had experienced pain around the neck and shoulders 2 weeks before, following which abdominal pain developed. Laboratory data were unremarkable, with a white blood cell count of 6600 cells/µL and a C-reactive protein level of 0.19 mg/dL. However, enhanced computed tomography (CT) revealed multiple infarctions in the kidney, liver, and spleen, suggesting IE. Although transthoracic echocardiography was negative, transoesophageal echocardiography revealed a vegetation on the aortic valve (Figure 1A). The blood cultures were positive for Streptococcus sanguinis. IE of the biological valve was confirmed, and AVR was performed. The postoperative course was favourable, and she was discharged 2 months after admission.
Platelet interactions with viruses and parasites
Published in Platelets, 2015
The role of platelets as part of the innate immune system has become well established, due to their role in responding to infection [1, 2]. Central to this is the ability of platelets to bind to pathogens and either kill them or clear them from the circulation [3]. This is not a novel concept and even in the early 1960’s there were reports of bacteria toxins activating platelets. Probably the earliest report of a pathogen activating platelets was by Zucker and Grant in 1974 where they showed platelet aggregation and secretion in response to zymosan (yeast-derived surface glucan) [4]. This was then expanded to include bacteria, especially the oral bacterial Streptococcus sanguinis by a series of studies from the Herzberg group [5] and the Douglas group [6]. Then, in a series of papers from our group, we dissected the mechanism of platelet aggregation induced by Staphylococcus aureus [7]. Subsequently, there has been a rapid increase in papers on bacteria-platelet interactions. Most of the research have focused on the interaction between platelets and Gram-positive bacteria although there have been a number of studies on the Gram-negative Helicobacter pylori [8]. Despite the earliest study reporting on yeast-induced platelet aggregation there is a paucity of studies on the interaction of pathogens other than bacteria with platelets. In this review we will focus on what is known about the interaction of platelets with non-bacterial pathogens.
The distinct effects of aspirin on platelet aggregation induced by infectious bacteria
Published in Platelets, 2020
Nadji Hannachi, Jean-Pierre Baudoin, Arsha Prasanth, Gilbert Habib, Laurence Camoin-Jau
The members of the viridians Streptococcus group represent the second-leading cause of IE. Among these bacteria, Streptococcus sanguinis is a predominant bacterium of the human oral cavity [9,10]. S. sanguinis causes platelet aggregation via membrane receptors involving platelet GPIIbIIIa and GPIb [11].