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Dental Disease, Inflammation, Cardiovascular Disease, Nutrition and Nutritional Supplements
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Douglas G. Thompson, Gregori M. Kurtzman, Chelsea Q. Watkins
Periodontal disease is generated by microorganisms which may enter the general circulation causing a bacteremia. Some species of these microorganism have been identified as high-risk pathogens. Those high-risk pathogens are currently understood as Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), Treponema denticola (Td) and Fusobacterium nucleatum (Fn). High-risk pathogens may adversely influence the atherosclerosis pathogenesis triad in three distinct ways. High-risk periodontal pathogens affect serum lipoprotein concentration, endothelial permeability and lipoprotein binding in the intima. Strong evidence also supports that periodontal bacteria affect vascular elasticity, lipid concentration, vascular biomarkers, HDL efflux and endothelial function. Therefore, the dental community has a substantial opportunity to assist in mitigating the number one cause of morbidity and mortality, namely cardiovascular disease, by effective management of periodontal disease and reduction or elimination of those high-risk pathogens.79–81
Commensal Flora
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
Poor dental hygiene is a risk factor for periodontitis involving bacteria such as Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola. Aggregatibacter actinomycetemcomitans has been linked to highly aggressive periodontitis. Transient bacterial translocation from oropharynx into the bloodstream is common. Poor dental hygiene and dental procedures are known contributors. Although often asymptomatic, in the presence of an abnormal heart valve, such bacteraemia can cause endocarditis. Common causes of endocarditis are viridans streptococci and bacteria from the HACEK group, all of which are part of the oropharyngeal commensal flora.
Ceftriaxone
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Baek-Nam Kim, Anna Maria Peri, David L. Paterson
Ceftriaxone is recommended for the treatment of HACEK endocarditis (Habib et al., 2015; Baddour et al., 2015). HACEK organisms, a group of fastidious Gram-negative bacilli, consist of Haemophilus spp., Aggregatibacter spp., Cardiobacterium hominis, Eikenella corrodens, and Kingella spp. (Baddour et al., 2015). For HACEK endocarditis, treatment guidelines recommend dosing of ceftriaxone 2 g daily i.v. for 4–6 weeks (Habib et al., 2015; Baddour et al., 2015). Ceftriaxone is preferred to cefotaxime for once-daily therapy on an outpatient basis (Wilson et al., 1995; Kaye, 1996). Previously, the HACEK group of microorganisms was uniformly susceptible to ampicillin; however, beta-lactamase-producing strains of HACEK are appearing with increased frequency (Habib et al., 2015; Baddour et al., 2015).
Diversity of site-specific microbes of occlusal and proximal lesions in severe- early childhood caries (S-ECC)
Published in Journal of Oral Microbiology, 2022
Kausar Sadia Fakhruddin, Lakshman Perera Samaranayake, Rifat Akram Hamoudi, Hien Chi Ngo, Hiroshi Egusa
We also noted several pathogens such as C. concisus, C. granulosa, Neisseria bacilliformis, and G. adiacens, implicated in the oral-systemic disease axis, amongst the caries microbiota. The two former organisms (C. granulosa, N. bacilliformis) are implicated in abscess development and bacteremia secondary to focal infections [89,90]. In addition, the oral C. concisus strains have been associated with human irritable bowel syndrome [91,92]. Furthermore, members of the ‘HACEK’ group bacteria, i.e. Haemophilus sp., Aggregatibacter sp., C. hominis, E. corrodens, Kingella sp., and G. adiacens, a nutritionally variant streptococcus, all known to cause bacterial endocarditis [93,94], were also prevalent in the dentinal caries samples. Thus, it is tempting to speculate that reservoirs of these microbes within cavitated lesions of S-ECC may act as potential reservoirs that may contribute to the foregoing systemic diseases in these children.
Ethnic variability associating gut and oral microbiome with obesity in children
Published in Gut Microbes, 2021
Baskar Balakrishnan, Vaithinathan Selvaraju, Jun Chen, Priscilla Ayine, Lu Yang, Jeganathan Ramesh Babu, Thangiah Geetha, Veena Taneja
Interestingly, the oral microbiome of EA children showed microbial variability between obese and non-obese children, whereas AA children did not show that variability. Salivary microbiota in obese EA children showed an abundance of Aggregatibacter and Eikenella, both associated with periodontitis and obesity.36–38Aggregatibacter has been described as an oral pathogen associated with obesity in AA and Japanese adults.37Eikenella was found to be increased in obese Brazilian patients with chronic periodontitis.38 Hence, the changes in oral microbiome may also have regional specificity. Gupta et al39 showed how geography, ethnicity, and subsistence play a role in the diversity of human microbiome composition. While many opportunistic pathogenic species, such as Streptococcus, Butyrivibrio, Capnocytophaga, Fusobacterium, Haemophilus, and Prevotella,40,41 showed differences in salivary microbiome between AA and EA children, Streptococcus are the only bacteria that differentiated with higher abundance in AA children, supporting a previous study of its increased presence in low-income AA populations.38 The present data suggest that the oral microbiome in obesity is much more relevant for EA children than AA children.
Peptidoglycan-associated lipoprotein of Aggregatibacter actinomycetemcomitans induces apoptosis and production of proinflammatory cytokines via TLR2 in murine macrophages RAW 264.7 in vitro
Published in Journal of Oral Microbiology, 2018
Riikka Ihalin, Kjell Eneslätt, Sirkka Asikainen
Periodontitis is a multifactorial inflammatory disease which destroys tooth-supporting tissues; however, it may also correlate with the development of systemic disorders such as cardiovascular diseases when bacteria and their inflammatory components are released to the circulation from inflamed periodontal pockets [1]. Gram-negative species are over-represented in periodontitis compared to healthy periodontium microbiota. Thus, the spread of lipopolysaccharide (LPS) from periodontal pockets eliciting systemic inflammatory host responses has been suggested to accelerate atherogenesis [2]. Aggregatibacter actinomycetemcomitans is a Gram-negative oral bacterium which is a major pathogen in aggressive periodontitis, especially in populations with North-West African descent when colonized by the highly leukotoxic serotype b JP2-clone of the bacterium. Thus, it has extensively been used as a model species in studies investigating the etiopathogenesis of this disease. Although A. actinomycetemcomitans is an oral bacterium, it can cause severe non-oral infections such as endocarditis and abscesses in brains and lungs on rare occasions [3–5]. LPS is the best-known pro-inflammatory outer membrane component in A. actinomycetemcomitans [6–8].