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Opsonization of Actinobacillus actinomycetemcomitans by LPS-Directed IgG Antibodies in Sera of Juvenile Periodontitis Patients
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Microbiological studies of LJP patients have revealed that the subgingival microflora of these patients differ from that of periodontally healthy individuals and patients with adult periodontitis. Actinobacillus actinomycetemcomitans, a capnophilic gram-negative coccobacillus that is closely related to the oral haemophili (6–8), has been identified as a prominent member of the subgingival microflora of these patients. A. actinomycetemcomitans is present, albeit in relatively low numbers, in the subgingival microflora of approximately 20% of periodontally healthy juveniles and adults and a similar percentage of patients with adult periodontitis (7). In contrast, more than 95% of LJP subjects examined harbor this organism in high numbers. Further evidence for an association between A. actinomycetemcomitans and LJP derives from studies showing that elimination of this organism from subgingival plaque following antibiotic therapy correlates with resolution of periodontal lesions in these patients (9). Moreover, recurrence of disease activity is accompanied by the reappearance of A. actinomycetem-comitans in periodontal lesions of LJP patients. Several studies have provided evidence that A. actinomycetem-comitans may be transmitted among members of families with LJP (10,11).
The Role of the Microbiota and the Application of Probiotics in Reducing the Risk of Cardiovascular Diseases
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Raquel Bedani, Susana Marta Isay Saad
Several studies have shown a relationship between the microbiota from the oral cavity and the atherosclerotic plaques of individuals with atherosclerosis (Kholy et al. 2015, Bui et al. 2019). The most common bacterial genera in the oral cavity are Treponema spp., Porphyromonas spp., Prevotella spp., Capnocytophaga spp., Peptostreptococcus spp., Fusobacterium spp., Actinobacillus spp., and Eikenella spp. (Bui et al. 2019). The oral microbiota is found in saliva, gingival epithelium, and other oral cavity surfaces, and concentrated in dental plaques (Bui et al. 2019).
Pathogens Causing Multisystem Infections
Published in Victor A. Bernstam, Pocket Guide to GENE LEVEL DIAGNOSTICS in Clinical Practice, 2019
The most prevalent species in periodontitis was found to be Prevotella intermedia. REA demonstrated different digestion patterns among all isolates of Actinobacillus actinomycetemcomitans, Prevotella gingivalis, and P. intermedia, suggesting that no cross-infection occurred among the subjects studied.
Microbially-derived cocktail of carbohydrases as an anti-biofouling agents: a ‘green approach’
Published in Biofouling, 2022
Harmanpreet Kaur, Arashdeep Kaur, Sanjeev Kumar Soni, Praveen Rishi
Dsp B is a promising antibiofilm enzyme capable of preventing biofilm formation and accelerating biofilm detachment (Kaplan 2009). Its production has been reported by Actinobacillus actinomycetecomitans, involved in the biofilm dispersion of Gram-negative periodontal pathogen (Izano et al. 2007; Blackledge et al. 2013). Dsp B explicitly targets and degrades the exopolysaccharide, PNAG, essential for intercellular adhesion (Thallinger et al. 2013). The enzyme disrupts the matrix of target biofilm formers, whether Gram-positive (S. aureus, S. epidermidis) or Gram-negative (E. coli, P. fluorescens) and drastically reduces the biofilm biomass (Kaplan 2009; Kaplan 2014). In all PNAG producing microbial species, Dsp B can prevent biofilm formation and accelerate biofilm detachment (Dobrynina et al. 2015). A study by Kaplan et al. (2004) reported that Dsp B efficiently removed S. epidermidis biofilms formed on plastic surfaces. Also, Dsp B has been marketed for the treatment of wounds, skin, and medical devices (Donelli et al. 2007). As Dsp B can inhibit and disperse biofilms without any bactericidal or bacteriostatic effect, combining the enzyme with other antimicrobial agents such as antibiotics, detergents, or other enzymes may be necessary to ensure the complete eradication of target biofilms.
Lasers in non-surgical periodontal treatment – a review
Published in Journal of Cosmetic and Laser Therapy, 2019
Nida Sumra, Rohit Kulshrestha, Vinay Umale, Kshama Chandurkar
Cobb et al. (1992) showed that Nd YAG laser at 1.75 watts (87.5 mJ) and 3 watts (150 mJ) exhibited some degree of laser induced root surface alteration and crater formation ranging in diameter from 0.1 to 1 mm. Calculus deposits exposed to laser and not removed by scaling and root planing were free of surface plaque and exhibited a texture characteristic of melt down and resolidification. The irregular topography of such deposits and the resultant porosity may provide a nidus for recolonization of subgingival bacteria. A post therapy reduction in levels of Actinobacillus Actinomycetemcomitans (AA), Porphyromonas Gingivalis (PG) and Prevotella Intermedia (PI) was suggested in microbial sampling (11). Miyazaki et al. (2003) compared Nd YAG laser with CO2 laser which showed Nd YAG laser at 100 mJ/pulse and 20 Hz is successful in reducing the clinical signs of periodontitis and PG over a 12 week period. CO2 laser at 2 watts (100 mJ) was found to be inefficient in removing the subgingival plaque (5).
Gingival epithelial barrier: regulation by beneficial and harmful microbes
Published in Tissue Barriers, 2019
Naoki Takahashi, Benso Sulijaya, Miki Yamada-Hara, Takahiro Tsuzuno, Koichi Tabeta, Kazuhisa Yamazaki
Aside from neutrophil-mediated epithelial barrier disruption, the strong contribution of periodontopathogens and their virulence factors to barrier disruption have been investigated. An in vitro study demonstrated that treatment with bacterial lipopolysaccharide (LPS) reduces claudin-1 expression in JE, reducing subsequent epithelial barrier disruption.40 Other studies have demonstrated an outer membrane protein of Actinobacillus actinomycetemcomitans decreases connexin-43 levels.17,19,41Porphyromonas gingivalis and A. actinomycetemcomitans decrease E-cadherin expression in gingival epithelial cells.10,18 Most recently, the authors reported that a P. gingivalis virulence factor degrades gingival epithelial-derived E-cadherin protein, and thus disrupts epithelial barrier functions in vitro. Furthermore, the authors suggested that E-cadherin degradation is involved in the pathogenesis of periodontitis in an experimental mouse model.35 Altogether, these findings suggest that the modulation of epithelial barrier function by microorganisms strongly contributes to the initiation and progression of periodontal diseases.