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Oral Health
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Ana Moura Teles, José Manuel Cabeda
Periodontitis is an evolution of gingivitis that can be described as an infection that involves all soft tissue and bone that support the periodontium and teeth structures (Horz and Conrads 2007). The pathologic mechanism is similar to the one described for caries: multiple opportunistic pathogens overgrow in dental plaque, become pathogenic (Horz and Conrads 2007), release proteolytic enzymes that break down host tissue, and may result in gingival inflammation, loss of gingival attachment, periodontal pocket formation, alveolar bone, and even, root resorption. The predominant pathogens involved in periodontitis are Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, Tannerella forsythia, Eikenellacorredens, and Treponema denticola (Filoche et al. 2010; Dashiff and Kadouri 2011).
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
Plaque is a community of microorganisms found on the tooth surface or within the gingival sulcus (periodontal pocket), which are embedded in a matrix of polymers of host and bacterial origin. This is much more of a complex bio-environment than previously recognized and has been re-termed a community called oral biofilm as a result.17,18 Between 700 and 1,500 different species of bacteria naturally reside in the mouth.19–22 Most of those oral bacteria are considered innocuous, but some of these microorganisms have been identified as pathogenic. This aggregation of bacteria work symbiotically together as a community, producing specific proteins and enzymes utilizing oral fluids as the vector for transmission and the source of nutrients.23 It has been long demonstrated that those microbial communities can display enhanced pathogenicity (pathogenic synergism) compared to bacteria that are planktonic (free floating). Additionally, unlike planktonic bacteria, those in biofilms are protected by the surrounding slime layer which restricts the host’s ability to remove them via an immunological action or from the penetration of antimicrobial agents. This means that biofilm infections are less susceptible to antimicrobials applied locally or administered systemically.24,25 To summarize, bacteria in these complex biofilms act and react differently than bacteria that are planktonic in nature which complicates management and treatment, and makes them potentially more harmful. In addition to oral bacteria, yeast and viruses are also found in the biofilm of some patients with periodontal disease. The composition of the biofilm in periodontal and periapical disease has long been ignored for any affects outside the oral cavity because the connection to systemic health had been poorly understood. Research has now linked pathogenic biofilm to the vascular disease process and negative effects on the biology of the blood vessels.26
Periodontitis: a newly identified comorbidity in psoriasis and psoriatic arthritis
Published in Expert Review of Clinical Immunology, 2020
Szandra Dalmády, Lajos Kemény, Márk Antal, Rolland Gyulai
Periodontitis is a multifactorial chronic inflammatory, infectious disease characterized by gingival bleeding, periodontal pocket formation, alveolar bone loss and the destruction of connective tissue attachment [12,13]. Local inflammation activates osteoclasts and results in tissue destruction. According to the pathogenic model of Kornman et al., there are two phases in the progress of periodontitis [14]. In the first phase, tissue inflammation is dominant, resulting in gingivitis. Pathogen-associated-molecular-pattern molecules from periodontal bacteria increase the production of proinflammatory cytokines, such as interleukin (IL) 1, IL-6, IL-8 and tumor necrosis factor α (TNF-α), as well as the activation of matrix metalloproteinase (MMPs). Although gingivitis can be reversed, the excessive long-lasting inflammation of chronic periodontitis (CP) results in irreversible changes. The local consequences of CP are increased epithelial permeability, periodontal bone absorption, extracellular matrix and collagen destruction, vasodilation and edema [15,16]. Approximately 20 bacteria species of the subgingival oral microflora have been identified in CP; among these, the most important are Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia and Aggregatibacter actinomycetemcomitans [17]. Some of these bacteria, especially P. gingivalis, induce the Th17 pathway, leading to chronic inflammation [18]. Some investigators identified specific HLA gene loci, HLA-DR4, in the pathogenesis of CP [19,20]. The clinical diagnosis of CP involves examination of the teeth and gums for bleeding in response to probing, clinical attachment and probing depth (Figures 1 and 2).
Biofilm-related disease
Published in Expert Review of Anti-infective Therapy, 2018
The oral microbiome is diverse and exists as multispecies microbial communities on oral surfaces in structurally and functionally organized biofilms [31]. The evidence seems to indicate that oral microorganisms and pathogenic species of medical importance interact within the periodontal microbiota in many different ways that can lead to conditions that affect periodontal health or periodontal disease. Whether these opportunistic pathogens play a role in periodontal diseases or are simply bystanders, their ability to colonize the oral microbiota provides a potential source for dissemination to distant body sites and the risk of developing systemic infections, mainly in those with immunodeficiency [32]. Periodontal disease (i.e. periodontitis and gingivitis) is one of the most common oral infectious diseases associated with the establishment of a highly pathogenic biofilm that triggers an immune/inflammatory host response that leads to the destruction of the supporting periodontal tissue and eventually tooth loss [33]. Several studies have shown considerable biodiversity in the supragingival and subgingival plaque in the healthy oral cavity. The bacterial composition differs markedly in the supragingival and subgingival plaque. In healthy adults, the supragingival bacterial microbiota is composed mainly of gram-positive cocci and anaerobic gram-positive rods with a predominance of streptococci and Actinomyces naeslundii, respectively, whereas in the subgingival plaque, anaerobic gram-negative rods and facultative anaerobic gram-positive cocci are the predominant microorganisms [34]. Due to the anatomical proximity of periodontal biofilm to the gingival bloodstream, periodontal pockets can act as reservoirs of microbial pathogens and their products, as well as inflammatory mediators and immune complexes that can disseminate to other sites of the human body [35]. Colonization helps microbes to alter the calcium flux, invade mucosal cells and release toxins [36]. Networks of multiple synergistic and antagonistic interactions generate microbial interdependencies and give biofilms resilience to minor environmental perturbations [31]. Interestingly, there seems to be a relationship between yeasts and other bacteria in oral biofilms. A metagenomic analysis of elderly patients, for example, showed that the increased Candida load favored the presence of oral streptococci [37].