Explore chapters and articles related to this topic
Bacteria
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
In periodontitis or pyorrhea, there is invasion and destruction of gingival tissue by a mixture of bacteria that includes spirochetes, Bacteroides and the bacteria listed above that cause the milder form of gingivitis. The most common causative agents appear to be Treponema vincentii and Bacteroides melaninogenicoccus. Eventually the growth of the bacteria can erode the bone holding the teeth, resulting in their loss.
The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
Necrotizing periodontal diseases include necrotizing gingivitis (NG) and necrotizing periodontitis (NP). These may occur in patients who are both chronically and/or severely compromised (e.g. immunosuppressed or severely malnourished) or patients who are temporarily and/or moderately compromised (such as those who smoke or are stressed). NG typically occurs in young adults and presents as painful, ulceration, and necrosis of the interdental papillae and halitosis. The condition involves the formation of an anaerobic fuso-spirochaetal complex including Fusobacterium nucleatum and Treponema vincentii among others, and responds to improved oral hygiene and appropriate anti-microbial therapy. In contrast, the disease in developing countries occurs most often in malnourished children and, if left untreated, can spread leading to extensive necrosis of orofacial tissue – ‘cancrum oris’ – and may be fatal. HIV infection may also present as necrotizing periodontal conditions. Periodontal disease may arise as a manifestation of systemic disease such as haematological disorders or genetic disorders, e.g. cyclic neutropenia or Ehlers–Danlos syndrome. There is emerging evidence which supports links between periodontal disease and acquired systemic conditions such as diabetes, and cardiovascular disease.
Carbon source utilization patterns in dental plaque and microbial responses to sucrose, lactose, and phenylalanine consumption in severe early childhood caries
Published in Journal of Oral Microbiology, 2020
Weihua Shi, Jing Tian, He Xu, Guiyan Wang, Qiong Zhou, Man Qin
Our study demonstrated that CF group metabolized phenylalanine more actively than S-ECC group, suggesting that phenylalanine might be related to caries free state. Previous studies also suggested that phenylalanine could have an inhibitory effect on caries development [23,24]. In bacteria, phenylalanine may first be deaminated then convert to phenylpropionate or phenylacetate, both generating alkali [53] which is an essential factor in maintaining plaque pH homeostasis. So we additionally analyzed the plaque microbiota cultured in phenylalanine well to reveal the microbial community structure and explore caries suppression potential of phenylalanine. The differentially abundant species of CF and S-ECC groups in response to phenylalanine have no reported connections to phenylalanine metabolism, probably because studies of the effect of phenylalanine on the oral microbiota are very limited. A previous study showed that phenylalanine was essential for the growth of oral anaerobes, such as Capnocytophaga gingivalis, Eubacterium timidurn, Fusobacterium nucleatum, Porphyromonas gingivalis, Treponema denticola, and Treponema vincentii [25]. However, none of these species showed a difference in relative abundance in response to phenylalanine compared with that to water in our results. Therefore, the relationship between phenylalanine and the S-ECC microbiota requires further study.