Original Article- "human microbiota".
Oral cavity
editThe environment present in the human mouth allows the growth of characteristic microorganisms found there. It provides a source of water and nutrients, as well as a moderate temperature.[1] Resident microbes of the mouth adhere to the teeth and gums to resist mechanical flushing from the mouth to stomach where acid-sensitive microbes are destroyed by hydrochloric acid.[1][2]
Anaerobic bacteria in the oral cavity include: Actinomyces, Arachnia, Bacteroides, Bifidobacterium, Eubacterium, Fusobacterium, Lactobacillus, Leptotrichia, Peptococcus, Peptostreptococcus, Propionibacterium, Selenomonas, Treponema, and Veillonella.[3][needs update] Genera of fungi that are frequently found in the mouth include Candida, Cladosporium, Aspergillus, Fusarium, Glomus, Alternaria, Penicillium, and Cryptococcus, among others.[4] Bacteria accumulate on both the hard and soft oral tissues in biofilms. Bacterial adhesion is particularly important for oral bacteria.
Oral bacteria have evolved mechanisms to sense their environment and evade or modify the host. Bacteria occupy the ecological niche provided by both the tooth surface and gingival epithelium. However, a highly efficient innate host defense system constantly monitors the bacterial colonization and prevents bacterial invasion of local tissues. A dynamic equilibrium exists between dental plaque bacteria and the innate host defense system.[5] Of particular interest is the role of oral microorganisms in the two major dental diseases: dental caries and periodontal disease.[5] Additionally, research has correlated poor oral heath and the resulting ability of the oral microbiota to invade the body to affect cardiac health as well as cognitive function.[6]
Edited Verison "human microbiota"
Oral cavity
editThe environment present in the human mouth allows the growth of characteristic microorganisms found there. It provides a source of water and nutrients, as well as a moderate temperature.[1] Resident microbes of the mouth adhere to the teeth and gums to resist mechanical flushing from the mouth to stomach where acid-sensitive microbes are destroyed by hydrochloric acid.[1][2]
Anaerobic bacteria in the oral cavity include: Actinomyces, Arachnia, Bacteroides, Bifidobacterium, Eubacterium, Fusobacterium, Lactobacillus, Leptotrichia, Peptococcus, Peptostreptococcus, Propionibacterium, Selenomonas, Treponema, and Veillonella.[3][needs update] Genera of fungi that are frequently found in the mouth include Candida, Cladosporium, Aspergillus, Fusarium, Glomus, Alternaria, Penicillium, and Cryptococcus, among others.[4] Bacteria accumulate on both the hard and soft oral tissues in biofilms. Bacterial adhesion is particularly important for oral bacteria.
The oral cavity contains diverse biofilms that form an ecosystem where an ecological change can shift the relationship from mutualistic to parasitic.[7] Induction, Accumulation, and Existence are three succession phases of biofilm formation. Induction phase is the formation of a linking film. This is followed by Accumulation where bacteria adheres and grows forming layers of colonies. The Existence phase is indicated by the balance between growth and removal of biofilm. Saliva plays this homeostatic role allowing recolonization of bacteria for biofilm formation and controlling growth by detaching biofilm buildup.[8] It also provides biofilms a means of nutrients and temperature regulation. The location of the biofilm determines the type of exposed nutrients it receives. [9]
Oral bacteria have evolved mechanisms to sense their environment and evade or modify the host. Bacteria occupy the ecological niche provided by both the tooth surface and gingival epithelium. However, a highly efficient innate host defense system constantly monitors the bacterial colonization and prevents bacterial invasion of local tissues. A dynamic equilibrium exists between dental plaque bacteria and the innate host defense system.[5] Of particular interest is the role of oral microorganisms in the two major dental diseases: dental caries and periodontal disease.[5] Additionally, research has correlated poor oral heath and the resulting ability of the oral microbiota to invade the body to affect cardiac health as well as cognitive function.[6] The relationship between host and microbe is mutually beneficially as the host provides microbes with a community they can flourish in. Ecological changes such as an increase of abundance, acquisition of virulence factors, and a shift from a mutual to parasitic relationship results in the host being prone to periodontal diseases.[7][8] Systemic disease at various sites of the body can result from oral microbes entering the blood bypassing periodontal pockets and oral membranes..[7] The use of antibiotics can treat already spreading infection and can only slow down the grown of biofilm bacteria. Persistent proper oral hygiene is crucial in preventing oral and systemic disease. It reduces the density of biofilm and overgrowth of potential pathogenic bacteria resulting in disease.[7] [9] Huigary (talk) 04:55, 8 October 2017 (UTC)
ASSIGNMENT#5 FINAL Oral Cavity
Oral cavity
editThe environment present in the human mouth allows the growth of characteristic microorganisms found there. It provides a source of water and nutrients, as well as a moderate temperature.[1] Resident microbes of the mouth adhere to the teeth and gums to resist mechanical flushing from the mouth to stomach where acid-sensitive microbes are destroyed by hydrochloric acid.[1][2]
Anaerobic bacteria in the oral cavity include: Actinomyces, Arachnia, Bacteroides, Bifidobacterium, Eubacterium, Fusobacterium, Lactobacillus, Leptotrichia, Peptococcus, Peptostreptococcus, Propionibacterium, Selenomonas, Treponema, and Veillonella.[3][needs update] Genera of fungi that are frequently found in the mouth include Candida, Cladosporium, Aspergillus, Fusarium, Glomus, Alternaria, Penicillium, and Cryptococcus, among others.[4]
Bacteria accumulate on both the hard and soft oral tissues in biofilms allowing them to adhere and strive in the oral environment while protected from environmental factors and anti-microbial agents.[10] Saliva plays a key homeostatic role allowing recolonization of bacteria for biofilm formation and controlling growth by detaching biofilm buildup.[8] It also provides a means of nutrients and temperature regulation. The location of the biofilm determines the type of exposed nutrients it receives.[9]
Oral bacteria have evolved mechanisms to sense their environment and evade or modify the host. However, a highly efficient innate host defense system constantly monitors the bacterial colonization and prevents bacterial invasion of local tissues. A dynamic equilibrium exists between dental plaque bacteria and the innate host defense system.[5]
This dynamic between host oral cavity and oral microbes plays a key role in health and disease as it provides microbes entry into the body.[7] A healthy equilibrium presents a symbiotic relationship where oral microbes limit growth and adherence of pathogens while the host provides an environment for them to flourish.[7][10] Ecological changes such as change of immune status, shift of resident microbes and nutrient availability shift from a mutual to parasitic relationship resulting in the host being prone to oral and systemic disease. [10] Systemic diseases such as diabetes and cardiovascular diseases has been correlated to poor oral health.[7] Of particular interest is the role of oral microorganisms in the two major dental diseases: dental caries and periodontal disease.[5] Pathogen colonization at the periodontium cause an excessive immune response resulting in a periodontal pocket- a deepened space between the tooth and gingiva.[10] This acts as a protected blood-rich reservoir with nutrients for anaerobic pathogens.[10] Systemic disease at various sites of the body can result from oral microbes entering the blood bypassing periodontal pockets and oral membranes.[7]
Persistent proper oral hygiene is the primary method for preventing oral and systemic disease.[7] It reduces the density of biofilm and overgrowth of potential pathogenic bacteria resulting in disease.[9] However, proper oral hygiene may not be enough as the oral microbiome, genetics, and changes to immune response play a factor in developing chronic infections.[9] Use of antibiotics could treat already spreading infection but ineffective against bacteria within biofilms.[9] Huigary (talk) 03:12, 20 November 2017 (UTC)
- ^ a b c d e f Cite error: The named reference
Prescottswas invoked but never defined (see the help page). - ^ a b c Cite error: The named reference
Wang2014revwas invoked but never defined (see the help page). - ^ a b c Sutter, V. L. (1984). "Anaerobes as normal oral flora". Reviews of infectious diseases. 6 Suppl 1: S62–S66. doi:10.1093/clinids/6.Supplement_1.S62. PMID 6372039.
- ^ a b c Cite error: The named reference
mycobiomewas invoked but never defined (see the help page). - ^ a b c d e f Rogers A H (editor). (2008). Molecular Oral Microbiology. Caister Academic Press. ISBN 978-1-904455-24-0.
{{cite book}}:|author=has generic name (help) - ^ a b Noble JM, Scarmeas N, Papapanou PN (2013). "Poor oral health as a chronic, potentially modifiable dementia risk factor: review of the literature". Curr Neurol Neurosci Rep. 13 (10): 384. doi:10.1007/s11910-013-0384-x. PMID 23963608.
- ^ a b c d e f g h i Zarco, MF; Vess, TJ; Ginsburg, GS (March 2012). "The oral microbiome in health and disease and the potential impact on personalized dental medicine". Oral Diseases. 18 (2): 109–120. doi:10.1111/j.1601-0825.2011.01851. Retrieved 8 October 2017.
- ^ a b c Arweiler, Nicole; Netuschil, Lutz (May 2016). The Oral Microbiota. Springer,Cham. pp. 45–60. ISBN 978-3-319-31248-4. Retrieved 8 October 2017.
- ^ a b c d e f Avila, Maria; Ojcius, David; Ozlem, Yilmaz. "The Oral Microbiota: Living with a Permanent Guest". 28: 405-11. doi:10.1089/dna.2009.0874. Retrieved 8 October 2017.
{{cite journal}}: Cite journal requires|journal=(help) - ^ a b c d e Purnima, Kumar (December 2013). "Oral microbiota and systemic disease". Anaerobe. 24: 90–93. Retrieved 19 November 2017.