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==Description and significance==
==Description and significance==
''Porphyromonas gingivalis'' is a gram-negative, obligate anaerobic, non-motile, non-spore-forming microorganism and is one of the predominant human oral microbiota (1). This rod-shaped, black-pigmented, asaccharolytic and highly proteolytic bacterium cannot grow in the existence of bile (20%) and on rabbit blood agar plates, they have an average size of diameter below 1.5 μm, living individually from each other (1-2). It is often found in a deep periodontal pocket, human subgingival plaque, living along with approximately other >500 species of bacteria (3). The organism has a multitude of virulence factors that can lead to the damage of human’s periodontal tissue which is achieved by modulating the host inflammatory response either directly or indirectly (3).
''Porphyromonas gingivalis'' is a gram-negative, obligate anaerobic, non-motile, non-spore-forming microorganism and is one of the predominant human oral microbiota. <sup>[[#References|[1]]]</sup> This rod-shaped, black-pigmented, asaccharolytic and highly proteolytic bacterium cannot grow in the existence of bile (20%) and on rabbit blood agar plates, they have an average size of diameter below 1.5 μm, living individually from each other. <sup>[[#References|[1]]]</sup>,<sup>[[#References|[2]]]</sup> It is often found in a deep periodontal pocket, human subgingival plaque, living along with approximately other >500 species of bacteria. <sup>[[#References|[3]]]</sup>


''P. gingivalis'' is a primary causative pathogen that contributed to a chronic periodontitis, a disease that is characterized by the demolition of tooth-supporting tissues, affecting about 50% of population >30 years of age in the United States and globally, it affects about 10-15% adult populations (1-4). The disease usually started as an acute gingival tissue inflammation, but then may advance to a creation of teeth pocket which may cause loss of teeth if it is not treated (3). Periodontitis is more susceptible among patient acquiring systemic diseases such as diabetes mellitus, AIDS, leukaemia, and Down’s syndrome (5-6).
''P. gingivalis'' is a primary causative pathogen that contributed to a chronic periodontitis, a disease that is characterized by the demolition of tooth-supporting tissues, affecting about 50% of population >30 years of age in the United States and globally, it affects about 10-15% adult populations. <sup>[[#References|[1]]]</sup>,<sup>[[#References|[4]]]</sup> The disease usually started as an acute gingival tissue inflammation, but then may advance to a creation of teeth pocket which may cause loss of teeth if it is not treated. <sup>[[#References|[3]]]</sup> Periodontitis is more susceptible among patient acquiring systemic diseases. <sup>[[#References|[5]]]</sup>,<sup>[[#References|[6]]]</sup>
Periodontitis has been linked with cardiovascular diseases such as coronary artery disease, heart attack and stroke; people with gum disease is more likely to acquire coronary artery disease compared to people with healthy gum (3,7). Recent studies have suggested that the pathogen may dilute the arteries by entering the bloodstream causing inflammation which increases the build up of plaque (8). Other than periodontitis, ''P. gingivalis'' has also been associated with pulpal infection, oral abscesses and it was also detected in women with bacterial vaginosis which may cause burning with urination (9-11).


''P. gingivalis'' can be classified into two strains; virulent and less virulent strains (12). An example of virulent strain is strain W83 while for less virulent is strain ATC 33277 (12). The bacteria of virulent strain, W83 was first discovered in the 1950s at Bonn, Germany by H.Werner, obtained from an undocumented oral disease and then in 1960s, it was brought by Madeleine Sebald to The Pasteur Institute (12). ''P. gingivalis'' has been cultured and was available at American Type Culture Collection (13).  
Periodontitis has been linked with cardiovascular diseases such as coronary artery disease, heart attack and stroke. <sup>[[#References|[3]]]</sup>,<sup>[[#References|[7]]]</sup> Other than periodontitis, ''P. gingivalis'' has also been associated with pulpal infection, oral abscesses and it was also detected in women with bacterial vaginosis which may cause burning with urination. <sup>[[#References|[8]]]</sup>,<sup>[[#References|[9]]]</sup>,<sup>[[#References|[10]]]</sup> The bacteria of virulent strain, W83 was first discovered in the 1950s at Bonn, Germany by H.Werner, obtained from an undocumented oral disease and then in 1960s, it was brought by Madeleine Sebald to The Pasteur Institute. <sup>[[#References|[11]]]</sup> ''P. gingivalis'' has been cultured and was available at American Type Culture Collection. <sup>[[#References|[12]]]</sup>


Capsules, fimbriae, lipopolysaccharide (LPS) and other membrane proteins in the outer membrane (OM) and inner membrane (IM) of ''P. gingivalis'' are all played a significant role in its pathogenicity. Although there have been numerous studies done to explain the mechanism of virulence factors secreted by ''P. gingivalis'' and how they interact with the host, investigating a gene or protein in isolation without considering other molecular components or networks is not truly insightful. This is because, in the actual in vivo environment, the genes may work as a system, hence may interact differently than a single virulence factor to the host cells. Adding to that, rather than working alone, ''P. gingivalis'' is also likely to interact with other microbes to survive in the harsh environment of the periodontal pocket. Therefore, further research needs to be performed to improve our understanding of the interaction between periodontal bacteria and host cells at the molecular and cellular level so that we can develop effective approaches to control the disease caused by this bacterium.  
Although there have been numerous studies done to explain the mechanism of virulence factors secreted by ''P. gingivalis'' and how they interact with the host, investigating a gene or protein in isolation without considering other molecular networks is not truly insightful because in the actual in vivo environment, the genes may work as a system, hence may interact differently than a single virulence factor to the host cells. Adding to that, rather than working alone, ''P. gingivalis'' is also likely to interact with other microbes to survive in the harsh environment of the periodontal pocket. <sup>[[#References|[3]]]</sup> Therefore, further research needs to be performed to improve our understanding of the interaction between periodontal bacteria and host cells at the molecular and cellular level so that effective approaches can be implemented to control the disease caused by this bacterium.  
 
 
Examples of citations <sup>[[#References|[2]]]</sup>, <sup>[[#References|[3]]]</sup>


==Genome structure==
==Genome structure==
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==References==
==References==


References examples
References examples <b></b>:
 
1. [https://www.google.ch/patents/US5710039 Porphyromonas gingivicanis strain ATCC 55562]
 
2. [https://www.ncbi.nlm.nih.gov/pubmed/18524787 Naito, M., Hirakawa, H., Yamashita, A., Ohara, N., Shoji, M., Yukitake, H., Nakayama, K., Toh, H., Yoshimura, F., Kuhara, S., Hattori, M., Hayashi, T., Nakayama, K. (2008) Determination of the genome sequence of Porphyromonas gingivalis strain ATCC 33277 and genomic comparison with strain W83 revealed extensive genome rearrangements in P. gingivalis. DNA Res <b>4</b>:215-25.]
 
3. [https://www.ncbi.nlm.nih.gov/pubmed/26903954 How, K.Y., Song, K.P., Chan, K.G. (2016) Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line. Front Microbiol <b>7</b>:53.]
 
4. [https://www.ncbi.nlm.nih.gov/pubmed/22909104 Petersen, P.E., Ogawa, H. (2012) The global burden of periodontal disease: towards integration with chronic disease prevention and control. <b>60</b>:15-39.]
 
5. [https://link.springer.com/chapter/10.1007%2F978-1-4614-9557-4_15#page-1 Oxidative stress and periodontal disease in Down Syndrome]
 
6. [http://www.ijcdmr.com/index.php/ijcdmr/article/view/74 Mehta, A. (2015) Risk factors associated with periodontal diseases and their clinical considerations. Int J Contemp Dent Med Rev.]
 
7. [https://www.ncbi.nlm.nih.gov/pubmed/16954266 Nakano, K. (2006) Detection of cariogenic Streptococcus mutans in extirpated heart valve and atheromatous plaque specimens. J Clin Microbiol <b>9</b>:3313-3317.]
 
8. [https://www.ncbi.nlm.nih.gov/pubmed/1313462 Loos, B.G. (1992) A statistical approach to the ecology of Porphyromonas gingivalis. J Dent Res <b>71</b>:353-358.]
 
9. [https://www.ncbi.nlm.nih.gov/pubmed/8276979 Wolff, L.F. (1993) Natural distribution of 5 bacteria associated with periodontal disease. J Clin Periodontol <b>20</b>:699-706.]


1. [http://www.bacterio.net/porphyromonas.html List of prokaryotic names with standing in nomenculture]
10. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113856/ Charlene, W.J. (2014) Anaerobes and Bacterial Vaginosis in Pregnancy: Virulence Factors Contributing to Vaginal Colonisation. Int J Environ Res Public Health <b>11</b>:6979-7000.]


2. [http://onlinelibrary.wiley.com/doi/10.1046/j.1462-2920.1999.00007.x/full Sahm, K., MacGregor, B.J., Jørgensen, B.B., and Stahl, D.A. (1999) Sulphate reduction and vertical distribution of sulphate-reducing bacteria quantified by rRNA slotblot hybridization in a coastal marine sediment. Environ Microbiol <b>1</b>: 65-74.]
11. [https://www.ncbi.nlm.nih.gov/pubmed/12949112 Nelson, K.E. (2003). Complete Genome Sequence of the Oral Pathogenic Bacterium Porphyromonas gingivalisStrain W83. J Bacteriol <b>185</b>:5591-5601.]


3. [http://www.homd.org Human Oral Microbiome]
12. [https://www.atcc.org/products/all/33277.aspx#generalinformation Porphyromonas gingivalis (Coykendall et al.) Shah and Collins]


<references/>
<references/>


This page is written by Muhammad Irfan Zulkifle for the MICR3004 course, Semester 2, 2016
This page is written by Muhammad Irfan Zulkifle for the MICR3004 course, Semester 2, 2016

Revision as of 15:48, 22 September 2016

Name Bench ID Date [1]

Classification

Higher order taxa

Bacteria (Kingdom) – Fibrobactere-Chlorobi-Bacteroidetes, FCB Group (Domain) – Bacteroidetes (Phylum) – Bacteroidia (Class) – Bacteroidales (Order) – Porphyromonadaceae (Family) – Porphyromonas (Genus)

Species

Porphyromonas gingivalis, Strain W83

Description and significance

Porphyromonas gingivalis is a gram-negative, obligate anaerobic, non-motile, non-spore-forming microorganism and is one of the predominant human oral microbiota. [1] This rod-shaped, black-pigmented, asaccharolytic and highly proteolytic bacterium cannot grow in the existence of bile (20%) and on rabbit blood agar plates, they have an average size of diameter below 1.5 μm, living individually from each other. [1],[2] It is often found in a deep periodontal pocket, human subgingival plaque, living along with approximately other >500 species of bacteria. [3]

P. gingivalis is a primary causative pathogen that contributed to a chronic periodontitis, a disease that is characterized by the demolition of tooth-supporting tissues, affecting about 50% of population >30 years of age in the United States and globally, it affects about 10-15% adult populations. [1],[4] The disease usually started as an acute gingival tissue inflammation, but then may advance to a creation of teeth pocket which may cause loss of teeth if it is not treated. [3] Periodontitis is more susceptible among patient acquiring systemic diseases. [5],[6]

Periodontitis has been linked with cardiovascular diseases such as coronary artery disease, heart attack and stroke. [3],[7] Other than periodontitis, P. gingivalis has also been associated with pulpal infection, oral abscesses and it was also detected in women with bacterial vaginosis which may cause burning with urination. [8],[9],[10] The bacteria of virulent strain, W83 was first discovered in the 1950s at Bonn, Germany by H.Werner, obtained from an undocumented oral disease and then in 1960s, it was brought by Madeleine Sebald to The Pasteur Institute. [11] P. gingivalis has been cultured and was available at American Type Culture Collection. [12]

Although there have been numerous studies done to explain the mechanism of virulence factors secreted by P. gingivalis and how they interact with the host, investigating a gene or protein in isolation without considering other molecular networks is not truly insightful because in the actual in vivo environment, the genes may work as a system, hence may interact differently than a single virulence factor to the host cells. Adding to that, rather than working alone, P. gingivalis is also likely to interact with other microbes to survive in the harsh environment of the periodontal pocket. [3] Therefore, further research needs to be performed to improve our understanding of the interaction between periodontal bacteria and host cells at the molecular and cellular level so that effective approaches can be implemented to control the disease caused by this bacterium.

Genome structure

The genome size of strain W83 (GenBank: AE015924.1) is 2,343,479 bp containing 4 ribosomal operons (5S-23S-tRNAAla-tRNAIle-16S), 2 structural RNA genes and 53 specific amino-acid tRNA genes, with an average G+C content of 48.3% and having a total ORF of 1990 (covered the complete genome by 85%) (1-2). 54% (1,075) of the 1,990 ORF consisted of biological role categories, 10.5% (208) of those have an unknown function, 9.2% (184) were conserved hypothetical proteins/domain proteins while the other 26.3% (523) were hypothetical proteins (2). Repetitive elements such as DNA repeats (which include clustered regularly interspaced short palindromic repeats (CRSPRs) and uninterrupted direct repeats) and transposable components (which include insertion sequence (IS) elements and miniature inverted-repeat transposable elements (MITEs)) made up 6% of the whole genome (2). However, the strain did not contain other classes of dispersed repetitive DNA sequence elements which include ERIC and REP elements (2).


Cell structure and metabolism

Cell wall, biofilm formation, motility, metabolic functions.

Ecology

Aerobe/anaerobe, habitat (location in the oral cavity, potential other environments) and microbe/host interactions.

Pathology

Application to biotechnology

Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,…

Current research

Summarise some of the most recent discoveries regarding this species.

References

References examples :

1. Porphyromonas gingivicanis strain ATCC 55562

2. Naito, M., Hirakawa, H., Yamashita, A., Ohara, N., Shoji, M., Yukitake, H., Nakayama, K., Toh, H., Yoshimura, F., Kuhara, S., Hattori, M., Hayashi, T., Nakayama, K. (2008) Determination of the genome sequence of Porphyromonas gingivalis strain ATCC 33277 and genomic comparison with strain W83 revealed extensive genome rearrangements in P. gingivalis. DNA Res 4:215-25.

3. How, K.Y., Song, K.P., Chan, K.G. (2016) Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line. Front Microbiol 7:53.

4. Petersen, P.E., Ogawa, H. (2012) The global burden of periodontal disease: towards integration with chronic disease prevention and control. 60:15-39.

5. Oxidative stress and periodontal disease in Down Syndrome

6. Mehta, A. (2015) Risk factors associated with periodontal diseases and their clinical considerations. Int J Contemp Dent Med Rev.

7. Nakano, K. (2006) Detection of cariogenic Streptococcus mutans in extirpated heart valve and atheromatous plaque specimens. J Clin Microbiol 9:3313-3317.

8. Loos, B.G. (1992) A statistical approach to the ecology of Porphyromonas gingivalis. J Dent Res 71:353-358.

9. Wolff, L.F. (1993) Natural distribution of 5 bacteria associated with periodontal disease. J Clin Periodontol 20:699-706.

10. Charlene, W.J. (2014) Anaerobes and Bacterial Vaginosis in Pregnancy: Virulence Factors Contributing to Vaginal Colonisation. Int J Environ Res Public Health 11:6979-7000.

11. Nelson, K.E. (2003). Complete Genome Sequence of the Oral Pathogenic Bacterium Porphyromonas gingivalisStrain W83. J Bacteriol 185:5591-5601.

12. Porphyromonas gingivalis (Coykendall et al.) Shah and Collins

  1. MICR3004

This page is written by Muhammad Irfan Zulkifle for the MICR3004 course, Semester 2, 2016